NEUROLOGIC EMERGENCIES 0733-8619 /98 $8.00 + .

OO

EMERGENCY DEPARTMENT
EVALUATION OF HEADACHE
Lawrence C. Newman, MD a n d Richard B. Lipton, MD

Headache is an extremely common complaint in the Emergency Department

(ED), accounting for 1-16% of all Although there are more than 300
medical conditions that can produce headache, fortunately, the majority of head-
ache disorders are benign.62Because headache can be a presenting symptom of
serious disorders, and serious disorders are more common in the ED, it is impor-
tant to have an orderly approach to the differential diagnosis of headache.
In the ED, when evaluating a patient who has a headache, the first task is to
idenhfy or to exclude secondary headache disorders based on the history and the
general medical and neurologic examinations (Fig. 1).When suspicious features
are present, diagnostic testing may be necessary. Once secondary headaches are
excluded, the task is to diagnose one (or more than one) specific primary headache
disorder. In the initial evaluation, the physician looks for diagnostic alarms that
suggest the possibility of a secondary headache disorder. Table 1 summarizes
some of these alarms, the differential diagnoses they suggest, and some consid-
erations in the workup.
Recent studies have demonstrated that computerized tomography (CT) and
magnetic resonance imaging (MRI) of the head have extremely low yields in head-
ache patients in the absence of a1arms.2,5,14,35
If patients do not fit neatly into the
International Headache Society (IHS)diagnostic categoriesz7or if response to treat-
ment is atypical, the issue of secondary headache should be revisited.
Patients present to the ED for a number of reasons. Although many patients
believe that their headaches are the result of very serious illnesses, migraine and
tension-type headaches account for between 25% and 55% of the patient^.^,^^,^^
Headaches associated with systemic illness account for 33-39% of the patient~,8.~~,~*
and headaches secondary to serious neurologic conditions [subarachnoid hem-
orrhage (SAH), mass lesion, meningitis or intracerebral hemorrhage] occur in 1-
16%of the patients.62

From The Department of Neurology (LCN, RBL), and the Department of Epidemiology and
Social Medicine (RBL), Albert Einstein College of Medicine; and the Montefiore Head-
ache Unit (LCN), Bronx, New York; and Innovative Medical Research (RBL), Stamford,
Connecticut

NEUROLOGIC CLINICS OF NORTH AMERICA

VOLUME 16 * NUMBER 2 MAY 1998 285
286 NEWMAN & LIPTON

Patient presents complaining of headache

I I

Evidence of P serious headache disorder?

Headache Warms. by history (TaMe 1)
Abnormalitieson medical exam
Abnormalitieson neurologicexam
N~ Yes
Diagnosls primary headachedirorden Work-up to identifyor exclude secondary headache
(Miiralne. Cluster. Tension-hlpe)

ReconsiderpossiMe secondary headache Treat primary headache

In this chapter, an approach is presented for distinguishing between primary

and secondary headache disorders in the ED setting through history and physical
examinations. Headache alarms are highlighted and diagnostic possibilities are
discussed. Next, the clinical features of headache disorders commonly encoun-
tered in the ED setting are described. Finally, treatment options for the primary
headache disorders are presented.

Table 1. DIAGNOSTIC ALARMS IN THE EVALUATION OF HEADACHE DISORDERS

Headache Alarm Differential Diagnosis Possible WorkUp
Headache begins after Temporal arteritis, mass lesion Erythrocyte sedimentation
age 50 rate, neuroimaging
Very sudden onset of Subarachnoid hemorrhage, Neuroimaging, lumbar
headache pituitary apoplexy, puncture, if CT is negative
hemorrhage into a mass
lesion or vascular
malformation, mass lesion
(especially posterior fossa)
Headaches increase in Mass lesions, subdural Neuroimaging, drug screen
frequency and hematoma, medication
severity overuse
New-onset headache in Meningitis (chronic or Neuroimaging, lumbar
patient who has risk carcinomatous), brain puncture, if neuroimaging
factors for HIV, abscess (including is negative
cancer toxoplasmosis), metastasis
Headache with Meningitis, encephalitis, Lyme Neuroimaging, lumbar
systemic illness disease, systemic infection, puncture, serology
(fever, stiff neck, collagen vascular disease
rash)
Focal neurological Mass lesion, vascular Neuroimaging, collagen
symptoms or signs of malformation, stroke, vascular evaluation
disease (other than collagen vascular disease (including antiphospholipid
typical aura) antibodies)
Papilledema Mass lesion, pseudotumor, Neuroimaging, lumbar
meningitis puncture
Headache following lntracranial hemorrhage, Neuroimaging of brain, skull,
head trauma subdural hematoma, epidural and possibly cervical spine
hematoma, posttraumatic
headache
 EMERGENCY DEPARTMENT EVALUATION OF HEADACHE 287

Since many patients complaining of headache have completely normal medi-

cal and neurologic examinations, a thorough history is the single most important
element for establishing the correct diagnosis.45In the ED, where time is limited,
several key questions regarding the headache should be addressed first. We begin
by discussing the three headache syndromes that most often bring patients to the
ED. We then discuss the critical elements of the headache history organizing the
discussion around a series of key questions. Finally, we discuss the diagnosis of
specific secondary headaches and the management of the common primary head-
ache disorders in the ED.

HEADACHE HISTORY

Why Did This Headache Bring You

to the Emergency Department?

Headache sufferers typically present to an ED for one of three reasons. They

may have a very severe headache that is unlike any previous headache (first-or-
worst syndr~rne).'~ They may have a headache accompanied by new or fright-
ening features like a change in mental status, fever, or focal neurologic findings
(frighteningaccompaniments).They may be suffering from yet another in a seem-
ingly endless string of headaches that do not respond to the treatments they have
at home (last-straw Though serious disease is possible in all of the
situations, it is much more likely in the first-or-worst syndrome or in the fright-
ening-accompaniment situations. The differential diagnosis of the first-or-worst
syndrome includes SAH, pituitary apoplexy, and intracerebral hemorrhage,
among other causes. The frightening-accompanimentsyndrome may result from
mass lesions and stroke. If the patient describes a 15-year history of near daily
headaches that become intolerable (not owing to a change in headache pattern or
associated features), serious disease is unlikely. If a chronic disorder has recently
progressed or acute headache occurs on top of chronic headache, an acute disorder
is more likely.

When Did This Headache Type Start?/Have You Had Previous

Similar Headaches?

Headaches beginning after 55 are much more likely to have a serious cause,
such as a mass lesion, giant-cell arteritis, or cerebrovascular disease.49Knowing
the age of onset of headaches can also aid in diagnosis. Migraine most commonly
begins before age 30.6,40,61 Cluster headaches typically have their onset between 20
and 50 years of age.32,42 Tension-type headaches usually begin before age 5056;40%
of tension-type headache sufferers report headache onset before age 20.55
In general, if a patient has a long history of previous similar attacks, a serious
cause is less likely. If a patient reports numerous identical attacks treated at home,
it is important to understand why this particular one led to an ED visit.

How Did the Headache Start?

The nature of the headache's onset may yield useful diagnostic clues. A head-
ache that awakens a patient from sleep for the first time may indicate an organic
etiology, such as cerebrovascular disease, a mass lesion, or an infection, although,
cluster and migraine may cause nocturnal awakenings.
288 NEWMAN & LIPTON

Inquiring about the rapidity of headache onset will also help the examiner to
establish headache etiology. Headaches of paroxysmal onset and sustained du-
ration (more than minutes) suggest the possibility of SAH.I7Though usually se-
vere, the sudden onset is more important than the agonizing pain. The headaches
associated with sexual activity may begin as a dull ache that rapidly intensifies
during orgasm or may present an explosive, severe h e a d a ~ h e . 4 ~When
, ~ * , ~sexual
~
headaches present abruptly, an aneurysmal rupture must be excluded. Benign
exertional headaches are of moderate severity and follow strenuous physical ac-
tivity such as lifting weights.9~~~
Migraine headaches usually begin gradually and
resolve slowly, often following sleep. Cluster headaches and the paroxysmal hem-
icranias have a rapid onset, climax quickly, and abruptly Tension-
type headaches are characterizedby dull aching that may wax and wane through-
out the day. Trigeminal neuralgia presents with excruciating pains that begin and
peak nearly instantaneously and occur in paroxysms lasting a minute or less.21,63
It is useful to inquire about events associated with the onset of the headache
syndrome. Headaches following a blow to the cranium suggest a postconcussive
headache disorderz3or intracranial hemorrhage (i.e., subdural hematoma; epidural
hematoma, posttraumatic intraparenchymal hemorrhage).I5However, both mi-
graine and cluster headaches may be triggered by head Headaches
occurring in the peripartum period may be caused by cortical vein or sagittal sinus
thrombosis.11Fever in association with headache onset suggests an infectious eti-
ology. Headaches triggered by stress, fatigue, depression, or hunger may be
caused by migraine or tension-type headaches. Pain arising following the inges-
tion of medications, alcohol, nitrites, or caffeine suggests headache of a toxic or
metabolic origin.@

Where Does the Head Hurt?

The localization of maximal pain and the pattern of pain radiation may pro-
vide diagnostic clues. Head pain may be localized or diffuse;it may be consistently
hemicranial; or it may demonstrate side shift. Pain may be reported as a superficial
annoyance or as a deep-seated discomfort.
The presence of unilateral, hemicranial headache usually suggests an under-
lying vascular etiology. Migraine headaches are usually unilateral and frontotem-
poral, but they can become diffuse. Approximately 20% of migraine sufferers re-
port bilateral pain at attack onset.33In the majority of migraineurs, head pain
randomly changes side from attack to attack, although there is usually a predilec-
tion for a particular side. The pain of migraine may radiate into the ipsilateral eye,
face, neck, shoulder, or arm. Cluster headaches are always unilateral, with the site
of maximal pain centered in or around the orbit, temple, or cheek. The pain of
cluster may spread to the other cranial regions ipsilaterally or into the neck, but,
unlike migraine, the pain does not generalize. Also, unlike migraine, only 15%of
cluster sufferers report side shift.32Tension-type headaches are usually bilateral,
encompassing the head in a bandlike fashion.
Localized pain may also occur with organic disease. The pain-sensitive struc-
tures in the supratentorial space are predominantly innervated by the trigeminal
nerve; infratentorial pain-sensitive structures receive information from the upper
cervical, glossopharyngeal, and vagus n e r ~ e sBecause
.~ of this pattern of inner-
vation, supratentorial lesions usually produce frontal headache, and lesions situ-
ated infratentorially cause occipital pain. When headaches are strictly limited to
the periorbital regions, ocular pathology should be considered. Lesions encroach-
ing on the falx or on midline intracranial structures may produce ocular pain. Pain
 EMERGENCY DEPARTMENT EVALUATION OF HEADACHE 289

experienced in the ear may be caused by local pathology or to cerebellopontine

angle tumors or lesions within the lateral sinus.
Trigeminal neuralgia may cause pain in any area of the face innervated by
the trigeminal nerve, although, the second and third divisions of the nerve are
most often affected.21In giant-cell arteritis the headache is often located in the
temple, but may occur anywhere.63Approximately 50% of the patients who have
brain tumors complain of headache,8,58 and in 80%of the patients, the site of pain
is ipsilateral to the mass.31,58
Headaches associated with cerebrovascular disease
may be global or lateralized. When lateralized, the headaches are ipsilateral to the
lesion only half of the time.49Carotid or middle cerebral artery occlusion may
cause ipsilateral retro-orbital or supraorbital pain.I3Basilar artery occlusion pro-
duces occipital or frontal headache, and retroauricular pain may follow vertebral
0cc1usions.~~

What Is the Character of the Pain?

It is essential to obtain a description of the pain, preferably in the patients

own words. It is best to start with an open-ended question; if the patient has
difficulty, it may be helpful to provide alternative descriptive terms, such as burn-
ing, throbbing, pulsating, pressurelike, stabbing, boring, or piercing to prompt a
useful response.
The characteristic headache of brain tumor is a dull ache not unlike that seen
in tension-type headache^.'^,^^ Headaches following the rupture of an aneurysm
or arteriovenous malformation are usually described as a continuous and intense
ache or throbbing pain.I7Headache is a frequent occurrence in patients who have
cerebrovascular disease; patients who have a previous history of recurrent throb-
bing headaches are more likely to report a throbbing sensation following a cere-
brovascular event.49The pain of giant-cell arteritis is usually dull and boring
though it may pulsate at times.63
The pain of migraine is characteristically throbbing or pulsatile but may begin
as a dull steady ache that gradually intensifies; it may not throb until the pain
reaches a high intensity. Cluster headaches usually produce a deep boring or
piercing sensation, occasionally likened to a hot poker thrust into the eye. Similar
intense pain is seen with the paroxysmal hemicranias. Dull bandlike or vicelike
pain is frequently described by sufferers of tension-type headaches. Trigeminal
neuralgia presents with paroxysms of brief electriclikeshocks. Idiopathic stabbing
headaches occur as brief, intense, sharp, jabbing pains occurring as single episodes
or in repeated volleys.53These ice-pick pains may occur as an isolated entity, but
they are commonly seen in association with other headache types such as migraine
or cluster headache.

Do You Have Any Ongoing or Recent Health Problems?

Specific features of the medical or social history suggest specific headache

etiologies. In a patient known to have cancer, brain metastases or infectionsrelated
to immunosuppression are more likely. In patients who are seropositive for the
human immunodeficiency virus (HIV), opportunistic infections, such as crypto-
coccal meningitis or toxoplasmosis brain abscess as well as primary lymphoma of
the central nervous system should be c o n ~ i d e r e d . In
~,~individuals
~ who have
recently spent time in the woods or in those who have an antecedent rash or flulike
illness, Lyme disease or other tic-borne illnesses are possibilities. Obesity in a
young woman suggests the possibility of pseudotumor cerebri.22
290 NEWMAN & LIFTON

What Other Symptoms Do You Experience

with Your Headache?

Sometimes the symptoms associated with the headache rather than the pain
itself prompt the patient to seek medical assistance. Associated symptoms may
occur before, together with, or following the headache; their temporal relationship
should be established. Neurologic deficits may accompany headaches of organic
illness; the deficits are usually related to the site of the lesion. Intracranial mass
lesions are often associated with nausea and vomiting or vomiting without nausea
(projectile vomiting) in 50% of all cases. Vomiting may also be present in other
organic disorders, such as meningitis, cerebrovascular disease, or intracranial
hemorrhage. Giant-cellarteritis may be associated with localized scalp tenderness,
malaise, myalgias, arthralgias, polymyalgia rheumatica, low-grade fevers, or other
constitutional symptoms.26Jaw claudication, if present, is strongly suggestive of
the disorder.28Posttraumatic headaches may be associated with nonspecific light-
headedness, malaise, or memory impairment.
Migraine may be associated with a multitude of symptoms such as photo-
phobia, phonophobia, or osmophobia, and nausea with or without vomiting. Vi-
sual disturbances frequently occur in migraine as a part of the aura. The migrain-
ous aura is a transient phenomenon that rarely lasts longer than 60 minutes.
Migraine auras classically include both positive visual abnormalities such as for-
tification spectra, photopsia, micropsia or macropsia, and teichopsias, as well as
negative features such as visual loss (scotomata).Migraine auras generally evolve
slowly to involve an increasing proportion of the visual field and then gradually
resolve.6 In contrast, the visual disturbances seen with epilepsy tend to be brief
and multicolored. Visual obscurations may also be described for the patient who
has increased intracranial pressure from mass lesions or who has pseudotumor
~erebri.,~~
Cluster headache sufferers experience one or more ipsilateral autonomic
symptoms, such as lacrimation, conjunctival injection, nasal congestion, ptosis,
miosis, eyelid edema, and forehead ~ w e a t i n g .Nausea
~ ~ , ~ ~may be experienced by
40% of the cluster sufferers, although, vomiting is rare.32,42 Similar autonomic fea-
tures accompany both the paroxysmal hemicranias and the hemicrania c0ntinua.4~
Tension-type headaches usually occur in the absence of associated features (see
below). Facial grimacing may be observed during a pain paroxysm in trigeminal
neuralgia (hence the term tic douZoureux).21

Harbingers of Serious Disease

Certain features of the headache history suggest the possibility of a serious

disorder requiring immediate attention (see Table 1). Headaches occurring with a
sudden explosive or apoplectic onset suggest SAH, pituitary apoplexy, or another
serious disorder and require immediate workup, including neuroimaging. For
pituitary apoplexy, special attention to the region of the sella is required, with
coronal cuts if CT is used. In the setting of explosive headaches, if neuroimaging
is negative, a lumbar puncture is needed to look for blood or xanthrochromia.
Though these serious conditions usually produce severe headache, the rapidity of
onset is more important than severity in suggesting the need for a diagnostic
workup.
A new headache or change in an established pattern of headache in a patient
who has a long-standing headache history must always be carefully evaluated.
Headaches that increase in frequency or severity require a careful evaluation. Any
new onset of headache occurring in a patient more than 55 years old must be
 EMERGENCY DEPARTMENT EVALUATION OF HEADACHE 291

considered to have an organic basis until proved otherwise. Elderly patients

should have a sedimentation rate and neuroimaging procedure to rule out giant-
cell arteritis and intracranial disease. Headaches associated with fever or nuchal
rigidity should elicit a search for an infectious or hemorrhagic source and may
warrant a lumbar puncture. Persistent neurologic deficits associated with head-
ache almost always require further investigation to exclude organic cerebral disease.

PHYSICAL AND NEUROLOGIC EXAMINATION

After completing the history, the patient must be throughly examined. Vitals
are obtained, followed by an examination of the heart and the lungs with auscu-
lation of the carotid and the vertebral arteries for bruits. The head and neck are
palpated for trigger points, tender areas, masses, bruises, and thickened blood
vessels. The pulses of the head and neck are examined for abnormalitiesespecially
in the elderly patient in whom temporal arteritis is considered. The eyes are ob-
served for injection or corneal clouding that may be present in cases of glaucoma.
The ear canals are examined for evidence of blood secondary to trauma, infections,
cholesteatomas, or vesicles. Fluid leaking from the nose or ears suggests possible
CSF leak. Battles sign or raccoon eyes indicate basilar skull fracture.
A complete neurologic examination should be performed. Detection of con-
fusion or a depressed level of consciousness may indicate a serious neurologic
lesion with co-existent mass effect. Funduscopy should be performed without
mydriatics, which mask pupillary dilation from brain herniation. Papilledema
suggests increased intracranial pressure and warrants an imaging procedure to
rule out a mass lesion. Visual field testing is performed to uncover defects. Frontal
headache in association with a bitemporal field cut suggests a pituitary mass.
Enlarged blind spots may be seen with glaucoma, optic-nerve disease, mass le-
sions, or migraine. Opthalmoplegia may result from increased intracranial pres-
sure, mass lesions, or compressionby aneurysms or arterio-venous malformations
(AVMs). Horners syndrome may be seen with cluster headache, the paroxysmal
hemicranias, or intracranial or carotid lesions. Focal neurologic deficits may in-
dicate structural brain disease and may require neuroimaging.

DIAGNOSIS OF SECONDARY HEADACHES

Following the history and the physical examination, the physician should be
able to determine if a secondary etiology is likely. After applying selected diag-
nostic tests, secondary causes of headache can be identified or excluded (Table2).

MASS LESIONS

Mass lesions in the central nervous system produce pain through several
m e ~ h a n i s m s . ~Direct
~ , ~ ~extension
,~~ into the pain-sensitive cranial structures, in-
cluding the larger cerebral vessels and the meninges, may give rise to pain. Al-
ternatively, mass lesions may produce pain indirectly by causing traction on the
pain-sensitive structures or through increasing intracranial pressure. The pain pat-
terns produced by.mass lesions are highly variable, depending in part upon the
location of the mass and the structures involved. Increased intracranial pressure
produces headache bifrontally or bioccipitally and is sometimes accompanied by
nausea and vomiting, or occasionally by projectile vomiting alone. Brain-tumor
headaches are often, but not strictly, on the same side as the tumor. Brain tumors
N
rD
N

Table 2. DIFFERENTIAL DIAGNOSIS OF SELECTED HEADACHE DISORDERS

Age of Onset Frequency1 Associated
HeadacheType (years) Location Duration Timing Severity Quality Features
Migraine 10-30 Hemicranial, 4-72 hours Variable Moderat+severe Throbbing > Nausea, vomiting,
but demon- steady ache photo/phono/osmo-
strates side- phobia, scotomata,
shift neurologicaldeficits
(rarely)
Tension-type 20-50 Bilateral 30 minutes->7 Variable Dull ache; may Vicelike, band- Nausea, photophobia
days wax/wane like, pressure or phonophobia, no
vomiting
Cluster 20-40 Unilateral peri/ 15-1 80 minutes 1-8 x/day, noc- Excruciating Boring, piercing lpsilateral conjunctival
retro-orbital turnal attacks injection, lacrima-
tion, nasal conges-
tion, rhinorrhea, mi-
osis, facial sweating
Mass lesion Any Variable Intermittent, noc- Moderate Dull steady/ Vomiting, nuchal rigid-
turnal, upon throbbing ity, neurologicaldef-
arising icits
Subarachnoidhem- Adult Global, often Variable Not applicable Excruciating Explosive Nausea, vomiting, nu-
orrhage occipitonu- chal rigidity, loss of
chal consciousness,
neurologicaldeficits
Trigeminal neuralgia 50-70 2nd-3rd > 1st Seconds, occur Paroxysmal Excruciating Electriclike Facial trigger points,
division in volleys ipsilateral spasm of
facial muscles (tic)
Giant-cell arteritis >55 Temporal, any Intermittentthen Constant ? worse Variable Variable Tender scalp arteries,
region continuous at night polymyalgia rheu-
matica, jaw claudi-
cation
 EMERGENCY DEPARTMENT EVALUATION OF HEADACHE 293

commonly disrupt sleep with headache pain worse upon arising in the morning
or awakening the patient from sleep during the night. However, the classic triad
of brain-tumor headache, sleep disturbances, severe pain, and nausea and vom-
iting, are seen in only one third of the patients with brain tumors.* The typical
clinical situation is a slowly progressive headache that may be accompanied by
progressive neurologic deficits. The most frequent types of primary brain tumors
are gliomas, meningiomas, and pituitary adenomas. The most frequent cause of
brain metastases are lung and breast carcinomas followed by malignant melano-
mas, and carcinomas of the kidney and gastrointestinal tract^.'^,^^,^^
Subdural hematomas also act as mass lesions and typically present with head-
ache symptoms similar to those seen in patients suffering from brain tumors.
Unlike brain tumors, subdural hematomas are rarely associated with focal neu-
rologic deficits because the hematomas collect extra-axially. Subdural hematomas
can arise at variable intervals following head trauma, and in many, an antecedent
history of head trauma is never elicited. The clinical diagnosis is based on the
presence of headache and either an overt change in mental status or a waxing and
waning sensorium. Elderly patients appear to be at greater risk of subdural he-
matomas, since the presence of brain atrophy increases the likelihood of venous
shearing following head trauma.39

BRAIN ABSCESS

Brain abscesses occur when infectious agents are implanted within the pa-
renchyma through trauma or contiguous extension of a nearby site or are carried
through the blood from a remote r e g i ~ n The . ~ majority of abscesses arise from
infections in the paranasal sinuses, ears, lungs, and oral cavity; cardiac sources
account for a smaller percentage of cases. Like other mass lesions, brain abscess
causes headache by compression and traction upon the pain-sensitive meningeal
structures and also by increasing intracranial pressure.
Clinically, patients who have brain abscesses present with headache, vomit-
ing, change in mental status, and focal neurologic deficit^.^ Headache is the usual
first clinical manifestation of the abscess. In acute cases, the headache is severe
and constant; chronic abscesses produce headaches that worsen with activities that
increase intracranial pressure (coughing, bending, straining). Headache location
varies with the site of the abscess. Cerebellar abscesses cause occipitonucal pain.
Frontal abscesses, which typically originate in the sinuses, produce frontal head-
aches. Abscesses that arise as a result of ear infections cause ear and temporal
pain. If the abscesses arise as a result of hematogenous spread, patients may de-
scribe headaches of insidious ~ n s e t . ~ , ~
The diagnosis is confirmed by neuroimaging. Blood cultures, lumbar punc-
ture, and routine blood tests are usually not helpful.

SUBARACHNOID HEMORRHAGE

Nontraumatic SAH usually result from the rupture of saccular aneurysms but
may also arise from arteriovenous malformations.1~17~6z The headache of SAH is
classically described as the worst headache of my life. Headaches are usually
excruciatingly severe, peaking rapidly and diminishing within hours to days.
Headaches are usually global radiating to the occipital and the nuchal regions. An
aseptic meningeal reaction that follows the rupture may produce back pain and
radicular pain in the limbs as well. Lateralized headaches occur in approximately
one third of the aneurysmal cases, most often occurring with carotid, posterior-
294 NEWMAN & LIPTON

communicating, and middle cerebral artery aneurysms. These lateralized head-

aches are usually retro-orbital, ipsilateral to the site of aneurysmal rupture. The
headaches are associated with disturbance of consciousness in approximately 50%
of the patients. Other associated features include nausea, vomiting, visual distur-
bances, neck and back stiffness, and, rarely, low-grade fevers. The majority of
patients with SAH have normal motor examinations and neurologic testing, al-
though focal signs may indicate the site of the ruptured aneurysm: bilateral lower-
extremity weakness from rupture of an anterior-communicatingartery aneurysm;
hemiparesis from middle cerebral artery aneurysm rupture; and third-nerve dys-
function from the rupture of a posterior communicating artery aneurysm.
Approximately 50% of the patients who have SAH experience a warning or
sentinel hemorrhage before their catastrophic bleed.12,36 This warning hemorrhage
tends to occur days to months before the major event and is characterized by a
headache of unusual severity and location that is similar to but less intense than
that occurring with the major bleed. These headaches caused by sentinel hemor-
rhages tend to resolve over 1or 2 days but may at times last for as long as 2 weeks.
Sentinel hemorrhages are associated with nausea and vomiting in approximately
20% of SAH patients, neck stiffness or neck pain in 30%, visual disturbances are
15%,and motor or sensory abnormalities in 15-20%. The warning headaches of
sentinel hemorrhages are so atypical and alarming that between 40% and 75% of
the patients seek medical a t t e n t i ~ n . ' ~
All
, ~too
~ commonly, however, these head-
aches are misdiagnosed as migraine, sinusitis, or tension-type headache, and the
patients are discharged from medical care without proper evaluation.
SAHs should be suspected in a patient who present to the ED with a severe,
unusual, or unremitting headache that is characterized by abrupt onset and ex-
cruciating severity. Patients with preexisting headaches who describe a new qual-
ity or pattern to their headaches should also be suspected of suffering from SAH.
Workup includes CT scanning of the brain, which will reveal the presence of
subarachnoid blood in approximately 90% of cases. If the initial CT reveals no
SAH, a lumbar puncture should then be performed. The presence of blood or
xanthochromia in the CSF confirms the diagnosis, and cerebral angiography
should be arranged.

HEADACHE AND STROKE

Headaches may accompany or follow an acute ischemic stroke and at times

may presage the event. Failure to recognize the warning headache of an impend-
ing stroke may have serious consequences for both the patient and the physician.
Headaches may be associated with transient ischemic attacks (TIAs), large cere-
brovascular occlusions, intracranial hemorrhages and lacunar The
nature and the location of the headaches varies with the type and the location of
the involved vessel.
Headache associated with ischemic strokes are most common with occlusions
of the larger cerebral vessels, occur less often with embolic events, and are rare
with lacunes. In general, headache location is of little clinical relevance in ischemic
stroke. Portenoy et a149found no -relationshipbetween headache location and sub-
type or location of stroke. The headache of ischemic stroke is usually of mild-to-
moderate intensity and overlies the lesion in half of cases. Headache accompanies
TIAs in 6 4 4 % of the cases, although the clinical patterns are ~ n r e v e a l i n g . ~ ~
Headache is reported in 2348% of the patients who have intraparenchymal
hemorrhage. Warning or sentinel headaches are reported by some patients before
the bleed.24Headaches most commonly occur in association with lobar and cere-
 EMERGENCY DEPARTMENT EVALUATION OF HEADACHE 295

bellar hemorrhages. Intraparenchymal hemorrhage may cause a moderate-to-

severe headache, the location of which varies with the site of the hematoma.

MENINGITIS

Inflammation of the meninges secondary to an acute infectious process is

another cause of ED visits. Meningitis should be suspected in any patient pre-
senting with headache and fever or a stiff neck.20Patients typically describe a
throbbing, global headache that may be associated with nausea, vomiting, pho-
tophobia, and nuchal rigidity. Meningeal irritation also may produce pain upon
movement of the eyes. Other clinical features of bacterial meningitis depend on
such factors as a causative agent, the patient's age, and the concomitant presence
of malnutrition, AIDS, or immunosuppression for other reasons. In children ages
2-5 Hemophilus influenza is the predominant organism. Pneumococcus, meningo-
coccus, and Listeria monocytogenes are the commonest causes of community-
acquired meningitis in adults. In patients suffering from acquired immunodefi-
ciency syndrome (AIDS) or those receiving steroids or chemotherapy, the most
likely etiology is cryptococcus or t u b e r c ~ l o s i s . ~ ~ ~ ~ ~ ~ ~ ~

AIDS

Headache is a frequent complaint among patients who have AIDS, occurring

in 11-55% of the patients and may occur in a number of AIDS-related conditions?*
Aseptic meningitis associated with lymphocytic pleocytosis is seen in patients at
the time of seroconversion. During acute HIV infections, patients may describe
headache in association with fever, lymphadenopathy, sore throat, and myalgias.
Between 60% and 100%of these patients describe headache associated with pho-
t o p h ~ b i a .In
~ ~patients
, ~ ~ who have AIDS and headache and who present to the
ED, serious causes are common. One series of 49 HIV-infected patients evaluated
in an ED or an AIDS clinic found that 82%of the patients had headaches secondary
to an identifiable cause.52
Toxoplasma gondii commonly produces lesions that lead to headache. Toxo-
plasmosis typically produces multiple brains abscesses and bilateral, persistent
headaches. Depending on the site of the abscesses, focal neurologic deficits may
be seen.38,52 The diagnosis of toxoplasmosis is made by CT, MR imaging, or by
brain biopsy. Other central nervous system lesions include B-cell lymphoma and
progressive multifocal leukoencephal~pathy.~~~~~ Cryptococcal meningitis is a
common cause of headache in AIDS patients, occurring in as much as 10%of the
patient^.^^,^^ Meningitis is characterized by fever, headache, and nausea. The pres-
ence of meningismus or mental status changes are uncommon. Patients who have
HIV and who present to the ED with persistent headache usually require neu-
roimaging, and if this is normal, then lumbar puncture.

GIANT-CELL ARTERITIS (TEMPORAL ARTERITIS)

Giant-cell arteritis is a systemic arterial vasculitis that is rare before age 50

and dramatically increases in incidence a f t e n v a r d ~Giant-cell
.~~ arteritis should be
suspected in any elderly patient who has a new headache onset or a change in an
established pattern of headache. The headache of giant-cell arteritis is typically
temporal in location but may occur anywhere in the head.26,63 The pain may be
296 NEWMAN & LIPTON

described as continuous, intermittent, throbbing, steady, boring, or aching. Many

patients complain of scalp tenderness and report that pain is exacerbated by local
pressure such as when resting their head on a pillow or wearing a hat.26,39,63
Systemic complications associated with giant-cell arteritis include myalgias
and arthralgias. When occurring without cranial arteritis, the syndrome is termed
polyrnyulgiu rheurnuticu.26 Giant-cell arteritis is also accompanied by dysphoric
mood, weight loss, and anorexia. Jaw claudication, when present, is virtually pa-
thognomonic of the disorder.28
Untreated, giant-cell arteritis produces visual loss in 7 4 0 % of the patients.
This visual loss is usually monocular, usually caused by ischemic optic neuropa-
thy.39Less commonly, visual loss may be caused by posterior ischemic optic neu-
ropathy, central retinal artery occlusion, or bilateral occipital lobe infarction.39 Vi-
sual loss is often rapid and irreversible but may be preceded by episodes of
transient visual loss.
The physical examination may reveal tender or indurated superficial arteries
with a diminished or absent Visual-acuity and visual-field testing should
be carried out, as well as a careful funduscopic examination. The most consistent
laboratory abnormality is an elevated erythrocyte sedimentation rate (ESR).Other
laboratory findings include mild-to-moderateanemia, elevated C-reactive protein
level, and liver function abnormalities.
Although the definitive diagnosis of giant-cell arteritis is based on a positive
temporal artery biopsy, treatment should be promptly initiated based on the clini-
cal presumption and results of the ESR. The initial doses of prednisone range from
60 to 80 mg daily. After several weeks of therapy, the prednisone dose can be
gradually reduced with careful monitoring of the ESR. Following discontinuation
of therapy, the ESR should be monitored periodically.

HEADACHES ASSOCIATED WITH DISORDERS OF CRANIUM,

NECK, EYES, EARS, AND NOSE

Acute sinusitis patients may present with headache associated with a puru-
lent nasal discharge.30The pattern of pain referral is dependent upon the infected
sinus. Retronasal pain and a sensation of nasal congestion is also seen with na-
sopharyngeal malignancies, and, if suspected, an otolaryngolic examination is
warranted.60Inflammation of the eye causes pain around the orbit. Ocular pain in
association with corneal clouding, scleral injection, and diminished vision sug-
gests acute angle closure glaucoma and requires prompt treatment to prevent
blindne~s.~
Infection of the teeth or mucous membranes of the mouth may also cause
pain in the adjacent areas of the face and mouth and may produce head and facial
pain, although dental disease is not a common cause of headache. When acute
pain occurs in the teeth or the supporting dental structures, patients often com-
plain of localized pain that may .be referred to adjacent regions, thus producing
headache.25
Temporomandibular disorders produce headache and facial pain as a result
of inflammation within the joint itself and concomitant myofascial pain.25The pain
is usually in the jaw, the preauricular region, and the muscles of mastication. It is
precipitated by movement and clenching of the jaw and is associated with a de-
creased range of motion of the jaw as well as noise upon jaw movement (clicking).
 EMERGENCY DEPARTMENT EVALUATION OF HEADACHE 297

PRIMARY HEADACHE DISORDERS

Once secondary headaches have been excluded, the next task is to diagnosis
and treat the primary headache disorder. In this section, diagnosis and manage-
ment of the major primary headache disorders are discussed.

Migraine Headaches

Differentiating migraine from an acute life-threatening medical emergency

may be difficult at times but should be made easier with an accurate history and
a physical examination. Be wary of the first-ever migraine and the patient who
has migraine and who has a new pattern of headache; secondary causes are more
likely in these contexts. Typically migraineurs present to the emergency room
because their usual medications are unhelpful in aborting a migraine attack. These
patients give a history of repeated stereotypical headache episodes characterized
by unilateral throbbing headaches that are associated with nausea, vomiting, pho-
tophobia, phonophobia, and osmophobia. Untreated migraine headaches last be-
tween 4 and 72 hours and may recur at varying intervals.6,61 Approximately 10-
15%of migraine sufferers report that their headaches are preceded by a migrain-
ous aura, which typically consists of visual phenomenon.6,61 Rarely, migraine suf-
ferers may present with neurologic deficits such as hemiparesis or hemisensory
loss. The patient who has a rare form of migraine known as basilar artery migraine
may present with bioccipital headache associated with dysarthria, vertigo, ataxia,
bilateral paresthesias or paresis, and altered consciousness. Patients who have
basilar artery migraine are often misdiagnosed in the ED as suffering from psy-
chiatric conditions, drug abuse, or mass lesions. Migraine does not confer im-
munity to serious headaches. Unless the patient makes a habit of using the ED, it
is therefore important to understand why the patient came and to consider the
possibility of secondary headache superimposed on a primary headache disorder.

Cluster Headache

Cluster headaches occur predominantly in men with initial onset usually be-
tween the third and the fifth decades. The most common type is episodic cluster,
in which headaches occur in groups or clusters, lasting from 3 weeks to 3 months
and are followed by headache-free periods or remission^.^^^^^ Cluster headaches
present as unilateral headaches without side shift. The pain is centered in, around,
and behind the eye, is excruciating in intensity, and is associated with at least one
of the following: eyelid edema, ptosis, miosis, conjunctival injection, lacrimation,
nasal congestion, rhinorrhea. The patient typically describes a stabbing or boring
sensation, similar to a hot poker being thrust into the eye. Headaches last, on
average, 20-180 minutes and may recur from once every other day to as many as
eight times per day.32,42 Headaches recur throughout the day, frequently awak-
ening the patient from a sound sleep. Unlike migraine headaches, in which the
patient prefers to lie down in a dark quiet room, the patient with cluster will pace,
rock, or bang his head against the wall. Cluster headache is usually not difficult
to diagnose by history and physical examination. Ocular disorders such as glau-
coma may occasionally mimic the features of cluster. The pain of acute glaucoma
is continuous and is typically associated with visual disturbances, ipsilateral pu-
pillary dilation, photophobia and a markedly increased intraocular pressure. The
clinical features of cluster, sporadic short-lived pain, lacrimation, ptosis, and rhi-
298 NEWMAN & LIPTON

norrhea are not present in glaucoma. Unilateral orbital pain and Horner's syn-
drome are also seen with carotid dissection. The pain associated with carotid dis-
section usually begins abruptly, varies in intensity, and lasts from hours to days.
Although frequently associated with signs of cerebrovascular ischemia, such as
ipsilateral amaurosis fugax or contralateral deficits, rarely, these are absent. The
absence of autonomic features and the presence of neurologic deficits differenti-
ates this disorder from cluster. Headache and ptosis also accompany aneurysms
of the posterior-communicatingartery. There the distinction is made by the ac-
companying pupillary dilation as well as other signs of third cranial-nerve dys-
function.

Tension-Type Headache

Tension-type headaches are characteristically bilateral, mild to moderate in

severity with a pressing or tightening quality, and not exacerbated by routine
physical activity. Patients may describe either nausea, phonophobia, or photo-
phobia. Tension-type headaches usually occur episodically, but in some patients
they may occur on a chronic basis. These patients describe a period of tightness
or soreness surrounding the head, not unlike a vise or tight headband. Patients
presenting to the ED with chronic tension headaches should be screened for co-
morbid depression and overuse of medications.62

Emergency DepartmentTreatment of Primary Headaches

In this section, we will deal with the therapy of primary headache disorders.
The treatment of secondary headache is determined by the etiology of the head-
ache. The ED treatment of headaches is divided into two phases: initial evaluation
and stabilization and therapy. Since most patients who present to the ED with a
chief complaint of headache are uncomfortable and may be restless, there may be
an initial temptation to medicate first. It is imperative that the appropriate diag-
nosis be established before initiating treatment.
Migraine patients who present to an ED tend either to have very severe at-
tacks or to have failed medications at home and require alternative therapies.
Many agents are currently available for the ED treatment of migraine. Sumatriptan
administered subcutaneously during an attack of migraine is effective in as much
as 87%of the sufferers. Sumatriptan treats not only the pain, but also relieves the
nausea and vomiting and is a useful alternative in this subset of migraineurs."
Sumatriptan is dosed as a 6-mg subcutaneous injection that may be repeated
1 hour later, if necessary, with a maximum of two injections per day. It should
not be given to patients who have uncontrolled hypertension, coronary artery
disease, renal or liver disease, pregnancy or in patients suffering from basilar or
hemiplegic migraine. It should not be used in patients who have headache and
persistent focal neurologic deficits. Although it is safe to administer during the
migraine aura, it is not effective. It is sometimes difficult to differentiate migraine
with aura from headache with evolving stroke early in the ED. Sumatriptan should
only be used after a diagnosis is established; it should not be employed as a di-
agnostic test, since the headaches associated with meningitis, SAH, and giant-cell
arteritis may respond to sumatriptan.
Patients requiring ED treatment have often had a protracted period of vom-
iting. If dehydration is suspected, hydration with intravenous fluids can be very
helpful. Since the patients are often photophobic and phonophobic, placing them
in a dark, quiet room will also make them more comfortable.
 EMERGENCY DEPARTMENT EVALUATION OF HEADACHE 299

Dihydroergotamine (DHE)given intravenously in combinationwith metoclo-

pramide or prochlorperazine is also useful in aborting a migraine a t t a ~ k . ~ ~
The
,,~~
patient is first pretreated with 10 mg of metoclopramide or 5 mg of prochlorper-
azine. Thirty minutes later, DHE 0.5-1.0 mg is given using a slow intravenous
push over 2 minutes. DHE may be repeated again 1 hour later, if needed. DHE is
contraindicated in vascular disease, sepsis, uncontrolled hypertension, and preg-
nancy. Side effects include nausea, vomiting, gastrointestinal upset, and muscle
cramping.
If sumatriptan and DHE are contraindicated, treatment with the intramus-
cular nonsteriodal anti-inflammatory agent (NSAID) ketorolac may be usefu1.62
Ketorolac is given as a 30-60 mg intramuscularly (IM) loading dose, and an ad-
ditional 30 mg may be repeated in 8 hours, although, given parenterally, ketorolac
has similar side effects and contraindications as other NSAIDs.
Dopamine antagonists such as metoclopramide, chlorpromazine,34and
prochlorperazinez9given orally, rectally, or parenterally have been successfully
used for many years to alleviate the nausea and vomiting associated with mi-
graine. In the ED, intravenous administration of these agents is often quite suc-
cessful alone or as an adjunctive therapy to DHE.
Prochlorperizine as a 10-mg intravenous dose may be given initially and re-
peated in 30 minutes, if necessary. Because of the high occurrence of orthostatic
hypotension associated with intravenous chlorpromazine, 500 mg of normal saline
should be given first and then the 10-mg intravenous chlorpromazine, repeated
again in 30-60 minutes if necessary. These agents may cause sedation, akathesia,
acute dystonic reactions, and other extrapyramidal symptoms, including torticollis
and oculogyric crisis.
Corticosteroids such as dexamethasone 10 mg given intravenously followed
by a 4-mg intravenous dose every 6 hours as needed is also useful, especially for
aborting status migrainous.62
Though narcotic agents are frequently employed in the ED setting, we reserve
them for patients who have contraindications, side effects, or lack of response to
the above agents. Injectable narcotics are difficult to dose and have only modest
efficacy; repeated dosing is sometimes necessary. Furthermore, narcotics may pro-
duce sedation or orthostatic hypotension prolonging the ED visit. Meperidine, 75-
100 mg, with promethazine 50 mg IM is the treatment most often used. Other
choices include morphine sulfate, codeine, and hydrocodone preparations.

Acute Cluster Headaches

For most patients suffering from an acute cluster episode, the use of oxygen
inhalation is the treatment of first choice, since it is easily administered, has no
side effects, and works rapidly. Using a nonrebreathing face mask, 8 L/min over
10-15 minutes is quite efficacious.16Subcutaneous sumatriptan has a rapid onset
and is considered by many to be the most effective agent available for treatment
of the acute attack. It is given as a 6-mg subcutaneous dose and may be repeated
at least 1 hour later but not more than twice daily. This limitation may pose a
problem. Furthermore, sumatriptan may not be taken within 24 hours of ergota-
mine preparation^.^^ DHE (0.5-1 .O mg) given intravenously or intramuscularly is
also useful as an abortive agent for a cluster headache.

Tension-Type Headaches

Sufferers of episodic tension headache rarely need ED visits as they can usu-
ally manage their headaches at home with a variety of over-the-counter or pre-
scription pain relievers.
300 NEWMAN & LIITON

A more challenging problem is the patient who has chronic tension-type

headaches who frequent the ED. Many sufferers of chronic tension-type headaches
overuse or abuse analgesics, including narcotics, which perpetuates their chronic
pain cycle. These patients require treatment with nonhabituating medications such
as NSAIDs and muscle relaxants. A referral to a physician with headache expertise
may be useful for these patients.

Follow-Up

The use of the ED for treatment of primary headache disorders is time con-
suming and expensive. Patients presenting to the ED for treatment should be
referred to a primary care physician for adequate follow-up care. Patients who
frequently require ED visits should be referred to headache specialists to establish
an effective program of care that explores prophylactic as well as home-based
abortive therapies. Repeated use of the ED for headache represents a failure of
outpatient management. Every effort should be made to provide effective treat-
ment of patients who have migraine and cluster headaches at home or in the
physician's office.

SUMMARY

Although headache is a common complaint in the ED, it is often considered

to be more of a nuisance than a true medical emergency. It is imperative for the
physician evaluating patients in the emergency setting to have a good understand-
ing of the many disorders that may have headache as a feature. It is of utmost
importance to first identify or eliminate the secondary causes of headache through
history taking and physical examinations as described in this chapter. If a second-
ary cause of headache is identified, appropriate steps aimed at treating the un-
derlying illness must be addressed. If the presenting complaint is the result of a
primary headache disorder, treatment options as described here should be em-
ployed, and referrals for follow-up care should be given to avoid repeated ED
visits. Although, the majority of patients presenting to the ED suffer from an acute
exacerbation of one of the primary headache disorders, care must be taken to rule
out more serious causes of headache, especially in patients who have new or
unusual symptoms. Diagnosis should always be established before initiation of
therapy.

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Address reprint requests to

Lawrence C. Newman, MD
Montefiore Headache Unit
111 East 210 Street
Bronx, NY 10467