Unspecified Trauma- and
Stressor-Related Disorder
309.9 (F43.9)
This category applies to presentations in which symptoms characteristic of a trauma- and
stressor-related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for any of the disorders in the trauma- and stressor-related disorders diagnostic class.
The unspecified trauma- or stressor-related disorder category is used in situations in which
the clinician chooses not to specify the reason that the criteria are not met for a specific
trauma- and stressor-related disorder, and includes presentations in which there is insufficient information to make a more specific diagnosis (e.g., in emergency room settings).
DiSSOCiâtiVG d isorders are characterized by a disruption of and/or discontinuity
in the normal integration of consciousness, memory, identity, emotion, perception, body
representation, motor control, and behavior. Dissociative symptoms can potentially disrupt every area of psychological functioning. This chapter includes dissociative identity
disorder, dissociative amnesia, depersonalization/derealization disorder, other specified
dissociative disorder, and unspecified dissociative disorder.
Dissociative symptoms are experienced as a) unbidden intrusions into awareness and
behavior, with accompanying losses of continuity in subjective experience (i.e., "positive"
dissociative symptoms such as fragmentation of identity, depersonalization, and derealization) and/or b) inability to access information or to control mental functions that normally are readily amenable to access or control (i.e., '"negative" dissociative symptoms such
as amnesia).
The dissociative disorders are frequently found in the aftermath of trauma, and many
of the symptoms, including embarrassment and confusion about the symptoms or a desire
to hide them, are influenced by the proximity to trauma. In DSM-5, the dissociative disorders are placed next to, but are not part of, the trauma- and stressor-related disorders, reflecting the close relationship between these diagnostic classes. Both acute stress disorder
and posttraumatic stress disorder contain dissociative symptoms, such as amnesia, flashbacks, numbing, and depersonalization/derealization.
Depersonalization/derealization disorder is characterized by clinically significant persistent or recurrent depersonalization (i.e., experiences of unreality or detachment from one's
mind, self, or body) and/or derealization (i.e., experiences of imreality or detachment from
one's surroundings). These alterations of experience are accompanied by intact reality
testing. There is no evidence of any distinction between individuals with predominantly
depersonalization versus derealization symptoms. Therefore, individuals with this disorder can have depersonalization, derealization, or both.
Dissociative amnesia is characterized by an inability to recall autobiographical information. This amnesia may be localized (i.e., an event or period of time), selective (i.e., a specific
aspect of an event), or generalized (i.e., identity and life history). Dissociative amnesia is fundamentally an inability to recall autobiographical information that is inconsistent with normal forgetting. It may or may not involve purposeful travel or bewildered wandering (i.e.,
fugue). Although some individuals with amnesia promptly notice that they have "lost time"
or that they have a gap in their memory, most individuals with dissociative disorders are initially unaware of their amnesias. For them, awareness of amnesia occurs only when personal
identity is lost or when circumstances make these individuals aware that autobiographical
information is missing (e.g., when they discover evidence of events they cannot recall or
when others tell them or ask them about events they cannot recall). Until and unless this happens, these individuals have "amnesia for their amnesia." Amnesia is experienced as an essential feature of dissociative amnesia; individuals may experience localized or selective
amnesia most commonly, or generalized amnesia rarely. Dissociative fugue is rare in persons with dissociative amnesia but common in dissociative identity disorder.
Dissociative identity disorder is characterized by a) the presence of two or more distinct
personality states or an experience of possession and b) recurrent episodes of amnesia. The
fragmentation of identity may vary v^ith culture (e.g., possession-form presentations) and circumstance. Thus, individuals may experience discontinuities in identity and memory that
may not be immediately evident to others or are obscured by attempts to hide dysfunction. Individuals with dissociative identity disorder experience a) recurrent, inexplicable intrusions
into their conscious functioning and sense of self (e.g., voices; dissociated actions and speech;
intrusive thoughts, emotions, and impulses), b) alterations of sense of self (e.g., attitudes, preferences, and feeling like one's body or actions are not one's own), c) odd changes of perception
(e.g., depersonalization or derealization, such as feeling detached from one's body while cutting), and d) intermittent functional neurological symptoms. Stress often produces transient
exacerbation of dissociative symptoms that makes them more evident.
The residual category of other specified dissociative disorder has seven examples: chronic
or recurrent mixed dissociative symptoms that approach, but fall short of, the diagnostic criteria for dissociative identity disorder; dissociative states secondary to brainwashing or
thought reform; two acute presentations, of less than 1 month's duration, of mixed dissociative
symptoms, one of which is also marked by the presence of psychotic symptoms; and three single-symptom dissociative presentations—dissociative trance, dissociative stupor or coma, and
Ganser's syndrome (the giving of approximate and vague answers).
Dissociative Identity Disorder
Diagnostic Criteria 300.14 (F44.81)
A. Disruption of identity characterized by two or more distinct personality states, which
may be described in some cultures as an experience of possession. The disruption in
identity involves marked discontinuity in sense of self and sense of agency, accompanied by related alterations in affect, behavior, consciousness, memory, perception,
cognition, and/or sensory-motor functioning. These signs and symptoms may be observed by others or reported by the individual.
B. Recurrent gaps in the recall of everyday events, important personal information, and/
or traumatic events that are inconsistent with ordinary forgetting.
C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The disturbance is not a normal part of a broadly accepted cultural or religious practice.
Note: In children, the symptoms are not better explained by imaginary playmates or
other fantasy play.
E. The symptoms are not attributable to the physiological effects of a substance (e.g.,
blacl<outs or chaotic behavior during alcohol intoxication) or another medical condition
(e.g., complex partial seizures).
Diagnostic Features
The defining feature of dissociative identity disorder is the presence of two or more distinct personality states or an experience of possession (Criterion A). The overtness or
covertness of these personality states, however, varies as a function of psychological
motivation, current level of stress, culture, internal conflicts and dynamics, and emotional
resilience. Sustained periods of identity disruption may occur when psychosocial pressures are severe and/or prolonged. In many possession-form cases of dissociative identity
disorder, and in a small proportion of non-possession-form cases, manifestations of alternate identities are highly overt. Most individuals with non-possession-form dissociative
identity disorder do not overtly display their discontinuity of identity for long periods of
time; only a small minority present to clinical attention with observable alternation of
identities. When alternate personality states are not directly observed, the disorder can be
identified by two clusters of symptoms: 1) sudden alterations or discontinuities in sense of
self and sense οί agency (Criterion A), and 2) recurrent dissociative amnesias (Criterion B).
Criterion A symptoms are related to discontinuities of experience that can affect any
aspect of an individual's functioning. Individuals v^ith dissociative identity disorder may
report the feeling that they have suddenly become depersonalized observers of their
"own" speech and actions, which they may feel powerless to stop (sense of self). Such individuals may also report perceptions of voices (e.g., a child's voice; crying; the voice of a
spiritual being). In some cases, voices are experienced as multiple, perplexing, independent thought streams over which the individual experiences no control. Strong emotions,
impulses, and even speech or other actions may suddenly emerge, without a sense of personal ownership or control (sense of agency). These emotions and impulses are frequently
reported as ego-dystonic and puzzling. Attitudes, outlooks, and personal preferences
(e.g., about food, activities, dress) may suddenly shift and then shift back. Individuals may
report that their bodies feel different (e.g., like a small child, like the opposite gender, huge
and muscular). Alterations in sense of self and loss of personal agency may be accompanied by a feeling that these attitudes, emotions, and behaviors—even one's body—are
"not mine" and/or are "not under my control." Although most Criterion A symptoms are
subjective, many of these sudden discontinuities in speech, affect, and behavior can be witnessed by family, friends, or the clinician. Non-epileptic seizures and other conversion
symptoms are prominent in some presentations of dissociative identity disorder, especially in some non-Westem settings.
The dissociative amnesia of individuals with dissociative identity disorder manifests in
three primary ways: as 1) gaps in remote memory of personal life events (e.g., periods of
childhood or adolescence; some important life events, such as the death of a grandparent,
getting married, giving birth); 2) lapses in dependable memory (e.g., of what happened
today, of well-leamed skills such as how to do their job, use a computer, read, drive); and
3) discovery of evidence of their everyday actions and tasks that they do not recollect doing (e.g., finding unexplained objects in their shopping bags or among their possessions;
finding perplexing writings or drawings that they must have created; discovering injuries;
"coming to" in the midst of doing something). Dissociative fugues, wherein the person
discovers dissociated travel, are common. Thus, individuals with dissociative identity disorder may report that they have suddenly found themselves at the beach, at work, in a nightclub, or somewhere at home (e.g., in the closet, on a bed or sofa, in the corner) with no
memory of how they came to be there. Amnesia in individuals with dissociative identity disorder is not limited to stressful or traumatic events; these individuals often cannot recall
everyday events as well.
Individuals with dissociative identity disorder vary in their awareness and attitude toward their amnesias. It is common for these individuals to minimize their amnestic symptoms. Some of their amnestic behaviors may be apparent to others—as when these persons
do not recall something they were witnessed to have done or said, when they cannot
remember their own name, or when they do not recognize their spouse, children, or close
friends.
Possession-form identities in dissociative identity disorder typically manifest as behaviors that appear as if a "spirit," supernatural being, or outside person has taken control,
such that the individual begins speaking or acting in a distinctly different manner. For example, an individual's behavior may give the appearance that her identity has been
replaced by the "ghost" of a girl who committed suicide in the same community years
before, speaking and acting as though she were still alive. Or an individual may be "taken
over" by a demon or deity, resulting in profound impairment, and demanding that the individual or a relative be punished for a past act, followed by more subtle periods of identity alteration. However, the majority of possession states around the world are normal,
usually part of spiritual practice, and do not meet criteria for dissociative identity disor-
der. The identities that arise during possession-form dissociative identity disorder present
recurrently, are unvs^anted and involuntary, cause clinically significant distress or impairment (Criterion C), and are not a normal part of a broadly accepted cultural or religious
practice (Criterion D).
Associated Features Supporting Diagnosis
Individuals with dissociative identity disorder typically present v^ith comorbid depression,
anxiety, substance abuse, self-injury, non-epileptic seizures, or another common symptom. They often conceal, or are not fully aware of, disruptions in consciousness, amnesia,
or other dissociative symptoms. Many individuals with dissociative identity disorder report dissociative flashbacks during which they undergo a sensory reliving of a previous
event as though it were occurring in the present, often with a change of identity, a partial
or complete loss of contact with or disorientation to current reality during the flashback,
and a subsequent amnesia for the content of the flashback. Individuals with the disorder
typically report multiple types of interpersonal maltreatment during childhood and adulthood. Nonmaltreatment forms of overwhelming early life events, such as multiple long,
painful, early-life medical procedures, also may be reported. Self-mutilation and suicidal
behavior are frequent. On standardized measures, these individuals report higher levels
of hypnotizability and dissociativity compared with other clinical groups and healthy control subjects. Some individuals experience transient psychotic phenomena or episodes.
Several brain regions have been implicated in the pathophysiology of dissociative identity
disorder, including the orbitofrontal cortex, hippocampus, parahippocampal gyrus, and
amygdala.
Prevalence
The 12-month prevalence of dissociative identity disorder among adults in a small U.S.
community study was 1.5%. The prevalence across genders in that study was 1.6% for
males and 1.4% for females.
Development and Course
Dissociative identity disorder is associated with overwhelming experiences, traumatic
events, and/or abuse occurring in childhood. The full disorder may first manifest at almost any age (from earliest childhood to late life). Dissociation in children may generate
problems with memory, concentration, attachment, and traumatic play. Nevertheless, children usually do not present with identity changes; instead they present primarily with overlap and interference among mental states (Criterion A phenomena), wiüi symptoms related
to discontinuities of experience. Sudden changes in identity during adolescence may appear to be just adolescent turmoil or the early stages of another mental disorder. Older
individuals may present to treatment with what appear to be late-life mood disorders, obsessive-compulsive disorder, paranoia, psychotic mood disorders, or even cognitive disorders due to dissociative amnesia. In some cases, disruptive affects and memories may
increasingly intrude into awareness with advancing age.
Psychological decompensation and overt changes in identity may be triggered by 1) removal from the traumatizing situation (e.g., through leaving home); 2) the individual's
children reaching the same age at which the individual was originally abused or traumatized; 3) later traumatic experiences, even seemingly inconsequential ones, like a minor
motor vehicle accident; or 4) the death of, or the onset of a fatal illness in, their abuser(s).
Risk and Prognostic Factors
Environmental. Inteφersonal physical and sexual abuse is associated with an increased
risk of dissociative identity disorder. Prevalence of childhood abuse and neglect in the
United States, Canada, and Europe among those with the disorder is about 90%. Other
forms of traumatizing experiences, including childhood medical and surgical procedures,
war, childhood prostitution, and terrorism, have been reported.
Course modifiers. Ongoing abuse, later-life retraumatization, comorbidity with mental
disorders, severe medical illness, and delay in appropriate treatment are associated with
poorer prognosis.
Culture-Related Diagnostic issues
Many features of dissociative identity disorder can be influenced by the individual's cultural background. Individuals with this disorder may present with prominent medically
unexplained neurological symptoms, such as non-epileptic seizures, paralyses, or sensory
loss, in cultural settings where such symptoms are common. Similarly, in settings where
normative possession is common (e.g., rural areas in the developing world, among certain
religious groups in the United States and Europe), the fragmented identities may take the
form of possessing spirits, deities, demons, animals, or mythical figures. Acculturation or
prolonged intercultural contact may shape the characteristics of the other identities (e.g.,
identities in India may speak English exclusively and wear Western clothes). Possessionform dissociative identity disorder can be distinguished from culturally accepted possession states in that the former is involuntary, distressing, uncontrollable, and often recurrent or persistent; involves conflict between the individual and his or her surrounding
family, social, or work milieu; and is manifested at times and in places that violate the
norms of the culture or religion.
Gender-Related Diagnostic issues
Females with dissociative identity disorder predominate in adult clinical settings but not
in child clinical settings. Adult males with dissociative identity disorder may deny their
symptoms and trauma histories, and this can lead to elevated rates of false negative diagnosis. Females with dissociative identity disorder present more frequently with acute
dissociative states (e.g., flashbacks, amnesia, fugue, functional neurological [conversion]
symptoms, hallucinations, self-mutilation). Males commonly exhibit more criminal or violent behavior than females; among males, common triggers of acute dissociative states include combat, prison conditions, and physical or sexual assaults.
Suicide Risk
Over 70% of outpatients with dissociative identity disorder have attempted suicide; multiple attempts are common, and other self-injurious behavior is frequent. Assessment of
suicide risk may be complicated when there is amnesia for past suicidal behavior or when
the presenting identity does not feel suicidal and is unaware that other dissociated identities do.
Functional Consequences of
Dissociative identity Disorder
Impairment varies widely, from apparently minimal (e.g., in high-functioning professionals) to profound. Regardless of level of disability, individuals with dissociative identity
disorder commonly minimize the impact of their dissociative and posttraumatic symptoms. The symptoms of higher-functioning individuals may impair their relational, marital, family, and parenting functions more than their occupational and professional life
(although the latter also may be affected). With appropriate treatment, many impaired individuals show marked improvement in occupational and personal functioning. However, some remain highly impaired in most activities of living. These individuals may only
respond to treatment very slowly, with gradual reduction in or improved tolerance of
their dissociative and posttraumatic symptoms. Long-term supportive treatment may
slowly increase these individuals' ability to manage their symptoms and decrease use of
more restrictive levels of care.
Differential Diagnosis
Other specified dissociative disorder. The core of dissociative identity disorder is the
division of identity, v^ith recurrent disruption of conscious functioning and sense of self.
This central feature is shared with one form of other specified dissociative disorder, which
may be distinguished from dissociative identity disorder by the presence of chronic or recurrent mixed dissociative symptoms that do not meet Criterion A for dissociative identity
disorder or are not accompanied by recurrent amnesia.
Major depressive disorder. Individuals with dissociative identity disorder are often depressed, and their symptoms may appear to meet the criteria for a major depressive episode.
Rigorous assessment indicates that this depression in some cases does not meet full criteria for
major depressive disorder. Other specified depressive disorder in individuals with dissociative identity disorder often has an important feature: the depressed mood and cognitions fluctuate because they are experienced in some identity states but not others.
Bipolar disorders. Individuals with dissociative identity disorder are often misdiagnosed with a bipolar disorder, most often bipolar II disorder. The relatively rapid shifts in
mood in individuals with this disorder—typically within minutes or hours, in contrast to
the slower mood changes typically seen in individuals with bipolar disorders—are due to
the rapid, subjective shifts in mood commonly reported across dissociative states, sometimes accompanied by fluctuation in levels of activation. Furthermore, in dissociative
identity disorder, elevated or depressed mood may be displayed in conjunction with overt
identities, so one or the other mood may predominate for a relatively long period of time
(often for days) or may shift within minutes.
Posttraumatic stress disorder. Some traumatized individuals have both posttraumatic
stress disorder (PTSD) and dissociative identity disorder. Accordingly, it is crucial to distinguish between individuals with PTSD only and individuals who have both PTSD and
dissociative identity disorder. This differential diagnosis requires that the clinician establish the presence or absence of dissociative symptoms that are not characteristic of acute
stress disorder or PTSD. Some individuals with PTSD manifest dissociative symptoms that
also occur in dissociative identity disorder: 1) amnesia for some aspects of trauma, 2) dissociative flashbacks (i.e., reliving of the trauma, with reduced awareness of one's current
orientation), and 3) symptoms of intrusion and avoidance, negative alterations in cognition and mood, and hyperarousal that are focused around the traumatic event. On the other
hand, individuals with dissociative identity disorder manifest dissociative symptoms that
are not a manifestation of PTSD: 1) amnesias for many everyday (i.e., nontraumatic) events,
2) dissociative flashbacks that may be followed by amnesia for the content of the flashback,
3) disruptive intrusions (unrelated to traumatic material) by dissociated identity states
into the individual's sense of self and agency, and 4) infrequent, full-blown changes
among different identity states.
Psychotic disorders. Dissociative identity disorder may be confused with schizophrenia or other psychotic disorders. The personified, internally communicative inner voices
of dissociative identity disorder, especially of a child (e.g., "I hear a little girl crying in a
closet and an angry man yelling at her"), may be mistaken for psychotic hallucinations.
Dissociative experiences of identity fragmentation or possession, and of perceived loss of
control over thoughts, feelings, impulses, and acts, may be confused with signs of formal
thought disorder, such as thought insertion or withdrawal. Individuals with dissociative
identity disorder may also report visual, tactile, olfactory, gustatory, and somatic hallucinations, which are usually related to posttraumatic and dissociative factors, such as partial
flashbacks. Individuals with dissociative identity disorder experience these symptoms as
caused by alternate identities, do not have delusional explanations for the phenomena,
and often describe the symptoms in a personified way (e.g., "I feel like someone else wants
to cry with my eyes"). Persecutory and derogatory internal voices in dissociative identity
disorder associated with depressive symptoms may be misdiagnosed as major depression
with psychotic features. Chaotic identity change and acute intrusions that disrupt thought
processes may be distinguished from brief psychotic disorder by the predominance of dissociative symptoms and amnesia for the episode, and diagnostic evaluation after cessation
of the crisis can help confirm the diagnosis.
Substance/medication-induced disorders. Symptoms associated with the physiological
effects of a substance can be distinguished from dissociative identity disorder if the substance in question is judged to be etiologically related to the disturbance.
Personality disorders. Individuals with dissociative identity disorder often present identities that appear to encapsulate a variety of severe personality disorder features, suggesting a
differential diagnosis of personality disorder, especially of tiie borderline type. Importantly,
however, the individual's longitudinal variability in personality style (due to inconsistency
among identities) differs from the pervasive and persistent dysfunction in affect management
and inteφersonal relationships typical of those with personality disorders.
Conversion disorder (functional neurological symptom disorder). This disorder may be
distinguished from dissociative identity disorder by the absence of an identity disruption
characterized by two or more distinct personality states or an experience of possession.
Dissociative amnesia in conversion disorder is more limited and circumscribed (e.g., amnesia for a non-epileptic seizure).
Seizure disorders. Individuals with dissociative identity disorder may present with seizurelike symptoms and behaviors that resemble complex partial seizures with temporal
lobe foci. These include déjà vu, jamais vu, depersonalization, derealization, out-of-body
experiences, amnesia, disruptions of consciousness, hallucinations, and other intrusion
phenomena of sensation, affect, and thought. Normal electroencephalographic findings,
including telemetry, differentiate non-epileptic seizures from the seizurelike symptoms of
dissociative identity disorder. Also, individuals with dissociative identity disorder obtain
very high dissociation scores, whereas individuals with complex partial seizures do not.
Factitious disorder and malingering. Individuals who feign dissociative identity disorder do not report the subtle symptoms of intrusion characteristic of the disorder; instead
they tend to overreport well-publicized symptoms of the disorder, such as dissociative
amnesia, while underreporting less-publicized comorbid symptoms, such as depression.
Individuals who feign dissociative identity disorder tend to be relatively undisturbed by
or may even seem to enjoy "having" the disorder. In contrast, individuals with genuine
dissociative identity disorder tend to be ashamed of and overwhelmed by their symptoms
and to underreport their symptoms or deny their condition. Sequential observation, corroborating history, and intensive psychometric and psychological assessment may be
helpful in assessment.
Individuals who malinger dissociative identity disorder usually create limited, stereotyped alternate identities, with feigned amnesia, related to the events for which gain is
sought. For example, they may present an "all-good" identity and an "all-bad" identity in
hopes of gaining exculpation for a crime.
Comorbidity
Many individuals with dissociative identity disorder present with a comorbid disorder. If
not assessed and treated specifically for the dissociative disorder, these individuals often
receive prolonged treatment for the comorbid diagnosis only, with limited overall treatment response and resultant demoralization, and disability.
Individuals with dissociative identity disorder usually exhibit a large number of comorbid disorders. In particular, most develop PTSD. Other disorders that are highly comorbid with dissociative identity disorder include depressive disorders, trauma- and
stressor-related disorders, personality disorders (especially avoidant and borderline personality disorders), conversion disorder (functional neurological symptom disorder),
somatic symptom disorder, eating disorders, substance-related disorders, obsessivecompulsive disorder, and sleep disorders. Dissociative alterations in identity, memory,
and consciousness may affect the symptom presentation of comorbid disorders.
Dissociative Amnesia
Diagnostic Criteria 300.12 (F44.0)
A. An inability to recall important autobiographical information, usually of a traumatic or
stressful nature, that is inconsistent with ordinary forgetting.
Note: Dissociative amnesia most often consists of localized or selective amnesia for a
specific event or events; or generalized amnesia for identity and life history.
B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
C. The disturbance is not attributable to the physiological effects of a substance (e.g., alcohol or other drug of abuse, a medication) or a neurological or other medical condition
(e.g., partial complex seizures, transient global amnesia, sequelae of a closed head injury/traumatic brain injury, other neurological condition).
D. The disturbance is not better explained by dissociative identity disorder, posttraumatic
stress disorder, acute stress disorder, somatic symptom disorder, or major or mild neurocognitive disorder.
Coding note: The code for dissociative amnesia without dissociative fugue is 300.12
(F44.0). The code for dissociative amnesia with dissociative fugue is 300.13 (F44.1).
Specify if ;
300.13 (F44.1) With dissociative fugue: Apparently purposeful travel or bewildered
wandering that is associated with amnesia for identity or for other important autobiographical information.___________________________________________________
Diagnostic Features
The defining characteristic of dissociative amnesia is an inability to recall important autobiographical information that 1) should be successfully stored in memory and 2) ordinarily would be readily remembered (Criterion A). Dissociative amnesia differs from the
permanent amnesias due to neurobiological damage or toxicity that prevent memory storage or retrieval in that it is always potentially reversible because the memory has been successfully stored.
Localized amnesia, a failure to recall events during a circumscribed period of time, is the
most common form of dissociative amnesia. Localized amnesia may be broader than amnesia for a single traumatic event (e.g., months or years associated with child abuse or intense combat). In selective amnesia, the individual can recall some, but not all, of the events
during a circumscribed period of time. Thus, the individual may remember part of a traumatic event but not other parts. Some individuals report both localized and selective amnesias.
Generalized amnesia, a complete loss of memory for one's life history, is rare. Individuals
with generalized amnesia may forget personal identity. Some lose previous knowledge
about the world (i.e., semantic knowledge) and can no longer access well-learned skills
(i.e., procedural knowledge). Generalized amnesia has an acute onset; the perplexity, disorientation, an4 purposeless wandering of individuals with generalized amnesia usually
bring them to the attention of the police or psychiatric emergency services. Generalized
amnesia may be more common among combat veterans, sexual assault victims, and individuals experiencing extreme emotional stress or conflict.
Individuals with dissociative amnesia are frequently unaware (or only partially aware)
of their memory problems. Many, especially those with localized amnesia, minimize the
importance of their memory loss and may become uncomfortable when prompted to address it. In systematized amnesia, the individual loses memory for a specific category of information (e.g., all memories relating to one's family, a particular person, or childhood
sexual abuse). In continuous amnesia, an individual forgets each new event as it occurs.
Associated Features Supporting Diagnosis
Many individuals with dissociative amnesia are chronically impaired in their ability to
form and sustain satisfactory relationships. Histories of trauma, child abuse, and victimization are common. Some individuals with dissociative amnesia report dissociative flashbacks (i.e., behavioral reexperiencing of traumatic events). Many have a history of selfmutilation, suicide attempts, and other high-risk behaviors. Depressive and functional
neurological symptoms are common, as are depersonalization, auto-hypnotic symptoms,
and high hypnotizability. Sexual dysfunctions are common. Mild traumatic brain injury
may precede dissociative amnesia.
Prevalence
The 12-month prevalence for dissociative amnesia among adults in a small U.S. community study was 1.8% (1.0% for males; 2.6% for females).
Development and Course
Onset of generalized amnesia is usually sudden. Less is known about the onset of localized
and selective amnesias because these amnesias are seldom evident, even to the individual.
Although overwhelming or intolerable events typically precede localized amnesia, its onset may be delayed for hours, days, or longer.
Individuals may report multiple episodes of dissociative amnesia. A single episode
may predispose to future episodes. In between episodes of amnesia, the individual may or
may not appear to be acutely symptomatic. The duration of the forgotten events can range
from minutes to decades. Some episodes of dissociative amnesia resolve rapidly (e.g.,
when the person is removed from combat or some other stressful situation), whereas other
episodes persist for long periods of time. Some individuals may gradually recall the dissociated memories years later. Dissociative capacities may decline with age, but not always. As the amnesia remits, there may be considerable distress, suicidal behavior, and
symptoms of posttrauma tic stress disorder (PTSD).
Dissociative amnesia has been observed in young children, adolescents, and adults.
Children may be the most difficult to evaluate because they often have difficulty understanding questions about amnesia, and interviewers may find it difficult to formulate childfriendly questions about memory and amnesia. Observations of apparent dissociative amnesia are often difficult to differentiate from inattention, absorption, anxiety, oppositional
behavior, and learning disorders. Reports from several different sources (e.g., teacher,
therapist, case worker) may be needed to diagnose amnesia in children.
Risl( and Prognostic Factors
Environmental. Single or repeated traumatic experiences (e.g., war, childhood maltreatment, natural disaster, internment in concentration camps, genocide) are common ante
cedents. Dissociative amnesia is more likely to occur with 1) a greater number of adverse
childhood experiences, particularly physical and/or sexual abuse, 2) interpersonal violence; and 3) increased severity, frequency, and violence of the trauma.
Genetic and physiological. There are no genetic studies of dissociative amnesia. Studies of dissociation report significant genetic and environmental factors in both clinical and
nonclinical samples.
Course modifiers. Removal from the traumatic circumstances underlying the dissociative
amnesia (e.g., combat) may bring about a rapid return of memory. The memory loss of individuals with dissociative fugue may be particularly refractory. Onset of PTSD symptoms may
decrease localized, selective, or systematized amnesia. The returning memory, however, may
be experienced as flashbacks that alternate with amnesia for the content of the flashbacks.
Culture-Related Diagnostic issues
In Asia, the Middle East, and Latin America, non-epileptic seizures and other functional
neurological symptoms may accompany dissociative amnesia. In cultures with highly restrictive social traditions, the précipitants of dissociative amnesia often do not involve
frank trauma. Instead, the amnesia is preceded by severe psychological stresses or conflicts (e.g., marital conflict, other family disturbances, attachment problems, conflicts due
to restriction or oppression).
Suicide Risk
Suicidal and other self-destructive behaviors are common in individuals with dissociative
amnesia. Suicidal behavior may be a particular risk when the amnesia remits suddenly
and overwhelms the individual with intolerable memories.
Functional Consequences of Dissociative Amnesia
The impairment of individuals with localized, selective, or systematized dissociative amnesia ranges from limited to severe. Individuals with chronic generalized dissociative amnesia usually have impairment in all aspects of functioning. Even when these individuals
"re-leam" aspects of their life history, autobiographical memory remains very impaired.
Most become vocationally and interpersonally disabled.
Differential Diagnosis
Dissociative identity disorder. Individuals with dissociative amnesia may report depersonalization and auto-hypnotic symptoms. Individuals with dissociative identity disorder report pervasive discontinuities in sense of self and agency, accompanied by many
other dissociative symptoms. The amnesias of individuals with localized, selective, and/
or systematized dissociative amnesias are relatively stable. Anmesias in dissociative identity disorder include amnesia for everyday events, finding of unexplained possessions,
sudden fluctuations in skills and knowledge, major gaps in recall of life history, and brief
amnesic gaps in interpersonal interactions.
Posttraumatic stress disorder. Some individuals with PTSD cannot recall part or all of
a specific traumatic event (e.g., a rape victim with depersonalization and/or derealization
symptoms who cannot recall most events for the entire day of the rape). When that amnesia extends beyond the immediate time of the trauma, a comorbid diagnosis of dissociative
amnesia is warranted.
Neurocognitive disorders. In neurocognitive disorders, memory loss for personal information is usually embedded in cognitive, linguistic, affective, attentional, and behavioral
disturbances. In dissociative amnesia, memory deficits are primarily for autobiographical
information; intellectual and cognitive abilities are preserved.
Substance-related disorders. In the context of repeated intoxication with alcohol or
other substances/medications, there may be episodes of "^lack outs" or periods for which the
individual has no memory. To aid in distinguishing these episodes from dissociative amnesia, a longitudinal history noting that the amnestic episodes occur only in the context of
intoxication and do not occur in other situations would help identify the source as substance-induced; however the distinction may be difficult when the individual with dissociative amnesia may also misuse alcohol or other substances in the context of stressful
situations that may also exacerbate dissociative symptoms. Some individuals with comorbid dissociative amnesia and substance use disorders will attribute their memory problems solely to the substance use. Prolonged use of alcohol or other substances may result in
a substance-induced neurocognitive disorder that may be associated with impaired cognitive function, but in this context the protracted history of substance use and the persistent deficits associated with the neurocognitive disorder would serve to distinguish it
from dissociative amnesia, where there is typically no evidence of persistent impairment in
intellectual functioning.
Posttraumatic amnesia due to brain injury. Amnesia may occur in the context of a traumatic brain injury (TBI) when there has been an impact to the head or other mechaiüsms of
rapid movement or displacement of the brain within the skull TBI. Other characteristics of
TBI include loss of consciousness, disorientation and confusion, or, in more severe cases,
neurological signs (e.g., abnormalities on neuroimaging, a new onset of seizures or a marked
worsening of a preexisting seizure disorder, visual field cuts, anosmia). A neurocognitive
disorder attributable to TBI must present either immediately after brain injury occurs or immediately after the individual recovers consciousness after the injury, and persist past the
acute post-injury period. The cognitive presentation of a neurocognitive disorder following
TBI is variable and includes difficulties in the domains of complex attention, executive function, learning and memory as well as slowed speed of information processing and disturbances in social cognition. These additional features help distinguish it from dissociative
amnesia.
Seizure disorders. Individuals with seizure disorders may exhibit complex behavior during seizures or post-ictally with subsequent amnesia. Some individuals with a seizure disorder
engage in nonpurposive wandering that is limited to the period of seizure activity. Conversely, behavior during a dissociative fugue is usually purposeful, complex, and goaldirected and may last for days, weeks, or longer. Occasionally, individuals with a seizure disorder will report that earlier autobiographical memories have been "wiped out" as the seizure
disorder progresses. Such memory loss is not associated with traumatic circumstances and appears to occur randomly. Serial electroencephalograms usually show abnormalities. Telemetric electroencephalographic monitoring usually shows an association between the episodes of
amnesia and seizure activity. Dissociative and epileptic amnesias may coexist.
Catatonic stupor. Mutism in catatonic stupor may suggest dissociative amnesia, but failure of recall is absent. Other catatonic symptoms (e.g., rigidity, posturing, negativism) are
usually present.
Factitious disorder and malingering. There is no test, battery of tests, or set of procedures
that invariably distinguishes dissociative amnesia from feigned amnesia. Individuals with
factitious disorder or malingering have been noted to continue their deception even during
hypnotic or barbiturate-facilitated interviews. Feigned amnesia is more common in individuals with 1) acute, florid dissociative amnesia; 2) financial, sexual, or legal problems; or 3) a
wish to escape stressful circumstances. True amnesia can be associated with those same circumstances. Many individuals who malinger confess spontaneously or when confronted.
Normal and age-related changes in memory. Memory decrements in major and mild
neurocognitive disorders differ from those of dissociative amnesia, which are usually associated with stressful events and are more specific, extensive, and/or complex.
Comorbidity
As dissociative anmesia begins to remit, a wide variety of affective phenomena may surface: dysphoria, grief, rage, shame, guilt, psychological conflict and turmoil, and suicidal
and homicidal ideation, impulses, and acts. These individuals may have symptoms that
then meet diagnostic criteria for persistent depressive disorder (dysthymia); major depressive disorder; other specified or unspecified depressive disorder; adjustment disorder, with depressed mood; or adjustment disorder, with mixed disturbance of emotions
and conduct. Many individuals with dissociative amnesia develop PTSD at some point
during their life, especially when the traumatic antecedents of their amnesia are brought
into conscious awareness.
Many individuals with dissociative amnesia have symptoms that meet diagnostic criteria for a comorbid somatic symptom or related disorder (and vice versa), including somatic symptom disorder and conversion disorder (functional neurological symptom
disorder). Many individuals with dissociative amnesia have symptoms that meet diagnostic criteria for a personality disorder, especially dependent, avoidant, and borderline.
Depersonalization/Dereallzation Disorder
Diagnostic Criteria 300.6 (F48.1)
A. The presence of persistent or recurrent experiences of depersonalization, derealization, or both:
1. Depersonalization: Experiences of unreality, detachment, or being an outside observer with respect to one’s thoughts, feelings, sensations, body, or actions (e.g.,
perceptual alterations, distorted sense of time, unreal or absent self, emotional and/
or physical numbing).
2. Derealization: Experiences of unreality or detachment with respect to surroundings (e.g., individuals or objects are experienced as unreal, dreamlike, foggy, lifeless, or visually distorted).
B. During the depersonalization or derealization experiences, reality testing remains intact.
C. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, medication) or another medical condition (e.g., seizures).
E. The disturbance is not better explained by another mental disorder, such as schizophrenia, panic disorder, major depressive disorder, acute stress disorder, posttraumatic stress disorder, or another dissociative disorder.
Diagnostic Features
The essential features of depersonalization/derealization disorder are persistent or recurrent episodes of depersonalization, derealization, or both. Episodes of depersonalization
are characterized by a feeling of unreality or detachment from, or unfamiliarity with, one's
whole self or from aspects of the self (Criterion Al). The individual may feel detached
from his or her entire being (e.g., "I am no one," "I have no self"). He or she may also feel
subjectively detached from aspects of the self, including feelings (e.g., hypoemotionality:
"I know I have feelings but I don't feel them"), thoughts (e.g., "My thoughts don't feel like
my own," "head^filled with cotton"), whole body or body parts, or sensations (e.g., touch,
proprioception, hunger, thirst, libido). There may also be a diminished sense of agency
(e.g., feeling robotic, like an automaton; lacking control of one's speech or movements).
The depersonalization experience can sometimes be one of a split self, with one part observing and one participating, known as an "out-of-body experience" in its most extreme
form. The unitary symptom of "depersonalization" consists of several symptom factors:
anomalous body experiences (i.e., unreality of the self and perceptual alterations); emotional or physical numbing; and temporal distortions with anomalous subjective recall.
Episodes of derealization are characterized by a feeling of unreality or detachment
from, or unfamiliarity with, the world, be it individuals, inanimate objects, or all surroundings (Criterion A2). TTie individual may feel as if he or she were in a fog, dream, or bubble, or
as if there were a veil or a glass wall between the individual and world around. Surroundings may be experienced as artificial, colorless, or lifeless. Derealization is commonly accompanied by subjective visual distortions, such as blurriness, heightened acuity, widened
or narrowed visual field, two-dimensionality or flatness, exaggerated three-dimensionality, or altered distance or size of objects (i.e., macropsia or micropsia). Auditory distortions
can also occur, whereby voices or sounds are muted or heightened. In addition. Criterion
C requires the presence of clinically significant distress or impairment in social, occupational, or other important areas of fimctioning, and Criteria D and E describe exclusionary
diagnoses.
Associated Features Supporting Diagnosis
Individuals with depersonalization/derealization disorder may have difficulty describing their symptoms and may think they are "crazy" or "going crazy". Another common
experience is the fear of irreversible brain damage. A commonly associated symptom is a
subjectively altered sense of time (i.e., too fast or too slow), as well as a subjective difficulty
in vividly recalling past memories and owning them as personal and emotional. Vague somatic symptoms, such as head fullness, tingling, or lightheadedness, are not uncommon.
Individuals may suffer extreme rumination or obsessional preoccupation (e.g., constantly
obsessing about whether they really exist, or checking their perceptions to determine
whether they appear real). Varying degrees of anxiety and depression are also common associated features. Individuals with the disorder have been found to have physiological
hyporeactivity to emotional stimuli. Neural substrates of interest include the hypothalamic-pituitary-adrenocortical axis, inferior parietal lobule, and prefrontal cortical-limbic
circuits.
Prevalence
Transient depersonalization/derealization symptoms lasting hours to days are common
in the general population. The 12-month prevalence of depersonalization/derealization
disorder is thought to be markedly less than for transient symptoms, although precise estimates for the disorder are unavailable. In general, approximately one-half of all adults
have experienced at least one lifetime episode of depersonalization/derealization. However, symptomatology that meets full criteria for depersonalization/derealization disorder is markedly less common than transient symptoms. Lifetime prevalence in U.S. and
non-U.S. countries is approximately 2% (range of 0.8% to 2.8%). TÎie gender ratio for the
disorder is 1:1.
Deveiopment and Course
The mean age at onset of depersonalization/derealization disorder is 16 years, although the
disorder can start in early or middle childhood; a minority cannot recall ever not having had
the symptoms. Less than 20% of individuals experience onset after age 20 years and only
5% after age 25 years. Onset in the fourth decade of life or later is highly unusual. Onset can
range from extremely sudden to gradual. Duration of depersonalization/derealization
disorder episodes can vary greatly, from brief (hours or days) to prolonged (weeks,
months, or years). Given the rarity of disorder onset after age 40 years, in such cases the individual should be examined more closely for underlying medical conditions (e.g., brain
lesions, seizure disorders, sleep apnea). The course of the disorder is often persistent.
About one-third of cases involve discrete episodes; another third, continuous symptoms
from the start; and still another third, an initially episodic course that eventually becomes
continuous.
While in some individuals the intensity of symptoms can wax and wane considerably,
others report an unwavering level of intensity that in extreme cases can be constantly present for years or decades. Internal and external factors that affect symptom intensity vary
between individuals, yet some typical patterns are reported. Exacerbations can be triggered by stress, worsening mood or anxiety symptoms, novel or overstimulating settings,
and physical factors such as lighting or lack of sleep.
Risk and Prognostic Factors
Temperamental. Individuals with depersonalization/derealization disorder are characterized by harm-avoidant temperament, immature defenses, and both disconnection and
overconnection schemata. Immature defenses such as idealization/devaluation, projection and acting out result in denial of reality and poor adaptation. Cognitive disconnection
schemata reflect defectiveness and emotional inhibition and subsume themes of abuse, neglect, and deprivation. Overconnection schemata involve impaired autonomy with themes
of dependency, vulnerability, and incompetence.
Environmental. There is a clear association between the disorder and childhood interpersonal traumas in a substantial portion of individuals, although this association is not as prevalent or as extreme in the nature of the traumas as in other dissociative disorders, such as
dissociative identity disorder. In particular, emotional abuse and emotional neglect have been
most strongly and consistently associated with the disorder. Other stressors can include physical abuse; witnessing domestic violence; growing up with a seriously impaired, mentally ill
parent; or unexpected death or suicide of a family member or close Wend. Sexual abuse is a
much less common antecedent but can be encountered. The most common proximal précipitants of the disorder are severe stress (interpersonal, financial, occupational), depression, anxiety (particularly panic attacks), and illicit drug use. Symptoms may be specifically induced by
substances such as tetrahydrocannabinol, hallucinogens, ketamine, MDMA (3,4-methylenedioxymethamphetamine; "ecstasy") and salvia. Marijuana use may precipitate new-onset
panic attacks and depersonalization/derealization symptoms simultaneously.
Culture-Reiated Diagnostic issues
Volitionally induced experiences of depersonalization/derealization can be a part of meditative practices that are prevalent in many religions and cultures and should not be diagnosed as a disorder. However, there are individuals who initially induce these states
intentionally but over time lose control over them and may develop a fear and aversion for
related practices.
Functionai Consequences of
Depersonaiization/Dereaiization Disorder
Symptoms of depersonalization/derealization disorder are highly distressing and are associated with major morbidity. The affectively flattened and robotic demeanor that these
individuals often demonstrate may appear incongruent with the extreme emotional pain
reported by those with the disorder. Impairment is often experienced in both interpersonal
and occupational spheres, largely due to the hypoemotionaHty with others, subjective difficulty in focusing and retaining information, and a general sense of disconnectedness from
life.
Differential Diagnosis
Illness anxiety disorder. Although individuals with depersonalization/derealization disorder can present with vague somatic complaints as well as fears of permanent brain damage, the diagnosis of depersonalization/derealization disorder is characterized by the
presence of a constellation of typical depersonalization/derealization symptoms and the absence of other manifestations of illness anxiety disorder.
Major depressive disorder. Feelings of numbness, deadness, apathy, and being in a
dream are not uncommon in major depressive episodes. However, in depersonalization/
derealization disorder, such symptoms are associated with further symptoms of the disorder. If the depersonalization/derealization clearly precedes the onset of a major depressive episode or clearly continues after its resolution, the diagnosis of depersonalization/
derealization disorder applies.
Obsessive-compulsive disorder. Some individuals with depersonalization/derealization disorder can become obsessively preoccupied with their subjective experience or
develop rituals checking on the status of their symptoms. However, other symptoms of
obsessive-compulsive disorder unrelated to depersonalization/derealization are not
present.
Other dissociative disorders. In order to diagnose depersonalization/derealization
disorder, the symptoms should not occur in the context of another dissociative disorder,
such as dissociative identity disorder. Differentiation from dissociative amnesia and conversion disorder (functional neurological symptom disorder) is simpler, as the symptoms
of these disorders do not overlap with those of depersonalization/derealization disorder.
Anxiety disorders. Depersonalization/derealization is one of the symptoms of panic attacks, increasingly common as panic attack severity increases. Therefore, depersonalization/dereahzation disorder should not be diagnosed when the symptoms occur only
during panic attacks that are part of panic disorder, social anxiety disorder, or specific
phobia. In addition, it is not uncommon for depersonalization/derealization symptoms
to first begin in the context of new-onset panic attacks or as panic disorder progresses and
worsens. In such presentations, the diagnosis of depersonalization/derealization disorder
can be made if 1) the depersonalization/derealization component of the presentation is
very prominent from the start, clearly exceeding in duration and intensity the occurrence
of actual panic attacks; or 2) the depersonalization/derealization continues after panic disorder has remitted or has been successfully treated.
Psychotic disorders. The presence of intact reality testing specifically regarding the
depersonalization/derealization symptoms is essential to differentiating depersonalization/derealization disorder from psychotic disorders. Rarely, positive-symptom
schizophrenia can pose a diagnostic challenge when nihilistic delusions are present. For
example, an individual may complain that he or she is dead or the world is not real; this
could be either a subjective experience that the individual knows is not true or a delusional
conviction.
Substance/medication-induced disorders. Depersonalization/derealization associated
with the physiological effects of substances during acute intoxication or withdrawal is not
diagnosed as depersonalization/derealization disorder. The most common precipitating
substances are the illicit drugs marijuana, hallucinogens, ketamine, ecstasy, and salvia. In
about 15% of all cases of depersonalization/derealization disorder, the symptoms are precipitated by ingestion of such substances. If the symptoms persist for some time in the absence of any further substance or medication use, the diagnosis of depersonalization/
derealization disorder applies. This diagnosis is usually easy to establish since the vast majority of individuals with this presentation become highly phobic and aversive to the triggering substance and do not use it again.
Mental disorders due to another medical condition. Features such as onset after age
40 years or the presence of atypical symptoms and course in any individual suggest the
possibility of an underlying medical condition. In such cases, it is essential to conduct a
thorough medical and neurological evaluation, which may include standard laboratory
studies, viral titers, an electroencephalogram, vestibular testing, visual testing, sleep studies, and/or brain imaging. When the suspicion of an underlying seizure disorder proves
difficult to confirm, an ambulatory electroencephalogram may be indicated; although
temporal lobe epilepsy is most commonly implicated, parietal and frontal lobe epilepsy
may also be associated.
Comorbidity
In a convenience sample of adults recruited for a number of depersonalization research
studies, lifetime comorbidities were high for unipolar depressive disorder and for any
anxiety disorder, with a significant proportion of the sample having both disorders. Comorbidity with posttraumatic stress disorder was low. The three most commonly co-occurring
personality disorders were avoidant, borderline, and obsessive-compulsive.
Other Specified Dissociative Disorder
300.15 (F44.89)
This category applies to presentations in which symptoms characteristic of a dissociative
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the dissociative disorders diagnostic class. The other specified dissociative disorder category is used in situations in which the clinician chooses to communicate
the specific reason that the presentation does not meet the criteria for any specific dissociative disorder. This is done by recording “other specified dissociative disorder” followed
by the specific reason (e.g., “dissociative trance”).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Chronic and recurrent syndromes of mixed dissociative symptoms: This category includes identity disturbance associated with less-than-marked discontinuities in
sense of self and agency, or alterations of identity or episodes of possession in an individual who reports no dissociative amnesia.
2. identity disturbance due to proionged and intense coercive persuasion: Individuals who have been subjected to intense coercive persuasion (e.g., brainwashing,
thought reform, indoctrination while captive, torture, long-term political imprisonment,
recruitment by sects/cults or by terror organizations) may present with prolonged
changes in, or conscious questioning of, their identity.
3. Acute dissociative reactions to stressfui events: This category is for acute, transient conditions that typically last less than 1 month, and sometimes only a few hours
or days. These conditions are characterized by constriction of consciousness; depersonalization; derealization; perceptual disturbances (e.g., time slowing, macropsia);
micro-amnesias; transient stupor; and/or alterations in sensory-motor functioning (e.g.,
analgesia, paralysis).
4. Dissociative trance: This condition is characterized by an acute narrowing or complete loss of awareness of immediate surroundings that manifests as profound unresponsiveness or insensitivity to environmental stimuli. The unresponsiveness may be
accompanied by minor stereotyped behaviors (e.g., finger movements) of which the individual is unaware and/or that he or she cannot control, as well as transient paralysis
or loss of consciousness. The dissociative trance is not a normal part of a broadly accepted collective cultural or religious practice.
Unspecified Dissociative Disorder
300.15 (F44.9)
This category applies to presentations in which symptoms characteristic of a dissociative
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the dissociative disorders diagnostic class. The unspecified dissociative
disorder category is used in situations in which the clinician chooses not to specify the reason that the criteria are not met for a specific dissociative disorder, and includes presentations for which there is insufficient information to make a more specific diagnosis (e.g.,
in emergency room settings).
Somatic Symptom
Related
SomStiC symptom disorder and other disorders with prominent somatic symptoms constitute a new category in DSM-5 called somatic symptom and related disorders. This
chapter includes the diagnoses of somatic symptom disorder, illness anxiety disorder, conversion disorder (functional neurological symptom disorder), psychological factors affecting other medical conditions, factitious disorder, other specified somatic sjnnptom and
related disorder, and unspecified somatic symptom and related disorder. All of the disorders in this chapter share a common feature: the prominence of somatic symptoms associated with significant distress and impairment. Individuals with disorders with prominent
somatic symptoms are commonly encoimtered in primary care and other medical settings
but are less commonly encountered in psychiatric and otiier mental health settings. These
reconceptualized diagnoses, based on a reorganization of DSM-IV somatoform disorder diagnoses, are more useful for primary care and other medical (nonpsychiatric) clinicians.
The major diagnosis in this diagnostic class, somatic symptom disorder, emphasizes
diagnosis made on the basis of positive symptoms and signs (distressing somatic symptoms plus abnormal thoughts, feelings, and behaviors in response to these symptoms)
rather than the absence of a medical explanation for somatic symptoms. A distinctive characteristic of many individuals with somatic symptom disorder is not the somatic symptoms per se, but instead the way they present and interpret them. Incorporating affective,
cognitive, and behavioral components into the criteria for somatic symptom disorder provides a more comprehensive and accurate reflection of the true clinical picture than can be
achieved by assessing the somatic complaints alone.
The principles behind the changes in the somatic symptom and related diagnoses from
DSM-IV are crucial in imderstanding the DSM-5 diagnoses. The DSM-IV term somatoform
disorders was confusing and is replaced by somatic symptom and related disorders. In DSM-IV
there was a great deal of overlap across the somatoform disorders and a lack of clarity
about the boundaries of diagnoses. Although individuals with these disorders primarily
present in medical rather than mental health settings, nonpsychiatric physicians foimd the
DSM-IV somatoform diagnoses difficult to understand and use. The current DSM-5 classification recogrüzes this overlap by reducing the total number of disorders as well as their
subcategories.
The previous criteria overemphasized the centrality of medically unexplained symptoms.
Such symptoms are present to various degrees, particularly in conversion disorder, but somatic symptom disorders can also accompany diagnosed medical disorders. The reliability of determining that a somatic symptom is medically unexplained is limited, and
grounding a diagnosis on the absence of an explanation is problematic and reinforces
mind-body dualism. It is not appropriate to give an individual a mental disorder diagnosis
solely because a medical cause cannot be demonstrated. Furthermore, the presence of a
medical diagnosis does not exclude the possibility of a comorbid mental disorder, including a somatic symptom and related disorder. Perhaps because of the predominant focus
on lack of medical explanation, individuals regarded these diagnoses as pejorative and demeaning, implying that their physical symptoms were not "real." The new classification
defines the major diagnosis, somatic symptom disorder, on the basis of positive symptoms
(distressing somatic symptoms plus abnormal thoughts, feelings, and behaviors in response
to these symptoms). However, medically unexplained symptoms remain a key feature in
conversion disorder and pseudocyesis (other specified somatic symptom and related disorder) because it is possible to demonstrate definitively in such disorders that the symptoms are not consistent with medical pathophysiology.
It is important to note that some other mental disorders may initially manifest with primarily somatic symptoms (e.g., major depressive disorder, panic disorder). Such diagnoses may account for the somatic symptoms, or they may occur alongside one of the somatic
symptom and related disorders in this chapter. There is also considerable medical comorbidity among somatizing individuals. Although somatic symptoms are frequently associated with psychological distress and psychopathology, some somatic symptom and
related disorders can arise spontaneously, and their causes can remain obscure. Anxiety
disorders and depressive disorders may accompany somatic symptom and related disorders. The somatic component adds severity and complexity to depressive and anxiety disorders and results in higher severity, functional impairment, and even refractoriness to
traditional treatments. In rare instances, the degree of preoccupation may be so severe as
to warrant consideration of a delusional disorder diagnosis.
A number of factors may contribute to somatic symptom and related disorders. These
include genetic and biological vulnerability (e.g., increased sensitivity to pain), early traumatic experiences (e.g., violence, abuse, deprivation), and learning (e.g., attention obtained from illness, lack of reinforcement of nonsomatic expressions of distress), as well as
cultural/social norms that devalue and stigmatize psychological suffering as compared
with physical suffering. Differences in medical care across cultures affect the presentation,
recognition, and management of these somatic presentations. Variations in symptom presentation are likely the result of the interaction of multiple factors within cultural contexts that affect how individuals identify and classify bodily sensations, perceive illness,
and seek medical attention for them. Thus, somatic presentations can be viewed as expressions of personal suffering inserted in a cultural and social context.
All of these disorders are characterized by the prominent focus on somatic concerns
and their iiütial presentation mainly in medical rather than mental health care settings. Somatic symptom disorder offers a more clinically useful method of characterizing individuals who may have been considered in the past for a diagnosis of somatization disorder.
Furthermore, approximately 75% of individuals previously diagnosed with hypochondriasis are subsumed under the diagnosis of somatic symptom disorder. However, about
25% of individuals with hypochondriasis have high health anxiety in the absence of somatic symptoms, and many such individuals' symptoms would not qualify for an anxiety
disorder diagnosis. The DSM-5 diagnosis of illness anxiety disorder is for this latter group
of individuals. Illness anxiety disorder can be considered either in this diagnostic section
or as an anxiety disorder. Because of the strong focus on somatic concerns, and because illness anxiety disorder is most often encountered in medical settings, for utility it is listed
with the somatic symptom and related disorders. In conversion disorder, the essential feature is neurological symptoms that are found, after appropriate neurological assessment,
to be incompatible with neurological pathophysiology. Psychological factors affecting
other medical conditions is also included in this chapter. Its essential feature is the presence of one or more clinically significant psychological or behavioral factors that adversely
affect a medical condition by increasing the risk for suffering, death, or disability. Like the
other somatic symptom and related disorders, factitious disorder embodies persistent
problems related to illness perception and identity. In the great majority of reported cases
of factitious disorder, both imposed on self and imposed on another, individuals present
with somatic symptoms and medical disease conviction. Consequently, DSM-5 factitious
disorder is included among the somatic symptom and related disorders. Other specified
somatic symptom and related disorder and unspecified somatic symptom and related disorder include conditions for which some, but not all, of the criteria for somatic symptom
disorder or illness anxiety disorder are met, as well as pseudocyesis.
Somatic Symptom Disorder
Diagnostic Criteria 300.82 (F45.1)
A. One or more somatic symptoms that are distressing or result in significant disruption
of daily life.
B. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated health concerns as manifested by at least one of the following:
1. Disproportionate and persistent thoughts about the seriousness of one’s symptoms.
2. Persistently high level of anxiety about health or symptoms.
3. Excessive time and energy devoted to these symptoms or health concerns.
C. Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months).
Specify if:
Witli predominant pain (previously pain disorder): This specifier is for individuals
whose somatic symptoms predominantly involve pain.
Specify if:
Persistent: A persistent course is characterized by severe symptoms, marked impairment, and long duration (more than 6 months).
Specify current severity:
Mild: Only one of the symptoms specified in Criterion B is fulfilled.
Moderate: Two or more of the symptoms specified in Criterion B are fulfilled.
Severe: Two or more of the symptoms specified in Criterion B are fulfilled, plus there
are multiple somatic complaints (or one very severe somatic symptom).
Diagnostic Features
Individuals with somatic symptom disorder typically have multiple, current, somatic symptoms that are distressing or result in significant disruption of daily life (Criterion A), although sometimes only one severe symptom, most commonly pain, is present. Symptoms
may be specific (e.g., localized pain) or relatively nonspecific (e.g., fatigue). The symptoms
sometimes represent normal bodily sensations or discomfort that does not generally signify serious disease. Somatic symptoms without an evident medical explanation are not
sufficient to make this diagnosis. The individual's suffering is authentic, whether or not it
is medically explained.
The symptoms may or may not be associated with another medical condition. The diagnoses of somatic symptom disorder and a concurrent medical illness are not mutually
exclusive, and these frequently occur together. For example, an individual may become seriously disabled by symptoms of somatic symptom disorder after an uncomplicated myocardial infarction even if the myocardial infarction itself did not result in any disability. If
another medical condition or high risk for developing one is present (e.g., strong family
history), the thoughts, feelings, and behaviors associated with this condition are excessive
(Criterion B).
Individuals with somatic symptom disorder tend to have very high levels of worry
about illness (Criterion B). They appraise their bodily symptoms as unduly threatening,
harmful, or troublesome and often think the worst about their health. Even when there is
evidence to the contrary, some patients still fear the medical seriousness of their symptoms. In severe somatic symptom disorder, health concerns may assume a central role in
the individual's life, becoming a feature of his or her identity and dominating interpersonal relationships.
Individuals typically experience distress that is principally focused on somatic symptoms and their significance. When asked directly about their distress, some individuals describe it in relation to other aspects of their lives, while others deny any source of distress
other than the somatic symptoms. Health-related quality of life is often impaired, both
physically and mentally. In severe somatic symptom disorder, the impairment is marked,
and when persistent, the disorder can lead to invalidism.
There is often a high level of medical care utilization, which rarely alleviates the individual's concerns. Consequently, the patient may seek care from multiple doctors for the same
symptoms. These individuals often seem unresponsive to medical interventions, and new
interventions may only exacerbate the presenting symptoms. Some individuals with the disorder seem unusually sensitive to medication side effects. Some feel that their medical assessment and treatment have been inadequate.
Associated Features Supporting Diagnosis
Cognitive features include attention focused on somatic symptoms, attribution of normal
bodily sensations to physical illness (possibly with catastrophic interpretations), worry
about illness, and fear that any physical activity may damage the body. The relevant associated behavioral features may include repeated bodily checking for abnormalities, repeated seeking of medical help and reassurance, and avoidance of physical activity. These
behavioral features are most pronounced in severe, persistent somatic symptom disorder.
These features are usually associated with frequent requests for medical help for different
somatic symptoms. This may lead to medical consultations in which individuals are so focused on their concerns about somatic symptom(s) that they cannot be redirected to other
matters. Any reassurance by the doctor that the symptoms are not indicative of serious
physical illness tends to be short-lived and/or is experienced by the individuals as the
doctor not taking their symptoms with due seriousness. As the focus on somatic symptoms is a primary feature of the disorder, individuals with somatic symptom disorder typically present to general medical health services rather than mental health services. The
suggestion of referral to a mental health specialist may be met with surprise or even frank
refusal by individuals with somatic symptom disorder.
Since somatic symptom disorder is associated with depressive disorders, there is an increased suicide risk. It is not known whether somatic symptom disorder is associated with
suicide risk independent of its association with depressive disorders.
Prevaience
The prevalence of somatic symptom disorder is not known. However, the prevalence of
somatic symptom disorder is expected to be higher than that of the more restrictive DSMIV somatization disorder (<1%) but lower than that of undifferentiated somatoform disorder (approximately 19%). The prevalence of somatic symptom disorder in the general
adult population may be around 5%-7%. Females tend to report more somatic symptoms
than do males, and the prevalence of somatic symptom disorder is consequently likely to
be higher in females.
Development and Course
In older individuals, somatic symptoms and concurrent medical illnesses are common,
and a focus on Criterion B is crucial for making the diagnosis. Somatic symptom disorder
may be underdiagnosed in older adults either because certain somatic symptoms (e.g.,
pain, fatigue) are considered part of normal aging or because illness worry is considered
"understandable" in older adults who have more general medical illnesses and medications than do younger people. Concurrent depressive disorder is common in older people
who present with numerous somatic symptoms.
In children, the most common symptoms are recurrent abdominal pain, headache, fatigue, and nausea. A single prominent symptom is more common in children than in
adults. While young children may have somatic complaints, they rarely worry about "illness" per se prior to adolescence. The parents' response to the symptom is important, as
this may determine the level of associated distress. It is the parent who may determine the
interpretation of symptoms and the associated time off school and medical help seeking.
Risk and Prognostic Factors
Temperamental. The personality trait of negative affectivity (neuroticism) has been identified as an independent correlate/risk factor of a high number of somatic symptoms. Comorbid
anxiety or depression is common and may exacerbate symptoms and impairment.
Environmental. Somatic symptom disorder is more frequent in individuals with few years
of education and low socioeconomic status, and in those who have recently experienced
stressful life events.
Course modifiers. Persistent somatic symptoms are associated with demographic features (female sex, older age, fewer years of education, lower socioeconomic status, unemployment), a reported history of sexual abuse or other childhood adversity, concurrent
chronic physical illness or psychiatric disorder (depression, anxiety, persistent depressive
disorder [dysthymia], panic), social stress, and reinforcing social factors such as illness
benefits. Cognitive factors that affect clinical course include sensitization to pain, heightened attention to bodily sensations, and attribution of bodily symptoms to a possible medical illness rather than recognizing them as a normal phenomenon or psychological stress.
Cuiture-Reiated Diagnostic issues
Somatic sjmnptoms are prominent in various "culture-bound syndromes." High numbers
of somatic symptoms are found in population-based and primary care studies aroimd the
world, with a similar pattern of the most commonly reported somatic symptoms, impairment, and treatment seeking. The relationship between number of somatic symptoms and
illness worry is similar in different cultures, and marked illness worry is associated with
impairment and greater treatment seeking across cultures. The relationship between numerous somatic symptoms and depression appears to be very similar around the world
and between different cultures within one country.
Despite these similarities, there are differences in somatic symptoms among cultures
and ethnic groups. The description of somatic symptoms varies with linguistic and other
local cultural factors. These somatic presentations have been described as "idioms of distress" because somatic symptoms may have special meanings and shape patient-clinician
interactions in the particular cultural contexts. "Burnout," the sensation of heaviness or
the complaints of "gas"; too much heat in the body; or burning in the head are examples of
symptoms that are common in some cultures or ethnic groups but rare in others. Explanatory models also vary, and somatic symptoms may be attributed variously to particular
family, work, or environmental stresses; general medical illness; the suppression of feelings of anger and resentment; or certain culture-specific phenomena, such as semen loss.
There may also be differences in medical treatment seeking among cultural groups, in addition to differences due to variable access to medical care services. Seeking treatment for
multiple somatic symptoms in general medical clinics is a worldwide phenomenon and
occurs at similar rates among ethnic groups in the same country.
Functional Consequences of Somatic Symptom Disorder
The disorder is associated with marked impairment of health status. Many individuals
with severe somatic symptom disorder are likely to have impaired health status scores
more than 2 standard deviations below population norms.
Differential Diagnosis
If the somatic symptoms are consistent with another mental disorder (e.g., panic disorder),
and the diagnostic criteria for that disorder are fulfilled, then that mental disorder should
be considered as an alternative or additional diagnosis. A separate diagnosis of somatic
symptom disorder is not made if the somatic symptoms and related thoughts, feelings, or
behaviors occur only during major depressive episodes. If, as commonly occurs, the criteria for both somatic symptom disorder and another mental disorder diagnosis are fulfilled, then both should be coded, as both may require treatment.
Other medical conditions. The presence of somatic symptoms of unclear etiology is not
in itself sufficient to make the diagnosis of somatic symptom disorder. The symptoms of
many individuals with disorders like irritable bowel syndrome or fibromyalgia would not
satisfy the criterion necessary to diagnose somatic symptom disorder (Criterion B). Conversely, the presence of somatic symptoms of an established medical disorder (e.g., diabetes or heart disease) does not exclude the diagnosis of somatic symptom disorder if the
criteria are otherwise met.
Panic disorder. In panic disorder, somatic symptoms and anxiety about health tend to
occur in acute episodes, whereas in somatic symptom disorder, anxiety and somatic symptoms are more persistent.
Generalized anxiety disorder. Individuals with generalized anxiety disorder worry about
multiple events, situations, or activities, only one of which may involve their health. The
main focus is not usually somatic symptoms or fear of illness as it is in somatic symptom
disorder.
Depressive disorders. Depressive disorders are commonly accompanied by somatic
symptoms. However, depressive disorders are differentiated from somatic symptom disorder by the core depressive symptoms of low (dysphoric) mood and anhedonia.
Illness anxiety disorder. If the individual has extensive worries about health but no or
minimal somatic symptoms, it may be more appropriate to consider illness anxiety disorder.
Conversion disorder (functional neurological symptom disorder). In conversion disorder, the presenting symptom is loss of function (e.g., of a limb), whereas in somatic symptom disorder, the focus is on the distress that particular symptoms cause. The features
listed under Criterion B of somatic symptom disorder may be helpful in differentiating the
two disorders.
Delusional disorder. In somatic symptom disorder, the individual's beliefs that somatic
symptoms might reflect serious underlying physical illness are not held with delusional
intensity. Nonetheless, the individual's beliefs concerning the somatic symptoms can be
firmly held. In contrast, in delusional disorder, somatic subtype, the somatic symptom beliefs and behavior are stronger than those found in somatic symptom disorder.
Body dysmorphic disorder. In body dysmorphic disorder, the individual is excessively
concerned about, and preoccupied by, a perceived defect in his or her physical features. In
contrast, in somatic symptom disorder, the concern about somatic symptoms reflects fear
of underlying illness, not of a defect in appearance.
Obsessive-compulsive disorder. In somatic symptom disorder, the recurrent ideas about
somatic symptoms or illness are less intrusive, and individuals with this disorder do not
exhibit the associated repetitive behaviors aimed at reducing anxiety that occur in obsessive-compulsive disorder.
Comorbidity
Somatic symptom disorder is associated with high rates of comorbidity with medical disorders as well as anxiety and depressive disorders. When a concurrent medical illness is
present, the degree of impairment is more marked than would be expected from the physical illness alone. When an individual's symptoms meet diagnostic criteria for somatic
symptom disorder, the disorder should be diagnosed; however, in view of the frequent comorbidity, especially with anxiety and depressive disorders, evidence for these concurrent diagnoses should be sought.
Illness Anxiety Disorder
Diagnostic Criteria 300.7 (F45.21)
A. Preoccupation with having or acquiring a serious illness.
B. Somatic symptoms are not present or, if present, are only mild in intensity. If another
medical condition is present or there is a high risk for developing a medical condition
(e.g., strong family history is present), the preoccupation is clearly excessive or disproportionate.
C. There is a high level of anxiety about health, and the individual is easily alarmed about
personal health status.
D. The individual performs excessive health-related behaviors (e.g., repeatedly checks
his or her body for signs of illness) or exhibits maladaptive avoidance (e.g., avoids doctor appointments and hospitals).
E. Illness preoccupation has been present for at least 6 months, but the specific illness
that is feared may change over that period of time.
F. The illness-related preoccupation is not better explained by another mental disorder, such
as somatic symptom disorder, panic disorder, generalized anxiety disorder, body dysmorphic disorder, obsessive-compulsive disorder, or delusional disorder, somatic type.
Specify whether:
Care-seeking type: Medical care, including physician visits or undergoing tests and
procedures, is frequently used.
Care-avoidant type: Medical care is rarely used.
Diagnostic Features
Most individuals with hypochondriasis are now classified as having somatic symptom
disorder; however, in a minority of cases, the diagnosis of illness anxiety disorder applies
instead. Illness anxiety disorder entails a preoccupation with having or acquiring a serious, undiagnosed medical illness (Criterion A). Somatic symptoms are not present or, if
present, are only mild in intensity (Criterion B). A thorough evaluation fails to identify a
serious medical condition that accounts for the individual's concerns. While the concern
may be derived from a nonpathological physical sign or sensation, the individual's distress emanates not primarily from the physical complaint itself but rather from his or her
anxiety about the meaning, significance, or cause of the complaint (i.e., the suspected medical diagnosis). If a physical sign or symptom is present, it is often a normal physiological
sensation (e.g., orthostatic dizziness), a benign and self-limited dysfunction (e.g., transient
tinnitus), or a bodily discomfort not generally considered indicative of disease (e.g., belching). If a diagnosable medical condition is present, the individual's anxiety and preoccupation are clearly excessive and disproportionate to the severity of the condition (Criterion
B). Empirical evidence and existing literature pertain to previously defined DSM hypochondriasis, and it is unclear to what extent and how precisely they apply to the description of this new diagnosis.
The preoccupation with the idea that one is sick is accompanied by substantial anxiety
about health and disease (Criterion C). Individuals with illness anxiety disorder are easily
alarmed about illness, such as by hearing about someone else falling ill or reading a healthrelated news story. Their concerns about undiagnosed disease do not respond to appropriate medical reassurance, negative diagnostic tests, or benign course. The physician's attempts at reassurance and symptom palliation generally do not alleviate the individual's
concerns and may heighten them. Illness concerns assume a prominent place in the individual's life, affecting daily activities, and may even result in invalidism. Illness becomes
a central feature of the individual's identity and self-image, a frequent topic of social discourse, and a characteristic response to stressful life events. Individuals with the disorder
often examine themselves repeatedly (e.g., examining one's throat in the mirror) (Criterion D). They research their suspected disease excessively (e.g., on the Internet) and repeatedly seek reassurance from family, friends, or physicians. This incessant worrying often
becomes frustrating for others and may result in considerable strain within the family. In
some cases, the anxiety leads to maladaptive avoidance of situations (e.g., visiting sick
family members) or activities (e.g., exercise) that these individuals fear might jeopardize
their health.
Associated Features Supporting Diagnosis
Because they believe they are medically ill, individuals with illness anxiety disorder are
encountered far more frequently in medical than in mental health settings. The majority of
individuals with illness anxiety disorder have extensive yet unsatisfactory medical care,
though some may be too anxious to seek medical attention. They generally have elevated
rates of medical utilization but do not utilize mental health services more than the general
population. They often consult multiple physicians for the same problem and obtain repeatedly negative diagnostic test results. At times, medical attention leads to a paradoxical
exacerbation of anxiety or to iatrogenic complications from diagnostic tests and procedures. Individuals with the disorder are generally dissatisfied with their medical care and
find it unhelpful, often feeling they are not being taken seriously by physicians. At times,
these concerns may be justified, since physicians sometimes are dismissive or respond
with frustration or hostility. This response can occasionally result in a failure to diagnose
a medical condition that is present.
Prevaience
Prevalence estimates of illness anxiety disorder are based on estimates of the DSM-III and
DSM-rV diagnosis hypochondriasis. The 1- to 2-year prevalence of health anxiety and/or
disease conviction in community surveys and population-based samples ranges fiOm 1.3%
to 10%. In ambulatory medical populations, the 6-month/1-year prevalence rates are between 3% and 8%. The prevalence of the disorder is similar in males and females.
Deveiopment and Course
The development and course of illness anxiety disorder are unclear. Illness anxiety disorder is generally thought to be a chronic and relapsing condition with an age at onset in
early and middle adulthood. In population-based samples, health-related anxiety increases with age, but the ages of individuals with high health anxiety in medical settings
do not appear to differ from those of other patients in those settings. In older individuals,
health-related anxiety often focuses on memory loss; the disorder is thought to be rare in
children.
Risic and Prognostic Factors
Environmental. Illness anxiety disorder may sometimes be precipitated by a major life
stress or a serious but ultimately benign threat to the individual's health. A history of child
hood abuse or of a serious childhood ilhiess may predispose to development of the disorder in adulthood^
Course modifiers. Approximately one-third to one-half of individuals with illness anxiety disorder have a transient form, which is associated with less psychiatric comorbidity,
more medical comorbidity, and less severe illness aiixiety disorder.
Culture-Related Diagnostic issues
The diagnosis should be made with caution in individuals whose ideas about disease are
congruent with widely held, culturally sanctioned beliefs. Little is known about the phenomenology of the disorder across cultures, although the prevalence appears to be similar
across different countries with diverse cultures.
Functional Consequences of Illness Anxiety Disorder
Illness anxiety disorder causes substantial role impairment and decrements in physical
function and health-related quality of life. Health concerns often interfere with interpersonal relationships, disrupt family life, and damage occupational performance.
Differential Diagnosis
Other medical conditions. The first differential diagnostic consideration is an underlying medical condition, including neurological or endocrine conditions, occult malignancies, and other diseases that affect multiple body systems. The presence of a medical
condition does not rule out the possibility of coexisting illness anxiety disorder. If a medical condition is present, the health-related anxiety and disease concerns are clearly disproportionate to its seriousness. Transient preoccupations related to a medical condition
do not constitute illness anxiety disorder.
Adjustment disorders. Health-related anxiety is a normal response to serious illness
and is not a mental disorder. Such nonpathological health anxiety is clearly related to the
medical condition and is typically time-limited. If the health anxiety is severe enough, an
adjustment disorder may be diagnosed. However, only when the health anxiety is of sufficient duration, severity, and distress can illness anxiety disorder be diagnosed. Thus, the
diagnosis requires the continuous persistence of disproportionate health-related anxiety
for at least 6 months.
Somatic symptom disorder. Somatic symptom disorder is diagnosed when significant
somatic symptoms are present. In contrast, individuals with illness anxiety disorder have
minimal somatic symptoms and are primarily concerned with the idea they are ill.
Anxiety disorders. In generalized anxiety disorder, individuals worry about multiple
events, situations, or activities, only one of which may involve health. In panic disorder,
the individual may be concerned that the panic attacks reflect the presence of a medical illness; however, although these individuals may have health anxiety, their anxiety is typically very acute and episodic. In illness anxiety disorder, the health anxiety and fears are
more persistent and enduring. Individuals with illness anxiety disorder may experience
panic attacks that are triggered by their illness concerns.
Obsessive-compulsive and related disorders. Individuals with illness anxiety disorder may have intrusive thoughts about having a disease and also may have associated
compulsive behaviors (e.g., seeking reassurance). However, in illness anxiety disorder, the
preoccupations are usually focused on having a disease, whereas in obsessive-compulsive
disorder (OCD), the thoughts are intrusive and are usually focused on fears of getting a
disease in the future. Most individuals with OCD have obsessions or compulsions involving other concerns in addition to fears about contracting disease. In body dysmorphic dis-
order, concerns are limited to the individual's physical appearance, which is viewed as
defective or flawed.
Major depressive disorder. Some individuals with a major depressive episode ruminate about their health and worry excessively about illness. A separate diagnosis of illness
anxiety disorder is not made if these concerns occur only during major depressive episodes. However, if excessive illness worry persists after remission of an episode of major
depressive disorder, the diagnosis of illness anxiety disorder should be considered.
Psychotic disorders. Individuals with illness anxiety disorder are not delusional and
can acknowledge the possibility that the feared disease is not present. Their ideas do not
attain the rigidity and intensity seen in the somatic delusions occurring in psychotic disorders (e.g., schizophrenia; delusional disorder, somatic type; major depressive disorder,
with psychotic features). True somatic delusions are generally more bizarre (e.g., that an
organ is rotting or dead) than the concerns seen in illness anxiety disorder. The concerns
seen in illness anxiety disorder, though not founded in reality, are plausible.
Comorbidity
Because illness anxiety disorder is a new disorder, exact comorbidities are unknown. Hypochondriasis co-occurs with anxiety disorders (in particular, generalized anxiety disorder, panic disorder, and OCD) and depressive disorders. Approximately two-thirds of
individuals with illness anxiety disorder are likely to have at least one other comorbid major mental disorder. Individuals with illness anxiety disorder may have an elevated risk
for somatic symptom disorder and personality disorders.
Conversion Disorder
(Functional Neurological Symptom Disorder)
Diagnostic Criteria
A. One or more symptoms of altered voluntary motor or sensory function.
B. Clinical findings provide evidence of incompatibility between the symptom and recognized neurological or medical conditions.
C. The symptom or deficit is not better explained by another medical or mental disorder.
D. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other important areas of functioning or warrants medical evaluation.
Coding note: The ICD-9-CM code for conversion disorder is 300.11, which is assigned
regardless of the symptom type. The ICD-10-CM code depends on the symptom type (see
below).
Specify symptom type:
(F44.4) With wealcness or paralysis
(F44.4) With abnormal movement (e.g., tremor, dystonie movement, myoclonus, gait
disorder)
(F44.4) With swallowing symptoms
(F44.4) With speech symptom (e.g., dysphonia, slurred speech)
(F44.5) With attacks or seizures
(F44.6) With anesthesia or sensory loss
(F44.6) With special sensory symptom (e.g., visual, olfactory, or hearing disturbance)
(F44.7) With mixed symptoms
Specify if:
Acute episode; Symptoms present for less than 6 months.
Persistent: Symptoms occurring for 6 months or more.
Specify if:
With psyctiological stressor (specify stressor)
Without psychoiogicai stressor
Diagnostic Features
Many clinicians use the alternative names of "functional" (referring to abnormal central
nervous system functioning) or "psychogenic" (referring to an assumed etiology) to describe the symptoms of conversion disorder (functional neurological symptom disorder). In conversion disorder, there may be one or more symptoms of various types. Motor
symptoms include weakness or paralysis; abnormal movements, such as tremor or dystonie movements; gait abnormalities; and abnormal limb posturing. Sensory symptoms
include altered, reduced, or absent skin sensation, vision, or hearing. Episodes of abnormal generalized limb shaking with apparent impaired or loss of consciousness may resemble epileptic seizures (also called psychogenic or non-epileptic seizures). There may be
episodes of unresponsiveness resembling syncope or coma. Other symptoms include reduced or absent speech volume (dysphonia/aphonia), altered articulation (dysarthria), a
sensation of a lump in the throat (globus), and diplopia.
Although the diagnosis requires that the symptom is not explained by neurological
disease, it should not be made simply because results from investigations are normal or
because the symptom is "bizarre." There must be clinical findings that show clear evidence
of incompatibility with neurological disease. Internal inconsistency at examination is one
way to demonstrate incompatibility (i.e., demonstrating that physical signs elicited
through one examination method are no longer positive when tested a different way). Examples of such examination findings include
• Hoover's sign, in which weakness of hip extension returns to normal strength with contralateral hip flexion against resistance.
• Marked weakness of ankle plantar-flexion when tested on the bed in an individual who
is able to walk on tiptoes;
• Positive findings on the tremor entrainment test. On this test, a unilateral tremor may
be identified as functional if the tremor changes when the individual is distracted away
from it. This may be observed if the individual is asked to copy the examiner in making
a rhythmical movement with their unaffected hand and this causes the functional
tremor to change such that it copies or "entrains" to the rhythm of the unaffected hand
or the functional tremor is suppressed, or no longer makes a simple rhythmical movement.
• In attacks resembling epilepsy or syncope ("psychogenic" non-epileptic attacks), the
occurrence of closed eyes with resistance to opening or a normal simultaneous electroencephalogram (although this alone does not exclude all forms of epilepsy or syncope).
• For visual symptoms, a tubular visual field (i.e., tunnel vision).
It is important to note that the diagnosis of conversion disorder should be based on the
overall clinical picture and not on a single clinical finding.
Associated Features Supporting Diagnosis
A number of associated features can support the diagnosis of conversion disorder. There
may be a history of multiple similar somatic symptoms. Onset may be associated with
stress or trauma, either psychological or physical in nature. The potential etiological rele
vance of this stress or trauma may be suggested by a close temporal relationship. However,
while assessment for stress and trauma is important, the diagnosis should not be withheld
if none is found.
Conversion disorder is often associated with dissociative symptoms, such as depersonalization, derealization, and dissociative amnesia, particularly at symptom onset or during
attacks.
The diagnosis of conversion disorder does not require the judgment that the symptoms
are not intentionally produced (i.e., not feigned), as the definite absence of feigning may
not be reliably discerned. The phenomenon of la belle indifférence (i.e., lack of concern about
the nature or implications of the symptom) has been associated with conversion disorder
but it is not specific for conversion disorder and should not be used to make the diagnosis.
Similarly the concept of secondary gain (i.e., when individuals derive external benefits such
as money or release from responsibilities) is also not specific to conversion disorder and
particularly in the context of definite evidence for feigning, the diagnoses that should be
considered instead would include factitious disorder or malingering (see the section "Differential Diagnosis" for this disorder).
Prevalence
Transient conversion symptoms are common, but the precise prevalence of the disorder is
unknown. This is partly because the diagnosis usually requires assessment in secondary
care, where it is found in approximately 5% of referrals to neurology clinics. The incidence
of individual persistent conversion symptoms is estimated to be 2-5/100,000 per year.
Development and Course
Onset has been reported throughout the life course. The onset of non-epileptic attacks
peaks in the third decade, and motor symptoms have their peak onset in the fourth decade.
The symptoms can be transient or persistent. The prognosis may be better in younger children than in adolescents and adults.
Risk and Prognostic Factors
Temperamental. Maladaptive personality traits are commonly associated with conversion disorder.
Environmental. There may be a history of childhood abuse and neglect. Stressful life
events are often, but not always, present.
Genetic and physiological. The presence of neurological disease that causes similar symptoms is a risk factor (e.g., non-epileptic seizures are more common in patients who also
have epilepsy).
Course modifiers. Short duration of symptoms and acceptance of the diagnosis are positive prognostic factors. Maladaptive personality traits, the presence of comorbid physical
disease, and the receipt of disability benefits may be negative prognostic factors.
Culture-Related Diagnostic Issues
Changes resembling conversion (and dissociative) symptoms are common in certain
culturally sanctioned rituals. If the symptoms are fully explained within the particular
cultural context and do not result in clinically significant distress or disability, then the diagnosis of conversion disorder is not made.
Gender-Related Diagnostic Issues
Conversion disorder is two to three times more common in females.
Functional Consequences of Conversion Disorder
Individuals with conversion symptoms may have substantial disability. The severity of disability can be similar to that experienced by individuals with comparable medical diseases.
Differential Diagnosis
If another mental disorder better explains the symptoms, that diagnosis should be made.
However the diagnosis of conversion disorder may be made in the presence of another
mental disorder.
Neurological disease. The main differential diagnosis is neurological disease that might
better explain the symptoms. After a thorough neurological assessment, an unexpected
neurological disease cause for the symptoms is rarely found at follow up. However, reassessment may be required if the symptoms appear to be progressive. Conversion disorder
may coexist with neurological disease.
Somatic symptom disorder. Conversion disorder may be diagnosed in addition to somatic symptom disorder. Most of the somatic symptoms encountered in somatic symptom
disorder cannot be demonstrated to be clearly incompatible with pathophysiology (e.g.,
pain, fatigue), whereas in conversion disorder, such incompatibility is required for the diagnosis. The excessive thoughts, feelings, and behaviors characterizing somatic symptom
disorder are often absent in conversion disorder.
Factitious disorder and malingering. The diagnosis of conversion disorder does not require the judgment that the symptoms are not intentionally produced (i.e., not feigned),
because assessment of conscious intention is unreliable. However definite evidence of
feigning (e.g., clear evidence that loss of function is present during the examination but not
at home) would suggest a diagnosis of factitious disorder if the individual's apparent aim
is to assume the sick role or malingering if the aim is to obtain an incentive such as money.
Dissociative disorders. Dissociative symptoms are common in individuals with conversion disorder. If both conversion disorder and a dissociative disorder are present, both
diagnoses should be made.
Body dysmorphic disorder. Individuals with body dysmorphic disorder are excessively concerned about a perceived defect in their physical features but do not complain of
symptoms of sensory or motor functioning in the affected body part.
Depressive disorders. In depressive disorders, individuals may report general heaviness of their limbs, whereas the weakness of conversion disorder is more focal and prominent. Depressive disorders are also differentiated by the presence of core depressive
symptoms.
Panic disorder. Episodic neurological symptoms (e.g., tremors and paresthesias) can
occur in both conversion disorder and panic attacks. In panic attacks, the neurological
symptoms are typically transient and acutely episodic with characteristic cardiorespiratory symptoms. Loss of awareness with amnesia for the attack and violent limb movements occur in non-epileptic attacks, but not in panic attacks.
Comorbidity
Anxiety disorders, especially panic disorder, and depressive disorders commonly co-occur
with conversion disorder. Somatic symptom disorder may co-occur as well. Psychosis, substance use disorder, and alcohol misuse are uncommon. Personality disorders are more
common in individuals with conversion disorder than in the general population. Neurological or other medical conditions commonly coexist with conversion disorder as well.
Psychological Factors Affecting
Other Medical Conditions
Diagnostic Criteria 316 (F54)
A. A medical symptom or condition (other than a mental disorder) is present.
B. Psychological or behavioral factors adversely affect the medical condition in one of the
following ways:
1. The factors have influenced the course of the medical condition as shown by a
close temporal association between the psychological factors and the development
or exacerbation of, or delayed recovery from, the medical condition.
2. The factors interfere with the treatment of the medical condition (e.g., poor adherence).
3. The factors constitute additional well-established health risks for the individual.
4. The factors influence the underlying pathophysiology, precipitating or exacerbating
symptoms or necessitating medical attention.
C. The psychological and behavioral factors in Criterion B are not better explained by another mental disorder (e.g., panic disorder, major depressive disorder, posttraumatic
stress disorder).
Specify current severity:
Mild: Increases medical risk (e.g., inconsistent adherence with antihypertension treatment).
Moderate: Aggravates underlying medical condition (e.g., anxiety aggravating
asthma).
Severe: Results in medical hospitalization or emergency room visit.
Extreme: Results in severe, life-threatening risk (e.g., ignoring heart attack symptoms).
Diagnostic Features
The essential feature of psychological factors affecting other medical conditions is the
presence of one or more clinically significant psychological or behavioral factors that adversely affect a medical condition by increasing the risk for suffering, death, or disability
(Criterion B). These factors can adversely affect the medical condition by influencing its
course or treatment, by constituting an additional well-established health risk factor, or by
influencing the underlying pathophysiology to precipitate or exacerbate symptoms or to
necessitate medical attention.
Psychological or behavioral factors include psychological distress, patterns of interpersonal interaction, coping styles, and maladaptive health behaviors, such as denial of symptoms or poor adherence to medical recommendations. Common clinical examples are
anxiety-exacerbating asthma, denial of need for treatment for acute chest pain, and manipulation of insulin by an individual v^ith diabetes wishing to lose weight. Many different
psychological factors have been demonstrated to adversely influence medical conditions—
for example, symptoms of depression or anxiety, stressful life events, relationship style,
personality traits, and coping styles. The adverse effects can range from acute, with immediate medical consequences (e.g., Takotsubo cardiomyopathy) to chronic, occurring over a
long period of time (e.g., chronic occupational stress increasing risk for hypertension). Affected medical conditions can be those with clear pathophysiology (e.g., diabetes, cancer,
coronary disease), functional syndromes (e.g., migraine, irritable bowel syndrome, fibromyalgia), or idiopathic medical symptoms (e.g., pain, fatigue, dizziness).
This diagnosis should be reserved for situations in which the effect of the psychological
factor on the medical condition is evident and the psychological factor has clinically significant effects on the course or outcome of the medical condition. Abnormal psychological or behavioral symptoms that develop in response to a medical condition are more
properly coded as an adjustment disorder (a clinically significant psychological response
to an identifiable stressor). There must be reasonable evidence to suggest an association
between the psychological factors and the medical condition, although it may often not be
possible to demonstrate direct causality or the mechanisms underlying the relationship.
Prevalence
The prevalence of psychological factors affecting other medical conditions is unclear. In
U.S. private insurance billing data, it is a more common diagnosis than somatic symptom
disorders.
Development and Course
Psychological factors affecting other medical conditions can occur across the lifespan. Particularly with young children, corroborative history from parents or school can assist the diagnostic evaluation. Some conditions are characteristic of particular life stages (e.g., in older
individuals, the stress associated with acting as a caregiver for an ill spouse or partner).
Culture-Related Diagnostic issues
Many differences between cultures may influence psychological factors and their effects
on medical conditions, such as those in language and communication style, explanatory
models of illness, patterns of seeking health care, service availability and organization,
doctor-patient relationships and other healing practices, family and gender roles, and attitudes toward pain and death. Psychological factors affecting other medical conditions
must be differentiated from culturally specific behaviors such as using faith or spiritual
healers or other variations in illness management that are acceptable within a culture and
represent an attempt to help the medical condition rather than interfere with it. These local
practices may complement rather than obstruct evidence-based interventions. If they do
not adversely affect outcomes, they should not be pathologized as psychological factors
affecting other medical conditions.
Functional Consequences of Psychological Factors
Affecting Other Medical Conditions
Psychological and behavioral factors have been demonstrated to affect the course of many
medical diseases.
Differential Diagnosis
Mental disorder due to another medical condition. A temporal association between
symptoms of a mental disorder and those of a medical condition is also characteristic of a
mental disorder due to another medical condition, but the presumed causality is in the opposite direction. In a mental disorder due to another medical condition, the medical
condition is judged to be causing the mental disorder through a direct physiological mechanism. In psychological factors affecting other medical conditions, the psychological or behavioral factors are judged to affect the course of the medical condition.
Adjustment disorders. Abnormal psychological or behavioral symptoms that develop in
response to a medical condition are more properly coded as an adjustment disorder (a clinically significant psychological response to an identifiable stressor). For example, an indi
vidual with angina that is precipitated whenever he becomes enraged would be diagnosed
as having psychological factors affecting other medical conditions, whereas an individual
with angina who developed maladaptive anticipatory anxiety would be diagnosed as having an adjustment disorder with anxiety. In clinical practice, however, psychological factors and a medical condition are often mutually exacerbating (e.g., anxiety as both a
precipitant and a consequence of angina), in which case the distinction is arbitrary. Other
mental disorders frequently result in medical complications, most notably substance use
disorders (e.g., alcohol use disorder, tobacco use disorder). If an individual has a coexisting
major mental disorder that adversely affects or causes another medical condition, diagnoses of the mental disorder and the medical condition are usually sufficient. Psychological
factors affecting other medical conditions is diagnosed when the psychological traits or
behaviors do not meet criteria for a mental diagnosis.
Somatic symptom disorder. Somatic symptom disorder is characterized by a combination of distressing somatic symptoms and excessive or maladaptive thoughts, feelings,
and behavior in response to these symptoms or associated health concerns. The individual
may or may not have a diagnosable medical condition. In contrast, in psychological factors
affecting other medical conditions, the psychological factors adversely affect a medical
condition; the individual's thoughts, feelings, and behavior are not necessarily excessive.
The difference is one of emphasis, rather than a clear-cut distinction. In psychological factors affecting other medical conditions, the emphasis is on the exacerbation of the medical
condition (e.g., an individual with angina that is precipitated whenever he becomes anxious). In somatic symptom disorder, the emphasis is on maladaptive thoughts, feelings,
and behavior (e.g., an individual with angina who worries constantly that she will have a
heart attack, takes her blood pressure multiple times per day, and restricts her activities).
Illness anxiety disorder. Illness anxiety disorder is characterized by high illness anxiety
that is distressing and/or disruptive to daily life with minimal somatic symptoms. The focus of clinical concern is the individual's worry about having a disease; in most cases, no
serious disease is present. In psychological factors affecting other medical conditions, anxiety may be a relevant psychological factor affecting a medical condition, but the clinical
concern is the adverse effects on the medical condition.
Comorbidity
By definition, the diagnosis of psychological factors affecting other medical conditions entails
a relevant psychological or behavioral syndrome or trait and a comorbid medical condition.
Factitious Disorder
Diagnostic Criteria 300.19 (F68.10)
Factitious Disorder Imposed on Self
A. Falsification of physical or psychological signs or symptoms, or induction of injury or
disease, associated with identified deception.
B. The individual presents himself or herself to others as ill, impaired, or injured.
C. The deceptive behavior is evident even in the absence of obvious external rewards.
D. The behavior is not better explained by another mental disorder, such as delusional
disorder or another psychotic disorder.
Specify:
Single episode
Recurrent episodes (two or more events of falsification of illness and/or induction of
injury)
Factitious Disorder Imposed on Another
(Previously Factitious Disorder by Proxy)
A. Falsification of physical or psychological signs or symptoms, or induction of injury or
disease, in another, associated with identified deception.
B. The individual presents another individual (victim) to others as ill, impaired, or injured.
C. The deceptive behavior is evident even in the absence of obvious external rewards.
D. The behavior is not better explained by another mental disorder, such as delusional
disorder or another psychotic disorder.
Note: The perpetrator, not the victim, receives this diagnosis.
Specify.
Single episode
Recurrent episodes (two or more events of falsification of illness and/or induction of
injury)
Recording Procedures
When an individual falsifies illness in another (e.g., children, adults, pets), the diagnosis is
factitious disorder imposed on another. The perpetrator, not the victim, is given the diagnosis. The victim may be given an abuse diagnosis (e.g., 995.54 [T74.12X]; see the chapter
'Other Conditions That May Be a Focus of Clinical Attention").
Diagnostic Features
The essential feature of factitious disorder is the falsification of medical or psychological signs
and symptoms in oneself or others that are associated with the identified deception. Individuals with factitious disorder can also seek treatment for themselves or another following
induction of injury or disease. The diagnosis requires demonstrating that the individual is
taking surreptitious actions to misrepresent, simulate, or cause signs or symptoms of illness or injury in the absence of obvious external rewards. Methods of illness falsification
can include exaggeration, fabrication, simulation, and induction. While a preexisting medical condition may be present, the deceptive behavior or induction of injury associated
with deception causes others to view such individuals (or another) as more ill or impaired,
and this can lead to excessive clinical intervention. Individuals with factitious disorder
might, for example, report feelings of depression and suicidality following the death of a
spouse despite the death not being true or the individual's not having a spouse; deceptively report episodes of neurological symptoms (e.g., seizures, dizziness, or blacking out);
manipulate a laboratory test (e.g., by adding blood to urine) to falsely indicate an abnormality; falsify medical records to indicate an illness; ingest a substance (e.g., insulin or
warfarin) to induce an abnormal laboratory result or illness; or physically injure themselves or induce illness in themselves or anotiier (e.g., by injecting fecal material to produce
an abscess or to induce sepsis).
Associated Features Supporting Diagnosis
Individuals with factitious disorder imposed on self or factitious disorder imposed on another are at risk for experiencing great psychological distress or functional impairment by
causing harm to themselves and others. Family, friends, and health care professionals are
also often adversely affected by their behavior. Factitious disorders have similarities to
substance use disorders, eating disorders, impulse-control disorders, pedophilic disorder,
and some other established disorders related to both the persistence of the behavior and
the intentional efforts to conceal the disordered behavior through deception. Whereas
some aspects of factitious disorders might represent criminal behavior (e.g., factitious dis-
order imposed on another, in which the parent's actions represent abuse and maltreatment of a child), such criminal behavior and mental illness are not mutually exclusive. The
diagnosis of factitious disorder emphasizes the objective identification of falsification of
signs and symptoms of illness, rather than an inference about intent or possible underlying motivation. Moreover, such behaviors, including the induction of injury or disease, are
associated with deception.
Prevalence
The prevalence of factitious disorder is unknown, likely because of the role of deception in
this population. Among patients in hospital settings, it is estimated that about 1% of individuals have presentations that meet the criteria for factitious disorder.
Development and Course
The course of factitious disorder is usually one of intermittent episodes. Single episodes
and episodes that are characterized as persistent and unremitting are both less common.
Onset is usually in early adulthood, often after hospitalization for a medical condition or a
mental disorder. When imposed on another, the disorder may begin after hospitalization
of the individual's child or other dependent. In individuals with recurrent episodes of falsification of signs and symptoms of illness and/or induction of injury, this pattern of successive deceptive contact with medical personnel, including hospitalizations, may become
lifelong.
Differential Diagnosis
Caregivers who lie about abuse injuries in dependents solely to protect themselves from liability are not diagnosed with factitious disorder imposed on anotiier because protection from
liability is an external reward (Criterion C, the deceptive behavior is evident even in the absence of obvious external rewards). Such caregivers who, upon observation, analysis of medical records, and/or interviews with others, are found to lie more extensively than needed for
immediate self-protection are diagnosed with factitious disorder imposed on another.
Somatic symptom disorder. In somatic symptom disorder, there may be excessive attention and treatment seeking for perceived medical concerns, but there is no evidence that
the individual is providing false information or behaving deceptively.
Malingering. Malingering is differentiated from factitious disorder by the intentional reporting of symptoms for personal gain (e.g., money, time off work). In contrast, the diagnosis of factitious disorder requires the absence of obvious rewards.
Conversion disorder (functional neurological symptom disorder). Conversion disorder
is characterized by neurological symptoms that are inconsistent with neurological pathophysiology. Factitious disorder with neurological symptoms is distinguished from conversion disorder by evidence of deceptive falsification of symptoms.
Borderiine personality disorder. Deliberate physical self-harm in the absence of suicidal
intent can also occur in association with other mental disorders such as borderline personality disorder. Factitious disorder requires that the induction of injury occur in association
with deception.
Medical condition or mental disorder not associated with intentional symptom falsification. Presentation of signs and symptoms of illness that do not conform to an identifiable medical condition or mental disorder increases the likelihood of the presence of a
factitious disorder. However, the diagnosis of factitious disorder does not exclude the
presence of true medical condition or mental disorder, as comorbid illness often occurs in
the individual along with factitious disorder. For example, individuals who might manipulate blood sugar levels to produce symptoms may also have diabetes.
Other Specified Somatic Symptom and
Related Disorder
300.89 (F45.8)
This category applies to presentations in which symptoms characteristic of a somatic
symptom and related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the
full criteria for any of the disorders in the somatic symptom and related disorders diagnostic class.
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Brief somatic symptom disorder: Duration of symptoms is less than 6 months.
2. Brief illness anxiety disorder: Duration of symptoms is less than 6 months.
3. Illness anxiety disorder without excessive health-related behaviors: Criterion D
for illness anxiety disorder is not met.
4. Pseudocyesis: A false belief of being pregnant that is associated with objective signs
and reported symptoms of pregnancy.
Unspecified Somatic Symptom and
Related Disorder
300.82 (F45.9)
This category applies to presentations in which symptoms characteristic of a somatic
symptom and related disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the
full criteria for any of the disorders in the somatic symptom and related disorders diagnostic class. The unspecified somatic symptom and related disorder category should not be
used unless there are decidedly unusual situations where there is insufficient information
to make a more specific diagnosis.
pGGdiriQ ând GSting disorders are characterized by a persistent disturbance of eating or eating-related behavior that results in the altered consumption or absorption of
food and that significantly impairs physical health or psychosocial functioning. Diagnostic criteria are provided for pica, rumination disorder, avoidant/restrictive food intake
disorder, anorexia nervosa, bulimia nervosa, and binge-eating disorder.
The diagnostic criteria for rumination disorder, avoidant/restrictive food intake disorder, anorexia nervosa, bulimia nervosa, and binge-eating disorder result in a classification scheme that is mutually exclusive, so that during a single episode, only one of these
diagnoses can be assigned. The rationale for this approach is that, despite a number of
common psychological and behavioral features, the disorders differ substantially in clinical course, outcome, and treatment needs. A diagnosis of pica, however, may be assigned
in the presence of any other feeding and eating disorder.
Some individuals with disorders described in this chapter report eating-related symptoms resembling those typically endorsed by individuals with substance use disorders,
such as craving and patterns of compulsive use. This resemblance may reflect the involvement of the same neural systems, including those implicated in regulatory self-control and
reward, in both groups of disorders. However, the relative contributions of shared and
distinct factors in the development and perpetuation of eating and substance use disorders remain insufficiently understood.
Finally, obesity is not included in DSM-5 as a mental disorder. Obesity (excess body fat)
results from the long-term excess of energy intake relative to energy expenditure. A range
of genetic, physiological, behavioral, and environmental factors that vary across individuals contributes to the development of obesity; thus, obesity is not considered a mental
disorder. However, there are robust associations between obesity and a number of mental
disorders (e.g., binge-eating disorder, depressive and bipolar disorders, schizophrenia).
The side effects of some psychotropic medications contribute importantly to the development of obesity, and obesity may be a risk factor for the development of some mental disorders (e.g., depressive disorders).
Pica
Diagnostic Criteria
A. Persistent eating of nonnutritive, nonfood substances over a period of at least 1 month.
B. The eating of nonnutritive, nonfood substances is inappropriate to the developmental
level of the individual.
C. The eating behavior is not part of a culturally supported or socially normative practice.
D. If the eating behavior occurs in the context of another mental disorder (e.g., intellectual
disability [intellectual developmental disorder], autism spectrum disorder, schizophrenia) or medical condition (including pregnancy), it is sufficiently severe to warrant additional clinical attention.
Coding note: The ICD-9-CIVI code for pica is 307.52 and is used for children or adults.
The ICD-10-CM codes for pica are (F98.3) in children and (F50.8) in adults.
Specify if:
In remission: After full criteria for pica were previously met, the criteria have not been
met for a sustained period of time.________________________________________
Diagnostic Features
The essential feature of pica is the eating of one or more nonnutritive, nonfood substances on a
persistent basis over a period of at least 1 month (Criterion A) that is severe enough to warrant
clinical attention. Typical substances ingested tend to vary with age and availability and might
include paper, soap, cloth, hair, string, wool, soil, chalk, talcum powder, paint, gum, metal,
pebbles, charcoal or coal, ash, clay, starch, or ice. The term nonfood is included because the diagnosis of pica does not apply to ingestion of diet products that have minimal nutritional content. There is typically no aversion to food in general. The eating of nonnutritive, nonfood
substances must be developmentally inappropriate (Criterion B) and not part of a culturally
supported or socially normative practice (Criterion C). A minimum age of 2 years is suggested
for a pica diagnosis to exclude developmentally normal mouthing of objects by infants that results in ingestion. The eating of nonnutritive, nonfood substances can be an associated feature
of other mental disorders (e.g., intellectual disability [intellectual developmental disorder],
autism spectrum disorder, schizophrenia). If the eating behavior occurs exclusively in the context of another mental disorder, a separate diagnosis of pica should be made only if the eating
behavior is sufficientiy severe to warrant additional clinical attention (Criterion D).
Associated Features Supporting Diagnosis
Although deficiencies in vitamins or minerals (e.g., zinc, iron) have been reported in some
instances, often no specific biological abnormalities are found. In some cases, pica comes
to clinical attention only following general medical complications (e.g., mechanical bowel
problems; intestinal obstruction, such as that resulting from a bezoar; intestinal perforation; infections such as toxoplasmosis and toxocariasis as a result of ingesting feces or dirt;
poisoning, such as by ingestion of lead-based paint).
Prevaience
The prevalence of pica is unclear. Among individuals with intellectual disability, the prevalence of pica appears to increase with the severity of the condition,
Deveiopment and Course
Onset of pica can occur in childhood, adolescence, or adulthood, although childhood onset
is most commonly reported. Pica can occur in otherwise normally developing children,
whereas in adults, it appears more likely to occur in the context of intellectual disability or
other mental disorders. The eating of nonnutritive, nonfood substances may also manifest
in pregnancy, when specific cravings (e.g., chalk or ice) might occur. The diagnosis of pica
during pregnancy is only appropriate if such cravings lead to the ingestion of nonnutritive, nonfood substances to the extent that the eating of these substances poses potential
medical risks. The course of the disorder can be protracted and can result in medical emergencies (e.g., intestinal obstruction, acute weight loss, poisoning). The disorder can potentially be fatal depending on substances ingested.
Risic and Prognostic Factors
Environmental. Neglect, lack of supervision, and developmental delay can increase the
risk for this condition.
Culture-Related Diagnostic Issues
In some populations, the eating of earth or other seemingly nonnutritive substances is believed
to be of spiritual, medicinal, or other social value, or may be a culturally supported or socially
normative practice. Such behavior does not warrant a diagnosis of pica (Criterion C).
Gender-Related Diagnostic Issues
Pica occurs in both males and females. It can occur in females during pregnancy; however,
little is known about the course of pica in the postpartum period.
Diagnostic Markers
Abdominal flat plate radiography, ultrasound, and other scanning methods may reveal
obstructions related to pica. Blood tests and other laboratory tests can be used to ascertain
levels of poisoning or the nature of infection.
Functional Consequences of Pica
Pica can significantly impair physical functioning, but it is rarely the sole cause of impairment in social functioning. Pica often occurs with other disorders associated with impaired social functioning.
Differential Diagnosis
Eating of nonnutritive, nonfood substances may occur during the course of other mental
disorders (e.g., autism spectrum disorder, schizophrenia) and in Kleine-Levin syndrome.
In any such instance, an additional diagnosis of pica should be given only if the eating behavior is sufficiently persistent and severe to warrant additional clinical attention.
Anorexia nervosa. Pica can usually be distinguished from the other feeding and eating
disorders by the consumption of nonnutritive, nonfood substances. It is important to note,
however, that some presentations of anorexia nervosa include ingestion of nonnutritive,
nonfood substances, such as paper tissues, as a means of attempting to control appetite. In
such cases, when the eating of nonnutritive, nonfood substances is primarily used as a
means of weight control, anorexia nervosa should be the primary diagnosis.
Factitious disorder. Some individuals with factitious disorder may intentionally ingest
foreign objects as part of the pattern of falsification of physical symptoms. In such instances, there is an element of deception that is consistent with deliberate induction of injury or disease.
Nonsuicidal self-injury and nonsuicidal self-injury behaviors in personality disorders.
Some individuals may swallow potentially harmful items (e.g., pins, needles, knives) in
the context of maladaptive behavior patterns associated with personality disorders or
nonsuicidal self-injury.
Comorbidity
Disorders most commonly comorbid with pica are autism spectrum disorder and intellectual disability (intellectual developmental disorder), and, to a lesser degree, schizophrenia
and obsessive-compulsive disorder. Pica can be associated with trichotillomania (hairpulling disorder) and excoriation (skin-picking) disorder. In comorbid presentations, the
hair or skin is typically ingested. Pica can also be associated with avoidant/restrictive food
intake disorder, particularly in individuals with a strong sensory component to their presentation. When an individual is known to have pica, assessment should include consideration of the possibility of gastrointestinal complications, poisoning, infection, and
nutritional deficiency.
Rumination Disorder
Diagnostic Criteria 307.53 (F98.21)
A. Repeated regurgitation of food over a period of at least 1 month. Regurgitated food
may be re-chewed, re-swallowed, or spit out.
B. The repeated regurgitation is not attributable to an associated gastrointestinal or other
medical condition (e.g., gastroesophageal reflux, pyloric stenosis).
C. The eating disturbance does not occur exclusively during the course of anorexia nervosa,
bulimia nervosa, binge-eating disorder, or avoidant/restrictive food intal<e disorder.
D. If the symptoms occur in the context of another mental disorder (e.g., intellectual disability [Intellectual developmental disorder] or another neurodevelopmental disorder),
they are sufficiently severe to warrant additional clinical attention.
Specify if:
In remission: After full criteria for rumination disorder were previously met, the criteria
have not been met for a sustained period of time.
Diagnostic Features
The essential feature of rumination disorder is the repeated regurgitation of food occurring after feeding or eating over a period of at least 1 month (Criterion A). Previously swallowed food that may be partially digested is brought up into the mouth without apparent
nausea, involuntary retching, or disgust. The food may be re-chewed and then ejected
from the mouth or re-swallowed. Regurgitation in rumination disorder should be frequent, occurring at least several times per week, typically daily. The behavior is not better
explained by an associated gastrointestinal or other medical condition (e.g., gastroesophageal reflux, pyloric stenosis) (Criterion B) and does not occur exclusively during the
course of anorexia nervosa, bulimia nervosa, binge-eating disorder, or avoidant/restrictive food intake disorder (Criterion C). If the symptoms occur in the context of another
mental disorder (e.g., intellectual disability [intellectual developmental disorder], neurodevelopmental disorder), they must be sufficiently severe to warrant additional clinical
attention (Criterion D) and should represent a primary aspect of the individual's presentation requiring intervention. The disorder may be diagnosed across the life span, particularly in individuals who also have intellectual disability. Many individuals with
rumination disorder can be directly observed engaging in the behavior by the clinician. In
other instances diagnosis can be made on the basis of self-report or corroborative information from parents or caregivers. Individuals may describe the behavior as habitual or outside of their control.
Associated Features Supporting Diagnosis
Infants with rumination disorder display a characteristic position of straining and arching
the back with the head held back, making sucking movements with their tongue. They
may give the impression of gaining satisfaction from the activity. They may be irritable
and hungry between episodes of regurgitation. Weight loss and failure to make expected
weight gains are common features in infants with rumination disorder. Malnutrition may
occur despite the infant's apparent hunger and the ingestion of relatively large amounts of
food, particularly in severe cases, when regurgitation immediately follows each feeding
episode and regurgitated food is expelled. Malnutrition might also occur in older children
and adults, particularly when the regurgitation is accompanied by restriction of intake.
Adolescents and adults may attempt to disguise the regurgitation behavior by placing a
hand over the mouth or coughing. Some will avoid eating with others because of the acknowledged soqal undesirability of the behavior. This may extend to an avoidance of eating prior to social situations, such as work or school (e.g., avoiding breakfast because it
may be followed by regurgitation).
Prevalence
Prevalence data for rumination disorder are inconclusive, but the disorder is commonly
reported to be higher in certain groups, such as individuals with intellectual disability.
Development and Course
Onset of rumination disorder can occur in infancy, childhood, adolescence, or adulthood.
The age at onset in infants is usually between ages 3 and 12 months. In infants, the disorder
frequently remits spontaneously, but its course can be protracted and can result in medical
emergencies (e.g., severe malnutrition). It can potentially be fatal, particularly in infancy.
Rumination disorder can have an episodic course or occur continuously until treated. In
infants, as well as in older individuals with intellectual disability (intellectual developmental disorder) or other neurodevelopmental disorders, the regurgitation and rumination behavior appears to have a self-soothing or self-stimulating function, similar to that of other
repetitive motor behaviors such as head banging.
Risk and Prognostic Factors
Environmental. Psychosocial problems such as lack of stimulation, neglect, stressful life
situations, and problems in the parent-child relationship may be predisposing factors in
infants and young children.
Functional Consequences of Rumination Disorder
Malnutrition secondary to repeated regurgitation may be associated with growth delay
and have a negative effect on development and learning potential. Some older individuals
with rumination disorder deliberately restrict their food intake because of the social undesirability of regurgitation. They may therefore present with weight loss or low weight.
In older children, adolescents, and adults, social functioning is more likely to be adversely
affected.
Differential Diagnosis
Gastrointestinal conditions. It is important to differentiate regurgitation in rumination
disorder from other conditions characterized by gastroesophageal reflux or vomiting. Conditions such as gastroparesis, pyloric stenosis, hiatal hernia, and Sandifer syndrome in infants should be ruled out by appropriate physical examinations and laboratory tests.
Anorexia nervosa and bulimia nervosa. Individuals with anorexia nervosa and bulimia
nervosa may also engage in regurgitation with subsequent spitting out of food as a means
of disposing of ingested calories because of concerns about weight gain.
Comorbidity
Regurgitation with associated rumination can occur in the context of a concurrent medical
condition or another mental disorder (e.g., generalized anxiety disorder). When the regurgitation occurs in this context, a diagnosis of rumination disorder is appropriate only when
the severity of the disturbance exceeds that routinely associated with such conditions or
disorders and warrants additional clinical attention.
Avoidant/Restrictive Food Intake Disorder
Diagnostic Criteria 307.59 (F50.8)
A. An eating or feeding disturbance (e.g., apparent lack of interest in eating or food; avoidance based on tlie sensory ciiaracteristics of food; concern about aversive consequences of eating) as manifested by persistent failure to meet appropriate nutritional
and/or energy needs associated with one (or more) of the following:
1. Significant weight loss (or failure to achieve expected weight gain or faltering
growth in children).
2. Significant nutritional deficiency.
3. Dependence on enteral feeding or oral nutritional supplements.
4. Marked interference with psychosocial functioning.
B. The disturbance is not better explained by lack of available food or by an associated
culturally sanctioned practice.
C. The eating disturbance does not occur exclusively during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which
one’s body weight or shape is experienced.
D. The eating disturbance is not attributable to a concurrent medical condition or not better explained by another mental disorder. When the eating disturbance occurs in the
context of another condition or disorder, the severity of the eating disturbance exceeds
that routinely associated with the condition or disorder and warrants additional clinical
attention.
Specify if:
In remission: After full criteria for avoidant/restrictive food intake disorder were previously met, the criteria have not been met for a sustained period of time.
Diagnostic Features
Avoidant/restrictive food intake disorder replaces and extends the DSM-IV diagnosis of
feeding disorder of infancy or early childhood. The main diagnostic feature of avoidant/
restrictive food intake disorder is avoidance or restriction of food intake (Criterion A)
manifested by clinically significant failure to meet requirements for nutrition or insufficient energy intake through oral intake of food. One or more of the following key features
must be present: significant weight loss, significant nutritional deficiency (or related
health impact), dependence on enteral feeding or oral nutritional supplements, or marked
interference with psychosocial functioning. The determination of whether weight loss is
significant (Criterion Al) is a clinical judgment; instead of losing weight, children and adolescents who have not completed growth may not maintain weight or height increases
along their developmental trajectory.
Determination of significant nutritional deficiency (Criterion A2) is also based on clinical assessment (e.g., assessment of dietary intake, physical examination, and laboratory
testing), and related impact on physical health can be of a similar severity to that seen in
anorexia nervosa (e.g., hypothermia, bradycardia, anemia). In severe cases, particularly in
infants, malnutrition can be life threatening. "Dependence" on enteral feeding or oral nutritional supplements (Criterion A3) means that supplementary feeding is required to sustain adequate intake. Examples of individuals requiring supplementary feeding include
infants with failure to thrive who require nasogastric tube feeding, children with neurodevelopmental disorders who are dependent on nutritionally complete supplements, and
individuals who rely on gastrostomy tube feeding or complete oral nutrition supplements
in the absence of an underlying medical condition. Inability to participate in normal social
activities, such as eating with others, or to sustain relationships as a result of the disturbance would inculcate marked interference with psychosocial functioning (Criterion A4).
Avoidant/restrictive food intake disorder does not include avoidance or restriction of
food intake related to lack of availability of food or to cultural practices (e.g., religious fasting or normal dieting) (Criterion B), nor does it include developmentally normal behaviors
(e.g., picky eating in toddlers, reduced intake in older adults). The disturbance is not better
explained by excessive concern about body weight or shape (Criterion C) or by concurrent
medical factors or mental disorders (Criterion D).
In some individuals, food avoidance or restriction may be based on the sensory characteristics of qualities of food, such as extreme sensitivity to appearance, color, smell,
texture, temperature, or taste. Such behavior has been described as "restrictive eating,"
"selective eating," "choosy eating," "perseverant eating," "chronic food refusal," and
"food neophobia" and may manifest as refusal to eat particular brands of foods or to tolerate the smell of food being eaten by others. Individuals with heightened sensory sensitivities associated with autism may show similar behaviors.
Food avoidance or restriction may also represent a conditioned negative response associated with food intake following, or in anticipation of, an aversive experience, such as
choking; a traumatic investigation, usually involving the gastrointestinal tract (e.g., esophagoscopy); or repeated vomiting. The terms frinctional dysphagia and globus hystericus have
also been used for such conditions.
Associated Features Supporting Diagnosis
Several features may be associated with food avoidance or reduced food intake, including
a lack of interest in eating or food, leading to weight loss or faltering growth. Very young
infants may present as being too sleepy, distressed, or agitated to feed. Infants and young
children may not engage with the primary caregiver during feeding or communicate hunger in favor of other activities. In older children and adolescents, food avoidance or restriction may be associated with more generalized emotional difficulties that do not meet
diagnostic criteria for an anxiety, depressive, or bipolar disorder, sometimes called "food
avoidance emotional disorder."
Deveiopment and Course
Food avoidance or restriction associated with insufficient intake or lack of interest in eating most commonly develops in infancy or early childhood and may persist in adulthood.
Likewise, avoidance based on sensory characteristics of food tends to arise in the first decade of life but may persist into adulthood. Avoidance related to aversive consequences
can arise at any age. The scant literature regarding long-term outcomes suggests that food
avoidance or restriction based on sensory aspects is relatively stable and long-standing,
but when persisting into adulthood, such avoidance/restriction can be associated with relatively normal functioning. There is currently insufficient evidence directly linking avoidant/restrictive food intake disorder and subsequent onset of an eating disorder.
Infants with avoidant/restrictive food intake disorder may be irritable and difficult to
console during feeding, or may appear apathetic and withdrawn. In some instances, parent-child interaction may contribute to the infant's feeding problem (e.g., presenting food
inappropriately, or interpreting the infant's behavior as an act of aggression or rejection).
Inadequate nutritional intake may exacerbate the associated features (e.g., irritability, developmental lags) and further contribute to feeding difficulties. Associated factors include
infant temperament or developmental impairments that reduce an infant's responsiveness
to feeding. Coexisting parental psychopathology, or child abuse or neglect, is suggested if
feeding and weight improve in response to changing caregivers. In infants, children, and
prepubertal adolescents, avoidant/restrictive food intake disorder may be associated with
growth delay, and the resulting malnutrition negatively affects development and learning
potential. In older children, adolescents, and adults, social functioning tends to be adversely affected. Regardless of the age, family function may be affected, with heightened
stress at mealtimes and in other feeding or eating contexts involving friends and relatives.
Avoidant/restrictive food intake disorder manifests more commonly in children than
in adults, and there may be a long delay between onset and clinical presentation. Triggers
for presentation vary considerably and include physical, social, and emotional difficulties.
Risk and Prognostic Factors
Temperamental. Anxiety disorders, autism spectrum disorder, obsessive-compulsive
disorder, and attention-deficit/hyperactivity disorder may increase risk for avoidant or
restrictive feeding or eating behavior characteristic of the disorder.
Environmental. Environmental risk factors for avoidant/restrictive food intake disorder include familial anxiety. Higher rates of feeding disturbances may occur in children of
mothers with eating disorders.
Genetic and physiological. History of gastrointestinal conditions, gastroesophageal reflux disease, vomiting, and a range of other medical problems has been associated with
feeding and eating behaviors characteristic of avoidant/restrictive food intake disorder.
Culture-Reiated Diagnostic issues
Presentations similar to avoidant/restrictive food intake disorder occur in various populations, including in the United States, Canada, Australia, and Europe. Avoidant/restrictive
food intake disorder should not be diagnosed when avoidance of food intake is solely related to specific religious or cultural practices.
Gender-Reiated Diagnostic issues
Avoidant/restrictive food intake disorder is equally common in males and females in infancy and early childhood, but avoidant/restrictive food intake disorder comorbid with
autism spectrum disorder has a male predominance. Food avoidance or restriction related
to altered sensory sensitivities can occur in some physiological conditions, most notably
pregnancy, but is not usually extreme and does not meet full criteria for the disorder.
Diagnostic iViaricers
Diagnostic markers include malnutrition, low weight, growth delay, and the need for artificial nutrition in the absence of any clear medical condition other than poor intake.
Functionai Consequences of Avoidant/Restrictive
Food Intaice Disorder
Associated developmental and functional limitations include impairment of physical development and social difficulties that can have a significant negative impact on family
function.
Differentiai Diagnosis
Appetite loss preceding restricted intake is a nonspecific symptom that can accompany a
number of mental diagnoses. Avoidant/restrictive food intake disorder can be diagnosed
concurrently with the disorders below if all criteria are met, and the eating disturbance requires specific clinical attention.
Other medical conditions (e.g., gastrointestinal disease, food allergies and Intolerances, occult malignancies). Restriction of food intake may occur in other medical condi-
tiens, especially those with ongoing symptoms such as vomiting, loss of appetite, nausea, abdominal pain, o^ diarrhea. A diagnosis of avoidant/restrictive food intake disorder requires
that the disturbance of intake is beyond that directly accounted for by physical symptoms consistent with a medical condition; tiie eating disturbance may also persist after being triggered
by a medical condition and following resolution of the medical condition.
Underlying medical or comorbid mental conditions may complicate feeding and eating.
Because older individuals, postsurgical patients, and individuals receiving chemotherapy
often lose their appetite, an additional diagnosis of avoidant/restrictive food intake disorder requires that the eating disturbance is a primary focus for intervention.
Specific neurological/neuromuscular, structural, or congenital disorders and conditions associated with feeding difficulties. Feeding difficulties are common in a number
of congenital and neurological conditions often related to problems with oral/esophageal/
pharyngeal structure and function, such as hypotonia of musculature, tongue protrusion,
and unsafe swallowing. Avoidant/restrictive food intake disorder can be diagnosed in individuals with such presentations as long as all diagnostic criteria are met.
Reactive attachment disorder. Some degree of withdrawal is characteristic of reactive
attachment disorder and can lead to a disturbance in the caregiver-child relationship that
can affect feeding and the child's intake. Avoidant/restrictive food intake disorder should
be diagnosed concurrently only if all criteria are met for both disorders and the feeding
disturbance is a primary focus for intervention.
Autism spectrum disorder. Individuals with autism spectrum disorder often present with
rigid eating behaviors and heightened sensory sensitivities. However, these features do
not always result in the level of impairment that would be required for a diagnosis of
avoidant/restrictive food intake disorder. Avoidant/restrictive food intake disorder should
be diagnosed concurrently only if all criteria are met for both disorders and when the eating disturbance requires specific treatment.
Specific phobia, social anxiety disorder (social phobia), and other anxiety disorders.
Specific phobia, other type, specifies "situations that may lead to choking or vomiting" and
can represent the primary trigger for the fear, anxiety, or avoidance required for diagnosis.
Distinguishing specific phobia from avoidant/restrictive food intake disorder can be difficult when a fear of choking or vomiting has resulted in food avoidance. Although avoidance or restriction of food intake secondary to a pronounced fear of choking or vomiting
can be conceptualized as specific phobia, in situations when the eating problem becomes
the primary focus of clinical attention, avoidant/restrictive food intake disorder becomes
the appropriate diagnosis. In social anxiety disorder, the individual may present with a
fear of being observed by others while eating, which can also occur in avoidant/restrictive
food intake disorder.
Anorexia nervosa. Restriction of energy intake relative to requirements leading to significantly low body weight is a core feature of anorexia nervosa. However, individuals
with anorexia nervosa also display a fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, as well as specific disturbances in relation to
perception and experience of their own body weight and shape. These features are not
present in avoidant/restrictive food intake disorder, and the two disorders should not be
diagnosed concurrently. Differential diagnosis between avoidant/restrictive food intake
disorder and anorexia nervosa may be difficult, especially in late childhood and early adolescence, because these disorders may share a number of common symptoms (e.g., food
avoidance, low weight). Differential diagnosis is also potentially difficult in individuals
with anorexia nervosa who deny any fear of fatness but nonetheless engage in persistent
behaviors that prevent weight gain and who do not recognize the medical seriousness of
their low weight—a presentation sometimes termed "non-fat phobic anorexia nervosa."
Full consideration of symptoms, course, and family history is advised, and diagnosis may
be best made in the context of a clinical relationship over time. In some individuals, avoidant/restrictive food intake disorder might precede the onset of anorexia nervosa.
Obsessive-compulsive disorder. Individuals with obsessive-compulsive disorder may
present with avoidance or restriction of intake in relation to preoccupations with food or
ritualized eating behavior. Avoidant/restrictive food intake disorder should be diagnosed
concurrently only if all criteria are met for both disorders and when the aberrant eating is
a major aspect of the clinical presentation requiring specific intervention.
Major depressive disorder. In major depressive disorder, appetite might be affected to
such an extent that individuals present with significantly restricted food intake, usually in
relation to overall energy intake and often associated with weight loss. Usually appetite
loss and related reduction of intake abate with resolution of mood problems. Avoidant/
restrictive food intake disorder should only be used concurrently if full criteria are met for
both disorders and when the eating disturbance requires specific treatment.
Schizophrenia spectrum disorders. Individuals with schizophrenia, delusional disorder, or other psychotic disorders may exhibit odd eating behaviors, avoidance of specific
foods because of delusional beliefs, or other manifestations of avoidant or restrictive intake. In some cases, delusional beliefs may contribute to a concern about negative consequences of ingesting certain foods. Avoidant/restrictive food intake disorder should be
used concurrently only if all criteria are met for both disorders and when the eating disturbance requires specific treatment.
Factitious disorder or factitious disorder imposed on another. Avoidant/restrictive
food intake disorder should be differentiated from factitious disorder or factitious disorder imposed on another. In order to assume the sick role, some individuals with factitious
disorder may intentionally describe diets that are much more restrictive than those they
are actually able to consume, as well as complications of such behavior, such as a need for
enteral feedings or nutritional supplements, an inability to tolerate a normal range of
foods, and/or an inability to participate normally in age-appropriate situations involving
food. The presentation may be impressively dramatic and engaging, and the symptoms reported inconsistently. In factitious disorder imposed on another, the caregiver describes
symptoms consistent with avoidant/restrictive food intake disorder and may induce
physical symptoms such as failure to gain weight. As with any diagnosis of factitious disorder imposed on another, the caregiver receives the diagnosis rather than the affected individual, and diagnosis should be made only on the basis of a careful, comprehensive
assessment of the affected individual, the caregiver, and their interaction.
Comorbidity
The most commonly observed disorders comorbid with avoidant/restrictive food intake
disorder are anxiety disorders, obsessive-compulsive disorder, and neurodevelopmental
disorders (specifically autism spectrum disorder, attention-deficit/hyperactivity disorder, and intellectual disability [intellectual developmental disorder]).
Anorexia Nervosa
Diagnostic Criteria
A. Restriction of energy intal<e relative to requirements, leading to a significantly low body
weigfit in tfie context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for
children and adolescents, less than that minimally expected.
B. Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes
with weight gain, even though at a significantly low weight.
C. Disturbance in tlie way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of
the seriousness of the current low body weight.
Coding note: The ICD-9-CM code for anorexia nervosa is 307.1, which is assigned regardless of the subtype. The ICD-10-CM code depends on the subtype (see below).
Specify whether:
(F50.01) Restricting type: During the last 3 months, the individual has not engaged in recurrent episodes of binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas). This subtype describes presentations in which
weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise.
(F50.02) Binge-eating/purging type: During the last 3 months, the individual has engaged in recurrent episodes of binge eating or purging behavior (i.e., self-induced
vomiting or the misuse of laxatives, diuretics, or enemas).
Specify if:
In partial remission: After full criteria for anorexia nervosa were previously met. Criterion A (low body weight) has not been met for a sustained period, but either Criterion
B (intense fear of gaining weight or becoming fat or behavior that interferes with weight
gain) or Criterion C (disturbances in self-perception of weight and shape) is still met.
In full remission: After full criteria for anorexia nervosa were previously met, none of
the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based, for adults, on current body mass index (BMI) (see
below) or, for children and adolescents, on BMI percentile. The ranges below are derived
from World Health Organization categories for thinness in adults; for children and adolescents, corresponding BMI percentiles should be used. The level of severity may be increased to reflect clinical symptoms, the degree of functional disability, and the need for
supervision.
Mild: BMI>17kg/m2
Moderate: BM116-16.99 kg/m^
Severe: BM115-15.99 kg/m^
Extreme: BMI < 15 kg/m^
Subtypes
Most individuals with the binge-eating/purging type of anorexia nervosa who binge eat
also purge through self-induced vomiting or the misuse of laxatives, diuretics, or enemas.
Some individuals with this subtype of anorexia nervosa do not binge eat but do regularly
purge after the consumption of small amounts of food.
Crossover between the subtypes over the course of the disorder is not uncommon;
therefore, subtype description should be used to describe current symptoms rather than
longitudinal course.
Diagnostic Features
There are three essential features of anorexia nervosa: persistent energy intake restriction;
intense fear of gaining weight or of becoming fat, or persistent behavior that interferes
with weight gain; and a disturbance in self-perceived weight or shape. The individual maintains a body weight that is below a minimally normal level for age, sex, developmental trajectory, and physical health (Criterion A). Individuals' body weights frequently meet this
criterion following a significant weight loss, but among children and adolescents, there
may alternatively be failure to make expected weight gain or to maintain a normal developmental trajectory (i.e., while growing in height) instead of weight loss.
Criterion A requires that the individual's weight be significantly low (i.e., less than
minimally normal or, for children and adolescents, less than that minimally expected).
Weight assessment can be challenging because normal weight range differs among individuals, and different thresholds have been published defining thinness or underweight
status. Body mass index (BMI; calculated as weight in kilograms/height in meters^) is a
useful measure to assess body weight for height. For adults, a BMI of 18.5 kg/m^ has been
employed by the Centers for Disease Control and Prevention (CDC) and the World Health
Organization (WHO) as the lower limit of normal body weight. Therefore, most adults with
a BMI greater than or equal to 18.5 kg/m^ would not be considered to have a significantly
low body weight. On the other hand, a BMI of lower than 17.0 kg/m^ has been considered
by the WHO to indicate moderate or severe thinness; therefore, an individual with a BMI
less than 17.0 kg/m^ would likely be considered to have a significantly low weight. An
adult with a BMI between 17.0 and 18.5 kg/m^, or even above 18.5 kg/m , might be considered to have a significantly low weight if clinical history or other physiological information supports this judgment.
For children and adolescents, determining a BMI-for-age percentile is useful (see, e.g.,
the CDC BMI percentile calculator for children and teenagers. As for adults, it is not possible to provide definitive standards forjudging whether a child's or an adolescent's weight
is significantly low, and variations in developmental trajectories among youth limit the
utility of simple numerical guidelines. The CDC has used a BMI-for-age below the 5th percentile as suggesting underweight; however, children and adolescents with a BMI above
this benchmark may be judged to be significantly underweight in light of failure to maintain their expected growth trajectory. In summary, in determining whether Criterion A is
met, the clinician should consider available numerical guidelines, as well as the individual's
body build, weight history, and any physiological disturbances.
Individuals with this disorder typically display an intense fear of gaining weight or of
becoming fat (Criterion B). This intense fear of becoming fat is usually not alleviated by
weight loss. In fact, concern about weight gain may increase even as weight falls. Younger
individuals with anorexia nervosa, as well as some adults, may not recognize or acknowledge a fear of weight gain. In the absence of another explanation for the significantly low
weight, clinician inference drawn from collateral history, observational data, physical and
laboratory findings, or longitudinal course either indicating a fear of weight gain or supporting persistent behaviors that prevent it may be used to establish Criterion B.
The experience and significance of body weight and shape are distorted in these individuals (Criterion C). Some individuals feel globally overweight. Others realize that they
are thin but are still concerned that certain body parts, particularly the abdomen, buttocks,
and thighs, are "too fat." They may employ a variety of techniques to evaluate their body
size or weight, including frequent weighing, obsessive measuring of body parts, and persistent use of a mirror to check for perceived areas of "fat." The self-esteem of individuals
with anorexia nervosa is highly dependent on their perceptions of body shape and weight.
Weight loss is often viewed as an impressive achievement and a sign of extraordinary selfdiscipline, whereas weight gain is perceived as an unacceptable failure of self-control. Although some individuals with this disorder may acknowledge being thin, they often do
not recognize the serious medical implications of their malnourished state.
Often, the individual is brought to professional attention by family members after marked
weight loss (or failure to make expected weight gains) has occurred. If individuals seek help
on their own, it is usually because of distress over the somatic and psychological sequelae
of starvation. It is rare for an individual with anorexia nervosa to complain of weight loss
per se. In fact, individuals with anorexia nervosa frequently either lack insight into or deny
the problem. It is therefore often important to obtain information from family members or
other sources to evaluate the history of weight loss and other features of the illness.
Associated Features Supporting Diagnosis
The semi-starvation of anorexia nervosa, and the purging behaviors sometimes associated
with it, can result in significant and potentially life-threatening medical conditions. The
nutritional compromise associated with this disorder affects most major organ systems
and can produce a variety of disturbances. Physiological disturbances, including amenorrhea and vital sign abnormalities, are common. While most of the physiological disturbances associated with malnutrition are reversible with nutritional rehabilitation, some,
including loss of bone mineral density, are often not completely reversible. Behaviors such
as self-induced vomiting and misuse of laxatives, diuretics, and enemas may cause a number of disturbances that lead to abnormal laboratory findings; however, some individuals
with anorexia nervosa exhibit no laboratory abnormalities.
When seriously underweight, many individuals with anorexia nervosa have depressive
signs and symptoms such as depressed mood, social withdrawal, irritability, insomnia, and
diminished interest in sex. Because these features are also observed in individuals without
anorexia nervosa who are significantly undernourished, many of the depressive features
may be secondary to the physiological sequelae of semi-starvation, although they may also
be sufficiently severe to warrant an additional diagnosis of major depressive disorder.
Obsessive-compulsive features, both related and unrelated to food, are often prominent.
Most individuals with anorexia nervosa are preoccupied with thoughts of food. Some collect recipes or hoard food. Observations of behaviors associated with other forms of starvation suggest that obsessions and compulsions related to food may be exacerbated by
imdemutrition. When individuals with anorexia nervosa exhibit obsessions and compulsions that are not related to food, body shape, or weight, an additional diagnosis of obsessive-compulsive disorder (OCD) may be warranted.
Other features sometimes associated with anorexia nervosa include concerns about
eating in public, feelings of ineffectiveness, a strong desire to control one's environment,
inflexible thinking, limited social spontaneity, and overly restrained emotional expression. Compared with individuals with anorexia nervosa, restricting type, those with
binge-eating/purging type have higher rates of impulsivity and are more likely to abuse
alcohol and other drugs.
A subgroup of individuals with anorexia nervosa show excessive levels of physical activity. Increases in physical activity often precede onset of the disorder, and over the
course of the disorder increased activity accelerates weight loss. During treatment, excessive activity may be difficult to control, thereby jeopardizing weight recovery.
Individuals with anorexia nervosa may misuse medications, such as by manipulating
dosage, in order to achieve weight loss or avoid weight gain. Individuals with diabetes
mellitus may omit or reduce insulin doses in order to minimize carbohydrate metabolism.
Prevalence
The 12-month prevalence of anorexia nervosa among young females is approximately
0.4%. Less is known about prevalence among males, but anorexia nervosa is far less common in males than in females, with clinical populations generally reflecting approximately
a 10:1 female-to-male ratio.
Development and Course
Anorexia nervosa commonly begins during adolescence or young adulthood. It rarely begins before puberty or after age 40, but cases of both early and late onset have been described. The onset of this disorder is often associated with a stressful life event, such as
leaving home for college. The course and outcome of anorexia nervosa are highly variable.
Younger individuals may manifest atypical features, including denying "fear of fat." Older
individuals more likely have a longer duration of illness, and their clinical presentation may
include more signs and symptoms of long-standing disorder. Clinicians should not exclude
anorexia nervosa from the differential diagnosis solely on the basis of older age.
Many individuals have a period of changed eating behavior prior to full criteria for the
disorder being met. Some individuals with anorexia nervosa recover fully after a single
episode, with some exhibiting a fluctuating pattern of weight gain followed by relapse,
and others experiencing a chronic course over many years. Hospitalization may be required to restore weight and to address medical complications. Most individuals with anorexia nervosa experience remission within 5 years of presentation. Among individuals
admitted to hospitals, overall remission rates may be lower. The crude mortality rate (CMR)
for anorexia nervosa is approximately 5% per decade. Death most commonly results from
medical complications associated with the disorder itself or from suicide.
Risk and Prognostic Factors
Temperamental. Individuals who develop anxiety disorders or display obsessional
traits in childhood are at increased risk of developing anorexia nervosa.
Environmental. Historical and cross-cultural variability in the prevalence of anorexia
nervosa supports its association with cultures and settings in which thinness is valued. Occupations and avocations that encourage thinness, such as modeling and elite athletics, are
also associated with increased risk.
Genetic and physiological. There is an increased risk of anorexia nervosa and bulimia
nervosa among first-degree biological relatives of individuals with the disorder. An increased risk of bipolar and depressive disorders has also been found among first-degree
relatives of individuals with anorexia nervosa, particularly relatives of individuals with
the binge-eating/purging type. Concordance rates for anorexia nervosa in monozygotic
twins are significantly higher than those for dizygotic twins. A range of brain abnormalities has been described in anorexia nervosa using functional imaging technologies (functional magnetic resonance imaging, positron emission tomography). The degree to which
these findings reflect changes associated with malnutrition versus primary abnormalities
associated with the disorder is unclear.
Cuiture-Related Diagnostic issues
Anorexia nervosa occurs across culturally and socially diverse populations, although available
evidence suggests cross-cultural variation in its occurrence and presentation. Anorexia nervosa is probably most prevalent in post-industrialized, high-income countries such as in the
United States, many European countries, Australia, New Zealand, and Japan, but its incidence
in most low- and middle-income countries is uncertain. Whereas the prevalence of anorexia
nervosa appears comparatively low among Latinos, African Americans, and Asians in the
United States, clinicians should be aware that mental health service utilization among individuals with an eating disorder is significantly lower in these ethnic groups and that the low rates
may reflect an ascertainment bias. The presentation of weight concerns among individuals
with eating and feeding disorders varies substantially across cultural contexts. The absence of
an expressed intense fear of weight gain, sometimes referred to as "fat phobia," appears to be
relatively more common in populations in Asia, where the rationale for dietary restriction is
commonly related to a more culturally sanctioned complaint such as gastrointestinal discomfort. Within the United States, presentations without a stated intense fear of weight gain may
be comparatively more common among Latino groups.
Diagnostic IVIaricers
The following laboratory abnormalities may be observed in anorexia nervosa; their presence may serve to increase diagnostic confidence.
Hematology. Leukopenia is common, with the loss of all cell types but usually with apparent lympho<^ytosis. Mild anemia can occur, as well as thrombocytopenia and, rarely,
bleeding problems.
Serum chemistry. Dehydration may be reflected by an elevated blood urea nitrogen
level. Hypercholesterolemia is common. Hepatic enzyme levels may be elevated. Hypomagnesemia, hypozincemia, hypophosphatemia, and hyperamylasemia are occasionally
observed. Self-induced vomiting may lead to metabolic alkalosis (elevated serum bicarbonate), hypochloremia, and hypokalemia; laxative abuse may cause a mild metabolic acidosis.
Endocrine. Serum thyroxine (T4) levels are usually in the low-normal range; triiodothyronine (T3) levels are decreased, while reverse T3 levels are elevated. Females have low serum estrogen levels, whereas males have low levels of serum testosterone.
Electrocardiography. Sinus bradycardia is common, and, rarely, arrhythmias are noted.
Significant prolongation of the QTc interval is observed in some individuals.
Bone mass. Low bone mineral density, with specific areas of osteopenia or osteoporosis, is often seen. The risk of fracture is significantly elevated.
Electroencephalography. Diffuse abnormalities, reflecting a metabolic encephalopathy, may result from significant fluid and electrolyte disturbances.
Resting energy expenditure. There is often a significant reduction in resting energy expenditure.
Physical signs and symptoms. Many of the physical signs and symptoms of anorexia
nervosa are attributable to starvation. Amenorrhea is commonly present and appears to
be an indicator of physiological dysfunction. If present, amenorrhea is usually a consequence of the weight loss, but in a minority of individuals it may actually precede the
weight loss. In prepubertal females, menarche maybe delayed. In addition to amenorrhea,
there may be complaints of constipation, abdominal pain, cold intolerance, lethargy, and
excess energy.
The most remarkable finding on physical examination is emaciation. Commonly, there
is also significant hypotension, hypothermia, and bradycardia. Some individuals develop
lanugo, a fine downy body hair. Some develop peripheral edema, especially during
weight restoration or upon cessation of laxative and diuretic abuse. Rarely, petechiae or
ecchymoses, usually on the extremities, may indicate a bleeding diathesis. Some individuals evidence a yellowing of the skin associated with hypercarotenemia. As may be seen in
individuals with bulimia nervosa, individuals with anorexia nervosa who self-induce
vomiting may have hypertrophy of the salivary glands, particularly the parotid glands, as
well as dental enamel erosion. Some individuals may have scars or calluses on the dorsal
surface of the hand from repeated contact with the teeth while inducing vomiting.
Suicide Risk
Suicide risk is elevated in anorexia nervosa, with rates reported as 12 per 100,000 per year.
Comprehensive evaluation of individuals with anorexia nervosa should include assessment of suicide-related ideation and behaviors as well as other risk factors for suicide, including a history of suicide attempt(s).
Functional Consequences of Anorexia Nervosa
Individuals with anorexia nervosa may exhibit a range of functional limitations associated
with the disorder. While some individuals remain active in social and professional functioning, others demonstrate significant social isolation and/or failure to fulfill academic or
career potential.
Differential Diagnosis
Other possible causes of either significantly low body weight or significant weight loss
should be considered in the differential diagnosis of anorexia nervosa, especially when the
presenting features are atypical (e.g., onset after age 40 years).
Medical conditions (e.g., gastrointestinal disease, hypeiihyroidism, occult malignancies, and acquired immunodeficiency syndrome [AIDS]). Serious weight loss may occur in medical conditions, but individuals with these disorders usually do not also manifest a disturbance in the way their body weight or shape is experienced or an intense fear
of weight gain or persist in behaviors that interfere with appropriate weight gain. Acute
weight loss associated with a medical condition can occasionally be followed by the onset
or recurrence of anorexia nervosa, which can initially be masked by the comorbid medical
condition. Rarely, anorexia nervosa develops after bariatric surgery for obesity.
Major depressive disorder. In major depressive disorder, severe weight loss may occur,
but most individuals with major depressive disorder do not have either a desire for excessive weight loss or an intense fear of gaining weight.
Schizophrenia. Individuals with schizophrenia may exhibit odd eating behavior and occasionally experience significant weight loss, but they rarely show the fear of gaining
weight and the body image disturbance required for a diagnosis of anorexia nervosa.
Substance use disorders. Individuals with substance use disorders may experience low
weight due to poor nutritional intake but generally do not fear gaining weight and do not
manifest body image disturbance. Individuals who abuse substances that reduce appetite
(e.g., cocaine, stimulants) and who also endorse fear of weight gain should be carefully
evaluated for the possibility of comorbid anorexia nervosa, given that the substance use
may represent a persistent behavior that interferes with weight gain (Criterion B).
Social anxiety disorder (social phobia), obsessive-compulsive disorder, and body dysmorphic disorder. Some of the features of anorexia nervosa overlap with the criteria for
social phobia, OCD, and body dysmorphic disorder. Specifically, individuals may feel humiliated or embarrassed to be seen eating in public, as in social phobia; may exhibit obsessions and compulsions related to food, as in OCD; or may be preoccupied with an imagined
defect in bodily appearance, as in body dysmorphic disorder. If the individual with anorexia
nervosa has social fears that are limited to eating behavior alone, the diagnosis of social phobia should not be made, but social fears unrelated to eating behavior (e.g., excessive fear of
speaking in public) may warrant an additional diagnosis of social phobia. Similarly, an additional diagnosis of OCD should be considered only if the individual exhibits obsessions
and compulsions unrelated to food (e.g., an excessive fear of contamination), and an additional diagnosis of body dysmorphic disorder should be considered only if the distortion is
unrelated to body shape and size (e.g., preoccupation that one's nose is too big).
Bulimia nervosa. Individuals with bulimia nervosa exhibit recurrent episodes of binge
eating, engage in inappropriate behavior to avoid weight gain (e.g., self-induced vomiting), and are overly concerned with body shape and weight. However, unlike individuals
with anorexia nervosa, binge-eating/purging type, individuals with bulimia nervosa maintain body weight at or above a minimally normal level.
Avoidant/restrictive food intake disorder. Individuals with this disorder may exhibit
significant weight loss or significant nutritional deficiency, but they do not have a fear of
gaining weight or of becoming fat, nor do they have a disturbance in the way they experience their body shape and weight.
Comorbidity
Bipolar, depressive, and anxiety disorders commonly co-occur with anorexia nervosa.
Many individuals with anorexia nervosa report the presence of either an anxiety disorder
or symptoms prior to onset of their eating disorder. OCD is described in some individuals
with anorexia nervosa, especially those with the restricting type. Alcohol use disorder and
other substance use disorders may also be comorbid with anorexia nervosa, especially
among those with the binge-eating/purging type.
Bulimia Nervosa
Diagnostic Criteria 307.51 (F50.2)
A. Recurrent episodes of binge eating. An episode of binge eating is characterized by
both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of
food that is definitely larger than what most individuals would eat in a similar period
of time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling that one
cannot stop eating or control what or how much one is eating).
B. Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such
as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting;
or excessive exercise.
C. The binge eating and inappropriate compensatory behaviors both occur, on average,
at least once a week for 3 months.
D. Self-evaluation is unduly influenced by body shape and weight.
E. The disturbance does not occur exclusively during episodes of anorexia nervosa.
Specify if:
In partial remission: After full criteria for bulimia nervosa were previously met, some,
but not all, of the criteria have been met for a sustained period of time.
In full remission: After full criteria for bulimia nervosa were previously met, none of
the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of inappropriate compensatory
behaviors (see below). The level of severity may be increased to reflect other symptoms
and the degree of functional disability.
lUlild: An average of 1-3 episodes of inappropriate compensatory behaviors per week.
■Moderate: An average of 4-7 episodes of inappropriate compensatory behaviors per
week.
Severe: An average of 8-13 episodes of inappropriate compensatory behaviors per
week.
Extreme: An average of 14 or more episodes of inappropriate compensatory behaviors per week.
Diagnostic Features
There are three essential features of bulimia nervosa: recurrent episodes of binge eating
(Criterion A), recurrent inappropriate compensatory behaviors to prevent weight gain
(Criterion B), and self-evaluation that is unduly influenced by body shape and weight
(Criterion D). To qualify for the diagnosis, the binge eating and inappropriate compensatory behaviors must occur, on average, at least once per week for 3 months (Criterion C).
An "episode of binge eating" is defined as eating, in a discrete period of time, an
amount of food that is definitely larger than most individuals would eat in a similar period
of time under similar circumstances (Criterion Al). The context in which the eating occurs
may affect the clinician's estimation of whether the intake is excessive. For example, a
quantity of food that might be regarded as excessive for a typical meal might be considered normal during a celebration or holiday meal. A "discrete period of time" refers to a
limited period, usually less than 2 hours. A single episode of binge eating need not be restricted to one setting. For example, an individual may begin a binge in a restaurant and
then continue to eat on returning home. Continual snacking on small amounts of food
throughout the day would not be considered an eating binge.
An occurrence of excessive food consumption must be accompanied by a sense of lack
of control (Criterion A2) to be considered an episode of binge eating. An indicator of loss
of control is the inability to refrain from eating or to stop eating once started. Some individuals describe a dissociative quality during, or following, the binge-eating episodes. The
impairment in control associated with binge eating may not be absolute; for example, an
individual may continue binge eating while the telephone is ringing but will cease if a
roommate or spouse unexpectedly enters the room. Some individuals report that their
binge-eating episodes are no longer characterized by an acute feeling of loss of control but
rather by a more generalized pattern of uncontrolled eating. If individuals report that they
have abandoned efforts to control their eating, loss of control should be considered as
present. Binge eating can also be planned in some instances.
The type of food consumed during binges varies both across individuals and for a
given individual. Binge eating appears to be characterized more by an abnormality in the
amount of food consumed than by a craving for a specific nutrient. However, during binges,
individuals tend to eat foods they would otherwise avoid.
Individuals with bulimia nervosa are typically ashamed of their eating problems and
attempt to conceal their symptoms. Binge eating usually occurs in secrecy or as inconspicuously as possible. The binge eating often continues until the individual is uncomfortably,
or even painfully, full. The most common antecedent of binge eating is negative affect.
Other triggers include interpersonal stressors; dietary restraint; negative feelings related
to body weight, body shape, and food; and boredom. Binge eating may minimize or mitigate factors that precipitated the episode in the short-term, but negative self-evaluation
and dysphoria often are the delayed consequences.
Another essential feature of bulimia nervosa is the recurrent use of inappropriate compensatory behaviors to prevent weight gain, collectively referred to as purge behaviors or
purging (Criterion B). Many individuals with bulimia nervosa employ several methods to
compensate for binge eating. Vomiting is the most common inappropriate compensatory
behavior. The immediate effects of vomiting include relief from physical discomfort and reduction of fear of gaining weight. In some cases, vomiting becomes a goal in itself, and the
individual will binge eat in order to vomit or will vomit after eating a small amount of food.
Individuals with bulimia nervosa may use a variety of methods to induce vomiting, including the use of fingers or instruments to stimulate the gag reflex. Individuals generally
become adept at inducing vomiting and are eventually able to vomit at will. Rarely, individuals consume syrup of ipecac to induce vomiting. Other purging behaviors include the
misuse of laxatives and diuretics. A number of other compensatory methods may also be
used in rare cases. Individuals with bulimia nervosa may misuse enemas following episodes of binge eating, but this is seldom the sole compensatory method employed. Individuals with this disorder may take thyroid hormone in an attempt to avoid weight gain.
Individuals with diabetes mellitus and bulimia nervosa may omit or reduce insulin doses in
order to reduce the metabolism of food consumed during eating binges. Individuals with
bulimia nervosa may fast for a day or more or exercise excessively in an attempt to prevent
weight gain. Exercise may be considered excessive when it significantly interferes with important activities, when it occurs at inappropriate times or in inappropriate settings, or
when the individual continues to exercise despite injury or other medical complications.
Individuals with bulimia nervosa place an excessive emphasis on body shape or weight
in their self-evaluation, and these factors are typically extremely important in determining
self-esteem (Criterion D). Individuals with this disorder may closely resemble those w^ith
anorexia nervosa in their fear of gaining weight, in their desire to lose weight, and in the
level of dissatisfaction with their bodies. However, a diagnosis of bulimia nervosa should
not be given when the disturbance occurs only during episodes of anorexia nervosa (Criterion E).
Associated Features Supporting Diagnosis
Individuals with bulimia nervosa typically are within the normal weight or overweight
range (body mass index [BMI] > 18.5 and < 30 in adults). The disorder occurs but is uncommon among obese individuals. Between eating binges, individuals with bulimia nervosa typically restrict their total caloric consumption and preferentially select low-calorie
("diet") foods while avoiding foods that they perceive to be fattening or likely to trigger a
binge.
Menstrual irregularity or amenorrhea often occurs among females with bulimia nervosa; it is uncertain whether such disturbances are related to weight fluctuations, to nutritional deficiencies, or to emotional distress. The fluid and electrolyte disturbances
resulting from the purging behavior are sometimes sufficiently severe to constitute medically serious problems. Rare but potentially fatal complications include esophageal tears,
gastric rupture, and cardiac arrhythmias. Serious cardiac and skeletal myopathies have
been reported among individuals following repeated use of syrup of ipecac to induce vomiting. Individuals who chronically abuse laxatives may become dependent on their use to
stimulate bowel movements. Gastrointestinal symptoms are commonly associated with
bulimia nervosa, and rectal prolapse has also been reported among individuals with this
disorder.
Prevalence
Twelve-month prevalence of bulimia nervosa among young females is 1%-1.5%. Point
prevalence is highest among young adults since the disorder peaks in older adolescence
and young adulthood. Less is known about the point prevalence of bulimia nervosa in
males, but bulimia nervosa is far less common in males than it is in females, with an approximately 10:1 female-to-male ratio.
Development and Course
Bulimia nervosa commonly begins in adolescence or young adulthood. Onset before puberty or after age 40 is uncommon. The binge eating frequently begins during or after an
episode of dieting to lose weight. Experiencing multiple stressful life events also can precipitate onset of bulimia nervosa.
Disturbed eating behavior persists for at least several years in a high percentage of
clinic samples. The course may be chronic or intermittent, with periods of remission
alternating with recurrences of binge eating. However, over longer-term follow-up, the
symptoms of many individuals appear to diminish with or without treatment, although
treatment clearly impacts outcome. Periods of remission longer than 1 year are associated
with better long-term outcome.
Significantly elevated risk for mortality (all-cause and suicide) has been reported for
individuals with bulimia nervosa. The CMR (crude mortality rate) for bulimia nervosa is
nearly 2% per decade.
Diagnostic cross-over from initial bulimia nervosa to anorexia nervosa occurs in a minority of cases (10%-15%). Individuals who do experience cross-over to anorexia nervosa
commonly will revert back to bulimia nervosa or have multiple occurrences of cross-overs
between these disorders. A subset of individuals with bulimia nervosa continue to binge
eat but no longer engage in inappropriate compensatory behaviors, and therefore their
symptoms meet criteria for binge-eating disorder or other specified eating disorder. Diagnosis should be based on the current (i.e., past 3 months) clinical presentation.
Risk and Prognostic Factors
Temperamental. Weight concerns, low self-esteem, depressive symptoms, social anxiety disorder, and overanxious disorder of childhood are associated with increased risk for
the development of bulimia nervosa.
Environmental. Internalization of a thin body ideal has been found to increase risk for
developing weight concerns, which in turn increase risk for the development of bulimia
nervosa. Individuals who experienced childhood sexual or physical abuse are at increased
risk for developing bulimia nervosa.
Genetic and physiological. Childhood obesity and early pubertal maturation increase
risk for bulimia nervosa. Familial transmission of bulimia nervosa may be present, as well
as genetic vulnerabilities for the disorder.
Course modifiers. Severity of psychiatric comorbidity predicts worse long-term outcome
of bulimia nervosa.
Culture-Related Diagnostic issues
Bulimia nervosa has been reported to occur with roughly similar frequencies in most industrialized countries, including the United States, Canada, many European countries,
Australia, Japan, New Zealand, and South Africa. In clinical studies of bulimia nervosa in
the United States, individuals presenting with this disorder are primarily white. However,
the disorder also occurs in other ethnic groups and with prevalence comparable to estimated prevalences observed in white samples.
Gender-Related Diagnostic issues
Bulimia nervosa is far more common in females than in males. Males are especially underrepresented in treatment-seeking samples, for reasons that have not yet been systematically examined.
Diagnostic IViarkers
No specific diagnostic test for bulimia nervosa currently exists. However, several laboratory abnormalities may occur as a consequence of purging and may increase diagnostic
certainty. These include fluid and electrolyte abnormalities, such as hypokalemia (which
can provoke cardiac arrhythmias), hypochloremia, and hyponatremia. The loss of gastric
acid through vomiting may produce a metabolic alkalosis (elevated serum bicarbonate),
and the frequent induction of diarrhea or dehydration through laxative and diuretic abuse
can cause metabolic acidosis. Some individuals with bulimia nervosa exhibit mildly elevated levels of serum amylase, probably reflecting an increase in the salivary isoenzyme.
Physical examination usually yields no physical findings. However, inspection of the
mouth may reveal significant and permanent loss of dental enamel, especially from lingual surfaces of the front teeth due to recurrent vomiting. These teeth may become
chipped and appear ragged and "moth-eaten." There may also be an increased frequency
of dental caries. In some individuals, the salivary glands, particularly the parotid glands,
may become notably enlarged. Individuals who induce vomiting by manually stimulating
the gag reflex may develop calluses or scars on the dorsal surface of the hand from repeated contact with the teeth. Serious cardiac and skeletal myopathies have been reported
among individuals following repeated use of syrup of ipecac to induce vomiting.
Suicide Risic
Suicide risk is elevated in bulimia nervosa. Comprehensive evaluation of individuals with
this disorder should include assessment of suicide-related ideation and behaviors as well
as other risk factors for suicide, including a history of suicide attempts.
Functional Consequences of Buiimia Nervosa
Individuals with bulimia nervosa may exhibit a range of functional limitations associated
with the disorder. A minority of individuals report severe role impairment, with the social-life domain most likely to be adversely affected by bulimia nervosa.
Differentiai Diagnosis
Anorexia nervosa, binge-eating/purging type. Individuals whose binge-eating behavior occurs only during episodes of anorexia nervosa are given the diagnosis anorexia nervosa, binge-eating/purging type, and should not be given the additional diagnosis of
bulimia nervosa. For individuals with an initial diagnosis of anorexia nervosa who binge
and purge but whose presentation no longer meets the full criteria for anorexia nervosa,
binge-eating/purging type (e.g., when weight is normal), a diagnosis of bulimia nervosa should be given only when all criteria for bulimia nervosa have been met for at least
3 months.
Binge-eating disorder. Some individuals binge eat but do not engage in regular inappropriate compensatory behaviors. In these cases, the diagnosis of binge-eating disorder
should be considered.
Kleine-Levin syndrome. In certain neurological or other medical conditions, such as
Kleine-Levin syndrome, there is disturbed eating behavior, but the characteristic psychological features of bulimia nervosa, such as overconcem with body shape and weight, are
not present.
Major depressive disorder, with atypical features. Overeating is common in major depressive disorder, with atypical features, but individuals with this disorder do not engage
in inappropriate compensatory behaviors and do not exhibit the excessive concern with
body shape and weight characteristic of bulimia nervosa. If criteria for both disorders are
met, both diagnoses should be given.
Borderline personality disorder. Binge-eating behavior is included in the impulsive behavior criterion that is part of the definition of borderline personality disorder. If the criteria for both borderline personality disorder and bulimia nervosa are met, both diagnoses
should be given.
Comorbidity
Comorbidity with mental disorders is common in individuals with bulimia nervosa, with
most experiencing at least one other mental disorder and many experiencing multiple comorbidities. Comorbidity is not limited to any particular subset but rather occurs across a
wide range of mental disorders. There is an increased frequency of depressive symptoms
(e.g., low self-esteem) and bipolar and depressive disorders (particularly depressive disorders) in individuals with bulimia nervosa. In many individuals, the mood disturbance
begins at the same time as or following the development of bulimia nervosa, and individuals often ascribe their mood disturbances to the bulimia nervosa. However, in some individuals, the mood disturbance clearly precedes the development of bulimia nervosa.
There may also be an increased frequency of anxiety symptoms (e.g., fear of social situations) or anxiety disorders. These mood and anxiety disturbances frequently remit follow
ing effective treatment of the bulimia nervosa. The lifetime prevalence of substance use,
particularly alcohol or stimulant use, is at least 30% among individuals with bulimia nervosa. Stimulant use often begins in an attempt to control appetite and weight. A substantial percentage of individuals with bulimia nervosa also have personality features that
meet criteria for one or more personality disorders, most frequently borderline personality
disorder.
Binge-Eating Disorder
Diagnostic Criteria 307.51 (F50.8)
A. Recurrent episodes of binge eating. An episode of binge eating is characterized
by both of the following:
1. Eating, in a discrete period of time (e.g., within any 2-hour period), an amount of
food that is definitely larger than what most people would eat in a similar period of
time under similar circumstances.
2. A sense of lack of control over eating during the episode (e.g., a feeling that one
cannot stop eating or control what or how much one is eating).
B. The binge-eating episodes are associated with three (or more) of the following:
1. Eating much more rapidly than normal.
2. Eating until feeling uncomfortably full.
3. Eating large amounts of food when not feeling physically hungry.
4. Eating alone because of feeling embarrassed by how much one is eating.
5. Feeling disgusted with oneself, depressed, or very guilty afterward.
C. Marked distress regarding binge eating is present.
D. The binge eating occurs, on average, at least once a week for 3 months.
E. The binge eating is not associated with the recurrent use of inappropriate compensatory behavior as in bulimia nen/osa and does not occur exclusively during the course
of bulimia nervosa or anorexia nervosa.
Specify if:
In partial remission: After full criteria for binge-eating disorder were previously met,
binge eating occurs at an average frequency of less than one episode per week for a
sustained period of time.
In full remission: After full criteria for binge-eating disorder were previously met, none
of the criteria have been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of episodes of binge eating (see
below). The level of severity may be increased to reflect other symptoms and the degree
of functional disability.
Mild: 1-3 binge-eating episodes per week.
lUloderate: 4-7 binge-eating episodes per week.
Severe: 8-13 binge-eating episodes per week.
Extreme: 14 or more binge-eating episodes per week.
Diagnostic Features
The essential feature of binge-eating disorder is recurrent episodes binge eating that must
occur, on average, at least once per week for 3 months (Criterion D). An "episode of binge
eating" is defined as eating, in a discrete period of time, an amount of food that is defi
nitely larger than most people would eat in a similar period of time under similar circumstances (Criterion Al). The context in which the eating occurs may affect the clinician's
estimation of whether the intake is excessive. For example, a quantity of food that might be
regarded as excessive for a typical meal might be considered normal during a celebration
or holiday meal. A ''discrete period of time" refers to a limited period, usually less than
2 hours. A single episode of binge eating need not be restricted to one setting. For example,
an individual may begin a binge in a restaurant and then continue to eat on returning
home. Continual snacking on small amounts of food throughout the day would not be considered an eating binge.
An occurrence of excessive food consumption must be accompanied by a sense of lack
of control (Criterion A2) to be considered an episode of binge eating. An indicator of loss
of control is the inability to refrain from eating or to stop eating once started. Some individuals describe a dissociative quality during, or following, the binge-eating episodes. The
impairment in control associated with binge eating may not be absolute; for example, an
individual may continue binge eating while the telephone is ringing but will cease if a
roommate or spouse unexpectedly enters the room. Some individuals report that their
binge-eating episodes are no longer characterized by an acute feeling of loss of control but
rather by a more generalized pattern of uncontrolled eating. If individuals report that they
have abandoned efforts to control their eating, loss of control may still be considered as
present. Binge eating can also be planned in some instances.
The type of food consumed during binges varies both across individuals and for a given
individual. Binge eating appears to be characterized more by an abnormality in the amount
of food consumed than by a craving for a specific nutrient.
Binge eating must be characterized by marked distress (Criterion C) and at least three
of the following features: eating much more rapidly than normal; eating until feeling uncomfortably full; eating large amoimts of food when not feeling physically hungry; eating
alone because of feeling embarrassed by how much one is eating; and feeling disgusted
with oneself, depressed, or very guilty afterward (Criterion B).
Individuals with binge-eating disorder are typically ashamed of their eating problems
and attempt to conceal their symptoms. Binge eating usually occurs in secrecy or as inconspicuously as possible. The most common antecedent of binge eating is negative affect.
Other triggers include inteφersonal stressors; dietary restraint; negative feelings related
to body weight, body shape, and food; and boredom. Binge eating may miriimize or mitigate factors that precipitated the episode in the short-term, but negative self-evaluation
and dysphoria often are the delayed consequences.
Associated Features Supporting Diagnosis
Binge-eating disorder occurs in normal-weight/overweight and obese individuals. It is reliably associated with overweight and obesity in treatment-seeking individuals. Nevertheless, binge-eating disorder is distinct from obesity. Most obese individuals do not
engage in recurrent binge eating. In addition, compared with weight-matched obese individuals without binge-eating disorder, those with the disorder consume more calories in
laboratory studies of eating behavior and have greater functional impairment, lower quality of life, more subjective distress, and greater psychiatric comorbidity.
Prevaience
Twelve-month prevalence of binge-eating disorder among U.S. adult (age 18 or older) females and males is 1.6% and 0.8%, respectively. The gender ratio is far less skewed in bingeeating disorder than in bulimia nervosa. Binge-eating disorder is as prevalent among females from racial or ethnic minority groups as has been reported for white females. The
disorder is more prevalent among individuals seeking weight-loss treatment than in the
general population.
Development and Course
Little is known about the development of binge-eating disorder. Both binge eating and
loss-of-control eating without objectively excessive consumption occur in children and are
associated with increased body fat, weight gain, and increases in psychological symptoms.
Binge eating is common in adolescent and college-age samples. Loss-of-control eating or
episodic binge eating may represent a prodromal phase of eating disorders for some individuals.
Dieting follows the development of binge eating in many individuals with bingeeating disorder. (This is in contrast to bulimia nervosa, in which dysfunctional dieting
usually precedes the onset of binge eating.) Binge-eating disorder typically begins in adolescence or young adulthood but can begin in later adulthood. Individuals with bingeeating disorder who seek treatment usually are older than individuals with either bulimia
nervosa or anorexia nervosa who seek treatment.
Remission rates in both natural course and treatment outcome studies are higher for
binge-eating disorder than for bulimia nervosa or anorexia nervosa. Binge-eating disorder
appears to be relatively persistent, and the course is comparable to that of bulimia nervosa
in terms of severity and duration. Crossover from binge-eating disorder to other eating
disorders is uncommon.
Risk and Prognostic Factors
Genetic and physiological. Binge-eating disorder appears to run in families, which may
reflect additive genetic influences.
Culture-Reiated Diagnostic issues
Binge-eating disorder occurs with roughly similar frequencies in most industrialized
countries, including the United States, Canada, many European countries, Australia, and
New Zealand. In the United States, the prevalence of binge-eating disorder appears comparable among non-Latino whites. Latinos, Asians, and African Americans.
Functionai Consequences of Binge-Eating Disorder
Binge-eating disorder is associated with a range of functional consequences, including social role adjustment problems, impaired health-related quality of life and life satisfaction,
increased medical morbidity and mortality, and associated increased health care utilization compared with body mass index (BMI)-matched control subjects. It may also be associated with an increased risk for weight gain and the development of obesity.
Differential Diagnosis
Bulimia neivosa. Binge-eating disorder has recurrent binge eating in common with bulimia nervosa but differs from the latter disorder in some fundamental respects. In terms of
clinical presentation, the recurrent inappropriate compensatory behavior (e.g., purging,
driven exercise) seen in bulimia nervosa is absent in binge-eating disorder. Unlike individuals with bulimia nervosa, individuals with binge-eating disorder typically do not
show marked or sustained dietary restriction designed to influence body weight and
shape between binge-eating episodes. They may, however, report frequent attempts at
dieting. Binge-eating disorder also differs from bulimia nervosa in terms of response to treatment. Rates of improvement are consistently higher among individuals with binge-eating
disorder than among those with bulimia nervosa.
Obesity. Binge-eating disorder is associated with overweight and obesity but has
several key features that are distinct from obesity. First, levels of overvaluation of body
weight and shape are higher in obese individuals with the disorder than in those without
the disorder. Second, rates of psychiatric comorbidity are significantly higher among
obese individuals with the disorder compared with those without the disorder. Third, the
long-term successful outcome of evidence-based psychological treatments for bingeeating disorder can be contrasted with the absence of effective long-term treatments for
obesity.
Bipolar and depressive disorders. Increases in appetite and weight gain are included
in the criteria for major depressive episode and in the atypical features specifiers for depressive and bipolar disorders. Increased eating in the context of a major depressive episode may or may not be associated with loss of control. If the full criteria for both disorders
are met, both diagnoses can be given. Binge eating and other symptoms of disordered eating are seen in association with bipolar disorder. If the full criteria for both disorders are
met, both diagnoses should be given.
Borderline personality disorder. Binge eating is included in the impulsive behavior criterion that is part of the definition of borderline personality disorder. If the full criteria for
both disorders are met, both diagnoses should be given.
Comorbidity
Binge-eating disorder is associated with significant psychiatric comorbidity that is comparable to that of bulimia nervosa and anorexia nervosa. The most common comorbid disorders are bipolar disorders, depressive disorders, anxiety disorders, and, to a lesser
degree, substance use disorders. The psychiatric comorbidity is linked to the severity of
binge eating and not to the degree of obesity.
Other Specified Feeding or Eating Disorder
307.59 (F50.8)
This category applies to presentations in which symptoms characteristic of a feeding and
eating disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for
any of the disorders in the feeding and eating disorders diagnostic class. The other specified feeding or eating disorder category is used in situations in which the clinician chooses
to communicate the specific reason that the presentation does not meet the criteria for any
specific feeding and eating disorder. This is done by recording “other specified feeding or
eating disorder” followed by the specific reason (e.g., “bulimia nervosa of low frequency”).
Examples of presentations that can be specified using the “other specified” designation
include the following:
1. Atypical anorexia nervosa: All of the criteria for anorexia nervosa are met, except
that despite significant weight loss, the individual’s weight is within or above the normal
range.
2. Bulimia nervosa (of low frequency and/or limited duration): All of the criteria for
bulimia nervosa are met, except that the binge eating and inappropriate compensatory
behaviors occur, on average, less than once a week and/or for less than 3 months.
3. Binge-eating disorder (of low frequency and/or limited duration): All of the criteria
for binge-eating disorder are met, except that the binge eating occurs, on average, less
than once a week and/or for less than 3 months.
4. Purging disorder: Recurrent purging behavior to influence weight or shape (e.g., selfinduced vomiting: misuse of laxatives, diuretics, or other medications) in the absence
of binge eating.
5. Night eating syndrome: Recurrent episodes of night eating, as manifested by eating
after awakening from sleep or by excessive food consumption after the evening meal.
There Is awareness and recall of the eating. The night eating is not better explained by
external influences such as changes in the individual’s sleep-wake cycle or by local social norms. The night eating causes significant distress and/or impairment in functioning. The disordered pattern of eating is not better explained by binge-eating disorder
or another mental disorder, including substance use, and is not attributable to another
medical disorder or to an effect of medication.
Unspecified Feeding or Eating Disorder
307.50 (F50.9)
This category applies to presentations in which symptoms characteristic of a feeding and
eating disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of functioning predominate but do not meet the full criteria for
any of the disorders in the feeding and eating disorders diagnostic class. The unspecified
feeding and eating disorder category is used in situations in which the clinician chooses
not to specify the reason that the criteria are not met for a specific feeding and eating disorder, and includes presentations in which there is insufficient information to make a more
specific diagnosis (e.g., in emergency room settings).
Elimination
Disorders
Elimin3tion diSOrdGrSall involve the inappropriate elimination of urine or feces
and are usually first diagnosed in childhood or adolescence. This group of disorders includes enuresis, the repeated voiding of urine into inappropriate places, and encopresis, the
repeated passage of feces into inappropriate places. Subtypes are provided to differentiate
nocturnal from diurnal (i.e., during waking hours) voiding for enuresis and the presence or
absence of constipation and overflow incontinence for encopresis. Although there are minimum age requirements for diagnosis of both disorders, these are based on developmental
age and not solely on chronological age. Both disorders may be volimtary or involuntary.
Although these disorders typically occur separately, co-occurrence may also be observed.
Enuresis
Diagnostic Criteria 307.6 (F98.0)
A. Repeated voiding of urine into bed or clothes, whether involuntary or intentional.
B. The behavior is clinically significant as manifested by either a frequency of at least twice a
week for at least 3 consecutive months or the presence of clinically significant distress or
impairment in social, academic (occupational), or other important areas of functioning.
C. Chronological age is at least 5 years (or equivalent developmental level).
D. The behavior is not attributable to the physiological effects of a substance (e.g., a diuretic, an antipsychotic medication) or another medical condition (e.g., diabetes, spina
bifida, a seizure disorder).
Specify whether:
Nocturnal only: Passage of urine only during nighttime sleep.
Diurnal only: Passage of urine during waking hours.
Nocturnal and diurnal: A combination of the two subtypes above.
Subtypes
The noctumal-only subtype of enuresis, sometimes referred to as monosymptomatic enuresis, is the most common subtype and involves incontinence only during nighttime sleep,
typically during the first one-third of the night. The diurnal-only subtype occurs in the
absence of nocturnal enuresis and may be referred to simply as urinary incontinence. Individuals with this subtype can be divided into two groups. Individuals with ''urge incontinence" have sudden urge symptoms and detrusor instability, whereas individuals with
"voiding postponement" consciously defer micturition urges until incontinence results.
The noctumal-and-diurnal subtype is also known as nonmonosymptomatic enuresis.
Diagnostic Features
The essential feature of enuresis is repeated voiding of urine during the day or at night into
bed or clothes (Criterion A). Most often the voiding is involuntary, but occasionally it may
be intentional. To qualify for a diagnosis of enuresis, the voiding of urine must occur at
least twice a week for at least 3 consecutive months or must cause clinically significant distress or impairment in social, academic (occupational), or other important areas of functioning (Criterion B). The individual must have reached an age at which continence is
expected (i.e., a chronological age of at least 5 years or, for children with developmental
delays, a mental age of at least 5 years) (Criterion C). The urinary incontinence is not attributable to the physiological effects of a substance (e.g., a diuretic, an antipsychotic medication) or another medical condition (e.g., diabetes, spina bifida, a seizure disorder)
(Criterion D).
Associated Features Supporting Diagnosis
Ehiring nocturnal enuresis, occasionally the voiding takes place during rapid eye movement
(REM) sleep, and the child may recall a dream that involved the act of urinating. During daytime (diurnal) enuresis, the child defers voiding until incontinence occurs, sometimes because
of a reluctance to use the toilet as a result of social anxiety or a preoccupation with school or
play activity. The enuretic event most commonly occurs in the early afternoon on school days
and may be associated with symptoms of disruptive behavior. The enuresis commonly persists after appropriate treatment of an associated infection.
Prevaience
The prevalence of enuresis is 5%-10% among 5-year-olds, 3%-5% among 10-year-olds,
and around 1% among individuals 15 years or older.
Deveiopment and Course
Two types of course of enuresis have been described: a "primary" type, in which the individual has never established urinary continence, and a "secondary" type, in which the disturbance develops after a period of established urinary continence. There are no differences
in prevalence of comorbid mental disorders between the two types. By definition, primary
enuresis begins at age 5 years. The most common time for the onset of secondary enuresis
is between ages 5 and 8 years, but it may occur at any time. After age 5 years, the rate of spontaneous remission is 5%-10% per year. Most children with the disorder become continent
by adolescence, but in approximately 1% of cases the disorder continues into adulthood.
Diurnal enuresis is uncommon after age 9 years. While occasional diurnal incontinence is
not uncommon in middle childhood, it is substantially more common in those who also
have persistent nocturnal enuresis. When enuresis persists into late childhood or adolescence, the frequency of incontinence may increase, whereas continence in early childhood
is usually associated with a declining frequency of wet nights.
Risic and Prognostic Factors
Environmental. A number of predisposing factors for enuresis have been suggested, including delayed or lax toilet training and psychosocial stress.
Genetic and physiological. Enuresis has been associated with delays in the development of normal circadian rhythms of urine production, with resulting nocturnal polyuria
or abnormalities of central vasopressin receptor sensitivity, and reduced functional bladder capacities with bladder hyperreactivity (unstable bladder syndrome). Nocturnal enuresis is a genetically heterogeneous disorder. Heritability has been shown in family, twin,
and segregation analyses. Risk for childhood nocturnal enuresis is approximately 3.6 times
higher in offspring of enuretic mothers and 10.1 times higher in the presence of paternal
urinary incontinence. The risk magnitudes for nocturnal enuresis and diurnal incontinence
are similar.
Culture-Related Diagnostic Issues
Enuresis has beeh reported in a variety of European, African, and Asian countries as well
as in the United States. At a national level, prevalence rates are remarkably similar, and
there is great similarity in the developmental trajectories found in different countries.
There are very high rates of enuresis in orphanages and other residential institutions,
likely related to the mode and environment in which toilet training occurs.
Gender-Related Diagnostic issues
Nocturnal enuresis is more common in males. Diurnal incontinence is more common in females. The relative risk of having a child who develops enuresis is greater for previously
enuretic fathers than for previously enuretic mothers.
Functional Consequences of Enuresis
The amount of impairment associated with enuresis is a function of the limitation on the
child's social activities (e.g., ineligibility for sleep-away camp) or its effect on the child's
self-esteem, the degree of social ostracism by peers, and the anger, punishment, and rejection on the part of caregivers.
Differential Diagnosis
Neurogenic bladder or another medical condition. The diagnosis of enuresis is not made
in the presence of a neurogenic bladder or another medical condition that causes polyuria or
urgency (e.g., untreated diabetes mellitus or diabetes insipidus) or during an acute urinary
tract infection. However, a diagnosis is compatible with such conditions if urinary incontinence was regularly present prior to the development of another medical condition or if it persists after the institution of appropriate treatment of the medical condition.
Medication side effects. Enuresis may occur during treatment with antipsychotic medications, diuretics, or other medications that may induce incontinence. In this case, the diagnosis should not be made in isolation but may be noted as a medication side effect.
However, a diagnosis of enuresis may be made if urinary incontinence was regularly present prior to treatment with the medication.
Comorbidity
Although most children with enuresis do not have a comorbid mental disorder, the prevalence
of comorbid behavioral symptoms is higher in children with enuresis than in children without
enuresis. Developmental delays, including speech, language, learning, and motor skills
delays, are also present in a portion of children with enuresis. Encopresis, sleepwalking, and
sleep terror disorder may be present. Urinary tract infections are more common in children
with enuresis, especially the diurnal subtype, than in those who are continent.
Encopresis
Diagnostic Criteria 307.7 (F98.1)
A. Repeated passage of feces into inappropriate places (e.g., clothing, floor), whether involuntary or intentional.
B. At least one such event occurs each month for at least 3 months.
C. Chronological age is at least 4 years (or equivalent developmental level).
D. The behavior is not attributable to the physiological effects of a substance (e.g., laxatives) or another medical condition except through a mechanism involving constipation.
Specify whether:
With constipation and overflow incontinence: There is evidence of constipation on
physical examination or by history.
Without constipation and overflow incontinence: There is no evidence of constipation on physical examination or by history.
Subtypes
Feces in the with constipation and overflow incontinence subtype are characteristically
(but not invariably) poorly formed, and leakage can be infrequent to continuous, occurring mostly during the day and rarely during sleep. Only part of the feces is passed during
toileting, and the incontinence resolves after treatment of the constipation.
In the without constipation and overflow incontinence subtype, feces are likely to be of
normal form and consistency, and soiling is intermittent. Feces may be deposited in a
prominent location. This is usually associated with the presence of oppositional defiant
disorder or conduct disorder or may be the consequence of anal masturbation. Soiling
without constipation appears to be less common than soiling with constipation.
Diagnostic Features
The essential feature of encopresis is repeated passage of feces into inappropriate places (e.g.,
clothing or floor) (Criterion A). Most often the passage is involimtary but occasionally may be
intentional. The event must occur at least once a month for at least 3 months (Criterion B), and
the chronological age of the child must be at least 4 years (or for children with developmental
delays, the mental age must be at least 4 years) (Criterion C). The fecal incontinence must not
be exclusively attributable to the physiological effects of a substance (e.g., laxatives) or another
medical condition except through a mechanism involving constipation (Criterion D).
When the passage of feces is involuntary rather than intentional, it is often related to
constipation, impaction, and retention with subsequent overflow. The constipation may
develop for psychological reasons (e.g., anxiety about defecating in a particular place, a
more general pattern of anxious or oppositional behavior), leading to avoidance of defecation. Physiological predispositions to constipation include ineffectual straining or paradoxical defecation dynamics, with contraction rather than relaxation of the external sphincter
or pelvic floor during straining for defecation. Dehydration associated with a febrile illness, hypothyroidism, or a medication side effect can also induce constipation. Once constipation has developed, it may be complicated by an anal fissure, painful defecation, and
further fecal retention. The consistency of the stool may vary. In some individuals the stool
may be of normal or near-normal consistency. In other individuals—such as those with
overflow incontinence secondary to fecal retention—it may be liquid.
Associated Features Supporting Diagnosis
The child with encopresis often feels ashamed and may wish to avoid situations (e.g.,
camp, school) that might lead to embarrassment. The amount of impairment is a function
of the effect on the child's self-esteem, the degree of social ostracism by peers, and the anger, punishment, and rejection on the part of caregivers. Smearing feces may be deliberate
or accidental, resulting from the child's attempt to clean or hide feces that were passed involuntarily. When the incontinence is clearly deliberate, features of oppositional defiant
disorder or conduct disorder may also be present. Many children with encopresis and
chronic constipation also have enuresis symptoms and may have associated urinary reflux
in the bladder or ureters that may lead to chronic urinary infections, the symptoms of
which may remit with treatment of the constipation.
Prevalence
It is estimated thiht approximately 1% of 5-year-olds have encopresis, and the disorder is
more common in males than in females.
Development and Course
Encopresis is not diagnosed until a child has reached a chronological age of at least 4 years
(or for children with developmental delays, a mental age of at least 4 years). Inadequate,
inconsistent toilet training and psychosocial stress (e.g., entering school, the birth of a sibling) may be predisposing factors. Two types of course have been described: a "primary"
type, in which the individual has never established fecal continence, and a "secondary"
type, in which the disturbance develops after a period of established fecal continence. Encopresis can persist, with intermittent exacerbations, for years.
Risk and Prognostic Factors
Genetic and physiological. Painful defecation can lead to constipation and a cycle of withholding behaviors that make encopresis more likely. Use of some medications (e.g., anticonvulsants, cough suppressants) may increase constipation and make encopresis more
likely.
Diagnostic IVIarkers
In addition to physical examination, gastrointestinal imaging (e.g., abdominal radiograph)
may be informative to assess retained stool and gas in the colon. Additional tests, such as
barium enema and anorectal manography, may be used to help exclude other medical
conditions, such as Hirschsprung's disease.
Differential Diagnosis
A diagnosis of encopresis in the presence of another medical condition is appropriate only
if the mechanism involves constipation that cannot be explained by other medical conditions. Fecal incontinence related to other medical conditions (e.g., chronic diarrhea, spina
bifida, anal stenosis) would not warrant a DSM-5 diagnosis of encopresis.
Comorbidity
Urinary tract infections can be comorbid with encopresis and are more common in females.
Other Specified Elimination Disorder
This category applies to presentations in which symptoms characteristic of an elimination
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the elimination disorders diagnostic class. The other specified elimination
disorder category is used in situations in which the clinician chooses to communicate the
specific reason that the presentation does not meet the criteria for any specific elimination
disorder. This is done by recording “other specified elimination disorder” followed by the
specific reason (e.g., “low-frequency enuresis”).
Coding note: Code 788.39 (N39.498) for other specified elimination disorder with urinary
symptoms: 787.60 (R15.9) for other specified elimination disorder with fecal symptoms.
Unspecified Elimination Disorder
This category applies to presentations in which symptoms characteristic of an elimination
disorder that cause clinically significant distress or impairment in social, occupational, or
other important areas of functioning predominate but do not meet the full criteria for any of
the disorders in the elimination disorders diagnostic class. The unspecified elimination disorder category is used in situations in which the clinician chooses nof to specify the reason
that the criteria are not met for a specific elimination disorder, and includes presentations
in which there is insufficient information to make a more specific diagnosis (e.g., in emergency room settings).
Coding note: Code 788.30 (R32) for unspecified elimination disorder with urinary symptoms; 787.60 (R15.9) for unspecified elimination disorder with fecal symptoms.
Sleep-W&k^
ThG DSM-5 Cl3SSifiC3tion of sleep-wake disorders is intended for use by general
mental health and medical clinicians (those caring for adult, geriatric, and pediatric patients). Sleep-wake disorders encompass 10 disorders or disorder groups: insomrüa disorder, hypersomjiolence disorder, narcolepsy, breathing-related sleep disorders, circadian
rhythm sleep-wake disorders, non-rapid eye movement (NREM) sleep arousal disorders,
nightmare disorder, rapid eye movement (REM) sleep behavior disorder, restless legs syndrome, and substance/medication-induced sleep disorder. Individuals with these disorders typically present with sleep-wake complaints of dissatisfaction regarding the quality,
timing, and amount of sleep. Resulting daytime distress and impairment are core features
shared by all of these sleep-wake disorders.
The organization of this chapter is designed to facilitate differential diagnosis of sleepwake complaints and to clarify when referral to a sleep specialist is appropriate for further
assessment and treatment planning. The DSM-5 sleep disorders nosology uses a simple,
clinically useful approach, while also reflecting scientific advances in epidemiology, genetics, pathophysiology, assessment, and interventions research since DSM-IV. In some
cases (e.g., insomnia disorder), a "lumping" approach has been adopted, whereas in others (e.g., narcolepsy), a "splitting" approach has been taken, reflecting the availability of
validators derived from epidemiological, neurobiological, and interventions research.
Sleep disorders are often accompanied by depression, anxiety, and cognitive changes
that must be addressed in treatment planning and management. Furthermore, persistent
sleep disturbances (both insomnia and excessive sleepiness) are established risk factors for
the subsequent development of mental illnesses and substance use disorders. They may
also represent a prodromal expression of an episode of mental illness, allowing the possibility of early intervention to preempt or to attenuate a full-blown episode.
The differential diagnosis of sleep-wake complaints necessitates a multidimensional
approach, with consideration of possibly coexisting medical and neurological conditions.
Coexisting clinical conditions are the rule, not the exception. Sleep disturbances furnish a
clinically useful indicator of medical and neurological conditions that often coexist with
depression and other common mental disorders. Prominent among these comorbidities
are breathing-related sleep disorders, disorders of the heart and lungs (e.g., congestive
heart failure, chronic obstructive pulmonary disease), neurodegenerative disorders (e.g.,
Alzheimer's disease), and disorders of the musculoskeletal system (e.g., osteoarthritis).
These disorders not only may disturb sleep but also may themselves be worsened during
sleep (e.g., prolonged apneas or electrocardiographic arrhythmias during REM sleep; confusional arousals in patients with dementing illness; seizures in persons with complex
partial seizures). REM sleep behavior disorder is often an early indicator of neurodegenerative disorders (alpha synucleinopathies) like Parkinson's disease. For all of these reasons—related to differential diagnosis, clinical comorbidity, and facilitation of treatment
planning—sleep disorders are included in DSM-5.
The approach taken to the classification of sleep-wake disorders in DSM-5 can be understood within the context of "lumping versus splitting." DSM-IV represented an effort to
simplify sleep-wake disorders classification and thus aggregated diagnoses under broader,
less differentiated labels. At the other pole, the International Classification of Sleep Disorders,
2nd Edition (ICSD-2) elaborated numerous diagnostic subtypes. DSM-IV was prepared for
use by mental health and general medical clinicians who are not experts in sleep medicine.
ICSD-2 reflected the science and opinions of the sleep specialist community and was prepared for use by specialists.
The weight of available evidence supports the superior performance characteristics
(interrater reliability, as well as convergent, discriminant, and face validity) of simpler, lessdifferentiated approaches to diagnosis of sleep-wake disorders. The text accompanying
each set of diagnostic criteria provides linkages to the corresponding disorders included in
ICSD-2. The DSM-5 sleep-wake disorders classification also specifies corresponding nonpsychiatric listings (e.g., neurology codes) from the International Classification of Diseases
(ICD).
The field of sleep disorders medicine has progressed in this direction since the publication of DSM-IV. The use of biological validators is now embodied in the DSM-5 classification of sleep-wake disorders, particularly for disorders of excessive sleepiness, such as
narcolepsy; for breathing-related sleep disorders, for which formal sleep studies (i.e.,
polysomnography) are indicated; and for restless legs syndrome, which can often coexist
with periodic limb movements during sleep, detectable via polysomnography.
Insomnia Disorder
Diagnostic Criteria 780.52 (G47.00)
A. A predominant complaint of dissatisfaction witli sleep quantity or quality, associated
with one (or more) of the following symptoms:
1. Difficulty initiating sleep. (In children, this may manifest as difficulty initiating sleep
without caregiver intervention.)
2. Difficulty maintaining sleep, characterized by frequent awakenings or problems returning to sleep after awakenings. (In children, this may manifest as difficulty returning to sleep without caregiver intervention.)
3. Early-morning awakening with inability to return to sleep.
B. The sleep disturbance causes clinically significant distress or impairment in social, occupational, educational, academic, behavioral, or other important areas of functioning.
C. The sleep difficulty occurs at least 3 nights per week.
D. The sleep difficulty is present for at least 3 months.
E. The sleep difficulty occurs despite adequate opportunity for sleep.
F. The insomnia is not better explained by and does not occur exclusively during the
course of another sleep-wake disorder (e.g., narcolepsy, a breathing-related sleep disorder, a circadian rhythm sleep-wake disorder, a parasomnia).
G. The insomnia is not attributable to the physiological effects of a substance (e.g., a drug
of abuse, a medication).
H. Coexisting mental disorders and medical conditions do not adequately explain the predominant complaint of insomnia.
Specify if:
With non-sleep disorder mental comorbidity, including substance use disorders
With other medical comorbidity
With other sleep disorder
Coding note: The code 780.52 (G47.00) applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder immediately after the code for insomnia disorder in order to indicate the association.
Specify if:
Episodic: Sy(nptoms last at least 1 month but less than 3 months.
Persistent: Symptoms last 3 months or longer.
Recurrent: Two (or more) episodes within the space of 1 year.
Note: Acute and short-term insomnia (i.e., symptoms lasting less than 3 months but othenA/ise meeting all criteria with regard to frequency, intensity, distress, and/or impairment)
should be coded as an other specified insomnia disorder.
Note. The diagnosis of insomnia disorder is given whether it occurs as an independent
condition or is comorbid with another mental disorder (e.g., major depressive disorder),
medical condition (e.g., pain), or another sleep disorder (e.g., a breathing-related sleep disorder). For instance, insomnia may develop its own course with some anxiety and depressive features but in the absence of criteria being met for any one mental disorder. Insomnia
may also manifest as a clinical feature of a more predominant mental disorder. Persistent
insomnia may even be a risk factor for depression and is a common residual symptom after treatment for this condition. With comorbid insomnia and a mental disorder, treatment
may also need to target both conditions. Given these different courses, it is often impossible to establish the precise nature of the relationship between these clinical entities, and
this relationship may change over time. Therefore, in the presence of insomnia and a comorbid disorder, it is not necessary to make a causal attribution between the two conditions. Rather, the diagnosis of insomnia disorder is made with concurrent specification of
the clinically comorbid conditions. A concurrent insomnia diagnosis should only be considered when the insomnia is sufficiently severe to warrant independent clinical attention;
otherwise, no separate diagnosis is necessary.
Diagnostic Features
The essential feature of insomnia disorder is dissatisfaction with sleep quantity or quality
with complaints of difficulty initiating or maintaining sleep. The sleep complaints are accompanied by clinically significant distress or impairment in social, occupational, or other
important areas of functioning. The sleep disturbance may occur during the course of another mental disorder or medical condition, or it may occur independently.
Different manifestations of insomnia can occur at different times of the sleep period. Sleeponset insomnia (or initial insomnia) involves difficulty initiating sleep at bedtime. Sleep maintenance insomnia (or middle insomnia) involves frequent or prolonged awakenings throughout
the night. Late insomnia involves early-morning awakening with an inability to return to sleep.
Difficulty maintaining sleep is the most common single symptom of insomnia, followed by
difficulty falling asleep, while a combination of these symptoms is the most common presentation overall. The specific type of sleep complaint often varies over time. Individuals who
complain of difficulty falling asleep at one time may later complain of difficulty maintaining
sleep, and vice versa. Symptoms of difficulty falling asleep and difficulty maintaining sleep
can be quantified by the individual's retrospective self-report, sleep diaries, or other methods,
such as actigraphy or polysomnography, but the diagnosis of insomnia disorder is based on
the individual's subjective perception of sleep or a caretaker's report.
Nonrestorative sleep, a complaint of poor sleep quality that does not leave the individual
rested upon awakening despite adequate duration, is a common sleep complaint usually
occurring in association with difficulty initiating or maintaining sleep, or less frequently in
isolation. This complaint can also be reported in association with other sleep disorders
(e.g., breathing-related sleep disorder). When a complaint of nonrestorative sleep occurs
in isolation (i.e., in the absence of difficulty initiating and/or maintaining sleep) but all diagnostic criteria with regard to frequency, duration, and daytime distress and impairments
are otherwise met, a diagnosis of other specified insomnia disorder or unspecified insomnia disorder is made.
Aside from the frequency and duration criteria required to make the diagnosis, additional criteria are useful to quantify insomnia severity. These quantitative criteria, while
arbitrary, are provided for illustrative purpose only. For instance, difficulty initiating sleep
is defined by a subjective sleep latency greater than 20-30 minutes, and difficulty maintaining sleep is defined by a subjective time awake after sleep onset greater than 20-30 minutes. Although there is no standard definition of early-morning awakening, this symptom
involves awakening at least 30 minutes before the scheduled time and before total sleep
time reaches hours. It is essential to take into account not only the final awakening time
but also the bedtime on the previous evening. Awakening at 4:00 A.M. does not have the
same clinical significance in those who go to bed at 9:00 P.M. as in those who go to bed at
11:00 P.M. Such a symptom may also reflect an age-dependent decrease in the ability to sustain sleep or an age-dependent shift in the timing of the main sleep period.
Insomnia disorder involves daytime impairments as well as nighttime sleep difficulties.
These include fatigue or, less commonly, daytime sleepiness; the latter is more common
among older individuals and when insomnia is comorbid with another medical condition
(e.g., chronic pain) or sleep disorder (e.g., sleep apnea). Impairment in cognitive performance
may include difficulties with attention, concentration and memory, and even with performing
simple manual skills. Associated mood disturbances are typically described as irritability or
mood lability and less commonly as depressive or anxiety symptoms. Not all individuals with
nighttime sleep disturbances are distressed or have functional impairment. For example, sleep
continuity is often interrupted in healthy older adults who nevertheless identify themselves
as good sleepers. A diagnosis of insomnia disorder should be reserved for those individuals
with significant daytime distress or impairment related to their nighttime sleep difficulties.
Associated Features Supporting Diagnosis
Insomnia is often associated with physiological and cognitive arousal and conditioning
factors that interfere with sleep. A preoccupation with sleep and distress due to the inability to sleep may lead to a vicious cycle: the more the individual strives to sleep, the more
frustration builds and further impairs sleep. Thus, excessive attention and efforts to sleep,
which override normal sleep-onset mechanisms, may contribute to the development of insomnia. Individuals with persistent insomnia may also acquire maladaptive sleep habits
(e.g., spending excessive time in bed; following an erratic sleep schedule; napping) and
cognitions (e.g., fear of sleeplessness; apprehensions of daytime impairments; clock monitoring) during the course of the disorder. Engaging in such activities in an environment in
which the individual has frequently spent sleepless nights may further compound the conditioned arousal and perpetuate sleep difficulties. Conversely, the individual may fall asleep
more easily when not trying to do so. Some individuals also report better sleep when away
from their own bedrooms and their usual routines.
Insomnia may be accompanied by a variety of daytime complaints and symptoms, including fatigue, decreased energy, and mood disturbances. Symptoms of anxiety or depression that do not meet criteria for a specific mental disorder may be present, as well as
an excessive focus on the perceived effects of sleep loss on daytime functioning.
Individuals with insomnia may have elevated scores on self-report psychological or
personality inventories with profiles indicating mild depression and anxiety, a worrisome
cognitive style, an emotion-focused and internalizing style of conflict resolution, and a somatic focus. Patterns of neurocognitive impairment among individuals with insomnia disorder are inconsistent, although there may be impairments in performing tasks of higher
complexity and those requiring frequent changes in performance strategy. Individuals
with insomnia often require more effort to maintain cognitive performance.
Prevalence
Population-based estimates indicate that about one-third of adults report insomnia symptoms, 10%-15% experience associated daytime impairments, and 6% -10% have symptoms
that meet criteria for insonmia disorder. Insomnia disorder is the most prevalent of all
sleep disorders. ù;i primary care settings, approximately 10%-20% of individuals complain
of significant insomnia symptoms. Insomnia is a more prevalent complaint among females than among males, with a gender ratio of about 1.44:1. Although insomnia can be a
symptom or an independent disorder, it is most frequently observed as a comorbid condition with another medical condition or mental disorder. For instance, 40%-50% of individuals with insomnia also present with a comorbid mental disorder.
Development and Course
The onset of insomnia symptoms can occur at any time during life, but the first episode is
more common in young adulthood. Less frequently, insomnia begins in childhood or adolescence. In women, new-onset insomnia may occur during menopause and persist even
after other symptoms (e.g., hot flashes) have resolved. Insomnia may have a late-life onset,
which is often associated with the onset of other health-related conditions.
Insomnia can be situational, persistent, or recurrent. Situational or acute insomnia usually lasts a few days or a few weeks and is often associated with life events or rapid changes
in sleep schedules or environment. It usually resolves once the initial precipitating event
subsides. For some individuals, perhaps those more vulnerable to sleep disturbances, insomnia may persist long after the initial triggering event, possibly because of conditioning
factors and heightened arousal. The factors that precipitate insomnia may differ from
those that perpetuate it. For example, an individual who is bedridden with a painful injury
and has difficulty sleeping may then develop negative associations for sleep. Conditioned
arousal may then persist and lead to persistent insomnia. A similar course may develop in
the context of an acute psychological stress or a mental disorder. For instance, insomnia that
occurs during an episode of major depressive disorder can become a focus of attention,
with consequent negative conditioning, and persist even after resolution of the depressive
episode. In some cases, insomnia may also have an insidious onset without any identifiable precipitating factor.
The course of insomnia may also be episodic, with recurrent episodes of sleep difficulties associated with the occurrence of stressful events. Chronicity rates range from 45%
to 75% for follow-ups of 1-7 years. Even when the course of the insomnia has become
chronic, there is night-to-night variability in sleep patterns, with an occasional restful night's
sleep interspersed with several nights of poor sleep. The characteristics of insomnia may
also change over time. Many individuals with insomnia have a history of "light" or easily
disturbed sleep prior to onset of more persistent sleep problems.
Insomnia complaints are more prevalent among middle-age and older adults. The type
of insomnia symptom changes as a function of age, with difficulties initiating sleep being
more common among young adults and problems maintaining sleep occurring more frequently among middle-age and older individuals.
Difficulties initiating and maintaining sleep can also occur in children and adolescents,
but there are more limited data on prevalence, risk factors, and comorbidity during these
developmental phases of the lifespan. Sleep difficulties in childhood can result from conditioning factors (e.g., a child who does not learn to fall asleep or return to sleep without
the presence of a parent) or from the absence of consistent sleep schedules and bedtime
routines. Insomnia in adolescence is often triggered or exacerbated by irregular sleep schedules (e.g., phase delay). In both children and adolescents, psychological and medical factors can contribute to insomnia.
The increased prevalence of insomnia in older adults is partly explained by the higher
incidence of physical health problems with aging. Changes in sleep patterns associated with
the normal developmental process must be differentiated from those exceeding age-related
changes. Although polysomnography is of limited value in the routine evaluation of insomnia, it may be more useful in the differential diagnosis among older adults because the
etiologies of insomnia (e.g., sleep apnea) are more often identifiable in older individuals.
Risk and Prognostic Factors
While the risk and prognostic factors discussed in this section increase vuhierability to insomnia, sleep disturbances are more likely to occur when predisposed individuals are exposed to precipitating events, such as major life events (e.g., illness, separation) or less
severe but more chronic daily stress. Most individuals resume normal sleep patterns after
the initial triggering event has disappeared, but others—perhaps those more vulnerable to
insomnia—continue experiencing persistent sleep difficulties. Perpetuating factors such as
poor sleep habits, irregular sleep scheduling, and the fear of not sleeping feed into the insomnia problem and may contribute to a vicious cycle that may induce persistent insomnia.
Temperamental. Anxiety or worry-prone personality or cognitive styles, increased arousal
predisposition, and tendency to repress emotions can increase vulnerability to insomnia.
Environmental. Noise, light, uncomfortably high or low temperature, and high altitude
may also increase vulnerability to insomnia.
Genetic and physiological. Female gender and advancing age are associated with increased vulnerability to insomnia. Disrupted sleep and insomnia display a familial disposition. The prevalence of insomnia is higher among monozygotic twins relative to
dizygotic twins; it is also higher in first-degree family members compared with the general
population. The extent to which this link is inherited through a genetic predisposition,
learned by observations of parental models, or established as a by-product of another psychopathology remains undetermined.
Course modifiers. Deleterious course modifiers include poor sleep hygiene practices
(e.g., excessive caffeine use, irregular sleep schedules).
Gender-Reiated Diagnostic issues
Insomnia is a more prevalent complaint among females than among males, with first onset
often associated with the birth of a new child or with menopause. Despite higher prevalence among older females, polysomnographic studies suggest better preservation of
sleep continuity and slow-wave sleep in older females than in older males.
Diagnostic iVlaricers
Polysomnography usually shows impairments of sleep continuity (e.g., increased sleep latency and time awake after sleep onset and decreased sleep efficiency [percentage of time
in bed asleep] and may show increased stage 1 sleep and decreased stages 3 and 4 sleep.
The severity of these sleep impairments does not always match the individual's clinical
presentation or subjective complaint of poor sleep, as individuals with insomnia often underestimate sleep duration and overestimate wakefulness relative to polysomnography.
Quantitative electroencephalographic analyses may indicate that individuals with insomnia have greater high-frequency electroencephalography power relative to good sleepers
both around the sleep onset period and during non-rapid eye movement sleep, a feature
suggestive of increased cortical arousal. Individuals with insomnia disorder may have a
lower sleep propensity and typically do not show increased daytime sleepiness on objective sleep laboratory measures compared with individuals without sleep disorders.
Other laboratory measures show evidence, although not consistently, of increased
arousal and a generalized activation of the hypothalamic-pituitary-adrenal axis (e.g., increased cortisol levels, heart rate variability, reactivity to stress, metabolic rate). In general,
findings are consistent with the hypothesis that increased physiological and cognitive
arousal plays a significant role in insomnia disorder.
Individuals with insomnia disorder may appear either fatigued or haggard or, conversely, overaroused and "wired." However, there are no consistent or characteristic
abnormalities on physical examination. There may be an increased incidence of stress-
related psychophysiological symptoms (e.g., tension headache, muscle tension or pain,
gastrointestinal symptoms).
Functional Consequences of Insomnia Disorder
Interpersonal, social, and occupational problems may develop as a result of insomnia or
excessive concern with sleep, increased daytime irritability, and poor concentration. Decreased attention and concentration are common and may be related to higher rates of accidents observed in insomnia. Persistent insomnia is also associated with long-term
consequences, including increased risks of major depressive disorder, hypertension, and
myocardial infarction; increased absenteeism and reduced productivity at work; reduced
quality of life; and increased economic burden.
Differential Diagnosis
Normal sleep variations. Normal sleep duration varies considerably across individuals.
Some individuals who require little sleep ("short sleepers") may be concerned about their
sleep duration. Short sleepers differ from individuals with insomnia disorder by the lack of
difficulty falling or staying asleep and by the absence of characteristic daytime symptoms
(e.g., fatigue, concentration problems, irritability). However, some short sleepers may desire
or attempt to sleep for a longer period of time and, by prolonging time in bed, may create an
insomnia-like sleep pattern. Clinical insomnia also should be distinguished from normal,
age-related sleep changes. Insomnia must also be distinguished from sleep deprivation due
to inadequate opportunity or circumstance for sleep resulting, for example, from an emergency or from professional or family obligations forcing the individual to stay awake.
Situational/acute insomnia. Situational/acute insomnia is a condition lasting a few days
to a few weeks, often associated with life events or with changes in sleep schedules. These
acute or short-term insomnia symptoms may also produce significant distress and interfere with social, personal, and occupational functioning. When such symptoms are frequent enough and meet all other criteria except for the 3-month duration, a diagnosis of
other specified insomnia disorder or unspecified insomnia disorder is made.
Delayed sleep phase and shift work types of circadian rhythm sleep-wake disorder.
Individuals with the delayed sleep phase type of circadian rhythm sleep-wake disorder report sleep-onset insomnia only when they try to sleep at socially normal times, but they do
not report difficulty falling asleep or staying asleep when their bed and rising times are
delayed and coincide with their endogenous circadian rhythm. Shift work type differs from
insomnia disorder by the history of recent shift work.
Restless legs syndrome. Restless legs syndrome often produces difficulties initiating
and maintaining sleep. However, an urge to move the legs and any accompanying unpleasant leg sensations are features that differentiate this disorder from insomnia disorder.
Breathing-related sleep disorders. Most individuals with a breathing-related sleep disorder have a history of loud snoring, breathing pauses during sleep, and excessive daytime
sleepiness. Nonetheless, as many as 50% of individuals with sleep apnea may also report
insomnia symptoms, a feature that is more common among females and older adults.
Narcolepsy. Narcolepsy may cause insomnia complaints but is distinguished from insomnia disorder by the predominance of symptoms of excessive daytime sleepiness, cataplexy, sleep paralysis, and sleep-related hallucinations.
Parasomnias. Parasomnias are characterized by a complaint of unusual behavior or events
during sleep that may lead to intermittent awakenings and difficulty resuming sleep.
However, it is these behavioral events, rather than the insomnia per se, that dominate the
clinical picture.
Substance/medication-induced sleep disorder, insomnia type. Substance/medicationinduced sleep disorder, insomnia type, is distinguished from insomnia disorder by the fact
that a substance (i.e., a drug of abuse, a medication, or exposure to a toxin) is judged to be
etiologically related to the insomnia (see "Substance/Medication-Induced Sleep Disorder" later in this chapter). For example, insomnia occurring only in the context of heavy
coffee consumption would be diagnosed as caffeine-induced sleep disorder, insomnia
type, with onset during intoxication.
Comorbidity
Insomnia is a common comorbidity of many medical conditions, including diabetes, coronary heart disease, chronic obstructive pulmonary disease, arthritis, fibromyalgia, and
other chronic pain conditions. The risk relationship appears to be bidirectional: insomnia
increases the risk of medical conditions, and medical problems increase the risk of insomnia. The direction of the relationship is not always clear and may change over time; for this
reason, comorbid insomnia is the preferred terminology in the presence of coexisting insomnia with another medical condition (or mental disorder).
Individuals with insomnia disorder frequently have a comorbid mental disorder, particularly bipolar, depressive, and anxiety disorders. Persistent insomnia represents a risk
factor or an early symptom of subsequent bipolar, depressive, anxiety, and substance use
disorders. Individuals with insomnia may misuse medications or alcohol to help with
nighttime sleep, anxiolytics to combat tension or anxiety, and caffeine or other stimulants
to combat excessive fatigue. In addition to worsening the insomnia, this type of substance
use may in some cases progress to a substance use disorder.
Relationship to international Classification of
Sleep Disorders
There are several distinct insomnia phenotypes relating to the perceived source of the insomnia that are recognized by the International Classification of Sleep Disorders, 2nd Edition
(ICSD-2). These include psychophysiological insomnia, idiopathic insomnia, sleep-state misperception, and inadequate sleep hygiene. Despite their clinical appeal and heuristic value, there is
limited evidence to support these distinct phenotypes.
Hypersomnolence Disorder
Diagnostic Criteria 780.54 (G47.10)
A. Self-reported excessive sleepiness (hypersomnolence) despite a main sleep period
lasting at least 7 hours, with at least one of the following symptoms:
1. Recurrent periods of sleep or lapses into sleep within the same day.
2. A prolonged main sleep episode of more than 9 hours per day that is nonrestorative
(i.e., unrefreshing).
3. Difficulty being fully awake after abrupt awakening.
B. The hypersomnolence occurs at least three times per week, for at least 3 months.
C. The hypersomnolence is accompanied by significant distress or impairment in cognitive, social, occupational, or other important areas of functioning.
D. The hypersomnolence is not better explained by and does not occur exclusively during
the course of another sleep disorder (e.g., narcolepsy, breathing-related sleep disorder, circadian rhythm sleep-wake disorder, or a parasomnia).
E. The hypersomnolence is not attributable to the physiological effects of a substance
(e.g., a drug of abuse, a medication).
F. Coexisting mental and medical disorders do not adequately explain the predominant
complaint of t^ypersomnolence.
Specify if:
With mental disorder, including substance use disorders
With medicai condition
With another sleep disorder
Coding note: The code 780.54 (G47.10) applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder immediately after the code for hypersomnolence disorder in order to indicate the association.
Specify if:
Acute: Duration of less than 1 month.
Subacute: Duration of 1-3 months.
Persistent: Duration of more than 3 months.
Specify current severity:
Specify severity based on degree of difficulty maintaining daytime alertness as manifested
by the occurrence of multiple attacks of irresistible sleepiness within any given day occurring, for example, while sedentary, driving, visiting with friends, or working.
Mild: Difficulty maintaining daytime alertness 1-2 days/week.
Moderate: Difficulty maintaining daytime alertness 3-^ days/week.
Severe: Difficulty maintaining daytime alertness 5-7 days/week.
Diagnostic Features
Hypersomnolence is a broad diagnostic term and includes symptoms of excessive quantity
of sleep (e.g., extended nocturnal sleep or involuntary daytime sleep), deteriorated quality
of wakefulness (i.e., sleep propensity during wakefulness as shown by difficulty awakening or inability to remain awake when required), and sleep inertia (i.e., a period of impaired performance and reduced vigilance following awakening from the regular sleep
episode or from a nap) (Criterion A). Individuals with this disorder fall asleep quickly and
have a good sleep efficiency (>90%). They may have difficulty waking up in the morning,
sometimes appearing confused, combative, or ataxic. This prolonged impairment of alertness at the sleep-wake transition is often referred to as sleep inertia (i.e., sleep drunkenness).
It can also occur upon awakening from a daytime nap. During that period, the individual
appears awake, but there is a decline in motor dexterity, behavior may be very inappropriate, and memory deficits, disorientation in time and space, and feelings of grogginess
may occur. This period may last some minutes to hours.
The persistent need for sleep can lead to automatic behavior (usually of a very routine,
low-complexity type) that the individual carries out with little or no subsequent recall. For
example, individuals may find themselves having driven several miles from where they
thought they were, unaware of the "automatic" driving they did in the preceding minutes.
For some individuals with hypersomnolence disorder, the major sleep episode (for most
individuals, nocturnal sleep) has a duration of 9 hours or more. However, the sleep is often
nonrestorative and is followed by difficulty awakening in the morning. For other individuals with hypersomnolence disorder, the major sleep episode is of normal nocturnal sleep
duration (6-9 hours). In these cases, the excessive sleepiness is characterized by several unintentional daytime naps. These daytime naps tend to be relatively long (often lasting 1 hour
or more), are experienced as nonrestorative (i.e., unrefreshing), and do not lead to improved
alertness. Individuals with hypersomnolence have daytime naps nearly everyday regardless of the nocturnal sleep duration. Subjective sleep quality may or may not be reported as
good. Individuals typically feel sleepiness developing over a period of time, rather than
experiencing a sudden sleep "attack." Unintentional sleep episodes typically occur in lowstimulation and low-activity situations (e.g., while attending lectures, reading, watching
television, or driving long distances), but in more severe cases they can manifest in highattention situations such as at work, in meetings, or at social gatherings.
Associated Features Supporting Diagnosis
Nonrestorative sleep, automatic behavior, difficulties awakening in the morning, and
sleep inertia, although common in hypersomnolence disorder, may also be seen in a variety
of conditions, including narcolepsy. Approximately 80% of individuals with hypersomnolence report that their sleep is nonrestorative, and as many have difficulties awakening in the morning. Sleep inertia, though less common (i.e., observed in 36%-50% of
individuals with hypersomnolence disorder), is highly specific to h)φersomnolence. Short
naps (i.e., duration of less than 30 minutes) are often unrefreshing. Individuals with hypersomnolence often appear sleepy and may even fall asleep in the clinician's waiting
area.
A subset of individuals with hypersomnolence disorder have a family history of hypersomnolence and also have symptoms of autonomic nervous system dysfunction, including recurrent vascular-type headaches, reactivity of the peripheral vascular system
(Raynaud's phenomenon), and fainting.
Prevaience
Approximately 5%-10% of individuals who consult in sleep disorders clinics with complaints of daytime sleepiness are diagnosed as having hypersomnolence disorder. It is estimated that about 1% of the European and U.S. general population has episodes of sleep
inertia. Hypersomnolence occurs with relatively equal frequency in males and females.
Deveiopment and Course
Hypersomnolence disorder has a persistent course, with a progressive evolution in the severity of symptoms. In most extreme cases, sleep episodes can last up to 20 hours. However, the average nighttime sleep duration is around 9Vi hours. While many individuals
with hypersomnolence are able to reduce their sleep time during working days, weekend
and holiday sleep is greatly increased (by up to 3 hours). Awakenings are very difficult
and accompanied by sleep inertia episodes in nearly 40% of cases. Hypersomnolence fully
manifests in most cases in late adolescence or early adulthood, with a mean age at onset of
17-24 years. Individuals with hypersomnolence disorder are diagnosed, on average, 10-15
years after the appearance of the first symptoms. Pediatric cases are rare.
Hypersomnolence has a progressive onset, with symptoms beginning between ages 15
and 25 years, with a gradual progression over weeks to months. For most individuals, the
course is then persistent and stable, unless treatment is initiated. The development of other
sleep disorders (e.g., breathing-related sleep disorder) may worsen the degree of sleepiness. Although hyperactivity may be one of the presenting signs of daytime sleepiness in
children, voluntary napping increases with age. This normal phenomenon is distinct from
hypersomnolence.
Risic and Prognostic Factors
Environmental. Hypersomnolence can be increased temporarily by psychological stress
and alcohol use, but they have not been documented as environmental precipitating
factors. Viral infections have been reported to have preceded or accompanied hypersomnolence in about 10% of cases. Viral infections, such as HIV pneumonia, infectious
mononucleosis, and Guillain-Barré syndrome, can also evolve into hypersomnolence within
months after the infection. Hypersomnolence can also appear within 6-18 months following a head traum;^.
Genetic and physiological. Hypersomnolence may be familial, with an autosomaldominant mode of inheritance.
Diagnostic iVlarlcers
Nocturnal polysomnography demonstrates a normal to prolonged sleep duration, short
sleep latency, and normal to increased sleep continuity. The distribution of rapid eye
movement (REM) sleep is also normal. Sleep efficiency is mostly greater than 90%. Some
individuals with hypersomnolence disorder have increased amounts of slow-wave sleep.
The multiple sleep latency test documents sleep tendency, typically indicated by mean
sleep latency values of less than 8 minutes. In hypersomnolence disorder, the mean sleep
latency is typically less than 10 minutes and frequently 8 minutes or less. Sleep-onset REM
periods (SOREMPs; i.e., the occurrence of REM sleep within 20 minutes of sleep onset)
may be present but occur less than two times in four to five nap opportunities.
Functional Consequences of Hypersomnoience Disorder
The low level of alertness that occurs while an individual fights the need for sleep can lead
to reduced efficiency, diminished concentration, and poor memory during daytime activities. Hypersomnoience can lead to significant distress and dysfunction in work and social
relationships. Prolonged nocturnal sleep and difficulty awakening can result in difficulty
in meeting morning obligations, such as arriving at work on time. Unintentional daytime
sleep episodes can be embarrassing and even dangerous, if, for instance, the individual is
driving or operating machinery when the episode occurs.
Differential Diagnosis
Normative variation in sleep. "Normal" sleep duration varies considerably in the general
population. "Long sleepers" (i.e., individuals who require a greater than average amount
of sleep) do not have excessive sleepiness, sleep inertia, or automatic behavior when they
obtain their required amount of nocturnal sleep. Sleep is reported to be refreshing. If social
or occupational demands lead to shorter nocturnal sleep, daytime symptoms may appear.
In hypersomnoience disorder, by contrast, symptoms of excessive sleepiness occur regardless of nocturnal sleep duration. An inadequate amount of nocturnal sleep, or behaviorally
induced insufficient sleep syndrome, can produce symptoms of daytime sleepiness very similar
to those of hypersomnoience. An average sleep duration of fewer than 7 hours per night
strongly suggests inadequate nocturnal sleep, and an average of more than 9-10 hours of
sleep per 24-hour period suggests hypersomnoience. Individuals with inadequate nocturnal sleep typically "catch up" with longer sleep durations on days when they are free from
social or occupational demands or on vacations. Unlike hypersomnoience, insufficient
nocturnal sleep is unlikely to persist unabated for decades. A diagnosis of hypersomnoience disorder should not be made if there is a question regarding the adequacy of nocturnal sleep duration. A diagnostic and therapeutic trial of sleep extension for 10-14 days can
often clarify the diagnosis.
Poor sleep quality and fatigue. Hypersomnoience disorder should be distinguished
from excessive sleepiness related to insufficient sleep quantity or quality and fatigue (i.e.,
tiredness not necessarily relieved by increased sleep and unrelated to sleep quantity or
quality). Excessive sleepiness and fatigue are difficult to differentiate and may overlap
considerably.
Breathing-related sleep disorders. Individuals with hypersomnoience and breathingrelated sleep disorders may have similar patterns of excessive sleepiness. Breathing-
related sleep disorders are suggested by a history of loud snoring, pauses in breathing
during sleep, brain injury, or cardiovascular disease and by the presence of obesity, oropharyngeal anatomical abnormalities, hypertension, or heart failure on physical examination. Polysomnographie studies can confirm the presence of apneic events in breathingrelated sleep disorder (and their absence in hypersomnolence disorder).
Circadian rhythm sleep-wake disorders. Circadian rhythm sleep-wake disorders are
often characterized by daytime sleepiness. A history of an abnormal sleep-wake schedule
(with shifted or irregular hours) is present in individuals with a circadian rhythm sleepwake disorder.
Parasomnias. Parasomnias rarely produce the prolonged, undisturbed nocturnal sleep
or daytime sleepiness characteristic of hypersomnolence disorder.
Other mental disorders. Hypersomnolence disorder must be distinguished from mental
disorders that include hypersomnolence as an essential or associated feature. In particular,
complaints of daytime sleepiness may occur in a major depressive episode, with atypical features, and in the depressed phase of bipolar disorder. Assessment for other mental disorders is
essential before a diagnosis of hypersomnolence disorder is considered. A diagnosis of hypersomnolence disorder can be made in the presence of another current or past mental disorder.
Comorbidity
H)φersomnolence can be associated with depressive disorders, bipolar disorders (during a
depressive episode), and major depressive disorder, with seasonal pattern. Many individuals with hypersomnolence disorder have symptoms of depression that may meet criteria for
a depressive disorder. This presentation may be related to the psychosocial consequences of
persistent increased sleep need. Individuals with hyper somnolence disorder are also at
risk for substance-related disorders, particularly related to self-medication with stimulants.
This general lack of specificity may contribute to very heterogeneous profiles among individuals whose symptoms meet the same diagnostic criteria for hypersomnolence disorder.
Neurodegenerative conditions, such as Alzheimer's disease, Parkinson's disease, and multiple system atrophy, may also be associated with hypersomnolence.
Reiationship to internatlonai Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates nine
subtypes of "hypersomnias of central origin," including recurrent hypersomnia (KleineLevin syndrome).
Narcolepsy
Diagnostic Criteria
A. Recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping occurring within the same day. These must have been occurring at least three times per
week over the past 3 months.
B. The presence of at least one of the following:
1. Episodes of cataplexy, defined as either (a) or (b), occurring at least a few times
per month:
a. In individuals with long-standing disease, brief (seconds to minutes) episodes
of sudden bilateral loss of muscle tone with maintained consciousness that are
precipitated by laughter or joking.
b. In children or in individuals within 6 months of onset, spontaneous grimaces or
jaw-opening episodes with tongue thrusting or a global hypotonia, without any
obvious emotional triggers.
2. Hypocretin deficiency, as measured using cerebrospinal fluid (CSF) hypocretin-1
immunoreactivity values (less than or equal to one-third of values obtained in
healthy subjects tested using the same assay, or less than or equal to 110 pg/mL).
Low CSF levels of hypocretin-1 must not be observed in the context of acute brain
injury, inflammation, or infection.
3. Nocturnal sleep polysomnography showing rapid eye movement (REM) sleep latency less than or equal to 15 minutes, or a multiple sleep latency test showing a
mean sleep latency less than or equal to 8 minutes and two or more sleep-onset
REM periods.
Specify whether:
347.00 (G47.419) Narcolepsy without cataplexy but with hypocretin deficiency: Criterion B requirements of low CSF hypocretin-1 levels and positive polysomnography/
multiple sleep latency test are met, but no cataplexy is present (Criterion B1 not met).
347.01 (G47.411) Narcolepsy with cataplexy but without hypocretin deficiency:
In this rare subtype (less than 5% of narcolepsy cases), Criterion B requirements of
cataplexy and positive polysomnography/multiple sleep latency test are met, but CSF
hypocretin-1 levels are normal (Criterion B2 not met).
347.00 (G47.419) Autosomal dominant cerebellar ataxia, deafness, and narcolepsy: This subtype is caused by exon 21 DNA (cytosine-5)-methyltransferase-1 mutations and is characterized by late-onset (age 30-40 years) narcolepsy (with low or
intermediate CSF hypocretin-1 levels), deafness, cerebellar ataxia, and eventually dementia.
347.00 (G47.419) Autosomal dominant narcolepsy, obesity, and type 2 diabetes:
Narcolepsy, obesity, and type 2 diabetes and low CSF hypocretin-1 levels have been
described in rare cases and are associated with a mutation in the myelin oligodendrocyte glycoprotein gene.
347.10 (G47.429) Narcolepsy secondary to another medical condition: This subtype is for narcolepsy that develops secondary to medical conditions that cause infectious (e.g., Whipple’s disease, sarcoidosis), traumatic, or tumoral destruction of
hypocretin neurons.
Coding note (for ICD-9-CM code 347.10 only): Code first the underlying medical condition (e.g., 040.2 Whipple’s disease; 347.10 narcolepsy secondary to Whipple’s disease).
Specify current severity:
IMild: Infrequent cataplexy (less than once per week), need for naps only once or twice
per day, and less disturbed nocturnal sleep.
Moderate: Cataplexy once daily or every few days, disturbed nocturnal sleep, and
need for multiple naps daily.
Severe: Drug-resistant cataplexy with multiple attacks daily, nearly constant sleepiness, and disturbed noctumal sleep (i.e., movements, insomnia, and vivid dreaming).
Subtypes
In narcolepsy without cataplexy but with hypocretin deficiency, unclear ''cataplexy-like"
symptoms may be reported (e.g., the symptoms are not triggered by emotions and are unusually long lasting). In extremely rare cases, cerebrospinal fluid (CSF) levels of hypocretin-1 are low, and polysomnographic/multiple sleep latency test (MSLT) results are
negative: repeating the test is advised before establishing the subtype diagnosis. In narco
lepsy with cataplexy but without hypocretin deficiency, test results for human leukocyte
antigen (HLA) DQBl’^06:02 may be negative. Seizures, falls of other origin, and conversion
disorder (functional neurological symptom disorder) should be excluded. In narcolepsy
secondary to infectious (e.g., Whipple's disease, sarcoidosis), traumatic, or tumoral destruction of hypocretin neurons, test results for HLA DQBl *06:02 may be positive and may
result from the insult triggering the autoimmune process. In other cases, the destruction of
hypocretin neurons may be secondary to trauma or hypothalamic surgery. Head trauma
or infections of the central nervous system can, however, produce transitory decreases in
CSF hypocretin-1 levels without hypocretin cell loss, complicating the diagnosis.
Diagnostic Features
The essential features of sleepiness in narcolepsy are recurrent daytime naps or lapses into
sleep. Sleepiness typically occurs daily but must occur at a minimum three times a week
for at least 3 months (Criterion A). Narcolepsy generally produces cataplexy, which most
commonly presents as brief episodes (seconds to minutes) of sudden, bilateral loss of muscle tone precipitated by emotions, typically laughing and joking. Muscles affected may
include those of the neck, jaw, arms, legs, or whole body, resulting in head bobbing, jaw
dropping, or complete falls. Individuals are awake and aware during cataplexy. To meet
Criterion Bl(a), cataplexy must be triggered by laughter or joking and must occur at least
a few times per month when the condition is untreated or in the past.
Cataplexy should not be confused with ''weakness" occurring in the context of athletic
activities (physiological) or exclusively after unusual emotional triggers such as stress or
anxiety (suggesting possible psychopathology). Episodes lasting hours or days, or those not
triggered by emotions, are unlikely to be cataplexy, nor is rolling on the floor while laughing hysterically.
In children close to onset, genuine cataplexy can be atypical, affecting primarily the
face, causing grimaces or jaw opening with tongue thrusting ("cataplectic faces"). Alternatively, cataplexy may present as low-grade continuous hypotonia, yielding a wobbling
walk. In these cases. Criterion Bl(b) can be met in children or in individuals within 6 months
of a rapid onset.
Narcolepsy-cataplexy nearly always results from the loss of hypothalamic hypocretin
(orexin)-producing cells, causing hypocretin deficiency (less than or equal to one-third of
control values, or 110 pg/mL in most laboratories). Cell loss is likely autoimmune, and approximately 99% of affected individuals carry HLA-DQBl*06:02 (vs. 12%-38% of control
subjects). Thus, checking for the presence of DQB1*06:02 prior to a lumbar puncture for evaluation of CSF hypocretin-1 immunoreactivity may be useful. Rarely, low CSF levels of hypocretin-1 occur without cataplexy, notably in youths who may develop cataplexy later. CSF
hypocretin-1 measurement represents the gold standard, excepting associated severe conditions (neurological, inflammatory, infectious, trauma) that can interfere with the assay.
A nocturnal polysonrmographic sleep study followed by an MSLT can also be used to
confirm the diagnosis (Criterion B3). These tests must be performed after the individual
has stopped all psychotropic medications, following 2 weeks of adequate sleep time (as
documented with sleep diaries, actigraphy). Short rapid eye movement (REM) latency
(sleep-onset REM period, REM latency less than or equal to 15 minutes) during polysomnography is sufficient to confirm the diagnosis and meets Criterion B3. Alternatively, the
MSLT result must be positive, showing a mean sleep latency of less than or equal to 8 minutes and two or more sleep-onset REM periods in four to five naps.
Associated Features Supporting Diagnosis
When sleepiness is severe, automatic behaviors may occur, with the individual continuing
his or her activities in a semi-automatic, hazelike fashion without memory or consciousness. Approximately 20%-60% of individuals experience vivid hypnagogic hallucinations
before or upon falling asleep or hypnopompic hallucinations just after awakening. These
hallucinations are distinct from the less vivid, nonhallucinatory dreamlike mentation at
sleep onset that occurs in normal sleepers. Nightmares and vivid dreaming are also frequent in narcolepsy, as is REM sleep behavior disorder. Approximately 20%-60% of individuals experience sleep paralysis upon falling asleep or awakening, leaving them awake
but unable to move or speak. However, many normal sleepers also report sleep paralysis,
especially with stress or sleep deprivation. Nocturnal eating may occur. Obesity is common. Nocturnal sleep disruption with frequent long or short awakenings is common and
can be disabling.
Individuals may appear sleepy or fall asleep in the waiting area or during clinical examination. During cataplexy, individuals may slump in a chair and have slurred speech or
drooping eyelids. If the clinician has time to check reflexes during cataplexy (most attacks
are less than 10 seconds), reflexes are abolished—an important finding distinguishing genuine cataplexy from conversion disorder.
Prevalence
Narcolepsy-cataplexy affects 0.02%-0.04% of the general population in most countries.
Narcolepsy affects both genders, with possibly a slight male preponderance.
Development and Course
Onset is typically in children and adolescents/young adults but rarely in older adults.
Two peaks of onset are suggested, at ages 15-25 years and ages 30-35 years. Onset can be
abrupt or progressive (over years). Severity is highest when onset is abrupt in children,
and then decreases with age or with treatment, so that symptoms such as cataplexy can occasionally disappear. Abrupt onset in young, prepubescent children can be associated
with obesity and premature puberty, a phenotype more frequently observed since 2009. In
adolescents, onset is more difficult to pinpoint. Onset in adults is often unclear, with some
individuals reporting having had excessive sleepiness since birth. Once the disorder has
manifested, the course is persistent and lifelong.
In 90% of cases, the first symptom to manifest is sleepiness or increased sleep, followed
by cataplexy (within 1 year in 50% of cases, within 3 years in 85%). Sleepiness, hypnagogic
hallucinations, vivid dreaming, and REM sleep behavior disorder (excessive movements
during REM sleep) are early symptoms. Excessive sleep rapidly progresses to an inability
to stay awake during the day, and to maintain good sleep at night, without a clear increase
in total 24-hour sleep needs. In the first months, cataplexy may be atypical, especially in
children. Sleep paralysis usually develops around puberty in children with prepubertal
onset. Exacerbations of symptoms suggest lack of compliance with medications or development of a concurrent sleep disorder, notably sleep apnea.
Young children and adolescents with narcolepsy often develop aggression or behavioral problems secondary to sleepiness and/or nighttime sleep disruption. Workload and
social pressure increase through high school and college, reducing available sleep time at
night. Pregnancy does not seem to modify symptoms consistently. After retirement, individuals typically have more opportunity for napping, reducing the need for stimulants.
Maintaining a regular schedule benefits individuals at all ages.
Risk and Prognostic Factors
Temperamental. Parasomnias, such as sleepwalking, bruxism, REM sleep behavior disorder, and enuresis, may be more common in individuals who develop narcolepsy. Individuals commonly report that they need more sleep than other family members.
Environmental. Group A streptococcal throat infection, influenza (notably pandemic
H lN l 2009), or other winter infections are likely triggers of the autoimmune process, pro
ducing narcolepsy a few months later. Head trauma and abrupt changes in sleep-wake
patterns (e.g., job changes, stress) may be additional triggers.
Genetic and physiological. Monozygotic twins are 25%-32% concordant for narcolepsy.
The prevalence of narcolepsy is l%-2% in first-degree relatives (a 10- to 40-fold increase
overall). Narcolepsy is strongly associated with DQB1*06:02 (99% vs. 12%-38% in control
subjects of various ethnic groups; 25% in the general U.S. population). DQB1*03:01 increases, while DQBl’OSiOl, DQBl’OôiOl, and DQB1*06:03 reduce risk in the presence of
DQB1’^06:02, but the effect is small. Polymorphisms within the T-cell receptor alpha gene
and other immune modulating genes also modulate risk slightly.
Culture-Related Diagnostic issues
Narcolepsy has been described in all ethnic groups and in many cultures. Among African
Americans, more cases present without cataplexy or with atypical cataplexy, complicating
diagnosis, especially in the presence of obesity and obstructive sleep apnea.
Diagnostic Markers
Functional imaging suggests impaired hypothalamic responses to humorous stimuli.
Nocturnal polysomnography followed by an MSLT is used to confirm the diagnosis of
narcolepsy, especially when the disorder is first being diagnosed and before treatment has
begun, and if hypocretin deficiency has not been documented biochemically. The polysomnography/MSLT should be performed after the individual is no longer taking any
psychotropic drugs and after regular sleep-wake patterns, without shift work or sleep deprivation, have been documented.
A sleep-onset REM period during the polysomnography (REM sleep latency less than
or equal to 15 minutes) is highly specific (approximately 1% positive in control subjects)
but moderately sensitive (approximately 50%). A positive MSLT result displays an average sleep latency of less than or equal to 8 minutes, and sleep-onset REM periods in two or
more naps on a four- or five-nap test. The MSLT result is positive in 90%-95% of individuals with narcolepsy versus 2%-4% of control subjects or individuals with other sleep disorders. Additional polysomnographic findings often include frequent arousals, decreased
sleep efficiency, and increased stage 1 sleep. Periodic limb movements (found in about
40% of individuals with narcolepsy) and sleep apnea are often noted.
Hypocretin deficiency is demonstrated by measuring CSF hypocretin-1 immunoreactivity. The test is particularly useful in individuals with suspected conversion disorder
and those without typical cataplexy, or in treatment-refractory cases. The diagnostic value
of the test is not affected by medications, sleep deprivation, or circadian time, but the findings are uninteφretable when the individual is severely ill with a concurrent infection or
head trauma or is comatose. CSF cytology, protein, and glucose are within normal range
even when sampled within weeks of rapid onset. CSF hypocretin-1 in these incipient cases
is typically already very diminished or undetectable.
Functional Consequences of Narcolepsy
Driving and working are impaired, and individuals with narcolepsy should avoid jobs
that place themselves (e.g., working with machinery) or others (e.g., bus driver, pilot) in
danger. Once the narcolepsy is controlled with therapy, patients can usually drive, although rarely long distances alone. Untreated individuals are also at risk for social isolation and accidental injury to themselves or others. Social relations may suffer as these
individuals strive to avert cataplexy by exerting control over emotions.
Differential Diagnosis
Other hypersomnias. Hypersomnolence and narcolepsy are similar with respect to the
degree of daytime sleepiness, age at onset, and stable course over time but can be distin
guished based on distinctive clinical and laboratory features. Individuals with hypersomnolence typically have longer and less disrupted nocturnal sleep, greater difficulty
awakening, more persistent daytime sleepiness (as opposed to more discrete "sleep attacks" in narcolepsy), longer and less refreshing daytime sleep episodes, and little or no
dreaming during daytime naps. By contrast, individuals with narcolepsy have cataplexy
and recurrent intrusions of elements of REM sleep into the transition between sleep and
wakefulness (e.g., sleep-related hallucinations and sleep paralysis). The MSLT typically
demonstrates shorter sleep latencies (i.e., greater physiological sleepiness) as well as the
presence of multiple sleep-onset REM periods in individuals with narcolepsy.
Sleep deprivation and insufficient nocturnal sleep. Sleep deprivation and insufficient
nocturnal sleep are common in adolescents and shift workers. In adolescents, difficulties
falling asleep at night are common, causing sleep deprivation. The MSLT result may be
positive if conducted while the individual is sleep deprived or while his or her sleep is
phase delayed.
Sleep apnea syndromes. Sleep apneas are especially likely in the presence of obesity.
Because obstructive sleep apnea is more frequent than narcolepsy, cataplexy may be overlooked (or absent), and the individual is assumed to have obstructive sleep apnea unresponsive to usual therapies.
Major depressive disorder. Narcolepsy or hypersomnia may be associated or confused
with depression. Cataplexy is not present in depression. The MSLT results are most often
normal, and there is dissociation between subjective and objective sleepiness, as measured
by the mean sleep latency during the MSLT.
Conversion disorder (functional neurological symptom disorder). Atypical features,
such as long-lasting cataplexy or unusual triggers, may be present in conversion disorder
(functional neurological symptom disorder). Individuals may report sleeping and dreaming, yet the MSLT does not show the characteristic sleep-onset REM period. Full-blown,
long-lasting pseudocataplexy may occur during consultation, allowing the examining
physician enough time to verify reflexes, which remain intact.
Attention-deficit/hyperactivity disorder or other behavioral problems. In children and
adolescents, sleepiness can cause behavioral problems, including aggressiveness and inattention, leading to a misdiagnosis of attention-deficit/hyperactivity disorder.
Seizures. In young children, cataplexy can be misdiagnosed as seizures. Seizures are not
conmionly triggered by emotions, and when they are, the trigger is not usually laughing or
joking. During a seizure, individuals are more likely to hurt themselves when falling. Seizures characterized by isolated atonia are rarely seen in isolation of other seizures, and
they also have signatures on the electroencephalogram.
Chorea and movement disorders. In young children, cataplexy can be misdiagnosed as
chorea or pediatric autoimmune neuropsychiatric disorders associated with streptococcal
infections, especially in the context of a strep throat infection and high antistreptolysin O
antibody levels. Some children may have an overlapping movement disorder close to onset of the cataplexy.
Schizophrenia. In the presence of florid and vivid hypnagogic hallucinations, individuals
may think these experiences are real—a feature that suggests schizophrenia. Similarly,
with stimulant treatment, persecutory delusions may develop. If cataplexy is present, the
clinician should first assume that these symptoms are secondary to narcolepsy before considering a co-occurring diagnosis of schizophrenia.
Comorbidity
Narcolepsy can co-occur with bipolar, depressive, and anxiety disorders, and in rare cases
with schizophrenia. Narcolepsy is also associated with increased body mass index or obe
sity, especially when the narcolepsy is untreated. Rapid weight gain is common in young
children with a sudden disease onset. Comorbid sleep apnea should be considered if there
is a sudden aggravation of preexisting narcolepsy.
Relationship to international Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates five
subtypes of narcolepsy.
Breathing-Related Sleep Disorders
The breathing-related sleep disorders category encompasses three relatively distinct disorders: obstructive sleep apnea hypopnea, central sleep apnea, and sleep-related hypoventilation.
Obstructive Sleep Apnea Hypopnea
Diagnostic Criteria 327.23 (G47.33)
A. Either (1) or (2):
1. Evidence by polysomnography of at least five obstructive apneas or hypopneas per
hour of sleep and either of the following sleep symptoms:
a. Nocturnal breathing disturbances: snoring, snorting/gasping, or breathing
pauses during sleep.
b. Daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportunities to sleep that is not better explained by another mental disorder (including a
sleep disorder) and is not attributable to another medical condition.
2. Evidence by polysomnography of 15 or more obstructive apneas and/or hypopneas
per hour of sleep regardless of accompanying symptoms.
Specify current severity:
Mild: Apnea hypopnea index is less than 15.
■Moderate: Apnea hypopnea Index is 15-30.
Severe: Apnea hypopnea index is greater than 30.
Specifiers
Disease severity is measured by a count of the number of apneas plus hypopneas per hour
of sleep (apnea hypopnea index) using polysomnography or other overnight monitoring.
Overall severity is also informed by levels of nocturnal desaturation and sleep fragmentation (measured by brain cortical arousal frequency and sleep stages) and degree of associated symptoms and daytime impairment. However, the exact number and thresholds
may vary according to the specific measurement techniques used, and these numbers may
change over time. Regardless of the apnea hypopnea index (count) per se, the disorder is
considered to be more severe when apneas and hypopneas are accompanied by significant
oxygen hemoglobin desaturation (e.g., when more than 10% of the sleep time is spent at
desaturation levels of less than 90%) or when sleep is severely fragmented as shown by an
elevated arousal index (arousal index greater than 30) or reduced stages in deep sleep (e.g.,
percentage stage N3 [slow-v^ave sleep] less than 5%).
Diagnostic Features
Obstructive sleep apnea hypopnea is the most common breathing-related sleep disorder.
It is characterized by repeated episodes of upper (pharyngeal) airw^ay obstruction (apneas
and hypopneas) during sleep. Apnea refers to the total absence of airflow, and hypopnea refers to a reduction in airflow. Each apnea or hypopnea represents a reduction in breathing
of at least 10 seconds in duration in adults or two missed breaths in children and is typically associated with drops in oxygen saturation of 3% or greater and/or an electroencephalographic arousal. Both sleep-related (nocturnal) and wake-time symptoms are common.
The cardinal symptoms of obstructive sleep apnea hypopnea are snoring and daytime
sleepiness.
Obstructive sleep apnea hypopnea in adults is diagnosed on the basis of polysomnographic findings and symptoms. The diagnosis is based on symptoms of 1) nocturnal
breathing disturbances (i.e., snoring, snorting/gasping, breathing pauses during sleep), or
2) daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportunities to
sleep that are not better explained by another mental disorder and not attributable to another medical condition, along with 3) evidence by polysomnography of five or more obstructive apneas or hypopneas per hour of sleep (Criterion Al). Diagnosis can be made in
the absence of these symptoms if there is evidence by polysomnography of 15 or more obstructive apneas and/or hypopneas per hour of sleep (Criterion A2).
Specific attention to disturbed sleep occurring in association with snoring or breathing
pauses and physical findings that increase risk of obstructive sleep apnea hypopnea (e.g.,
central obesity, crowded pharyngeal airway, elevated blood pressure) is needed to reduce
the chance of misdiagnosing this treatable condition.
Associated Features Supporting Diagnosis
Because of the frequency of nocturnal awakenings that occur with obstructive sleep apnea
hypopnea, individuals may report symptoms of insomnia. Other common, though nonspecific, symptoms of obstructive sleep apnea hypopnea are heartburn, nocturia, morning
headaches, dry mouth, erectile dysfunction, and reduced libido. Rarely, individuals may
complain of difficulty breathing while lying supine or sleeping. Hypertension may occur
in more than 60% of individuals with obstructive sleep apnea hypopnea.
Prevalence
Obstructive sleep apnea hypopnea is a very common disorder, affecting at least l% -2% of
children, 2%-15% of middle-age adults, and more than 20% of older individuals. In the
general community, prevalence rates of undiagnosed obstructive sleep apnea hypopnea
may be very high in elderly individuals. Since the disorder is strongly associated with obesity, increases in obesity rates are likely to be accompanied by an increased prevalence of
this disorder. Prevalence may be particularly high among males, older adults, and certain
racial/ethnic groups. In adults, the male-to-female ratio of obstructive sleep apnea hypopnea ranges from 2:1 to 4:1. Gender differences decline in older age, possibly because of an
increased prevalence in females after menopause. There is no gender difference among
prepubertal children.
Deveiopment and Course
The age distribution of obstructive sleep apnea hypopnea likely follows a J-shaped distribution. There is a peak in children ages 3-8 years when the nasopharynx may be compromised by a relatively large mass of tonsillar tissue compared with the size of the upper
airway. With growth of the airway and regression of lymphoid tissue during later childhood, there is reduction in prevalence. Then, as obesity prevalence increases in midlife and
females enter menopause, obstructive sleep apnea hypopnea again increases. The course
in older age is unclear; the disorder may level off after age 65 years, but in other individuals, prevalence may increase with aging. Because there is some age dependency of the occurrence of apneas and hypopneas, polysomnographic results must be interpreted in light
of other clinical data. In particular, significant clinical symptoms of insomnia or hypersomnia should be investigated regardless of the individual's age.
Obstructive sleep apnea hypopnea usually has an insidious onset, gradual progression,
and persistent course. Typically the loud snoring has been present for many years, often since
childhood, but an increase in its severity may lead the individual to seek evaluation. Weight
gain may precipitate an increase in symptoms. Although obstructive sleep apnea hypopnea
can occur at any age, it most commonly manifests among individuals ages 40-60 years. Over
4-5 years, the average apnea hypopnea index increases in adults and older individuals by approximately two apneas/hypopneas per hour. The apnea hypopnea index is increased and incident obstructive sleep apnea hypopnea is greater among individuals who are older, who are
male, or who have a higher baseline body mass index (BMI) or increase their BMI over time.
Spontaneous resolution of obstructive sleep apnea hypopnea has been reported with weight
loss, particularly after bariatric surgery. In children, seasonal variation in obstructive sleep apnea hypopnea has been observed, as has improvement with overall growth.
In young children, the signs and symptoms of obstructive sleep apnea hypopnea may be
more subtle than in adults, making diagnosis more difficult to establish. Polysomnography is
useful in confirming diagnosis. Evidence of fragmentation of sleep on the polysomnogram
may not be as apparent as in studies of older individuals, possibly because of the high homeostatic drive in young individuals. Symptoms such as snoring are usually parent-reported and
thus have reduced sensitivity. Agitated arousals and unusual sleep postures, such as sleeping
on the hands and knees, may occur. Nocturnal enuresis also may occur and should raise the
suspicion of obstructive sleep apnea hypopnea if it recurs in a child who was previously dry at
night. Children may also manifest excessive daytime sleepiness, although this is not as common or pronounced as in adults. Daytime mouth breathing, difficulty in swallowing, and poor
speech articulation are also common features in children. Children younger than 5 years more
often present with nighttime symptoms, such as observed apneas or labored breathing, than
with l^havioral symptoms (i.e., the nighttime symptoms are more noticeable and more often
bring the child to clinical attention). In children older than 5 years, daytime symptoms such as
sleepiness and behavioral problems (e.g., impulsivity and hyperactivity), attention-deficit/
hyperactivity disorder, learning difficulties, and morning headaches are more often the focus
of concern. Children with obstructive sleep apnea hypopnea also may present with failure to
thrive and developmental delays. In young children, obesity is a less common risk factor,
while delayed growth and "failure to thrive" may be present.
Risk and Prognostic Factors
Genetic and physiological. The major risk factors for obstructive sleep apnea hypopnea
are obesity and male gender. Others include maxillary-mandibular retrognathia or micrognathia, positive family history of sleep apnea, genetic syndromes that reduce upper
airway patency (e.g., Down's syndrome, Treacher Collin's syndrome), adenotonsillar hypertrophy (especially in young children), menopause (in females), and various endocrine
syndromes (e.g., acromegaly). Compared with premenopausal females, males are at increased risk for obstructive sleep apnea hypopnea, possibly reflecting the influences of sex
hormones on ventilatory control and body fat distribution, as well as because of gender
differences in airway structure. Medications for mental disorders and medical conditions
that tend to induce somnolence may worsen the course of apnea symptoms if these medications are not managed carefully.
Obstructive sleep apnea hypopnea has a strong genetic basis, as evidenced by the significant familial aggregation of the apnea hypopnea index. The prevalence of obstructive
sleep apnea hypopnea is approximately twice as high among the first-degree relatives of
probands with obstructive sleep apnea hypopnea as compared with members of control
families. One-third of the variance in the apnea hypopnea index is explained by shared familial factors. Although genetic markers with diagnostic or prognostic value are not yet
available for use, eliciting a family history of obstructive sleep apnea hypopnea should increase the clinical suspicion for the disorder.
Culture-Related Diagnostic Issues
There is a potential for sleepiness and fatigue to be reported differently across cultures. In
some groups, snoring may be considered a sign of health and thus may not trigger concerns. Individuals of Asian ancestry may be at increased risk for obstructive sleep apnea
hypopnea despite relatively low BMI, possibly reflecting the influence of craniofacial risk
factors that narrow the nasopharynx.
Gender-Related Issues
Females may more commonly report fatigue rather than sleepiness and may underreport
snoring.
Diagnostic Markers
Polysomnography provides quantitative data on frequency of sleep-related respiratory
disturbances and associated changes in oxygen saturation and sleep continuity. Polysomnographie findings in children differ from those in adults in that children demonstrate
labored breathing, partial obstructive hypoventilation with cyclical desaturations, hypercapnia and paradoxical movements. Apnea hypopnea index levels as low as 2 are used to
define thresholds of abnormality in children.
Arterial blood gas measurements while the individual is awake are usually normal, but
some individuals can have waking hypoxemia or hypercapnia. This pattern should alert the
clinician to the possibility of coexisting lung disease or hypoventilation. Imaging procedures
may reveal narrowing of the upper airway. Cardiac testing may show evidence of impaired
ventricular function. Individuals with severe nocturnal oxygen desaturation may also have elevated hemoglobin or hematocrit values. Validated sleep measures (e.g., multiple sleep latency test [MSLT], maintenance of wakefulness test) may identify sleepiness.
Functional Consequences of
Obstructive Sleep Apnea Hypopnea
More than 50% of individuals with moderate to severe obstructive sleep apnea hypopnea
report symptoms of daytime sleepiness. A twofold increased risk of occupational accidents
has been reported in association with symptoms of snoring and sleepiness. Motor vehicle
crashes also have been reported to be as much as sevenfold higher among individuals with
elevated apnea hypopnea index values. Clinicians should be cognizant of state government requirements for reporting this disorder, especially in relationship to commercial
drivers. Reduced scores on measures of health-related quality of life are common in individuals with obstructive sleep apnea hypopnea, with the largest decrements observed in the
physical and vitality subscales.
Differential Diagnosis
Primary snoring and other sleep disorders. Individuals with obstructive sleep apnea
hypopnea must be differentiated from individuals with primary snoring (i.e., otherwise
asjnnptomatic individuals who snore and do not have abnormalities on overnight polysomnography). Individuals with obstructive sleep apnea hypopnea may additionally report
nocturnal gasping and choking. The presence of sleepiness or other daytime symptoms
not explained by other etiologies suggests the diagnosis of obstructive sleep apnea hypopnea, but this differentiation requires polysomnography. Definitive differential diagnosis
between hypersomnia, central sleep apnea, sleep-related hypoventilation, and obstructive
sleep apnea hypopnea also requires polysomnographic studies.
Obstructive sleep apnea hypopnea must be differentiated from other causes of sleepiness, such as narcolepsy, hypersonmia, and circadian rhythm sleep disorders. Obstructive
sleep apnea hypopnea can be differentiated from narcolepsy by the absence of cataplexy,
sleep-related hallucinations, and sleep paralysis and by the presence of loud snoring,
gasping during sleep, or observed apneas in sleep. Daytime sleep episodes in narcolepsy
are characteristically shorter, more refreshing, and more often associated with dreaming.
Obstructive sleep apnea hypopnea shows characteristic apneas and hypopneas and oxygen desaturation during nocturnal polysomnographic studies. Narcolepsy results in multiple sleep-onset rapid eye movement (REM) periods during the MSLT. Narcolepsy, like
obstructive sleep apnea hypopnea, may be associated with obesity, and some individuals
have concurrent narcolepsy and obstructive sleep apnea hypopnea. A diagnosis of narcolepsy does not exclude the diagnosis of obstructive sleep apnea hypopnea, as the two conditions may co-occur.
Insomnia disorder. For individuals complaining of difficulty initiating or maintaining
sleep or early-moming awakenings, insomnia disorder can be differentiated from obstructive sleep apnea hypopnea by the absence of snoring and the absence of the history, signs,
and symptoms characteristic of the latter disorder. However, insomnia and obstructive
sleep apnea hypopnea may coexist, and if so, both disorders may need to be addressed
concurrently to improve sleep.
Panic attacks. Nocturnal panic attacks may include symptoms of gasping or choking
during sleep that may be difficult to distinguish clinically from obstructive sleep apnea hypopnea. However, the lower frequency of episodes, intense autonomic arousal, and lack of
excessive sleepiness differentiate nocturnal panic attacks from obstructive sleep apnea hypopnea. Polysomnography in individuals with nocturnal panic attacks does not reveal the
typical pattern of apneas or oxygen desaturation characteristic of obstructive sleep apnea
hypopnea. Individuals with obstructive sleep apnea hypopnea do not provide a history of
daytime panic attacks.
Attention-deficit/hyperactivity disorder. Attention-defidt/hyperactivity disorder in children may include symptoms of inattention, academic impairment, hyperactivity, and internalizing behaviors, all of which may also be symptoms of childhood obstructive sleep
apnea hypopnea. The presence of other symptoms and signs of childhood obstructive
sleep apnea hypopnea (e.g., labored breathing or snoring during sleep and adenotonsillar
hypertrophy) would suggest the presence of obstructive sleep apnea hypopnea. Obstructive sleep apnea hypopnea and attention-deficit/hyperactivity disorder may commonly
co-occur, and there may be causal links between them; therefore, risk factors such as enlarged tonsils, obesity, or a family history of sleep apnea may help alert the clinician to
their co-occurrence.
Substance/medication-induced insomnia or hypersomnia. Substance use and substance
withdrawal (including medications) can produce insomnia or hypersomnia. A careful history is usually sufficient to identify the relevant substance/medication, and follow-up
shows improvement of the sleep disturbance after discontinuation of the substance/medication. In other cases, the use of a substance/medication (e.g., alcohol, barbiturates, benzodiazepines, tobacco) has been shown to exacerbate obstructive sleep apnea hypopnea.
An individual with symptoms and signs consistent with obstructive sleep apnea hypop-
nea should receive that diagnosis, even in the presence of concurrent substance use that is
exacerbating the condition.
\
Comorbidity
Systemic hypertension, coronary artery disease, heart failure, stroke, diabetes, and increased
mortality are consistently associated with obstructive sleep apnea hypopnea. Risk estimates vary from 30% to as much as 300% for moderate to severe obstructive sleep apnea
hypopnea. Evidence of pulmonary hypertension and right heart failure (e.g., cor pulmonale, ankle edema, hepatic congestion) are rare in obstructive sleep apnea hypopnea and
when present indicate either very severe disease or associated hypoventilation or cardiopulmonary comorbidities. Obstructive sleep apnea hypopnea also may occur with increased frequency in association with a number of medical or neurological conditions (e.g.,
cerebrovascular disease, Parkinson's disease). Physical findings reflect the co-occurrence of
these conditions.
As many as one-third of individuals referred for evaluation of obstructive sleep apnea
hypopnea report symptoms of depression, with as many of 10% having depression scores
consistent with moderate to severe depression. Severity of obstructive sleep apnea hypopnea, as measured by the apnea hypopnea index, has been foimd to be correlated w i^ severity of symptoms of depression. This association may be stronger in males than in
females.
Reiationsliip to internationai Ciassification of
Sieep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates 11 subtypes of "sleep-related breathing disorders," including primary central sleep apnea, obstructive sleep apnea, and sleep-related hypoventilation.
Central Sleep Apnea
Diagnostic Criteria
A. Evidence by polysomnography of five or more central apneas per hour of sleep.
B. The disorder is not better explained by another current sleep disorder.
Specify whether:
327.21 (G47.31) Idiopathic central sleep apnea: Characterized by repeated episodes of apneas and hypopneas during sleep caused by variability in respiratory effort
but without evidence of ainway obstruction.
786.04 (R06.3) Clieyne-Stokes breathing: A pattern of periodic crescendodecrescendo variation in tidal volume that results in central apneas and hypopneas at
a frequency of at least five events per hour, accompanied by frequent arousal.
780.57 (G47.37) Central sleep apnea comorbid with opioid use: The pathogenesis
of this subtype is attributed to the effects of opioids on the respiratory rhythm generators in the medulla as well as the differential effects on hypoxic versus hypercapnic respiratory drive.
Coding note (for 780.57 [G47.37] code only): When an opioid use disorder is present, first
code the opioid use disorder: 305.50 (F11.10) mild opioid use disorder or 304.00 (F11.20)
moderate or severe opioid use disorder; then code 780.57 (G47.37) central sleep apnea
comorbid with opioid use. When an opioid use disorder is not present (e.g., after a onetime heavy use of the substance), code only 780.57 (G47.37) central sleep apnea comorbid with opioid use.
Note: See the section “Diagnostic Features” in text.
Specify current severity:
Severity of central sleep apnea is graded according to the frequency of the breathing
disturbances as well as the extent of associated oxygen desaturation and sleep fragmentation that occur as a consequence of repetitive respiratory disturbances.
Subtypes
Idiopathic central sleep apnea and Cheyne-Stokes breathing are characterized by increased
gain of the ventilatory control system, also referred to as high loop gain, which leads to instability in ventilation and PaC02 levels. This instability is termed periodic breathing and
can be recognized by hyperventilation alternating with hypoventilation. Individuals with
these disorders typically have pC02 levels while awake that are slightly hypocapneic or
normocapneic. Central sleep apnea may also manifest during initiation of treatment of obstructive sleep apnea hypopnea or may occur in association with obstructive sleep apnea
hypopnea syndrome (termed complex sleep apnea). The occurrence of central sleep apnea in
association with obstructive sleep apnea is also considered to be due to high loop gain. In
contrast, the pathogenesis of central sleep apnea comorbid with opioid use has been attributed to the effects of opioids on the respiratory rhythm generators in the medulla as
well as to its differential effects on hypoxic versus hypercapneic respiratory drive. These
individuals may have elevated pC02 levels while awake. Individuals receiving chronic
methadone maintenance therapy have been noted to have increased sonmolence and depression, although the role of breathing disorders associated with opioid medication in causing these problems has not been studied.
Specifiers
An increase in the central apnea index (i.e., number of central apneas per hour of sleep) reflects an increase in severity of central sleep apnea. Sleep continuity and quality may be
markedly impaired with reductions in restorative stages of non-rapid eye movement (REM)
sleep (i.e., decreased slow-wave sleep [stage N3]). In individuals with severe CheyneStokes breathing, the pattern can also be observed during resting wakefulness, a finding
that is thought to be a poor prognostic marker for mortality.
Diagnostic Features
Central sleep apnea disorders are characterized by repeated episodes of apneas and hypopneas during sleep caused by variability in respiratory effort. These are disorders of
ventilatory control in which respiratory events occur in a periodic or intermittent pattern.
Idiopathic central sleep apnea is characterized by sleepiness, insomnia, and awakenings due
to dyspnea in association with five or more central apneas per hour of sleep. Central sleep
apnea occurring in individuals with heart failure, stroke, or renal failure typically have a
breathing pattern called Cheyne-Stokes breathing, which is characterized by a pattern of
periodic crescendo-decrescendo variation in tidal volume that results in central apneas
and hypopneas occurring at a frequency of at least five events per hour that are accompanied by frequent arousals. Central and obstructive sleep apneas may coexist; the ratio of
central to obstructive apneas/hypopneas may be used to identify which condition is predominant.
Alterations in neuromuscular control of breathing can occur in association with medications or substances used in individuals with mental health conditions, which can cause
or exacerbate impairments of respiratory rhythm and ventilation. Individuals taking these
medications have a sleep-related breathing disorder that could contribute to sleep disturbances and symptoms such as sleepiness, confusion, and depression. Specifically, chronic
use of long-acting opioid medications is often associated with impairment of respiratory control leading to central sleep apnea.
Associated Features Supporting Diagnosis
Individuals with central sleep apnea hypopneas can manifest with sleepiness or insomnia.
There can be complaints of sleep fragmentation, including awakening with dyspnea.
Some individuals are asymptomatic. Obstructive sleep apnea hypopnea can coexist with
Cheyne-Stokes breathing, and thus snoring and abruptly terminating apneas may be observed during sleep.
Prevaience
The prevalence of idiopathic central sleep apnea is unknown but thought to be rare. The
prevalence of Cheyne-Stokes breathing is high in individuals with depressed cardiac ventricular ejection fraction. In individuals with an ejection fraction of less than 45%, the prevalence has been reported to be 20% or higher. The male-to-female ratio for prevalence is
even more highly skewed toward males than for obstructive sleep apnea hypopnea. Prevalence increases with age, and most patients are older than 60 years. Cheyne-Stokes breathing occurs in approximately 20% of individuals with acute stroke. Central sleep apnea
comorbid with opioid use occurs in approximately 30% of individuals taking chronic opioids for nonmalignant pain and similarly in individuals receiving methadone maintenance therapy.
Development and Course
The onset of Cheyne-Stokes breathing appears tied to the development of heart failure. The
Cheyne-Stokes breathing pattern is associated with oscillations in heart rate, blood pressure and oxygen desaturation, and elevated sympathetic nervous system activity that can
promote progression of heart failure. The clinical significance of Cheyne-Stokes breathing
in the setting of stroke is not known, but Cheyne-Stokes breathing may be a transient finding that resolves with time after acute stroke. Central sleep apnea comorbid with opioid
use has been documented with chronic use (i.e., several months).
Risic and Prognostic Factors
Genetic and physiological. Cheyne-Stokes breathing is frequently present in individuals with heart failure. The coexistence of atrial fibrillation further increases risk, as do older
age and male gender. Cheyne-Stokes breathing is also seen in association with acute stroke
and possibly renal failure. The underlying ventilatory instability in the setting of heart failure has been attributed to increased ventilatory chemosensitivity and hyperventilation
due to pulmonary vascular congestion and circulatory delay. Central sleep apnea is seen
in individuals taking long-acting opioids.
Diagnostic l\/larl(ers
Physical findings seen in individuals with a Cheyne-Stokes breathing pattern relate to its
risk factors. Findings consistent with heart failure, such as jugular venous distension, S3
heart sound, lung crackles, and lower extremity edema, may be present. Polysonmography is used to characterize the breathing characteristics of each breathing-related sleep
disorder subtype. Central sleep apneas are recorded when periods of breathing cessation
for longer than 10 seconds occur. Cheyne-Stokes breathing is characterized by a pattern of
periodic crescendo-decrescendo variation in tidal volume that results in central apneas
and hypopneas occurring at a frequency of at least five events per hour that are accompanied by frequent arousals. The cycle length of Cheyne-Stokes breathing (or time from end
of one central apnea to the end of the next apnea) is about 60 seconds.
Functional Consequences of Central Sleep Apnea
Idiopathic central sleep apnea has been reported to cause symptoms of disrupted sleep, including insomnia and sleepiness. Cheyne-Stokes breathing with comorbid heart failure
has been associated with excessive sleepiness, fatigue, and insomnia, although many individuals may be asymptomatic. Coexistence of heart failure and Cheyne-Stokes breathing may be associated with increased cardiac arrhythmias and increased mortality or
cardiac transplantation. Individuals with central sleep apnea comorbid with opioid use
may present with symptoms of sleepiness or insomnia.
Differential Diagnosis
Idiopathic central sleep apnea must be distinguished from other breathing-related sleep
disorders, other sleep disorders, and medical conditions and mental disorders that cause
sleep fragmentation, sleepiness, and fatigue. This is achieved using polysomnography.
Other breathing-related sleep disorders and sleep disorders. Central sleep apnea can
be distinguished from obstructive sleep apnea hypopnea by the presence of at least five
central apneas per hour of sleep. These conditions may co-occur, but central sleep apnea is
considered to predominate when the ratio of central to obstructive respiratory events exceeds 50%.
Cheyne-Stokes breathing can be distinguished from other mental disorders, including
other sleep disorders, and other medical conditions that cause sleep fragmentation, sleepiness, and fatigue based on the presence of a predisposing condition (e.g., heart failure or
stroke) and signs and polysomnographic evidence of the characteristic breathing pattern.
Polysomnographie respiratory findings can help distinguish Cheyne-Stokes breathing
from insomnia due to other medical conditions. High-altitude periodic breathing has a
pattern that resembles Cheyne-Stokes breathing but has a shorter cycle time, occurs only
at high altitude, and is not associated with heart failure.
Central sleep apnea comorbid with opioid use can be differentiated from other types of
breathing-related sleep disorders based on the use of long-acting opioid medications in
conjunction with polysomnographic evidence of central apneas and periodic or ataxic
breathing. It can be distinguished from insomnia due to drug or substance use based on
polysomnographic evidence of central sleep apnea.
Comorbidity
Central sleep apnea disorders are frequently present in users of long-acting opioids, such
as methadone. Individuals taking these medications have a sleep-related breathing disorder that could contribute to sleep disturbances and symptoms such as sleepiness, confusion, and depression. While the individual is asleep, breathing patterns such as central
apneas, periodic apneas, and ataxic breathing may be observed. Obstructive sleep apnea
hypopnea may coexist with central sleep apnea, and features consistent with this condition can also be present (see 'Obstructive Sleep Apnea Hypopnea" earlier in this chapter).
Cheyne-Stokes breathing is more commonly observed in association with conditions that
include heart failure, stroke, and renal failure and is seen more frequently in individuals
with atrial fibrillation. Individuals with Cheyne-Stokes breathing are more likely to be
older, to be male, and to have lower weight than individuals with obstructive sleep apnea
hypopnea.
Sleep-Related Hypoventilation
--------------------1-------------------------------------------------------------------------------------------
Diagnostic Criteria
A. Polysomnograpy demonstrates episodes of decreased respiration associated with elevated CO2 levels. (Note: In the absence of objective measurement of CO2 , persistent
low levels of hemoglobin oxygen saturation unassociated with apneic/hypopneic
events may indicate hypoventilation.)
B. The disturbance is not better explained by another current sleep disorder.
Specify whether:
327.24 (G47.34) Idiopathic liypoventilation: This subtype is not attributable to any
readily identified condition.
327.25 (G47.35) Congenital central alveolar hypoventilation: This subtype is a rare
congenital disorder in which the individual typically presents in the perinatal period with
shallow breathing, or cyanosis and apnea during sleep.
327.26 (G47.36) Comorbid sleep-related hypoventilation: This subtype occurs as a
consequence of a medical condition, such as a pulmonary disorder (e.g., interstitial
lung disease, chronic obstructive pulmonary disease) or a neuromuscular or chest wall
disorder (e.g., muscular dystrophies, postpolio syndrome, cervical spinal cord injury,
kyphoscoliosis), or medications (e.g., benzodiazepines, opiates). It also occurs with
obesity (obesity hypoventilation disorder), where it reflects a combination of increased
work of breathing due to reduced chest wall compliance and ventilation-perfusion mismatch and variably reduced ventilatory drive. Such individuals usually are characterized by body mass index of greater than 30 and hypercapnia during wakefulness (with
a PCO2 of greater than 45), without other evidence of hypoventilation.
Specify current severity:
Severity is graded according to the degree of hypoxemia and hypercarbia present during sleep and evidence of end organ impairment due to these abnormalities (e.g., rightsided heart failure). The presence of blood gas abnormalities during wakefulness is an
indicator of greater severity.
Subtypes
Regarding obesity hypoventilation disorder, the prevalence of obesity hypoventilation in
the general population is not known but is thought to be increasing in association with the
increased prevalence of obesity and extreme obesity.
Diagnostic Features
Sleep-related hypoventilation can occur independently or, more frequently, comorbid
with medical or neurological disorders, medication use, or substance use disorder. Although symptoms are not mandatory to make this diagnosis, individuals often report
excessive daytime sleepiness, frequent arousals and awakenings during sleep, morning
headaches, and insomnia complaints.
Associated Features Supporting Diagnosis
Individuals with sleep-related hypoventilation can present with sleep-related complaints
of insomnia or sleepiness. Episodes of orthopnea can occur in individuals with diaphragm
weakness. Headaches upon awakening may be present. During sleep, episodes of shallow
breathing may be observed, and obstructive sleep apnea hypopnea or central sleep apnea
may coexist. Consequences of ventilatory insufficiency, including pulmonary hypertension, cor pulmonale (right heart failure), polycythemia, and neurocognitive dysfunction.
can be present. With progression of ventilatory insufficiency, blood gas abnormalities extend into wakefulness. Features of the medical condition causing sleep-related hypoventilation can also be present. Episodes of hypoventilation may be associated with frequent
arousals or bradytachycardia. Individuals may complain of excessive sleepiness and insomnia or morning headaches or may present with findings of neurocognitive dysfunction
or depression. Hypoventilation may not be present during wakefulness.
Prevalence
Idiopathic sleep-related hypoventilation in adults is very uncommon. The prevalence of
congenital central alveolar hypoventilation is unknown, but the disorder is rare. Comorbid sleep-related hypoventilation (i.e., hypoventilation comorbid with other conditions,
such as chronic obstructive pulmonary disease [COPD], neuromuscular disorders, or obesity) is more common.
Development and Course
Idiopathic sleep-related hypoventilation is thought to be a slowly progressive disorder of
respiratory impairment. When this disorder occurs comorbidly with other disorders (e.g.,
COPD, neuromuscular disorders, obesity), disease severity reflects the severity of the underlying condition, and the disorder progresses as the condition worsens. Complications
such as pulmonary hypertension, cor pulmonale, cardiac dysrhythmias, polycythemia,
neurocognitive dysfunction, and worsening respiratory failure can develop with increasing severity of blood gas abnormalities.
Congenital central alveolar hypoventilation usually manifests at birth with shallow,
erratic, or absent breathing. This disorder can also manifest during infancy, childhood,
and adulthood because of variable penetrance of the PHOX2B mutation. Children with
congenital central alveolar hypoventilation are more likely to have disorders of the autonomic nervous system, Hirschsprung's disease, neural crest tumors, and characteristic boxshaped face (i.e., the face is short relative to its width).
Risk and Prognostic Factors
Environmental. Ventilatory drive can be reduced in individuals using central nervous
system depressants, including benzodiazepines, opiates, and alcohol.
Genetic and physiological. Idiopathic sleep-related hypoventilation is associated with
reduced ventilatory drive due to a blunted chemoresponsiveness to CO2 (reduced respiratory drive; i.e., "won't breathe"), reflecting underlying neurological deficits in centers
governing the control of ventilation. More commonly, sleep-related hypoventilation is comorbid with another medical condition, such as a pulmonary disorder, a neuromuscular
or chest wall disorder, or hypothyroidism, or with use of medications (e.g., benzodiazepines, opiates). In these conditions, the hypoventilation may be a consequence of increased work of breathing and/or impairment of respiratory muscle function (i.e., "can't
breathe") or reduced respiratory drive (i.e., "won't breathe").
Neuromuscular disorders influence breathing through impairment of respiratory motor innervation or respiratory muscle function. They include conditions such as amyotrophic lateral sclerosis, spinal cord injury, diaphragmatic paralysis, myasthenia gravis,
Lambert-Eaton syndrome, toxic or metabolic myopathies, postpolio syndrome, and Charcot-Marie-Tooth syndrome.
Congenital central alveolar hypoventilation is a genetic disorder attributable to mutations of PH0X2B, a gene that is crucial for the development of the embryonic autonomic
nervous system and neural crest derivatives. Children with congenital central alveolar hypoventilation show blunted ventilatory responses to hypercapnia, especially in non-rapid
eye movement sleep.
Gender-Related Diagnostic Issues
Gender distributions for sleep-related hypoventilation occurring in association with comorbid conditions reflect the gender distributions of the comorbid conditions. For example, COPD is more frequently present in males and with increasing age.
Diagnostic Markers
Sleep-related hypoventilation is diagnosed using polysomnography showing sleep-related
hypoxemia and hypercapnia that is not better explained by another breathing-related sleep
disorder. The documentation of increased arterial pC02 levels to greater than 55 mmHg
during sleep or a 10 mmHg or greater increase in pC02 levels (to a level that also exceeds
50 mmHg) during sleep in comparison to awake supine values, for 10 minutes or longer, is
the gold standard for diagnosis. However, obtaining arterial blood gas determinations during sleep is impractical, and non-invasive measures of pC02 have not been adequately validated during sleep and are not widely used during polysomnography in adults. Prolonged
and sustained decreases in oxygen saturation (oxygen saturation of less than 90% for more
than 5 minutes with a nadir of at least 85%, or oxygen saturation of less than 90% for at least
30% of sleep time) in the absence of evidence of upper airway obstruction are often used as
an indication of sleep-related hypoventilation; however, this finding is not specific, as there
are other potential causes of hypoxemia, such as that due to lung disease.
Functional Consequences of
Sleep-Related Hypoventilation
The consequences of sleep-related hypoventilation are related to the effects of chronic exposure to hypercapnia and hypoxemia. These blood gas derangements cause vasoconstriction of the pulmonary vasculature leading to pulmonary hypertension, which, if
severe, can result in right-sided heart failure (cor pulmonale). Hypoxemia can lead to dysfunction of organs such as the brain, blood, and heart, leading to outcomes such as cognitive dysfunction, polycythemia, and cardiac arrhythmias. Hypercapnia can depress
ventilatory drive, leading to progressive respiratory failure.
Differential Diagnosis
Other medical conditions affecting ventilation. In adults, the idiopathic variety of sleeprelated hypoventilation is very uncommon and is determined by excluding the presence of
lung diseases, skeletal malformations, neuromuscular disorders, and other medical and
neurological disorders or medications that affect ventilation. Sleep-related hypoventilation must be distinguished from other causes of sleep-related hypoxemia, such as that due
to lung disease.
Other breathing-related sleep disorders. Sleep-related hypoventilation can be distinguished from obstructive sleep apnea hypopnea and central sleep apnea based on clinical
features and findings on polysomnography. Sleep-related hypoventilation typically shows
more sustained periods of oxygen desaturation rather that the periodic episodes seen in
obstructive sleep apnea hypopnea and central sleep apnea. Obstructive sleep apnea hypopnea and central sleep apnea also show a pattern of discrete episodes of repeated airflow decreases that can be absent in sleep-related hypoventilation.
Comorbidity
Sleep-related hypoventilation often occurs in association with a pulmonary disorder (e.g., interstitial lung disease, COPD), with a neuromuscular or chest wall disorder (e.g., muscular
dystrophies, post-polio syndrome, cervical spinal cord injury, obesity, kyphoscoliosis), or.
most relevant to the mental health provider, with medication use (e.g., benzodiazepines, opiates). Congenital central alveolar hypoventilation often occurs in association with autonomic
dysfunction and may occur in association with Hirschsprung's disease. COPD, a disorder of
lower airway obstruction usually associated with cigarette smoking, can result in sleeprelated hypoventilation and hypoxemia. The presence of coexisting obstructive sleep apnea
hypopnea is thought to exacerbate hypoxemia and hypercapnia during sleep and wakefulness. The relationship between congenital central alveolar hypoventilation and idiopathic
sleep-related hypoventilation is unclear; in some individuals, idiopathic sleep-related hypoventilation may represent cases of late-onset congenital central alveolar hypoventilation.
Relationship to internationai Ciassification of
Sieep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), combines sleeprelated hypoventilation and sleep-related hypoxemia under the category of sleep-related
hypoventilation/hypoxemic syndromes. This approach to classification reflects the frequent co-occurrence of disorders that lead to hypoventilation and hypoxemia. In contrast,
the classification used in DSM-5 reflects evidence that there are distinct sleep-related
pathogenetic processes leading to hypoventilation.
Circadian Rhythm Sleep-Wake Disorders
Diagnostic Criteria
A. A persistent or recurrent pattern of sleep disruption that is primarily due to an alteration
of the circadian system or to a misalignment between the endogenous circadian
rhythm and the sleep-wake schedule required by an individual’s physical environment
or social or professional schedule.
B. The sleep disruption leads to excessive sleepiness or insomnia, or both.
C. The sleep disturbance causes clinically significant distress or impairment in social, occupational, and other important areas of functioning.
Coding note: For ICD-9-CM, code 307.45 for all subtypes. For ICD-10-CM, code is based
on subtype.
Specify whether:
307.45 (G47.21) Delayed sleep phase type: A pattern of delayed sleep onset and
awakening times, with an inability to fall asleep and awaken at a desired or conventionally acceptable earlier time.
Specify if:
Familial: A family history of delayed sleep phase is present.
Specify if:
Overlapping with non-24-hour sleep-wake type: Delayed sleep phase type
may overlap with another circadian rhythm sleep-wake disorder, non-24-hour
sleep-wake type.
307.45 (G47.22) Advanced sleep phase type: A pattern of advanced sleep onset and
awakening times, with an inability to remain awake or asleep until the desired or conventionally acceptable later sleep or wake times.
Specify if:
Familial: A family history of advanced sleep phase is present.
307.45 (G47.23) Irregular sleep-walte type: A temporally disorganized sleep-wake
pattern, such that the timing of sleep and wake periods is variable throughout the 24-
hour period.
307.45 (G47.24) Non-24-hour sleep-wake type: A pattern of sleep-wal<e cycles that
is not synchronized to the 24-hour environment, with a consistent daily drift (usually to
later and later times) of sleep onset and wake times.
307.45 (G47.26) Shift work type: Insomnia during the major sleep period and/or excessive sleepiness (including inadvertent sleep) during the major awake period associated with a shift work schedule (i.e., requiring unconventional work hours).
307.45 (G47.20) Unspecified type
Specify if:
Episodic: Symptoms last at least 1 month but less than 3 months.
Persistent: Symptoms last 3 months or longer.
Recurrent: Two or more episodes occur within the space of 1 year.
Delayed Sleep Phase Type
Diagnostic Features
The delayed sleep phase type is based primarily on a history of a delay in the timing of the
major sleep period (usually more than 2 hours) in relation to the desired sleep and wakeup time, resulting in symptoms of insomnia and excessive sleepiness. When allowed to set
their own schedule, individuals with delayed sleep phase type exhibit normal sleep quality and duration for age. Symptoms of sleep-onset insomnia, difficulty waking in the
morning, and excessive early day sleepiness are prominent.
Associated Features Supporting Diagnosis
Common associated features of delayed sleep phase type include a history of mental disorders or a concurrent mental disorder. Extreme and prolonged difficulty awakening with
morning confusion is also common. Psychophysiological insomnia may develop as a result of maladaptive behaviors that impair sleep and increase arousal because of repeated
attempts to fall asleep at an earlier time.
Prevaience
Prevalence of delayed sleep phase type in the general population is approximately 0.17%
but appears to be greater than 7% in adolescents. Although the prevalence of familial delayed sleep phase type has not been established, a family history of delayed sleep phase is
present in individuals with delayed sleep phase type.
Development and Course
Course is persistent, lasting longer than 3 months, with intermittent exacerbations throughout adulthood. Although age at onset is variable, symptoms begin typically in adolescence
and early adulthood and persist for several months to years before diagnosis is established. Severity may decrease with age. Relapse of symptoms is common.
Clinical expression may vary across the lifespan depending on social, school, and work
obligations. Exacerbation is usually triggered by a change in work or school schedule that
requires an early rise time. Individuals who can alter their work schedules to accommodate the delayed circadian sleep and wake timing can experience remission of symptoms.
Increased prevalence in adolescence may be a consequence of both physiological and behavioral factors. Hormonal changes may be involved specifically, as delayed sleep phase is associated with the onset of puberty. Thus, delayed sleep phase type in adolescents should be
differentiated from the common delay in the timing of circadian rhythms in this age group. In
the familial form, the course is persistent and may not improve sig^iificantly with age.
Risk and Prognostic Factors
Genetic and physiological. Predisposing factors may include a longer than average circadian period, changes in light sensitivity, and impaired homeostatic sleep drive. Some individuals with delayed sleep phase type may be hypersensitive to evening light, which
can serve as a delay signal to the circadian clock, or they may be hyposensitive to morning
light such that its phase-advancing effects are reduced. Genetic factors may play a role in
the pathogenesis of familial and sporadic forms of delayed sleep phase type, including
mutations in circadian genes (e.g., PER3, CKle).
Diagnostic i\/larl(ers
Confirmation of the diagnosis includes a complete history and use of a sleep diary or actigraphy (i.e., a wrist-wom motion detector that monitors motor activity for prolonged periods and
can be used as a proxy for sleep-wake patterns for at least 7 days). The period covered should
include weekends, when social and occupational obligations are less strict, to ensure that the
individual exhibits a consistently delayed sleep-wake pattern. Biomarkers such as salivary
dim light melatonin onset should be obtained only when the diagnosis is unclear.
Functional Consequences of Delayed Sleep Phase Type
Excessive early day sleepiness is prominent. Extreme and prolonged difficulty awakening
with morning confusion (i.e., sleep inertia) is also common. The severity of insomnia and
excessive sleepiness symptoms varies substantially among individuals and largely depends on the occupational and social demands on the individual.
Differential Diagnosis
Normative variations in sleep. Delayed sleep phase type must be distinguished from
"normal" sleep patterns in which an individual has a late schedule that does not cause
personal, social, or occupational distress (most commonly seen in adolescents and young
adults).
Other sleep disorders. Insomnia disorder and other circadian rhythm sleep-wake disorders should be included in the differential. Excessive sleepiness may also be caused by
other sleep disturbances, such as breathing-related sleep disorders, insomnias, sleeprelated movement disorders, and medical, neurological, and mental disorders. Overnight
polysomnography may help in evaluating for other comorbid sleep disorders, such as
sleep apnea. The circadian nature of delayed sleep phase type, however, should differentiate it from other disorders with similar complaints.
Comorbidity
Delayed sleep phase type is strongly associated with depression, personality disorder, and
somatic symptom disorder or illness anxiety disorder. In addition, comorbid sleep disorders, such as insomnia disorder, restless legs syndrome, and sleep apnea, as well as depressive and bipolar disorders and anxiety disorders, can exacerbate symptoms of insomnia
and excessive sleepiness. Delayed sleep phase type may overlap with another circadian
rhythm sleep-wake disorder, non-24-hour sleep-wake type. Sighted individuals with non24-hour sleep-wake type disorder commonly also have a history of delayed circadian sleep
phase.
Advanced Sleep Phase Type
\
Specifiers
Advanced sleep phase type may be documented with the specified "famihal." Although
the prevalence of familial advanced sleep phase type has not been established, a family
history of advanced sleep phase is present in individuals with advanced sleep phase type.
In this type, specific mutations demonstrate an autosomal dominant mode of inheritance.
In the familial form, onset of symptoms may occur earlier (during childhood and early
adulthood), the course is persistent, and the severity of symptoms may increase with age.
Diagnostic Features
Advanced sleep phase type is characterized by sleep-wake times that are several hours
earlier than desired or conventional times. Diagnosis is based primarily on a history of an
advance in the timing of the major sleep period (usually more than 2 hours) in relation to
the desired sleep and wake-up time, with symptoms of early morning insomnia and excessive daytime sleepiness. When allowed to set their schedule, individuals with advanced sleep phase type will exhibit normal sleep quality and duration for age.
Associated Features Supporting Diagnosis
Individuals with advanced sleep phase type are "morning types," having earlier sleepwake times, with the timing of circadian biomarkers such as melatonin and core body temperature rhythms occurring 2-A hours earlier than normal. When required to keep a conventional schedule requiring a delay of bedtime, these individuals will continue to have an
early rise time, leading to persistent sleep deprivation and daytime sleepiness. Use of hypnotics or alcohol to combat sleep-maintenance insomnia and stimulants to reduce daytime
sleepiness may lead to substance abuse in these individuals.
Prevaience
The estimated prevalence of advanced sleep phase type is approximately 1% in middleage adults. Sleep-wake times and circadian phase advance in older individuals, probably
accounting for increased prevalence in this population.
Deveiopment and Course
Onset is usually in late adulthood. In the familial form, onset can be earlier. The course is typically persistent, lasting more than 3 months, but the severity may increase depending on work
and social schedules. The advanced sleep phase type is more common in older adults.
Clinical expression may vary across the lifespan depending on social, school, and work
obligations. Individuals who can alter their work schedules to accommodate the advanced
circadian sleep and wake timing can experience remission of symptoms. Increasing age
tends to advance the sleep phase, however, it is unclear whether the common age-associated advanced sleep phase type is due solely to a change in circadian timing (as seen in the
familial form) or also to age-related changes in the homeostatic regulation of sleep, resulting in earlier awakening. Severity, remission, and relapse of symptoms suggest lack of adherence to behavioral and environmental treatments designed to control sleep and wake
structure and light exposure.
Risk and Prognostic Factors
Environmental. Decreased late aftemoon/early evening exposure to light and/or exposure to early morning light due to early morning awakening can increase the risk of advanced sleep phase type by advancing circadian rhythms. By going to bed early, these
individuals are not exposed to light in the phase delay region of the curve, resulting in perpetuation of advanced phase. In familial advanced sleep phase type, a shortening of the
endogenous circadian period can result in an advanced sleep phase, although circadian period does not appear to systematically decrease with age.
Genetic and physiological. Advanced sleep phase type has demonstrated an autosomal dominant mode of inheritance, including a PER2 gene mutation causing hypophosphorylation of the PER2 protein and a missense mutation in CKL
Culture-Reiated Diagnostic issues
African Americans may have a shorter circadian period and larger magnitude phase advances to light than do Caucasians, possibly increasing the risk for development of advanced sleep phase type in this population.
Diagnostic iVlaricers
A sleep diary and actigraphy may be used as diagnostic markers, as described earlier for
delayed sleep phase type.
Functionai Consequences of Advanced Sieep Pliase Type
Excessive sleepiness associated with advanced sleep phase can have a negative effect on
cognitive performance, social interaction, and safety. Use of wake-promoting agents to
combat sleepiness or sedatives for early morning awakening may increase potential for
substance abuse.
Differentiai Diagnosis
Other sleep disorders. Behavioral factors such as irregular sleep schedules, voluntary
early awakening, and exposure to light in the early morning should be considered, particularly in older adults. Careful attention should be paid to rule out other sleep-wake disorders, such as insomnia disorder, and other mental disorders and medical conditions that
can cause early morning awakening.
Depressive and bipolar disorders. Because early morning awakening, fatigue, and sleepiness are prominent features of major depressive disorder, depressive and bipolar disorders must also be considered.
Comorbidity
Medical conditions and mental disorders with the symptom of early morning awakening,
such as insomnia, can co-occur with the advance sleep phase type.
Irregular Sleep-Wake Type
Diagnostic Features
The diagnosis of irregular sleep-wake type is based primarily on a history of symptoms of
insomnia at night (during the usual sleep period) and excessive sleepiness (napping) during the day. Irregular sleep-wake type is characterized by a lack of discernable sleep-wake
circadian rhythm. There is no major sleep period, and sleep is fragmented into at least
three periods d\iring the 24-hour day.
Associated Features Supporting Diagnosis
Individuals with irregular sleep-wake type typically present with insomnia or excessive
sleepiness, depending on the time of day. Sleep and wake periods across 24 hours are fragmented, although the longest sleep period tends to occur between 2:00 A.M. and 6:00 A.M.
and is usually less than 4 hours. A history of isolation or reclusion may occur in association
with the disorder and contribute to the symptoms via a lack of external stimuli to help entrain a normal pattern. Individuals or their caregivers report frequent naps throughout the
day. Irregular sleep-wake type is most commonly associated with neurodegenerative disorders, such as major neurocognitive disorder, and many neurodevelopmental disorders
in children.
Prevalence
Prevalence of irregular sleep-wake type in the general population is unknown.
Deveiopment and Course
The course of irregular sleep-wake type is persistent. Age at onset is variable, but the disorder is more common in older adults.
Risic and Prognostic Factors
Temperamental. Neurodegenerative disorders, such as Alzheimer's disease, Parkinson's
disease, and Huntington's disease, and neurodevelopmental disorders in children increase the risk for irregular sleep-wake type.
Environmental. Decreased exposure to environmental light and structured daytime activity can be associated with a low-amplitude circadian rhythm. Hospitalized individuals
are especially prone to such weak external entraining stimuli, and even outside the hospital setting, individuals with major neurocognitive disorder (i.e., dementia) are exposed to
significantly less bright light.
Diagnostic iViaricers
A detailed sleep history and a sleep diary (by a caregiver) or actigraphy help confirm the
irregular sleep-wake pattern.
Functional Consequences of
irregular Sleep-Wake Type
Lack of a clearly discernible major sleep and wake period in irregular sleep-wake type results in insomnia or excessive sleepiness, depending on the time of day. Disruption of the
caregiver's sleep also often occurs and is an important consideration.
Differential Diagnosis
Normative variations in sleep. Irregular sleep-wake type should be distinguished from
a voluntary irregular sleep-wake schedule and poor sleep hygiene, which can result in insomnia and excessive sleepiness.
Other medical conditions and mental disorders. Other causes of insomnia and daytime
sleepiness, including comorbid medical conditions and mental disorders or medication,
should be considered.
Comorbidity
Irregular sleep-wake type is often comorbid with neurodegenerative and neurodevelopmental disorders, such as major neurocognitive disorder, intellectual disability (intellectual developmental disorder), and traumatic brain injury. It is also comorbid with other
medical conditions and mental disorders in which there is social isolation and/or lack of
light and structured activities.
Non-24-Hour Sleep-Wake Type
Diagnostic Features
The diagnosis of non-24-hour sleep-wake type is based primarily on a history of symptoms of insomnia or excessive sleepiness related to abnormal synchronization between the
24-hour light-dark cycle and the endogenous circadian rhythm. Individuals typically present with periods of insomnia, excessive sleepiness, or both, which alternate with short
asymptomatic periods. Starting with the asymptomatic period, when the individual's
sleep phase is aligned to the external environment, sleep latency will gradually increase
and the individual will complain of sleep-onset insomnia. As the sleep phase continues to
drift so that sleep time is now in the daytime, the individual will have trouble staying
awake during the day and will complain of sleepiness. Because the circadian period is not
aligned to the external 24-hour environment, symptoms will depend on when an individual tries to sleep in relation to the circadian rhythm of sleep propensity.
Associated Features Supporting Diagnosis
Non-24-hour sleep-wake type is most common among blind or visually impaired individuals who have decreased light perception. In sighted individuals, there is often a history of
delayed sleep phase and of decreased exposure to light and structured social and physical
activity. Sighted individuals with non-24-hour sleep-wake type also demonstrate increased sleep duration.
Prevaience
Prevalence of non-24-hour sleep-wake type in the general population is unclear, but the
disorder appears rare in sighted individuals. The prevalence in blind individuals is estimated to be 50%.
Deveiopment and Course
Course of non-24-hour sleep-wake type is persistent, with intermittent remission and exacerbations due to changes in work and social schedules throughout the lifespan. Age at
onset is variable, depending on the onset of visual impairment. In sighted individuals, because of the overlap with delayed sleep phase type, non-24-hour sleep-wake type may develop in adolescence or early adulthood. Remission and relapse of symptoms in blind and
sighted individuals largely depend on adherence to treatments designed to control sleep
and wake structure and light exposure.
Clinical expression may vary across the lifespan depending on social, school, and work
obligations. In adolescents and adults, irregular sleep-wake schedules and exposure to
light or lack of light at critical times of the day can exacerbate the effects of sleep loss and
disrupt circadian entrainment. Consequently, symptoms of insomnia, daytime sleepiness,
and school, professional, and interpersonal functioning may worsen.
Risk and Prognostic Factors
Environmental. In sighted individuals, decreased exposure or sensitivity to light and social and physical activity cues may contribute to a free-running circadian rhythm. With the
high frequency of mental disorders involving social isolation and cases of non-24-hour
sleep-wake type developing after a change in sleep habits (e.g., night shift work, job loss),
behavioral factors in combination with physiological tendency may precipitate and perpetuate this disorder in sighted individuals. Hospitalized individuals with neurological and
psychiatric disorders can become insensitive to social cues, predisposing them to the development of non-24-hour sleep-wake type.
Genetic and physiological. Blindness is a risk factor for non-24-hour sleep-wake type.
Non-24-hour sleep-wake type has been associated with traumatic brain injury.
Diagnostic iVlarlcers
Diagnosis is confirmed by history and sleep diary or actigraphy for an extended period.
Sequential measurement of phase markers (e.g., melatonin) can help determine circadian
phase in both sighted and blind individuals.
Functionai Consequences of
Non-24-Hour Sieep-Walce Type
Complaints of insomnia (sleep onset and sleep maintenance), excessive sleepiness, or both
are prominent. The unpredictability of sleep and wake times (typically a daily delay drift)
results in an inability to attend school or maintain a steady job and may increase potential
for social isolation.
Differentiai Diagnosis
Circadian rhythm sleep-wake disorders. In sighted individuals, non-24-hour sleep-wake
type should be differentiated from delayed sleep phase type, as individuals with delayed
sleep phase type may display a similar progressive delay in sleep period for several days.
Depressive disorders. Depressive symptoms and depressive disorders may result in
similar circadian dysregulation and symptoms.
Comorbidity
Blindness is often comorbid with non-24-hour sleep-wake type, as are depressive and bipolar disorders with social isolation.
Shift Work Type
Diagnostic Features
Diagnosis is primarily based on a history of the individual working outside of the normal
8:00 A.M. to 6:00 P.M. daytime window (particularly at night) on a regularly scheduled (i.e.,
non-overtime) basis. Symptoms of excessive sleepiness at work, and impaired sleep at
home, on a persistent basis are prominent. Presence of both sets of symptoms are usually
required for a diagnosis of shift work type. Typically, when the individual reverts to a daywork routine, symptoms resolve. Although the etiology is slightly different, individuals
who travel across many time zones on a very frequent basis may experience effects similar
to those experienced by individuals with shift work type who work rotating shifts.
Prevalence
The prevalence of shift work type is unclear, but the disorder is estimated to affect 5%-10%
of the night worker population (16%-20% of the workforce). Prevalence rises with advancement into middle-age and beyond (Drake et al. 2004).
Development and Course
Shift work type can appear in individuals of any age but is more prevalent in individuals
older than 50 years and typically worsens with the passage of time if the disruptive work
hours persist. Although older adults may show similar rates of circadian phase adjustment to a change in routine as do younger adults, they appear to experience significantly
more sleep disruption as a consequence of the circadian phase shift.
Risk and Prognostic Factors
Temperamental. Predisposing factors include a morning-type disposition, a need for
long (i.e., more than 8 hours) sleep durations in order to feel well rested, and strong competing social and domestic needs (e.g., parents of young children). Individuals who are able
to commit to a nocturnal lifestyle, with few competing day-oriented demands, appear at
lower risk for shift work type.
Genetic and physiological. Because shift workers are more likely than day workers to
be obese, obstructive sleep apnea may be present and may exacerbate the symptoms.
Diagnostic iVlarlcers
A history and sleep diary or actigraphy may be useful in diagnosis, as discussed earlier for
delayed sleep phase type.
Functional Consequences of Shift Worl( Type
Individuals with shift work type not only may perform poorly at work but also appear to
be at risk for accidents both at work and on the drive home. They may also be at risk for
poor mental health (e.g., alcohol use disorder, substance use disorder, depression) and
physical health (e.g., gastrointestinal disorders, cardiovascular disease, diabetes, cancer).
Individuals with a history of bipolar disorder are particularly vulnerable to shift work
type-related episodes of mania resulting from missed nights of sleep. Shift work type often results in interpersonal problems.
Differential Diagnosis
Normative variations in sleep with shift work. The diagnosis of shift work type, as opposed to the ''normal" difficulties of shift work, must depend to some extent on the severity of symptoms and/or level of distress experienced by the individual. Presence of shift
work type symptoms even when the individual is able to live on a day-oriented routine for
several weeks at a time may suggest the presence of other sleep disorders, such as sleep apnea, insomnia, and narcolepsy, which should be ruled out.
Comorbidity
Shift work type has been associated with increased alcohol use disorder, other substance
use disorders, and depression. A variety of physical health disorders (e.g., gastrointestinal
disorders, cardiovascular disease, diabetes, cancer) have been found to be associated with
prolonged exposure to shift work.
Relationship to International Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition (ICSD-2), differentiates nine
circadian rhythm sleep disorders, including jet lag type.
Parasomnias
Parasomnias are disorders characterized by abnormal behavioral, experiential, or physiological events occurring in association with sleep, specific sleep stages, or sleep-wake transitions. The most common parasomnias—non-rapid eye movement (NREM) sleep
arousal disorders and rapid eye movement (REM) sleep behavior disorder—represent admixtures of wakefulness and NREM sleep and wakefulness and REM sleep, respectively.
These conditions serve as a reminder that sleep and wakefulness are not mutually exclusive and that sleep is not necessarily a global, whole-brain phenomenon.
Non-Rapid Eye Movement
Sleep Arousal Disorders
Diagnostic Criteria
A. Recurrent episodes of incomplete awakening from sleep, usually occurring during the
first third of the major sleep episode, accompanied by either one of the following:
1. Sleepwalking: Repeated episodes of rising from bed during sleep and walking
about. While sleepwalking, the individual has a blank, staring face; is relatively unresponsive to the efforts of others to communicate with him or her; and can be
awakened only with great difficulty.
2. Sleep terrors: Recurrent episodes of abrupt terror arousals from sleep, usually beginning with a panicky scream. There is intense fear and signs of autonomic
arousal, such as mydriasis, tachycardia, rapid breathing, and sweating, during
each episode. There is relative unresponsiveness to efforts of others to comfort the
individual during the episodes.
B. No or little (e.g., only a single visual scene) dream imagery is recalled.
C. Amnesia for the episodes is present.
D. The episodes cause clinically significant distress or impairment in social, occupational,
or other important areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (e.g., a
drug of abuse, a medication).
F. Coexisting mental and medical disorders do not explain the episodes of sleepwalking
or sleep terrors.
Coding note: For ICD-9-CM, code 307.46 for all subtypes. For ICD-10-CM, code is based
on subtype.
Specify whether:
307.46 (F51.3) Sleepwalking type
Specify if:
With sleep-related eating
With sleep-related sexual behavior (sexsomnia)
307.46 (F51.4) Sleep terror type
Diagnostic Features
The essential feature of non-rapid eye movement (NREM) sleep arousal disorders is the
repeated occurrence of incomplete arousals, usually beginning during the first third of the
major sleep episode (Criterion A), that typically are brief, lasting 1-10 minutes, but may be
protracted, lasting up to 1 hour. The maximum duration of an event is unknown. The eyes
are typically open during these events. Many individuals exhibit both subtypes of arousals
on different occasions, which underscores the unitary underlying pathophysiology. The
subtypes reflect varying degrees of simultaneous occurrence of wakefulness and NREM
sleep, resulting in complex behaviors arising from sleep with varying degrees of conscious
awareness, motor activity, and autonomic activation.
The essential feature of sleepwalking is repeated episodes of complex motor behavior
initiated during sleep, including rising from bed and walking about (Criterion Al). Sleepwalking episodes begin during any stage of NREM sleep, most commonly during slowwave sleep and therefore most often occurring during the first third of the night. During
episodes, the individual has reduced alertness and responsiveness, a blank stare, and relative unresponsiveness to communication with others or efforts by others to awaken the
individual. If awakened during the episode (or on awakening the following morning), the
individual has limited recall for the episode. After the episode, there may initially be a brief
period of confusion or difficulty orienting, followed by full recovery of cognitive function
and appropriate behavior.
The essential feature of sleep terrors is the repeated occurrence of precipitous awakenings from sleep, usually beginning with a panicky scream or cry (Criterion A2). Sleep terrors usually begin during the first third of the major sleep episode and last 1-10 minutes,
but they may last considerably longer, particularly in children. The episodes are accompanied by impressive autonomic arousal and behavioral manifestations of intense fear.
During an episode, the individual is difficult to awaken or comfort. If the individual awakens after the sleep terror, little or none of the dream, or only fragmentary, single images,
are recalled. During a typical episode of sleep terrors, the individual abruptly sits up in
bed screaming or crying, with a frightened expression and autonomic signs of intense anxiety (e.g., tachycardia, rapid breathing, sweating, dilation of the pupils). The individual
may be inconsolable and is usually unresponsive to the efforts of others to awaken or comfort him or her. Sleep terrors are also called "night terrors" or "pavor nocturnus."
Associated Features Supporting Diagnosis
Sleepwalking episodes can include a wide variety of behaviors. Episodes may begin with
confusion: the individual may simply sit up in bed, look about, or pick at the blanket or
sheet. This behavior then becomes progressively complex. The individual may actually
leave the bed and walk into closets, out of the room, and even out of buildings. Individuals
may use the bathroom, eat, talk, or engage in more complex behaviors. Running and frantic attempts to escape some apparent threat can also occur. Most behaviors during sleepwalking episodes are routine and of low complexity. However, cases of unlocking doors
and even operating machinery (driving an automobile) have been reported. Sleepwalking
can also include inappropriate behavior (e.g., commonly, urinating in a closet or wastebasket). Most episodes last for several minutes to a half hour but may be more protracted.
Inasmuch as sleep is a state of relative analgesia, painful injuries sustained during sleepwalking may not be appreciated until awakening after the fact.
There are two "specialized" forms of sleepwalking: sleep-related eating behavior and
sleep-related sexual behavior (sexsomnia or sleep sex). Individuals with sleep-related eating
experience unwanted recurrent episodes of eating with varying degrees of amnesia, ranging from no awareness to full awareness without the ability to not eat. During these episodes, inappropriate foods may be ingested. Individuals witii sleep-related eating disorder
may find evidence of their eating only the next morning. In sexsomnia, varying degrees of
sexual activity (e.g., masturbation, fondling, groping, sexual intercourse) occur as complex
behaviors arising from sleep without conscious awareness. This condition is more common
in males and may result in serious interpersonal relationship problems or medicolegal
consequences.
During a typical episode of sleep terrors, there is often a sense of overwhelming dread,
with a compulsion to escape. Although fragmentary vivid dream images may occur, a storylike dream sequence (as in nightmares) is not reported. Most commonly, the individual does
not awaken fully, but returns to sleep and has amnesia for the episode on awakening the next
morning. Usually only one episode will occur on any one night. Occasionally several episodes
may occur at intervals throughout the night. These events rarely arise during daytime naps.
Prevalence
Isolated or infrequent NREM sleep arousal disorders are very common in the general population. From 10% to 30% of children have had at least one episode of sleepwalking, and
2%-3% sleepwalk often. The prevalence of sleepwalking disorder, marked by repeated episodes and impairment or distress, is much lower, probably in the range of l%-5%. The
prevalence of sleepwalking episodes (not sleepwalking disorder) is 1.0%-7.0% among
adults, with weekly to monthly episodes occurring in 0.5%-0.7%. The lifetime prevalence
of sleepwalking in adults is 29.2%, with a past-year prevalence of sleepwalking of 3.6%.
The prevalence of sleep terrors in the general population is unknown. The prevalence
of sleep terror episodes (as opposed to sleep terror disorder, in which there is recurrence
and distress or impairment) is approximately 36.9% at 18 months of age, 19.7% at 30 months
of age, and 2.2% in adults.
Development and Course
NREM sleep arousal disorders occur most commonly in childhood and diminish in frequency with increasing age. The onset of sleepwalking in adults with no prior history of
sleepwalking as children should prompt a search for specific etiologies, such as obstructive sleep apnea, nocturnal seizures, or effect of medication.
Risk and Prognostic Factors
Environmental. Sedative use, sleep deprivation, sleep-wake schedule disruptions, fatigue, and physical or emotional stress increase the likelihood of episodes. Fever and sleep
deprivation can produce an increased frequency of NREM sleep arousal disorders.
Genetic and physiological. A family history for sleepwalking or sleep terrors may occur in up to 80% of individuals who sleepwalk. The risk for sleepwalking is further increased (to as much as 60% of offspring) when both parents have a history of the disorder.
Individuals with sleep terrors frequently have a positive family history of either sleep
terrors or sleepwalking, with as high as a 10-fold increase in the prevalence of the disorder
among first-degree biological relatives. Sleep terrors are much more common in monozygotic twins as compared with dizygotic twins. The exact mode of inheritance is unknown.
Gender-Related Diagnostic Issues
Violent or sexual activity during sleepwalking episodes is more likely to occur in adults.
Eating during sleepwalking episodes is more commonly seen in females. Sleepwalking occurs more often in females during childhood but more often in males during adulthood.
Older children and adults provide a more detailed recollection of fearful images associated with sleep terrors than do younger children, who are more likely to have complete
amnesia or report only a vague sense of fear. Among children, sleep terrors are more common in males than in females. Among adults, the sex ratio is even.
Diagnostic IVIaricers
NREM sleep arousal disorders arise from any stage of NREM sleep but most commonly
from deep NREM sleep (slow-wave sleep). They are most likely to appear in the first third
of the night and do not commonly occur during daytime naps. During the episode, the
polysomnogram may be obscured with movement artifact. In the absence of such artifact,
the electroencephalogram typically shows theta or alpha frequency activity during the episode, indicating partial or incomplete arousal.
Polysomnography in conjunction with audiovisual monitoring can be used to document
episodes of sleepwalking. In the absence of actually capturing an event during a polysomnographic recording, there are no polysomnographic features that can serve as a marker for
sleepwalking. Sleep deprivation may increase the likelihood of capturing an event. As a group,
individuals who sleepwalk show instability of deep NREM sleep, but the overlap in findings
with individuals who do not sleepwalk is great enough to preclude use of this indicator in establishing a diagnosis. Unlike arousals from REM sleep associated with nightmares, in which
there is an increase in heart rate and respiration prior to the arousal, the NREM sleep arousals
of sleep terrors begin precipitously from sleep, without anticipatory autonomic changes. The
arousals are associated with impressive autonomic activity, with doubling or tripling of
the heart rate. The pathophysiology is poorly understood, but there appears to be instability in
the deeper stages of NREM sleep. Absent capturing an event during a formal sleep study,
there are no reliable polysomnographic indicators of the tendency to experience sleep terrors.
Functional Consequences of
Non-REIVI Sleep Arousal Disorders
For the diagnosis of a NREM sleep arousal disorder to be made, the individual or household members must experience clinically significant distress or impairment, although parasomnia symptoms may occur occasionally in nonclinical populations and would be
subthreshold for the diagnosis. Embarrassment concerning the episodes can impair social
relationships. Social isolation or occupational difficulties can result. The determination of a
"disorder" depends on a number of factors, which may vary on an individual basis and
will depend on the frequency of events, potential for violence or injurious behaviors, embarrassment, or disruption/distress of other household members. Severity determination
is best made based on the nature or consequence of the behaviors rather than simply on frequency. Uncommonly, NREM sleep arousal disorders may result in serious injury to the
individual or to someone trying to console the individual. Injuries to others are confined to
those in close proximity; individuals are not "sought out." Typically, sleepwalking in both
children and adults is not associated with significant mental disorders. For individuals
with sleep-related eating behaviors, unknowingly preparing or eating food during the
sleep period may create problems such as poor diabetes control, weight gain, injury (cuts
and bums), or consequences of eating dangerous or toxic inedibles. NREM sleep arousal
disorders may rarely result in violent or injurious behaviors with forensic implications.
Differential Diagnosis
Nightmare disorder. In contrast to individuals with NREM sleep arousal disorders, individuals with nightmare disorder typically awaken easily and completely, report vivid
storyhke dreams accompanying the episodes, and tend to have episodes later in the night.
NREM sleep arousal disorders occur during NREM sleep, whereas nightmares usually occur during REM sleep. Parents of children with NREM sleep arousal disorders may misinterpret reports of fragmentary imagery as nightmares.
Breathing-related sleep disorders. Breathing disorders during sleep can also produce
confusional arousals with subsequent amnesia. However, breathing-related sleep disorders are also characterized by characteristic symptoms of snoring, breathing pauses, and
daytime sleepiness. In some individuals, a breathing-related sleep disorder may precipitate episodes of sleepwalking.
\
REM sleep behavior disorder. REM sleep behavior disorder may be difficult to distinguish from NREM sleep arousal disorders. REM sleep behavior disorder is characterized
by episodes of prominent, complex movements, often involving personal injury arising
from sleep. In contrast to NREM sleep arousal disorders, REM sleep behavior disorder occurs during REM sleep. Individuals v^ith REM sleep behavior disorder awaken easily and
report more detailed and vivid dream content than do individuals with NREM sleep arousal
disorders. They often report that they "act out dreams."
Parasomnia overlap syndrome. Parasomnia overlap syndrome consists of clinical and
polysomnographic features of both sleepwalking and REM sleep behavior disorder.
Sleep-related seizures. Some types of seizures can produce episodes of very unusual
behaviors that occur predominantly or exclusively during sleep. Nocturnal seizures may
closely mimic NREM sleep arousal disorders but tend to be more stereotypic in nature, occur multiple times nightly, and be more likely to occur from daytime naps. The presence of
sleep-related seizures does not preclude the presence of NREM sleep arousal disorders.
Sleep-related seizures should be classified as a form of epilepsy.
Alcohol-induced blackouts. Alcohol-induced blackouts may be associated with extremely
complex behaviors in the absence of other suggestions of intoxication. They do not involve
the loss of consciousness but rather reflect an isolated disruption of memory for events
during a drinking episode. By history, these behaviors may be indistinguishable from those
seen in NREM sleep arousal disorders.
Dissociative amnesia, with dissociative fugue. Dissociative fugue may be extremely
difficult to distinguish from sleepwalking. Unlike all other parasomnias, nocturnal dissociative fugue arises from a period of wakefulness during sleep, rather than precipitously
from sleep without intervening wakefulness. A history of recurrent childhood physical or
sexual abuse is usually present (but may be difficult to obtain).
Malingering or other voluntary behavior occurring during wakefulness. As with dissociative fugue, malingering or other voluntary behavior occurring during wakefulness
arises from wakefulness.
Panic disorder. Panic attacks may also cause abrupt awakenings from deep NREM sleep
accompanied by fearfulness, but these episodes produce rapid and complete awakening without the confusion, amnesia, or motor activity typical of NREM sleep arousal disorders.
Medication-induced complex behaviors. Behaviors similar to those in NREM sleep
arousal disorders can be induced by use of, or withdrawal from, substances or medications (e.g., benzodiazepines, nonbenzodiazepine sedative-hypnotics, opiates, cocaine, nicotine, antipsychotics, tricyclic antidepressants, chloral hydrate). Such behaviors may arise
from the sleep period and may be extremely complex. The underlying pathophysiology
appears to be a relatively isolated amnesia. In such cases, substance/medication-induced
sleep disorder, parasomnia type, should be diagnosed (see "Substance/MedicationInduced Sleep Disorder" later in this chapter).
Night eating syndrome. The sleep-related eating disorder form of sleepwalking is to be
differentiated from night eating syndrome, in which there is a delay in the circadian rhythm
of food ingestion and an association with insomnia and/or depression.
Comorbidity
In adults, there is an association between sleepwalking and major depressive episodes and
obsessive-compulsive disorder. Children or adults with sleep terrors may have elevated
scores for depression and anxiety on personality inventories.
Relationship to international Classification of
Sleep Disorders
The International Classification of Sleep Disorders, 2nd Edition, includes "confusional
arousal" as a NREM sleep arousal disorder.
Nightmare Disorder
Diagnostic Criteria 307.47 (F51.5)
A. Repeated occurrences of extended, extremely dysphoric, and well-remembered
dreams that usually involve efforts to avoid threats to survival, security, or physical integrity and that generally occur during the second half of the major sleep episode.
B. On awakening from the dysphoric dreams, the individual rapidly becomes oriented and
alert.
0. The sleep disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The nightmare symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication).
E. Coexisting mental and medical disorders do not adequately explain the predominant
complaint of dysphoric dreams.
Specify if:
During sleep onset
Specify if:
With associated non-sleep disorder, including substance use disorders
With associated other medical condition
With associated other sleep disorder
Coding note: The code 307.47 (F51.5) applies to all three specifiers. Code also the
relevant associated mental disorder, medical condition, or other sleep disorder immediately after the code for nightmare disorder in order to indicate the association.
Specify if:
Acute: Duration of period of nightmares is 1 month or less.
Subacute: Duration of period of nightmares is greater than 1 month but less than
6 months.
Persistent: Duration of period of nightmares is 6 months or greater.
Specify current severity:
Severity can be rated by the frequency with which the nightmares occur:
Mild: Less than one episode per week on average.
Moderate: One or more episodes per week but less than nightly.
Severe: Episodes nightly.
Diagnostic Features
Nightmares are typically lengthy, elaborate, story like sequences of dream imagery that
seem real and that incite anxiety, fear, or other dysphoric emotions. Nightmare content
typically focuses on attempts to avoid or cope with imminent danger but may involve
themes that evoke other negative emotions. Nightmares occurring after traumatic experiences may replicate the threatening situation ("'replicative nightmares"), but most do not.
On awakening, nightmares are well remembered and can be described in detail. They arise
almost exclusively during rapid eye movement (REM) sleep and can thus occur throughout sleep but are; more likely in the second half of the major sleep episode when dreaming
is longer and more intense. Factors that increase early-night REM intensity, such as sleep
fragmentation or deprivation, jet lag, and REM-sensitive medications, might facilitate
nightmares earlier in the night, including at sleep onset.
Nightmares usually terminate with awakening and rapid return of full alertness. However, the dysphoric emotions may persist into wakefulness and contribute to difficulty returning to sleep and lasting daytime distress. Some nightmares, known as "bad dreams,"
may not induce awakening and are recalled only later. If nightmares occur during sleeponset REM periods (hypnagogic), the dysphoric emotion is frequently accompanied by a
sense of being both awake and unable to move voluntarily {isolated sleep paralysis).
Associated Features Supporting Diagnosis
Mild autonomic arousal, including sweating, tachycardia, and tachypnea, may characterize nightmares. Body movements and vocalizations are not characteristic because of REM
sleep-related loss of skeletal muscle tone, but such behaviors may occur under situations
of emotional stress or sleep fragmentation and in posttraumatic stress disorder (PTSD).
When talking or emoting occurs, it is typically a brief event terminating the nightmare.
Individuals with frequent nightmares are at substantially greater risk for suicidal ideation and suicide attempts, even when gender and mental illness are taken into account.
Prevalence
Prevalence of nightmares increases through childhood into adolescence. From 1.3% to
3.9% of parents report that their preschool children have nightmares "often" or "always".
Prevalence increases from ages 10 to 13 for both males and females but continues to increase to ages 20-29 for females (while decreasing for males), when it can be twice as high
for females as for males. Prevalence decreases steadily with age for both sexes, but the gender difference remains. Among adults, prevalence of nightmares at least monthly is 6%,
whereas prevalence for frequent nightmares is l%-2%. Estimates often combine idiopathic and posttraumatic nightmares indiscriminately.
Development and Course
Nightmares often begin between ages 3 and 6 years but reach a peak prevalence and severity in late adolescence or early adulthood. Nightmares most likely appear in children
exposed to acute or chronic psychosocial stressors and thus may not resolve spontaneously. In a minority, frequent nightmares persist into adulthood, becoming virtually a lifelong disturbance. Although specific nightmare content may reflect the individual's age,
the essential features of the disorder are the same across age groups.
Risk and Prognostic Factors
Temperamental. Individuals who experience nightmares report more frequent past adverse events, but not necessarily trauma, and often display personality disturbances or
psychiatric diagnosis.
Environmental. Sleep deprivation or fragmentation, and irregular sleep-wake schedules
that alter the timing, intensity, or quantity of REM sleep, can put individuals at risk for
nightmares.
Genetic and physiological. Twin studies have identified genetic effects on the disposition to nightmares and their co-occurrence with other parasomnias (e.g., sleeptalking).
Course modifiers. Adaptive parental bedside behaviors, such as soothing the child following nightmares, may protect against developing chronic nightmares.
Culture-Related Diagnostic issues
The significance attributed to nightmares may vary by culture, and sensitivity to such beliefs may facilitate disclosure.
Gender-Related Diagnostic Issues
Adult females report having nightmares more frequently than do adult males. Nightmare
content differs by sex, with adult females tending to report themes of sexual harassment or
of loved ones disappearing/dying, and adult males tending to report themes of physical
aggression or war/terror.
Diagnostic Markers
Polysomnographie studies demonstrate abrupt awakenings from REM sleep, usually during
the second half of the night, prior to report of a nightmare. Heart, respiratory, and eye movement rates may quicken or increase in variability before awakening. Nightmares following
traumatic events may also arise during non-REM (NREM), particularly stage 2, sleep. The typical sleep of individuals with nightmares is mildly impaired (e.g., reduced efficiency, less slowwave sleep, more awakenings), with more frequent periodic leg movements in sleep and relative sympathetic nervous system activation after REM sleep deprivation.
Functional Consequences of Niglitmare Disorder
Nightmares cause more significant subjective distress than demonstrable social or occupational impairment. However, if awakenings are frequent or result in sleep avoidance,
individuals may experience excessive daytime sleepiness, poor concentration, depression,
anxiety, or irritability. Frequent childhood nightmares (e.g., several per week), may cause
significant distress to parents and child.
Differential Diagnosis
Sleep terror disorder. Both nightmare disorder and sleep terror disorder include awakenings or partial awakenings with fearfulness and autonomic activation, but the two disorders are differentiable. Nightmares typically occur later in the night, during REM sleep,
and produce vivid, storylike, and clearly recalled dreams; mild autonomic arousal; and
complete awakenings. Sleep terrors typically arise in the first third of the night during
stage 3 or 4 NREM sleep and produce either no dream recall or images without an elaborate storylike quality. The terrors lead to partial awakenings that leave the individual confused, disoriented, and only partially responsive and with substantial autonomic arousal.
There is usually amnesia for the event in the morning.
REM sleep behavior disorder. The presence of complex motor activity during frightening dreams should prompt further evaluation for REM sleep behavior disorder, which
occurs more typically among late middle-age males and, unlike nightmare disorder, is associated with often violent dream enactments and a history of nocturnal injuries. The
dream disturbance of REM sleep behavior disorder is described by patients as nightmares
but is controlled by appropriate medication.
Bereavement. Dysphoric dreams may occur during bereavement but typically involve
loss and sadness and are followed by self-reflection and insight, rather than distress, on
awakening.
Narcolepsy. Nightmares are a frequent complaint in narcolepsy, but the presence of excessive sleepiness and cataplexy differentiates this condition from nightmare disorder.
Nocturnal seizures. Seizures may rarely manifest as nightmares and should be evaluated with polysomnography and continuous video electroencephalography. Nocturnal
seizures usually involve stereotypical motor activity. Associated nightmares, if recalled
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