50

30

10

3-8

• Never delay administering antibiotics while wa iting for

a CT scan or lumbar puncture (LP) when considering the

diagnosis of bacterial meningitis.

• When subarachnoid hemorrhage is suspected, follow a

normal CT scan with LP.

sinuses, the dura, cranial nerves, or extracranial sources

(muscle tension). In emergent headaches, pain may

arise from mass effect (tumor or subdural hematoma),

inflammation of the meninges (meningitis and SAH),

vascular inflammation (temporal arteritis), vascular

dissection (carotid and vertebral artery dissection) , or

extracranial sources ( dental caries, otitis media,

sinusitis).

...... Emergent Secondary Headaches

Subarachnoid Hemorrhage

Although SAH represents <1% of headaches in patients

who present to the ED, it occurs in approximately 12% of

patients with a severe sudden headache. Pain is often

maximal at onset, in the occipital region, and may resolve

spontaneously in the ED. The median age at presentation

is 50 years. More than 50% of patients have a normal

neurologic examination. Rupture of an aneurysm is the

most common cause.

Meningitis

Classic triad of headache, fever, and meningismus is often

not present. It is more difficult to diagnose at extremes of

age. Immunosuppression can cause atypical subacute

presentations.

336

Intracranial Bleed

Subdural bleed can occur with minimal or unrecognized

trauma (warfarin use, elderly). Epidural bleed usually

occurs with significant trauma. Intracerebral bleed is often

associated with severe hypertension.

Temporal Arteritis

Occurs in patients older than 50 years and is more fre ­

quent in women. It is caused by a systemic panarteritis.

Patients present with frontotemporal throbbing headache,

jaw claudication, and a nonpulsatile or tender temporal

artery. It may cause visual loss from ischemic optic

neuritis.

Carotid And Vertebral Artery Dissection

Together these entities cause 20% of strokes in patients

younger than 45 years. Carotid dissections occur twice as

often as vertebral dissections. Classically, they present as

acute unilateral headache and/or neck pain, but may present atypically (lower cranial nerve deficits or C5/6 radiculopathy). The median age of onset is 40 years. Sometimes

dissection occurs in association with minor trauma (yawning) or may be spontaneous.

Pseudotumor Cerebri

Benign intracranial hypertension of unclear cause. It has

been linked to the use of oral contraceptives, vitamin A,

tetracyclines, and thyroid disorders. Often occurs in

young, obese females with chronic headaches. Papilledema

is usually the only abnormal examination finding, but

cranial nerve abnormalities, visual field deficits, or

decreased visual acuity may also be present.

Stroke

Although 55% of patients with an intracerebral hemor ­

rhage have a headache, less than 1 7% of ischemic stroke

patients complain of pain. However, cerebellar infarction

often presents as acute pain in the occipital area. Because

of its location in the posterior fossa, there is risk of herniation as surrounding brain edema occurs.

Other

Pituitary apoplexy, acute angle-closure glaucoma, hyper ­

tensive encephalopathy, pheochromocytoma, CO poison ­

ing, preeclampsia, venous sinus thrombosis (often in the

setting of a hypercoagulable state).

� Primary Headaches

Migraine

Abnormal vascular actlvtty is thought to be causal.

Migraines are more common in females, with onset

HEADACHE

usually in teen years, and less commonly after age 40

years. The patient presents with unilateral pulsating

headache that may have an associated aura. The pain usually follows a typical pattern for individual patients and

improves during pregnancy (estrogen excess). Associated

symptoms include nausea and vomiting with photophobia and phonophobia.

Tension

The most common type of primary headache. Often presents with bitemporal nonpulsating pain without associated

nausea, vomiting, photophobia, or phonophobia.

Cluster

Uncommon in the general population, but more common

in men beginning after age 20 years. They present with

acute, severe, unilateral retro-orbital pain with associated

lacrimation, eye injection, and rhinorrhea and usually

occur in "clusters" over days to weeks and resolve spontaneously.

CLINICAL PRESENTATION

� History

A detailed history is most important to make the correct

diagnosis and guide therapy. Headache pattern should be

sought. Patterns that raise concern for a secondary headache

include sudden onset, first ever, or a change in frequency or

intensity from previous. Sudden onset of a severe headache

suggests SAH, but may also be present in venous sinus

thrombosis, cervical artery dissection, cerebellar infarct, and

pituitary apoplexy. A headache that is worse in the mornings

may indicate a tumor, whereas a headache that is worse on

standing is characteristic of a post-lumbar puncture (LP)

headache. Headache location is usually nonspecific.

However, migraines are typically unilateral, tension headaches are bilateral, and SAH is usually occipital or nuchal.

Neck pain with or without neurologic deficits may represent

a carotid or vertebral artery dissection. Headache character

may be pulsatile or throbbing (migraine), squeezing (ten ­

sion), or sharp and acute (cluster and SAH).

Associated symptoms that may point to an emergent

secondary cause include syncope, altered mental status

(AMS), neck pain or stiffness, fever, hypertension, visual

disturbance, weakness, seizures, or trauma. Consider

carbon monoxide poisoning when multiple family

members are concurrently affected during the fall or win ­

ter. Important elements of the past medical history include

immunocompromise, malignancy, coagulopathy

(warfarin), uncontrolled hypertension, aneurysm, connective tissue disease (cervical artery dissection), and cerebrovascular accident (CVA). Family history is also important.

Migraines, SAH, and carotid/vertebral dissections are all

more common if a first-degree relative has been affected.

CHAPTER 80

..... Physical Examination

Vital signs are often normal in patients with headache.

However, fever may indicate meningitis or sinusitis, and

severe hypertension suggests encephalopathy or intracra ­

nial bleed. General appearance should be appreciated and

may aid in diagnosing a life-threatening headache or severe

presentation of a primary headache syndrome. Head and

neck examination should assess for sinus tenderness, dental caries, otitis media or externa, temporal artery tenderness, and meningismus. Eye exam should include visual

acuity, pupil reactivity and funduscopy (papilledema from

increased ICP, subhyaloid hemorrhage from SAH). On the

neurologic examination, include mental status, cranial

nerves, strength, sensation, reflexes, cerebellar and gait if

possible. AMS or focal neurologic deficits often indicate

increased ICP.

DIAGNOSTIC STUDIES

..... Laboratory

General laboratory studies (complete blood count, chemistry

panel, urinalysis) add little to the diagnosis of emergent

headaches. Elevated white blood cell (WBC) count may

point to an infection; elevated erythrocyte sedimentation

rate (>50 mm/h) is present in cases of temporal arteritis.

Figure 80-1. Noncontrast head CT scan showi ng

SAH. Note the blood (white areas) in the basal cisterns

and interhemispheric fissure. This is referred to as the

"star sign" (arrow).

.... Imaging

Noncontrast head computed tomography (CT) scan is the

test of choice when evaluating emergent causes of head ­

ache. It can assess for acute SAH (sensitivity 98o/o within 12

hours, 93o/o within 24 hours); acute intracerebral, subdural,

and epidural hematomas; and lesions causing mass effect

(Figure 80-1). Intravenous (IV) contrast is added in

patients with immunocompromise, or when subacute or

chronic subdural, venous sinus thrombosis, or central nervous system infections are suspected. CT scan does not

diagnose idiopathic intracranial hypertension, meningitis,

and some cases of venous sinus thrombosis. When considering carotid or vertebral dissection, CT angiogram of the

neck, duplex ultrasonography, or magnetic resonance

imaging (MRI)/magnetic resonance angiogram (MRA) of

the neck should be performed.

PROCEDURES

LP should be performed when considering meningitis or

SAH (if the head CT scan is nondiagnostic). It can also be

performed to check the opening pressure (normal <20

em H2

0) in patients with suspected pseudotumor cerebri. Opening pressure should also be assessed for

suspected SAH; two thirds of patients will have elevated

pressure. CT should be performed before LP for patients

with any of the following: age >60 years, AMS, focal

neurologic deficit, signs of increased ICP (papilledema),

seizures, immunocompromise, or meningeal signs.

Cerebrospinal fluid ( CSF) findings in acute meningitis

and SAH are listed in Table 80-2. Interpreting CSF results

in the face of a traumatic LP can be difficult. A decrease in

red blood cells (RBCs) to near zero from tubes 1-4 suggests that the blood in tube 1 was from LP-induced trauma,

not SAH. In general, there will be 1 WBC in the CSF for

every 700 RBCs when from a traumatic LP. Xanthochromia

(due to lysis of erythrocytes in CSF), when present, is

indicative of SAH.

Table 80-2. CSF findings in mening itis and SAH.

CSF Normal Bacterial Viral SAH

Cells <5 WBCs 200·5,000 <1,000 1 oos-million

PMN monocytes RBCs

CSF/serum glu- 0.6 Low Normal Normal

cose ratio

Protein 1 5-45 High High Normal to

mg/dl increased

Gram stain Negative Positive Negative Negative

Xanthochromia* Negative Negative Negative Positive

'''Usually present 12 hours after SAH bleed and lasts 2-3 weeks,

MEDICAL DECISION MAKING

History and physical examination may be sufficient to

arrive at a benign diagnosis (tension, migraine, cluster

headache). However, when serious secondary headaches

are considered, CT imaging ± lumbar puncture should be

performed. Treatment of possible meningitis should not be

delayed by CT or LP (Figure 80-2).

TREATMENT

For patients with a presumed benign headache, oral pain

medications (nonsteroidal anti-inflammatory drug,

acetaminophen, hydrocodone) may be sufficient to relieve

pain. For more severe pain, especially when a migraine is s uspected, N antiemetics (prochlorperazine 5-10 mg N) often

provide relief. Sensory stimuli should be decreased (dark quiet

room). N opioids may be used for continued pain.

Patients with a presumed emergent headache usually

require IV medications for pain relief concurrently with

diagnostic tests (CT ± LP) and other treatments (N

antibiotics for meningitis). In general, N antiemetics and

opioids are safe for emergent headaches.

HEADACHE

Subarachnoid Hemorrhage

Emergent neurosurgical consultation is required for

aneurysm clipping or coiling. Nimodipine ( 60 mg by

mouth [PO]) is often given to reduce subsequent vasospasm.

Meningitis

Do not delay antibiotics for CT scan or LP ( ceftriaxone

+ vancomycin). Perform CT scan before LP if the patient

meets criteria as listed previously. N steroids should be

given empirically to adult patients in whom meningitis is

strongly suspected.

Intracranial Bleed

Emergent neurosurgical consultation is required for evacuation of subdural or epidural bleed. Fresh-frozen plasma

should be administered if the patient is coagulopathic.

Severe uncontrolled hypertension should be treated.

General recommendations include reduction of the mean

arterial pressure by 25% or to < 150/90.

Complaint of

headache

History & physical exam

Red flags present?

Benign headache

Treat symptoms

and refer

A. Figure 80-2. Headache Diagnostic algorithm. CT, computed

tomography; ESR, erythrocyte sedimentation rate; LP, lumbar puncture.