Common presenting symptoms 122
Assessment of conscious level 124
Optic (II), oculomotor (III), trochlear (IV) and abducens (VI) nerves 128
Vestibulocochlear (VIII) nerve 131
Glossopharyngeal (IX) and vagus (X) nerves 131
Inspection and palpation of the muscles 136
Common presenting symptoms 143
Lateral cutaneous nerve of the thigh 147
Interpretation of the findings 147
OSCE example 1: Headache history 149
Integrated examination sequence for the nervous system 150
For many common neurological symptoms such as headache,
numbness, disturbance/loss of consciousness and memory loss,
the history is the key to diagnosis, as the examination may be
either normal or unhelpful. Some symptoms, including loss of
consciousness or amnesia, require an additional witness history;
make every effort to contact such witnesses.
Remember the two key questions: where (in the nervous
system) is the lesion and what is the lesion?
Neurological symptoms may be difficult for patients to describe,
so clarify exactly what they tell you. Words such as ‘blackout’,
‘dizziness’, ‘weakness’ and ‘numbness’ may have different
meanings for different patients, so ensure you understand what
Ask patients what they think or fear might be wrong with
them, as neurological symptoms cause much anxiety. Patients
commonly research their symptoms on the internet; searches
on common benign neurological symptoms, like numbness or
weakness, usually list the most alarming (and unlikely) diagnoses
such multiple sclerosis, motor neurone disease or brain tumours
first, and almost never mention more common conditions such
as carpal tunnel syndrome or functional disorders.
The onset, duration and pattern of symptoms over time often
provide diagnostic clues: for example, in assessing headache
(Box 7.1) or vertigo (see Box 9.3).
• When did the symptoms start (or when was the patient
• Are they persistent or intermittent?
• If persistent, are they getting better, getting worse or
The nervous system consists of the brain and spinal cord (central
nervous system, CNS) and the peripheral nerves (peripheral
nervous system, PNS). The PNS includes the autonomic nervous
system, responsible for control of involuntary functions.
The neurone is the functional unit of the nervous system. Each
neurone has a cell body and axon terminating at a synapse,
supported by astrocytes and microglial cells. Astrocytes provide
the structural framework for the neurones, control their biochemical
environment and form the blood–brain barrier. Microglial cells
are blood-derived mononuclear macrophages with immune and
scavenging functions. In the CNS, oligodendrocytes produce
and maintain a myelin sheath around the axons. In the PNS,
myelin is produced by Schwann cells.
The brain consists of two cerebral hemispheres, each with
four lobes (frontal, parietal, temporal and occipital), the brainstem
and the cerebellum. The brainstem comprises the midbrain, pons
and medulla. The cerebellum lies in the posterior fossa, with two
hemispheres and a central vermis attached to the brainstem by
three pairs of cerebellar peduncles. Between the brain and the
skull are three membranous layers called the meninges: dura mater
next to the bone, arachnoid and pia mater next to the nervous
tissue. The subarachnoid space between the arachnoid and pia
is filled with cerebrospinal fluid (CSF) produced by the choroid
plexuses. The total volume of CSF is between 140 and 270 mL
and there is a turnover of the entire volume 3–4 times a day;
thus CSF is produced at a rate of approximately 700 mL per day.
The spinal cord contains afferent and efferent fibres arranged
in discrete bundles (pathways running to and from the brain),
which are responsible for the transmission of motor and sensory
information. Peripheral nerves have myelinated and unmyelinated
axons. The sensory cell bodies of peripheral nerves are situated in
the dorsal root ganglia. The motor cell bodies are in the anterior
horns of the spinal cord (Fig. 7.1).
7.1 Clinical characteristics of headache syndromes
Onset Duration/periodicity Pain location Associated features
Aura (usually visual), nausea/vomiting,
Cluster headache Rapid onset, often
conjunctival injection, tearing, nasal
stuffiness, ptosis, miosis, agitation
Meningitis Usually evolves over a
Fever, meningism, rash, false localising
signs, signs of raised intracranial
20% isolated headache only; nausea/
vomiting, reduced consciousness, false
localising signs, III nerve palsies
Temporal arteritis Gradual onset of temple
Continuous Temple and scalp Usually in those >55 years; unwell, jaw
pain on chewing, visual symptoms, tender
temporal arteries, elevated erythrocyte
sedimentation rate and C-reactive protein
Anterior spinocerebellar tract
Posterior spinocerebellar tract
An epileptic seizure is caused by paroxysmal electrical discharges
from either the whole brain (generalised seizure) or part of the
brain (focal seizure). A tonic–clonic seizure (convulsion) is the
most common form of generalised seizure, and typically follows a
stereotyped pattern with early loss of consciousness associated
with body stiffening (tonic phase) succeeded by rhythmical jerking
crescendoing and subsiding over 30–120 seconds (clonic phase);
this is followed by a period of unresponsiveness (often with
heavy breathing, the patient appearing to be deeply asleep) and
finally confusion as the patient reorientates (postictal phase).
The history from the patient and witnesses can help distinguish
syncope from epilepsy (Box 7.2). Focal seizures may or may not
involve loss of awareness (complete loss of consciousness is less
typical) and are characterised by whichever part of the brain is
involved: for example, a focal motor seizure arising from the motor
cortex, or temporal lobe seizures characterised by autonomic
and/or psychic symptoms, often associated with automatisms
such as lip smacking or swallowing. Functional dissociative
attacks (also known as non-epileptic or psychogenic attacks, or
pseudoseizures) are common, and may be difficult to distinguish
from epileptic seizures. These attacks are often more frequent
than epilepsy, sometimes occurring multiple times in a day, and
may last considerably longer, with symptoms waxing and waning.
Other features may include asynchronous movements, pelvic
thrusts, side-to-side rather than flexion/extension movements
and absence of postictal confusion. The widespread availability
of videophones allows witnesses to capture such events and
• If intermittent, how long do they last, and how long does
the patient remain symptom-free in between episodes?
• Was the onset sudden or gradual/evolving?
Precipitating, exacerbating or
• What was the patient doing when the symptoms
• Does anything make the symptoms better or worse,
such as time of day, menstrual cycle, posture or
Associated symptoms can aid diagnosis. For example, headache
may be associated with nausea, vomiting, photophobia (aversion
to light) and/or phonophobia (aversion to sound) in migraine;
headache with neck stiffness, fever and rash may be associated
Headache is the most common neurological symptom and
may be either primary or secondary to other pathology. Primary
• trigeminal autonomic cephalalgias (including cluster
• primary stabbing, cough, exertional or sex headache
• primary thunderclap headache
• new daily persistent headache.
Secondary (or symptomatic) headaches are less common,
but include potentially life-threatening or disabling causes such
as subarachnoid haemorrhage or temporal arteritis. One of the
key history aspects is rapidity of onset; isolated headache with
a truly abrupt onset may represent a potentially serious cause
such as subarachnoid haemorrhage or cerebral vein thrombosis,
whereas recurrent headache is much more likely to be migraine,
particularly if associated with other migrainous features like aura,
nausea and/or vomiting, photophobia and phonophobia (Box
7.1). Asking patents what they do when they have a headache
can be instructive. For example, abandoning normal tasks and
seeking a bed in a dark, quiet room suggest migraine, whereas
pacing around the room in an agitated state, or even head
banging, suggests cluster headache.
Transient loss of consciousness
Syncope is loss of consciousness due to inadequate cerebral
perfusion and is the most common cause of transient loss of
consciousness (TLOC). Vasovagal (or reflex) syncope (fainting)
is the most common type and precipitated by stimulation of the
parasympathetic nervous system, as with pain or intercurrent
illness. Exercise-related syncope, or syncope with no warning or
trigger, suggests a possible cardiac cause. TLOC on standing
is suggestive of orthostatic (postural) hypotension and may be
caused by drugs (antihypertensives or levodopa) or associated
with autonomic neuropathies, which may complicate conditions
7.2 Features that help discriminate vasovagal syncope
Feature Vasovagal syncope Seizure
Triggers Typically pain, illness,
Convulsion May occur but usually
Colour Pale/grey Flushed/cyanosed, may
Recovery Rapid, no confusion Gradual, over 30 mins;
than ischaemia include use of anticoagulation, headache, vomiting,
seizures and early reduced consciousness. Haemorrhagic stroke
is much more frequent in Asian populations. Spinal strokes are
very rare; patients typically present with abrupt bilateral paralysis,
depending on the level of spinal cord affected. The anterior
spinal artery syndrome is most common and causes loss of
motor function and pain/temperature sensation, with relative
sparing of joint position and vibration sensation below the level
Patients use ‘dizziness’ to describe many sensations. Recurrent
‘dizzy spells’ affect approximately 30% of those over 65 years
and can be due to postural hypotension, cerebrovascular disease,
cardiac arrhythmia or hyperventilation induced by anxiety and
panic. Vertigo (the illusion of movement) specifically indicates a
problem in the vestibular apparatus (peripheral) or, much less
commonly, the brain (central) (see Box 9.3 and p. 174). TIAs
do not cause isolated vertigo. Identifying a specific cause of
dizziness is often challenging but may be rewarding in some
cases, including benign paroxysmal positional vertigo (BPPV),
which is eminently treatable. As a guide, recurrent episodes of
vertigo lasting a few seconds are most likely to be due to BPPV;
vertigo lasting minutes or hours may be caused by Ménière’s
disease (with associated symptoms including hearing loss, tinnitus,
nausea and vomiting) or migrainous vertigo (with or without
Functional neurological symptoms
Many neurological symptoms are not due to disease. These
symptoms are often called ‘functional’ but other (less useful
and more pejorative) terms include psychogenic, hysterical,
somatisation or conversion disorders. Presentations include
blindness, tremor, weakness and collapsing attacks, and patients
will often describe numerous other symptoms, with fatigue,
lethargy, pain, anxiety and other mood disorders commonly
associated. Diagnosing functional symptoms requires experience
and patience (p. 363). Clues include symptoms not compatible
with disease (such as retained awareness of convulsing during
non-epileptic attacks, or being able to walk normally backwards
but not forwards), considerable variability in symptoms (such
as intermittent recovery of a hemiparesis), multiple symptoms
(often with numerous previous assessments by other specialties,
particularly gynaecology, gastroenterology, ear, nose and throat
and cardiorespiratory) and multiple unremarkable investigations,
leading to numerous different diagnoses. The size of a patient’s
case notes can sometimes be a clue in itself! Beware of labelling
symptoms as functional simply because they appear odd or
inexplicable. Like disease, most functional neurological disorders
follow recognisable patterns, so be cautious when the pattern
Symptoms that the patient has forgotten about or overlooked may
be important; for example, a history of previous visual loss (optic
neuritis) in someone presenting with numbness suggests multiple
sclerosis. Birth history and development may be significant, as
in epilepsy. Contact parents or family doctors to obtain such
information. If considering a vascular cause of neurological
symptoms, ask about important risk factors, such as other
vascular disease, hypertension, family history and smoking.
Stroke and transient ischaemic attack
A stroke is a focal neurological deficit of rapid onset that is
due to a vascular cause. A transient ischaemic attack (TIA) is
the same but symptoms resolve within 24 hours. TIAs are an
important risk factor for impending stroke and demand urgent
assessment and treatment. Hemiplegia following middle cerebral
artery occlusion is a typical example but symptoms are dictated by
the vascular territory involved. Much of the cerebral hemispheres
are supplied by the anterior circulation (the anterior and middle
cerebral arteries are derived from the internal carotid artery), while
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