Acute Headache in The ED Evidence-Based Evaluation and Treatment Options

EMERGENCY MEDICINE PRACTICE
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
June 2001
Acute Headache In The ED:

Evidence-Based Evaluation
And Treatment Options
Volume 3, Number 6
Authors
Steven A. Godwin, MD, FACEP
Assistant Professor and Residency Director, Department
of Emergency Medicine, University of Florida HSC/
Jacksonville, Jacksonville, FL.
John Villa, MD
Emergency Medicine Resident, University of Florida
HSC/Jacksonville, Jacksonville, FL.
Its 6:30 a.m.almost quitting time. But then a 40-year-old woman comes in
complaining of a terrible headache following an argument with her family.
The headache developed over approximately 15 minutes. Her pain is much
better since she took two hydrocodone tablets before coming to the ED. She has
mild photophobia without any focal neurological complaints and minimal neck
pain that probably came from gardening yesterday. The headache is almost like
her typical migraine. The neuro exam? Stone-cold normal. Its decision time
CT? LP? Some IM pain meds and discharge? Or should I turn her over to the
next doc coming on?
Peer Reviewers
Thomas W. Lukens, MD, PhD, FACEP
Operations Director, Department of Emergency
Medicine, MetroHealth Medical Center, Cleveland, OH.
M.C. Burke, MD
Los Angeles, CA.
CME Objectives
When your head did but ache, I knit a handkercher about my brows.
William Shakespeare (1554-1616), King John, IV, I, 41
HE majority of patients who come to the ED with a headache do not

have a life-threatening problem. The challenge is to identify the
small but significant percent that do. The differential diagnosis of
headache is hugeby the time some work-ups are complete, the emergency physician suffers greater agony than the patient.
This issue of Emergency Medicine Practice uses an evidence-based
approach for evaluating acute non-traumatic headache in the ED. The
article emphasizes life-threatening causes and discusses the management
of both benign and malignant headaches.
Clinical Practice Guidelines And Systematic Reviews

Despite legions of studies on headache, most research fails to define how
historical and physical information were collected or how these data
Editor-in-Chief
Stephen A. Colucciello, MD, FACEP,
Assistant Chair, Director of
Clinical Services, Department of
Emergency Medicine, Carolinas
Medical Center, Charlotte, NC;
Associate Clinical Professor,
Department of Emergency
Medicine, University of North
Carolina at Chapel Hill, Chapel
Hill, NC.
Associate Editor
Andy Jagoda, MD, FACEP, Professor
of Emergency Medicine; Director,
International Studies Program,
Mount Sinai School of Medicine,
New York, NY.
Editorial Board
Judith C. Brillman, MD, Residency
Director, Associate Professor,
Medicine, The University of

New Mexico Health Sciences
Center School of Medicine,
Albuquerque, NM.
W. Richard Bukata, MD, Assistant
Clinical Professor, Emergency
Medicine, Los Angeles County/
USC Medical Center, Los Angeles,
CA; Medical Director, Emergency
Department, San Gabriel Valley
Medical Center, San Gabriel, CA.
Francis M. Fesmire, MD, FACEP,
Director, Chest PainStroke
Center, Erlanger Medical Center;
Assistant Professor of Medicine,
UT College of Medicine,
Chattanooga, TN.
Valerio Gai, MD, Professor and Chair,
Medicine, University of Turin, Italy.
Michael J. Gerardi, MD, FACEP,
Clinical Assistant Professor,
Medicine, University of Medicine
and Dentistry of New Jersey;
Director, Pediatric Emergency
Medicine, Childrens Medical
Center, Atlantic Health System;

Vice-Chairman, Department of
Emergency Medicine, Morristown
Memorial Hospital.
Michael A. Gibbs, MD, FACEP,
Residency Program Director;
Medical Director, MedCenter Air,
Medicine, Carolinas Medical
Center; Associate Professor of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor,
MI; Clinical Professor, Department
of Emergency Medicine, University
of Michigan Medical School, Ann
Arbor, MI; President, American
Physicians Assurance Society, Ltd.,
Bridgetown, Barbados, West Indies;
Past President, ACEP.
Jerome R. Hoffman, MA, MD, FACEP,
Professor of Medicine/
Emergency Medicine, UCLA
Upon completing this article, you should be able to:

1. obtain a focused history and then classify the many
types of headaches into major categories;
2. discuss the pathophysiology of migraine and
understand its relevance to treatment decisions;
3. set priorities in the evaluation of the patient with
acute cephalalgia and explain the rationale behind
selection of specific diagnostic modalities;
4. discuss clinical pathways for evaluating both immunocompetent and immunosuppressed patients;
5. describe treatment options, including identifying
the medications considered to be first-line
agents; and
6. list specific circumstances in the evaluation
of the headache that should be treated with
special considerations.
Date of original release: June 7, 2001.

Date of most recent review: June 5, 2001.
See Physician CME Information on back page.
School of Medicine; Attending

Physician, UCLA Emergency
Medicine Center; Co-Director,
The Doctoring Program,
UCLA School of Medicine,
Los Angeles, CA.
John A. Marx, MD, Chair and Chief,
Medicine, Carolinas Medical
Center, Charlotte, NC; Clinical
Professor, Department of
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Michael S. Radeos, MD, MPH, FACEP,
Attending Physician in
Emergency Medicine, Lincoln
Hospital, Bronx, NY; Research
Fellow in Emergency Medicine,
Massachusetts General Hospital,
Boston, MA; Research Fellow in
Respiratory Epidemiology,
Channing Lab, Boston, MA.
Steven G. Rothrock, MD, FACEP,
FAAP, Associate Professor
of Emergency Medicine,
University of Florida; Orlando

Regional Medical Center; Medical
Director of Orange County
Emergency Medical Service,
Orlando, FL.
Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Medicine, Vanderbilt University
Hospital, Nashville, TN.
Mark Smith, MD, Chairman,
Medicine, Washington Hospital
Center, Washington, DC.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
of Alabama at Birmingham,
Birmingham, AL.
pathology. In one series, only 3.8% of patients who

presented to the ED for headache had a serious
intracranial process such as SAH, tumor, meningitis,
encephalitis, intracranial hypertension (ICH), or
cerebral infarction. 15
According to a study by Rasmussen et al, the
lifetime prevalence of headache, including migraines
and tension-type headaches, for men and women 25-64
years old is 96%. 13 In this study, tension-type headaches accounted for 78% and migraines for 16% of the
headaches. Women get more headaches than men, both
tension (88% vs 69%) and migraine (25% vs 8%).13
Several other population-based studies have noted this
gender difference.16-19
Age is a factor in the development of migraines;
they become more prevalent until age 45 years, after
which new-onset migraines become rare.17 Unlike
migraines, tension-type headaches do not correlate
with age.18
should be used to make decisions. Due to the lack of

prospective, randomized trials regarding the clinical
evaluation of patients, there are no consistent standards for assessing the headache patient.
Discrepancies in study methodology are a recurring problem in the headache literature. While one
study may use a visual analog scale to quantify the
efficacy of treatment, another study may employ a
different scale or no objective measurement at all.
Many studies claim efficacy, yet they do not follow
patients past some arbitrary time period. Despite the
common phenomenon of rebound headaches, few
trials evaluate relapse after ED discharge.
The frequent lack of a placebo arm also detracts
from the literature on headache management. In one
prospective, double-blind, randomized study, an
intramuscular placebo performed as well as either
ketorolac 60 mg IM or meperidine 50 mg plus
promethazine 25 mg IM in the treatment of acute
headache crises. 1 Data on many medications are
difficult to interpret because the study drug is often
used in combination with other agents (DHE and
promethazine, in particular).
Additional confusion arises due to the phenomenon of spectrum bias. This glitch in the evidencebased literature is based on the fact that a test may
perform differently based on the severity of the
disease. For instance, CT may be more accurate in
those with large subarachnoid hemorrhage (SAH) than
in those with small bleeds.2
There are several English-language guidelines on
the management of acute headache. These include
policies from the American Academy of Neurology
(AAN), 3 the National Headache Foundation,4 the
Canadian Association of Emergency Physicians,5 and
the American College of Emergency Physicians.6
Pathophysiology
When the head aches, all the body is the worse.
English proverb
Current thinking holds that there is a common
pathway for headache pain, regardless of the
Table 1. Major Categories Of Headache Disorders.

Primary causes
Migraine
Tension-type headaches
Cluster headache
Chronic paroxysmal hemicrania
Miscellaneous headaches unassociated with structural
lesion (idiopathic stabbing, external compression, cold
stimulus, benign cough, benign exertional, associated
with sexual activity)
Categorization Of Headaches
In 1988, the International Headache Society (IHS)
finalized the classification and diagnostic criteria
for headache disorders.7 More than a decade later,
it still provides an important framework for categorizing headaches.
The etiologies of headaches are divided into
primary and secondary.8-12 (See Table 1.) Primary
headaches, including disorders such as migraines,
tension-type, and cluster headache, are responsible for
the majority of all cases. Secondary headaches are far
less common and include headaches associated with
diverse underlying pathology such as tumor, aneurysm, meningitis, or giant cell arteritis.8,13
Secondary causes
Head trauma
Vascular disorders (CVA, intracranial hematoma, SAH,
unruptured vascular malformation, arteritis, venous
thrombosis, arterial hypertension)
Nonvascular intracranial disorder (high or low cerebrospinal fluid pressure, noninfectious inflammatory disease,
intracranial neoplasm)
Substance use or withdrawal
Infection (cephalic or meningeal infection,
non-cephalic infection)
Metabolic disorders (hypoxia, hypercapnia, hypoglycemia,
dialysis, other metabolic abnormalities)
Cranial-facial disorder (pathology of cranium, neck,
eyes, ears, nose, sinuses, teeth, mouth, or other facial or
cranial structures)
Neuralgias (persistent pain of cranial nerve origin, nervus
intermedius neuralgia, superior laryngeal neuralgia,
occipital neuralgia)
Epidemiology
Headache is one of the most common complaints seen
in the ED, accounting for 1% of all ED visits, or
approximately 1 million patients per year.14 Fortunately, few of these patients will have life-threatening
Emergency Medicine Practice
June 2001
The headache in migraine without an aura is

moderate to severe in intensity. In addition to the
nausea, vomiting, photophobia and/or phonophobia,
patients may demonstrate recurrent yawning, drowsiness, and difficulty concentrating. The IHS requires
five previous attacks to make a firm diagnosis. Though
there is no specific aura, a nonspecific prodrome may
precede the headache by hours or days.
While migraines without aura have no specific
prodrome before the headache, a migraine with aura is
preceded by a variety of symptoms. These commonly
include visual disturbances, especially flashing lights
(scintilla) or jagged lines in the patients field of vision
(like the ramparts of a castle). Patients may also
experience unilateral paresthesias and/or numbness,
unilateral weakness, aphasia, or speech difficulty.24 An
aura typically occurs one hour before the headache and
is completely reversible.7 (See Table 2.)
Diagnosis of migraine with aura requires at least
two attacks having at least three of the following
four characteristics:26
1. fully reversible focal cerebral, cortical, or
brainstem dysfunction;
2. at least one aura symptom;
3. no aura symptom lasting more than 60
minutes; and
4. the headache follows aura with a symptom-free
interval of less than 60 minutes.
underlying etiology. A variety of mechanisms may be

responsible, including: 10
distention or traction of intra- or extracranial arteries;
traction on intracranial veins or the dura;
irritation of cranial and spinal nerves;
irritation of cranial and cervical muscles;
meningeal irritation and raised intracranial
pressure; and
disturbance of intracerebral serotonergic
projections.
Headache pain is probably transmitted via the
trigeminal nerve from the blood vessels of the pia
mater and dura mater.11 The exact trigger of the pain
may be multifactorial, but once it occurs, the
trigemino-vascular axons are stimulated, resulting in
immediate pain and release of neurogenic peptides.
These vasoactive neuropeptides stimulate endothelial
cells, mast cells, and platelets, creating an inflammatory cascade known as neurogenic inflammation. This
results in vasodilatation, enhanced permeability of
plasma proteins, and a perivascular reaction.20
The aim of most migraine therapy is to prevent or
abort the neurogenic inflammation. Neurogenic peptide
release is modulated by serotonin (5-HT) receptors,
which have become the major focus of pain management.21 Currently, the 5-HT1 receptor is believed to be the
most important of the subtype receptors in the final
common pathway of headache. Agents such as the
triptans are specific agonists at the 5-HT1 receptor, while
other medications, such as dihydroergotamine (DHE),
prochlorperazine, and metoclopramide, act more globally
on these receptors.21-23
Atypical migraines may present with a variety of

neurologic deficits. Typical variants include:
Basilar migraines: accompanied by balance
disorder, syncope, and difficulty speaking.
Ophthalmoplegic migraines: associated with
paralysis of an extraocular muscle.
Ophthalmic migraines: involve visual disturbances (usually a lateral field deficit).
Hemiplegic migraines: accompanied by
unilateral weakness.
Differential Diagnosis
...an attack of the periodical head-ache which came
on me about a week ago rendering me unable as yet
either to write or read without great pain...
Thomas Jefferson, in a letter to
Thomas M. Randolph, Jr., May 9, 1790
Tension Headaches
Tension headaches are the most common presenting
headache in the ED and other primary care settings.
They probably exist on a continuum with migraines.27
The IHS divides tension headaches into episodic and
chronic, depending on the length of symptoms. The
presence or absence of pericranial muscle tenderness is
Migraine Headaches
Migraines may occur with or without an aura. They
usually last 4-72 hours, start on one side (but may
later spread bilaterally), and are pulsatile or
pounding. Symptoms may be aggravated by exertion.
Almost all patients with migraine will have nausea,
photophobia, or phonophobia.24 If the patient with a
presumed migraine does not complain of light hurting
their eyes, sound hurting their ears, or nausea, consider an alternative diagnosis.
Migraines may be triggered by stress, fatigue,
concurrent illness, and even certain foods.
(Thankfully, recent research shows that chocolate
is unlikely to be a precipitant. 25)
June 2001
Table 2. Aura Symptoms Frequently Associated

With Migraine.
Scotoma (blind spots)

Teichopsia (bright, wavy lines)
Fortification (zigzag patterns)
Photopsia (flashing lights)
Visual and auditory hallucinations
Paresthesias
Metamorphopsia (distorted size of objects)
key in classifying this form of headache.24,28

Tension headaches are typically episodic, with
mild to moderate pain intensity lasting minutes to
days. The discomfort is frequently described as
constricting in nature, bilateral in location, and is
normally not worsened with exertion. Typical migraine
symptoms of nausea, vomiting, and photophobia are
normally absent.28
Meningitis is another life-threatening cause of

secondary headache. The introduction of the Haemophilus
influenzae vaccine markedly changed the demographics
of bacterial meningitis. What was once a childhood
disease is now seen more frequently in adults.34
Post-traumatic conditions are an important cause
of headache. SAH is one of the most common, while
subdural and epidural are among the most serious.The
elderly, alcoholics, epileptics, patients on dialysis or
warfarin, and those with coagulopathies are at highest
risk for chronic subdural hematomas.
Post-traumatic headache can occur in up to 80% of
patients in the first three months post head trauma.
Symptoms include headache, dizziness, sleep disturbances, nausea, and difficulty concentrating.35
Post lumbar puncture (LP) headaches could be
considered iatrogenic trauma. They occur in as many
as 35% of patients undergoing dural puncture and are
especially common in thin, young women. 36 The
headache is much worse upon standing and is relieved
to a large extent by lying down.
Cerebral venous thrombosis (CVT) is an
important cause of headache that is more common
than once thought.37 CVT may present with a suddenonset headache, often associated with nausea and
vomiting, 38 clinically mimicking SAH. 39 The diagnosis
is often missed or delayed; CTs may be misinterpreted,
and the failure to measure cerebrospinal fluid (CSF)
pressure when performing an LP (which should be
high in CVT) may add to the diagnostic lag. CVT is an
especially feared complication of pregnancy and the
postpartum period.
Temporal arteritis, also known as giant cell
arteritis, is an important cause of headache in the
elderly and can lead to visual loss. Patients usually
present with headache, along with visual problems
(31.5%), blindness (9.7%), jaw claudication (40.8%),
and either tenderness or induration of the temporal
artery (61.3%).40
Dissection of the vertebral arteries is often characterized by a sudden, severe occipital headache, associated
with neck pain. The pain can occur several days before
the onset of neurologic deficits. About half of patients
complain of dizziness or vertigo and experience nausea
or vomiting. Some have unilateral facial numbness and
diplopia.41 Minor trauma (e.g., from sporting activities,
chiropractic manipulation, or even head-turning to park a
car) frequently occurs within six hours prior to the onset
of head and neck pain.42
Cluster Headaches
Over 90% of patients suffering from cluster
headaches are male, and many have a family history
of the same. 29 Attacks frequently come at night and
may wake the patient from sleep. They are often
precipitated by alcohol.30
Characteristic findings include severe, strictly
unilateral pain located about the eye. The pain
may last from 15-180 minutes and may occur 1-8
times per day. Attacks are usually clustered in a
short time period, followed by weeks to months of no
headaches. Associated symptoms often include
conjunctival injection, lacrimation, nasal congestion,
rhinorrhea, forehead and facial sweating, miosis, and
eyelid edema. As many as 30% of such patients may
display ptosis. 31
Secondary Headaches
Headache may accompany almost any systemic or
intracranial process. Some of the more common
secondary causes include sinusitis, systemic infections,
and dehydration.8,28
Non-traumatic SAH usually occurs from the
spontaneous rupture of a cerebral aneurysm. The
presentation is traditionally graded using the Hunt
and Hess classification, based upon mental status, neck
stiffness, and the neurologic exam.32 (See Table 3.)
As many as one-quarter of SAH cases may be
misdiagnosed in the ED, mostly in patients with
isolated headache and no neurological findings.33 The
ED physician may mistake SAH for viral meningitis,
migraine, or headache of uncertain etiology. Patients
with a missed diagnosis do significantly worse than
those in whom the bleed is detected on the initial visit.
Table 3. Hunt And Hess Classification Of

Subarachnoid Hemorrhage.
Grade 1: Asymptomatic, or minimal headache; slight
nuchal rigidity.
Grade 2: Moderate to severe headache, nuchal rigidity;
no neurological deficit (apart from cranial nerve palsy).
Grade 3: Drowsiness, confusion, or mild focal deficit.
Grade 4: Stupor, moderate to severe hemiparesis;
possible early decerebrate posturing.
Grade 5: Deep coma, decerebrate posturing, moribund.
Prehospital Care
Prehospital identification of headache complaints
may help risk stratification. Although somewhat
intuitive, at least one study has suggested that
patients with headache who arrive by ambulance
have a higher incidence of dangerous pathology
compared to walk-in patients.43
Adapted from: Hunt WE, Hess RM. Surgical risk as related to time of
intervention in the repair of intracranial aneurysms. J Neurosurg
1968;28:14-20.
June 2001
ED Evaluation
A basic unit can transport patients with stable vital

signs and a history of similar headaches. Patients with
abnormal vital signs, focal neurologic deficits, or
abnormal mental status require transport in an advanced unit with intravenous access, oxygen, and
cardiac rhythm monitoring. Some believe that upright
positioning at 30, unless contraindicated by suspicion
of cervical spine injury, can improve cerebral perfusion. If carbon monoxide poisoning is suspected,
medics should provide 100% oxygen by non-rebreather
facemask. Prehospital care providers must consider the
possibilities of hypoxia and hypoglycemia and treat
when appropriate.
In general, medics must resist the temptation to
lower the blood pressure in the headache patient.
Elevated blood pressure is a normal physiologic
response to pain and usually requires no special
treatment. High blood pressure is protective in those
with intracranial bleeds, as these patients require high
cerebral perfusion pressures.
The American Heart Associations Stroke Council
has published consensus-based guidelines for blood
pressure management during stroke,44 but these are not
necessarily applicable to the unselected headache
patient in the prehospital setting. However, if the
stroke guidelines were extrapolated to this setting, the
medics should not attempt blood pressure reduction
unless they have two readings 10-15 minutes apart
confirming a systolic pressure greater than 220 mmHg
or a diastolic pressure greater than 120 mmHg.
When confronted by the headache patient, the wary

emergency physician (who instinctively thinks of the
catastrophic), must consider SAH, meningitis, Rocky
Mountain spotted fever, carbon monoxide poisoning,
glaucoma, temporal arteritis, and rapidly expanding
mass lesions. A meticulous history and physical alone
can often rule out these concerns.
Approximately 1%-4% of patients presenting to the
ED with a chief complaint of headache have significant
underlying pathology that requires emergent, or at
least urgent, diagnosis. 14 Important clinical questions
include: Which patients need emergent
neuroimaging? Which patients must have an LP
performed? and Which patients need both? The
issue of early and empiric antibiotics for suspected
bacterial meningitis is also crucial. The history and
physical examination are key to answering these
questions. (See also Table 4.)
History
Though the presentations of ominous headaches vary,
most authors agree that the most important factors
include severity, onset and quality of pain, and associated symptoms.2,45 (See Table 5.)
Worst Headache
In clinical practice, the chief complaint of the worst
headache of ones life is suspicious for significant
intracranial pathology. One study found that 17% of
patients (18/107) with the worst headache of their
life had a bleed.46 In a prospective study, Mills et al
reported a 29% yield for positive head CT in patients
complaining of the worst headache of their life or
severe, persistent headache.47 These positive findings
included a variety of clinically significant intracranial
pathology. (Some wags have noted that any person
who has ever had a headache, by definition, has had a
worst headache of their life.)
Table 4. Pearls In The Clinical Evaluation Of The

Patient With Headache.
Finding
Consideration
Thunderclap headache
Subarachnoid hemorrhage
Worst headache
SAH, cerebral venous

thrombosis
Use of space heater
Carbon monoxide
Time To Maximal Onset
Pregnancy
Eclampsia, cerebral venous

thrombosis
Some data suggest that the suddenness of a headache
Change in vision
Glaucoma, optic neuritis
Pain with eye movement
Optic neuritis
Fever
Infection (CNS vs systemic)
Double vision
Intracranial mass, idiopathic

intracranial hypertension
Ptosis, miosis
Carotid artery dissection
Papilledema
Mass lesion, optic neuritis,

pseudotumor
Dilated pupil
Aneurysm compressing
third nerve
Age greater than 50 years
Temporal arteritis, mass

lesion, glaucoma
June 2001
Table 5. Danger Signals In Headache.

Historical features
Sudden-onset headache (thunderclap)
Worst headache of life
Headache dramatically different from past headaches
Immunocompromise
New onset of headache after age 50
Headache that begins with exertion
Physical findings
Altered mental status
Meningeal signs
Positive jolt test (see text)
Focal neurologic signs
Rash suspicious for spotted fever, meningococcemia
associated with SAH. 50 As many as half of all patients

with SAH may present with syncope. 53 Although
usually present with migraines, photophobia also
occurs with meningitis. Protracted or recurrent vomiting is often seen with an intracranial bleed. Jaw
claudication and pain in the shoulder muscles are
associated with temporal arteritis.
is an even more important factor than severity. The

term thunderclap headache is used to describe a
headache with sudden onset of excruciating pain that
reaches its maximal intensity within seconds. In one
prospective study, 70% of patients (35/49) presenting
with a thunderclap headache had an SAH.48 Another
study prospectively examined all patients presenting
with severe headache of sudden onset with no past
history of the same. Of 27 patients enrolled, nine had
SAH, one had intraventricular hemorrhage, and two
had meningitis. 49 One additional prospective study
interviewed 102 patients presenting with symptoms
consistent with a thunderclap headache. Symptoms
most often associated with an intracerebral bleed or
SAH were sudden onset, vomiting, exertional onset,
female sex, seizure, or focal neurologic findings,
including loss of consciousness. Although these
findings are often associated with SAH, they
also occur with the entity known as benign
thunderclap headache.50
Additional Aspects Of The History Of Present Illness

Additional components of the history focus on exacerbating and alleviating factors. Headaches can be food-,
stress-, or position-related. Concurrent pregnancy,
especially in the third trimester, should prompt
evaluation for preeclampsia. 6
Age
Be suspicious when an older patient complains of a
new-onset headache (i.e., no prior history of similar
pain). In a review of 468 ED patients who presented to
the ED with headaches, the authors found that age
greater than 55 years old was a strong predictor of
intracranial pathology.15 A new headache in patients
over 50 years of age raises concern for glaucoma,
intracranial lesions, and temporal arteritis. Of note, in
one study spanning a 42-year time period, no person
younger than 50 years old was diagnosed with temporal arteritis.54
Conflicting Data
Other studies suggest little correlation between worst
or sudden headache and final diagnosis.15,51,52 However,
each of these studies suffers from a variety of methodological flaws.
Although neither sensitive nor specific, there is
some evidence that the worst headache and especially sudden-onset headache are important historical findings. When present, the physician should
consider further diagnostic evaluation.
Past Medical History

Prior Headaches
Obtain a history and description of past headaches. In
particular, a significant change in character from prior
headaches can indicate serious new pathology.
A recent severe headache may represent a
sentinel bleed. One case-controlled study found
that of 30 patients admitted with SAH, 13 (43%)
had a recent history of previous sudden headache.55
The interval between the warning headache and
admission with ruptured aneurysm ranged from one
week to two months.
Headache Quality And Location

Headache quality and location are at times helpful, but
rarely diagnostic. Throbbing quality suggests vascular
etiologies such as migraine. Headaches due to mass
lesions, such as tumors or hydrocephalus, tend to be
dull and steady. Migraines usually begin unilaterally,
while tension headaches are frequently bandlike.
Occipital headaches often suggest cerebellar lesions,
muscle spasm, or cervical radiculopathy. However, the
presence of an acute headache located in the occipitonuchal region has been associated with increased
intracranial pathologyespecially when accompanied
by other symptoms.15 Vertex headaches are seen in
sphenoid sinusitis and supratentorial lesions, while
orbital headaches suggest glaucoma, optic neuritis,
cluster headache, or cavernous sinus thrombosis.
Unilateral facial pain is seen in trigeminal neuralgia,
sinusitis, and carotid artery dissection. Glossopharyngeal neuralgia is characterized by pain in the pharynx,
tonsils, and ear and is usually precipitated by swallowing, yawning, or eating.
History Of Intracranial Pathology Or Malignancy

Patients with history of previous neurosurgery
including shunt, arteriovenous malformation or
aneurysm, and non-CNS malignancyare at increased
risk for serious underlying pathology with the complaint of headache. 6,56
Likewise, a history of malignancy should raise
concern for metastatic brain or skull lesions. However,
the classic brain-tumor headache, described as
severe, present in the morning, and associated with
nausea and vomiting, is rare. In one series of 111
patients with brain tumors, headache was present in
only 48%, was most frequently bifrontal, and was
present during the morning in only 36% of patients.57
Associated Symptoms
Determine whether the patient has other symptoms.
Neurologic complaints are especially important. Visual
field deficits, double vision, or seizures may be
Immunocompromise
HIV infection and other immunocompromised states,
June 2001
such as alcoholism and transplants, raise additional

concerns. Such patients may suffer from lesions such as
toxoplasmosis or progressive multifocal leukoencephalopathy as well as being more susceptible to a variety
of meningeal infections.
can occur in a variety of infections, ranging from the

benign to the lethal. It can also occur with SAH.2
Head And Scalp

Palpation of the scalp may be quite valuable in the
patient with headache. Nearly all patients with tension
headache will have pericranial muscle tenderness.24,28
In addition to evaluating the scalp musculature,
determine whether the patient has any trigger points.
Tender areas that exactly reproduce the head pain may
indicate neuralgia. Occipital neuralgia is a common cause
of headache. Such patients have unilateral aching pain of
the head, and pain in the distribution of the occipital
nerve.64 The pain or tingling may radiate forward in the
scalp with tapping on the nerve as it exits beneath the
occipital bone (Tinels sign). Those with temporal arteritis
may demonstrate induration or tenderness of the
temporal artery. Other patients with headache may show
signs of trauma, including Battles sign.
Trauma
A history of trauma introduces the possibility of
chronic subdural hematoma or post-traumatic headache syndrome. However, patients can be amnestic to
the event, or the trauma can have occurred sufficiently
long ago that an accurate history is unobtainable. Up to
20% of patients with chronic subdural hematoma have no
identifiable etiology or can present with symptoms up to
three months from a known traumatic event.58
Toxin Exposure
Take an occupational history to uncover a toxin
exposure, such as carbon monoxide. During cold
weather, ask how the patients home is heated. Headache and dizziness are the two most common complaints in occult carbon monoxide poisoning and are
seen in 90% and 82% of patients, respectively.59 Exposure to products of combustion is not necessary for
carbon monoxide poisoning. Methylene chloride,
which is found in paint strippers, is metabolized to
carbon monoxide. 60
Eyes
While the eyes may or may not be the window
to the soul, they certainly provide a view of
headache etiology. Inspection of the lids, sclera,
cornea, eye movements, pupil, and retina often
provide essential information.
Look at the patients lids. Ptosis may occur with
cluster headaches as well as with more serious pathology such as Horner s syndrome (droopy lid, small
pupil, and an absence of facial sweating on the involved side). The presence of Horner s syndrome in
conjunction with a headache may represent a carotid
dissection.65 Periorbital ecchymosis (raccoons eyes)
suggests basilar skull fracture.
Test the patients visual fields by confrontation; a
field cut may occur with a complicated migraine or,
more ominously, an intracranial catastrophe. Similarly,
a disorder of extraocular motions in the presence of a
headache can reflect a CNS bleed, mass lesion, or
neuropathy of a cranial nerveoften from diabetes or
Lyme disease.
Inspect the eye for scleral injection. A unilateral
red eye is often seen with either glaucoma or cluster
headache. In glaucoma, the cornea is usually
cloudy and the pupil mid-position and unreactive.
Such patients need measurement of their
intraocular pressure.
The pupil size and reactivity are also revealing. A
dilated, unresponsive pupil in a conscious patient may
indicate a host of concerns, including an aneurysm
pressing on the third nerve, use of mydriatic eye drops,
or a glass eye.
The funduscopic exam of the headache patient can
reflect elevated intracranial pressure, manifesting as
papilledema. The sophisticated emergency physician
will train him- or herself to look for spontaneous
venous pulsations (SVPs). This is a subtle throbbing of
the central retinal vein (the fattest, darkest vessel in the
Medication Use
Chronic use or abuse of ergotamine, analgesics,
sympathomimetics, or cocaine is a known cause of
headache. Recent medication changes, including
initiation of oral contraceptives and withdrawal of
medications, may incite headaches.6,61,62 Withdrawal
from caffeine is an especially common precipitant.
(Clues to this diagnosis include persistent tremor in
conjunction with a Starbucks tattoo or finding a photo
of Juan Valdez in the patients wallet.)
Miscellaneous
SAH may be associated with polycystic kidney disease,
fibromuscular dysplasia, or a family history of SAH.2
Physical Exam
The physical examination provides important clues to
the underlying pathology. The first impression of the
patient may demonstrate toxicity or signs of physiologic stress, such as diaphoresis.
Vital Signs
Vital signs in the headache patient can be especially
revealing. The diagnosis of a hypertensive emergency
cannot be made without measuring the blood pressure.
Obtain an accurate temperature, using the rectal
approach if necessary. A normal temperature is very
unlikely in patients with meningitis. Ninety-five
percent of patients with bacterial meningitis will have
fever upon presentation to the ED. 63 Fever, of course,
June 2001
or her neck. Kernigs sign is produced by flexing one

hip and knee and then extending the knee (with the
hip still flexed). In the presence of significant
meningeal irritation, the lumbar roots will be irritated,
causing pain in the hamstring and paraspinous
muscles. Full extension of the knee may be impossible
due to spasm. In severe cases, a contralateral sign
occurs. This occurs when passive flexion of one hip
and knee causes flexion of the contralateral leg.
However, the spotty performance of Brudzinskis and
Kernigs signs in recent studies undermines their
utility; recent data indicate that these tests are neither
sensitive nor specific.70
A more promising examination involves the jolt
maneuver. To perform this test, ask the patient to
rapidly (2-3 times per second) shake his or her head
from side to side. In one study, accentuation of the
headache by this maneuver was 100% sensitive and
54% specific for meningitis; the studys authors claim
that the test is the most useful adjunctive maneuver for
evaluating headache in the presence of fever.71
There are some data to suggest that worsening of a
headache with the Valsalva maneuver increases the
likelihood of a positive finding on cranial CT.72
retina) just where it emerges from the disc. One study

correlated eye findings with pressure measurements
obtained using LP. (The author actually performed LPs
on numerous patients known to have brain tumors.)
No patient with SVPs had increased intracranial
pressure.66 While the presence of SVP essentially rules
out ICH, pulsations may be absent in about 12% of
normal patients.
Funduscopy may also reveal retinal hemorrhages
in the patient with SAH.
Mouth
Why look in the mouth of a patient with a headache?
To check for oral thrush. Children with headache may
have exudative tonsillitis. In one study, streptococcal
pharyngitis was responsible for 5% of all pediatric
headaches presenting to the ED.67
Sinuses
If the patient has facial or frontal pain, tap on the
sinuses to elicit tenderness. Similarly, having the
patient lean forward will often exacerbate the head
pain. However, of all physical findings, studies show
that purulent nasal secretion and abnormal sinus
transillumination are the best clinical predictors
of sinusitis.68
Diagnostic Testing
Neck
Lord, how my head aches! What a head have I!

It beats as it would fall into 20 pieces.
William Shakespeare (1554-1616),
in Romeo and Juliet, II, v, 49
Perhaps the most important aspect of the neck exam is

to determine whether the neck is supple. Place the
patient supine on the gurney and gently flex the neck
to detect any resistance against flexion.
Blood tests rarely reveal the cause of a headache.

In older patients with any combination of jaw
claudication, proximal muscle pain, visual
complaints, or tender temporal arteries, an
erythrocyte sedimentation rate (ESR) may suggest
the need for a temporal artery biopsy and empiric
treatment for temporal arteritis. In one study of
patients with biopsy-proven temporal arteritis, the
Westergren ESR was elevated (above 40 mm/h) in all
patients who were not on steroid therapy at the time
of biopsy (average, 108 mm/h). 73
The CBC should never be used to rule out meningitis; nearly one-third of patients with meningitis have
a normal white count and differential.74-76
While electrolytes are similarly unhelpful, a
bedside test of blood glucose may reveal hypoglycemia
in headache patients with altered mental status.
A carboxyhemoglobin level is essential in patients
in whom carbon monoxide poisoning is suspected. It is
especially useful in the winter months and when
people living in the same household complain of
dizziness and headache. One study showed that the
number of cigarettes smoked daily, use of stoves for
heat, and concurrently symptomatic cohabitants can
predict an elevated carboxyhemoglobin level.59
But of all of the laboratory tests available to the
Neurologic Exam
The neurologic exam has special significance in the
patient with headache, because a new neurologic
deficit mandates imaging and/or LP.
One of the first assessments should be the patients
mental status. What is the patients level of alertness?
Is he or she oriented to person, place, and time? The
neurologic examination should also evaluate the
cranial nerves, motor deficits, and gait. A pronator
drift is one of the most sensitive and commonly
employed tests for motor deficit. 69 While a sensory
exam is often suggested, there is little evidence to
show that it is helpful.
Skin
On occasion, inspection of the skin may reveal important
findings such as a rash associated with meningococcemia, vasculitis, or Rocky Mountain spotted fever. The
presence of skin tracks should raise concern for HIV.
Physical Examination Maneuvers

The most familiar maneuvers in the evaluation of
headache involve testing for Brudzinskis and Kernigs
signs. Brudzinskis sign is positive when the supine
patient bends both knees in response to flexion of his
June 2001
New-onset headache in patients older than

50 years
New-onset headache in patients with malignancy
or HIV
Headaches associated with neurological deficits
(other than migraines with aura)
Headaches associated with papilledema
or confusion
emergency physician, the most valuable is

analysis of the CSF. In patients suspected of
meningitis, a cell count, Grams stain, protein,
and glucose evaluation of the spinal fluid are
essential for diagnosis. The typical pattern in
bacterial meningitis may show a positive Grams
stain, a high CSF white count (usually PMNs), high
protein, and low glucose. In those who are suspected
of, or known to have, HIV, additional studies on CSF
may be helpful. Such tests include an India ink smear
for Cryptococcus, a cryptococcal antigen test, and
possibly a CSF VDRL.
Normal CSF pressure ranges from 5-15 cmH 2O
when the patient is in the usual decubitus position.
Measuring the pressure may occasionally be helpful,
as CSF pressures may be significantly elevated in a
variety of headache conditions. These include SAH,
CVT, bacterial and cryptococcal meningitis, and
pseudotumor cerebri. Of course, CSF pressures
may be elevated in the presence of a space-occupying
tumor, but hopefully you will not be measuring them
in that circumstance.
With the possible exception of detecting SAH,

neuroimaging in patients who have a normal neurologic examination is rarely productive. One review
examining multiple studies involving more than 3000
scans revealed the following positive scans: brain
tumors, 0.8%; arteriovenous malformations, 0.2%;
hydrocephalus, 0.3%; aneurysm, 0.1%; subdural
hematoma, 0.2%; and strokes, including chronic
ischemic processes, 1.2%. 81
A number of specialty societies, including the
American College of Emergency Physicians (ACEP),
have developed practice guidelines to identify which
headache patients may benefit from emergent
neuroimaging. There does seem to be some agreement
between specialties with the basic practice parameters.
The first of these practice parameters, titled Practice
parameter: The utility of neuroimaging in the evaluation of headache in patients with normal neurologic
examinations, was published in 1994 by the American
Academy of Neurology (AAN). 82 In this review, 17
identified studies are graded in an evidence-based
format, and the panel made three recommendations
supported by moderate clinical certainty.The authors
made the following recommendations:82
Neuroimaging is not warranted in patients
with a diagnosis of migraine who present
with a typical event.
Neuroimaging should be considered in patients
with atypical headaches, history of seizures, or
focal neurologic signs or symptoms.
There is insufficient evidence to define
the role of CT vs. MRI in headache patients
without migraine.
The Role Of Neuroimaging

The non-contrast CT scan is the most widely available
and useful neuroimaging test available to the emergency physician. A contrast scan is rarely necessary in
the evaluation of headache, but it may be helpful if the
physician suspects a subacute subdural hemorrhage
(2-3 weeks old) or complications of HIV disease, such
as toxoplasmosis.
While MRI is more sensitive than CT for some
lesions (particularly those in the posterior fossa), it is
not immediately available to most emergency physicians. In addition, CT is generally able to demonstrate
any neurosurgical emergency or determine whether LP
is contraindicated.
Possible indications for emergent MRI in the
patient with headache include suspicion of CVT
despite a non-diagnostic CT as well as suspected
vertebral or carotid artery dissection.77
Who Benefits From Neuroimaging?

In 1996, ACEP published a clinical policy for the
initial approach to headache. Its authors graded
literature and suggested certain actions in the presence
of various clinical findings. These actions were classified as either a rule or guideline. The authors recommended CT as a rule for patients with severe,
sudden-onset headache, suspected intracranial infection, and neurologic deficits. CT was recommended as
a guideline for a large number of historical or
physical findings, thus recognizing the need to place
the patients complaint in context.6
In 2000, the U.S. Headache Consortium published
Evidence-based guidelines in the primary care setting:
neuroimaging in patients with nonacute headache.79
(See Table 6 on page 10.)
The answer to this important question is not always

clear. The main objectives in obtaining neuroimaging
in the ED are to identify a potentially treatable lesion
and to determine whether performing an LP would be
safe. A number of authors have suggested various
criteria guide the need for urgent neuroimaging and/
or LP.78-80 However, no large, prospective trials have
validated these criteria, nor do the various authorities agree
with each other regarding these indications. Nonetheless,
the following have been suggested as indications for
performing a CT or LP:
The first/worst headache
Thunderclap headaches
Headache associated with fever, stiff neck, nausea,
and vomiting
June 2001
CT And SAH
missed on neuroimaging.
What is the correct answer? Clearly, numerous
small series and case reports document the phenomenon of an SAH diagnosed by LP despite a negative
cranial CT scan.2 However, the experienced emergency
physician knows that many patients with a negative
CT who feel well after ED therapy will refuse an LP.
These same physicians also recognize the importance
of documenting that the patients sensorium was clear
when he or she signs out against medical advice.
The accuracy of a CT scan in SAH depends on a

number of factorsnot the least of which includes the
generation of the scanner and the ability of the reader.
The timing of the CT is also very important. CT
appears most accurate in the first 12 hours after
aneurysmal rupture. In one study, a third-generation
CT was 100% sensitive to SAH if the patient was
scanned within 12 hours of symptom onset but fell to
81% after that time.83 The ability of CT to detect SAH
further degrades with time, decreasing to 50% by one
week and to less than 30% after two weeks. 84
Can LP Be Used Before Or Instead Of CT

To Evaluate SAH?
Does A Patient Suspected Of SAH Need An LP

After A Negative CT?
One author used a decision analysis to evaluate

the safety and utility of an LP-first strategy.
Assuming that an LP needs to be performed every
time a CT is ordered (and found negative) for SAH,
he argues that an LP-first strategy makes best use of
available resources. The author further suggests this
strategy be limited to young to middle-aged adults
without known cancer or HIV infection and that the LP
be performed at least 12 hours after symptom onset.87
This strategy, however, has not been subjected to
prospective trials.
Recent advances with the newer third-generation

scanners raise questions of whether an LP should be
performed following a negative CT. One recent
evidence-based review evaluated the available literature to answer the question: How good is a negative
CT result in excluding SAH within the first 24
hours? 45 The authors identified two studies that they
believed most closely addressed this question but
discarded several others, claiming bias in study design
or other problems. Based on one retrospective85 and
one prospective study,46 the authors calculated that a
person with a sudden-onset, severe headache and a
normal neurologic exam has a 6%-7% chance of having
a false-negative CT.45 For this reason, they recommend
an LP in patients suspected of SAH despite a
negative CT.
Others dispute this assertion and believe that
when patients have a low pretest probability of
SAH, a negative CT can obviate the need for subsequent LP.86 The counter-argument is that it is the wellappearing patient with a negative scan who needs the
subsequent LP.2 They argue that because of spectrum
bias, patients with minor symptoms are likely to have
less blood on CT and therefore are more likely to be
LP And Spinal Fluid Evaluation:

What Do You Do With A Bloody Tap?
Bloody CSF does not always equal CNS pathology.
While every ED physician dreams of the pristine
champagne tap, blood from an injured vein contaminates up to 20% of LPs. 2,88 A decreasing erythrocyte
count from the first tube to the last tube is only slightly
comforting. Patients with SAH may have fewer RBCs
in tube #4 compar ed to tube #1, while RBCs may
remain constant in face of a traumatic bleed. 81,89 The
clinical practice of comparing the erythrocyte count in
sequential tubes has never been validated and should
be considered unreliable.2,90 Some authors have
suggested that a measurement of the D-dimer in the
CSF can distinguish between a traumatic tap and true
SAH.2,46,91 However, D-dimer levels within CSF have
been shown to be inconsistent and thus unreliable in
identifying the etiology of bloody CSF. 2,46,91
Most authors agree that the presence of xanthochromia as determined by spectrophotometry (and not
by visual examination) is the primary criterion for
diagnosis of SAH.2,90 Xanthochromia suggests that
blood has been present in the spinal fluid for at least 12 hours.81,84,92 Because the naked eye can identify
xanthochromia in only half of the cases, the use of
spectrophotometry is critical in reliably diagnosing
SAH.2,93,94 Spectrophotometry is essentially 100%
accurate in detecting SAH from 12 hours to two weeks
after the incident. However, its sensitivity drops to
40% at 2-4 weeks.2,84
During the LP, measure the opening pressure when
feasible. Elevated intracranial pressure may indicate
CVT or pseudotumor cerebri and can help distinguish
a bloody tap from a true SAH.2
Table 6. U.S. Headache Consortium Guidelines For

Neuroimaging In Patients With Non-acute Headache.
Neuroimaging should be considered in patients with
non-acute headache and an unexplained abnormality on
neurologic examination.
There is insufficient evidence to make neuroimaging
recommendations based on the presence or absence of
neurological symptoms (note that this guideline addresses chronic headache, not acute).
Neuroimaging is usually not warranted in patients
presenting with a typical migraine headache with no
neurologic deficits.
There are insufficient data for an evidence-based
recommendation on the use of neuroimaging for
tension-type headaches.
There are insufficient data for evidence-based recommendations regarding CT vs. MRI in the evaluation of
non-acute headache.
10
June 2001
Is A CT Necessary Prior To Obtaining An LP?
headache. CVT is occasionally found in patients

presenting with an acute severe headache without
neurologic deficits.37,39,102 These patients often have a
normal head CT. Although the LP may be negative for
blood or xanthochromia in the CSF, the opening
pressure is likely to be elevated.
The most feared complication of LP is brain herniation.

This can occur in some patients with an intracranial
mass lesion. When the pressure below the brain is
suddenly decreased by the spinal tap, herniation can
occur. The phenomenon, also known as coning, is
quite rare. It is almost unheard of in the presence of a
nonfocal neurologic exam. If a patient is not comatose,
has a nonfocal neurologic examination, and has no
papilledema, LP is considered safe.95,96
There have been several reports of patients with
SAH who deteriorated shortly after LP. Post-mortem
examination in some showed cerebral dislocation.97,98
However, since none of the patients in the largest
study had CT prior to LP, it is difficult to say whether
prior CT could have warned of this complication.
Pharmacotherapy
The pharmacotherapy of headaches is an extraordinarily vast and, on occasion, controversial topic.
During the past 40 years, over 500 reports on the
efficacy of various medications for headache have
been published. 103
This section emphasizes the treatment of primary
headaches, such as tension and migraine. While
treatment of all secondary headaches is beyond the
scope of this article, it does address important issues
related to the emergency care of patients with SAH,
temporal arteritis, and CVT.
Thunderclap Headache With A Negative CT/LP:

Is Angiography Indicated?
A history of thunderclap headaches should trigger
the emergency physician to consider SAH. But
what if such a patient has a negative CT and a
negative LPdoes he or she need cranial angiography
as well? Although no prospective cohort studies
provide a definitive answer, a number of articles
address this dilemma.
In 1986, Day and Raskin reported the case of a 42year-old woman who presented with three thunderclap
headaches within one week.99 The patients evaluation
revealed a negative CT and bloodless CSF. Angiography showed diffuse marked vasospasm and an
unruptured aneurysm. The authors concluded that
hemorrhage into the wall of the aneurysm or rapid
expansion of the aneurysm might have been the cause
of the patients headaches. This case report led some to
argue that a normal CT scan and LP are not sufficiently
sensitive to exclude aneurysm in thunderclap headache. Others claim that the case report means nothing;
an aneurysm found on angiography could have
represented an incidental finding, since the prevalence
of inconsequential intracranial aneurysms at autopsy is
between 2% and 5%.100
There is a far more robust study by Wijdicks et al
that addresses this issue of how far does one go
when faced with a thunderclap headache in the ED. It
involved a more-than-three-year follow-up on 71
patients, each of whom presented with a thunderclap
headache and had a negative CT scan and LP.101 Each of
the six angiograms performed was negative. None of
these 71 patients suffered from SAH over the 3.3-year
follow-up period. Seventeen percent had identical
recurrences of their headaches; 44% developed tension
headaches or common migraines. The authors concluded from the study that angiography is not recommended for the work-up of these patients. Another
prospective study confirmed this finding. 48
Recognize, however, that SAH is not the only
serious condition that presents with a thunderclap
June 2001
Migraine Headache
Many agents can be considered in the treatment of
migraine. (See Table 7 on page 14.)
Antiemetics
Antiemetics are a mainstay of migraine treatment.
Generally, they are most effective when given intravenously, but they may also be administered intramuscularly, by mouth, or as a suppository. Antiemetics
generally cause some drowsiness, and patients to
whom these medications are given should not drive
home afterwards. Most antiemetics can also cause a
variety of side effects, including akathisia (restlessness
or feeling antsy) and dystonia (torticollis or other
posturing). These side effects can be controlled with a
benzodiazapine (such as lorazepam 1-2 mg IV) or
diphenhydramine (Benadryl).
Metoclopramide: Several randomized,
placebo-controlled studies show that 10 mg
of IV metoclopramide (Reglan) is effective in
relieving migraine headaches. 104,105 In comparison
studies, however, prochlorperazine proves better
than metoclopramide.106,107
Prochlorperazine: Prochlorperazine (Compazine)
is a very effective treatment for migraine, especially
when given as 10 mg IV.106-110 When compared to other
agents, it is more effective than sumatriptan,111
metoclopramide,106,107 and ketorolac.112 Patients who
experience relief can use suppositories in case of future
attacks. In one study, a 25 mg suppository was significantly better than placebo in controlling migraine
pain.113 However, the IV route may be more appropriate for the ED setting. In one study, only 8.7% of
patients treated with IV prochlorperazine needed
rescue medications, as opposed to 26.1% of those
treated via the rectum. 114
The rate of adverse reactions with parenteral
11
effective in migraineurs. 121
prochlorperazine may be higher than once thought. A

recent study of 229 adults showed that about 20% of
patients develop either akathisia (16%) or dystonia
(4%) requiring pharmacologic intervention.115
Promethazine: A number of studies show that
promethazine (Phenergan) is useful in the treatment of
migraine when combined with other agents, such as
narcotics.116,117 However, there are no randomized,
double-blind, placebo-controlled studies on the use
of promethazine alone for the acute treatment of
migraine headaches.
Granisetron/Zatosetron/Ondansetron: These
powerful antiemetics have gained some renown in
treating the nausea associated with chemotherapy.
However, they have not been well studied in the
treatment of headache. In one trial, IV granisetron was
more effective than placebo in reducing headache pain,
but 65% of the patients receiving this drug needed
rescue medication at two hours.118
Droperidol (IM And IV): One retrospective study
showed symptomatic relief in 81% of patients at 30
minutes with a 2.5 mg IM dose of droperidol. 119
Another study (prospective) showed that, when
titrated intravenously, droperidol can successfully treat
refractory migraine.120 Some evidence suggests that IV/
IM prochlorperazine and droperidol may be equally
Neuroleptics
IV Haloperidol: While no randomized, double-blind,
placebo-controlled studies exist, there appears to be a
molecular basis for the use of dopamine antagonists in
the treatment of migraine headaches.122 In one small
case series, all six patients treated with intravenous
saline and 5 mg haloperidol (Haldol) showed
clinical improvement.123
IV Chlorpromazine: Success rates for the IV use of
chlorpromazine (Thorazine) for migraine vary from
89% to 95%. 124-126 Dosages range from 0.1 mg/kg (given
up to three times as needed) to 12.5 mg IV, given twice
if necessary. In a variety of studies, IV chlorpromazine
was reported to be superior to meperidine,127
metaclopramide, 3 and DHE, 125 while its success was
equivalent to ketorolac.128 Because of its tendency to
cause orthostatic hypotension, patients to whom IV
chlorpromazine is given should be kept supine for a
period of time.
Barbiturate-Hypnotics
There is no strong evidence to suggest the value of
butalbital-containing compounds for the acute treatment of migraine headaches.129 Furthermore, barbitu-
Cost-Effective Strategies In Headache Management

criterion be replaced by a more objective Glasgow Coma
Scale score less than 14. Using these modified criteria, they
reported 100% sensitivity while increasing specificity.
Risk-Management Caveat: Certainly neuroimaging is
essential in some patients. Those with a thunderclap
headache, papilledema, unexplained altered mental status,
or an abnormal neurologic examination will need cranial
CT. HIV-infected patients with a new or worsening
headache are also candidates for such a study.
1. Minimize laboratory tests.

Most patients with headache need no laboratory tests. They
will require only a targeted history and physical examination.
Risk-Management Caveat: On occasion, the clinical exam
will suggest the need for further testing. The elderly patient
with jaw claudication or tender temporal arteries may need
an ESR. Obtaining carbon monoxide levels is crucial if
carbon monoxide poisoning is suspected. However, of all
laboratory tests performed in the patient with headache,
analysis of the CSF may be the most crucial.
3. Use oral medications when appropriate.

Not every patient with a headache needs parenteral
medication.222 If the history and physical examination are
consistent with tension headache, an oral analgesic may be
all that is indicated.
Risk-Management Caveat: Patients who are vomiting
or those suffering severe migrainous attacks will likely
benefit from subcutaneous, intramuscular, or
intravenous medications.
2. Minimize neuroimaging.
Not every patient with a headache needs a CT scan. In an
illuminating study by Rothrock et al, the authors looked at
the indications for emergent CT in the ED. They did not
include patients with acute head trauma. Important variables
included: age greater than 59, focal neurologic findings,
headache with nausea or vomiting, and altered mental
status.220 (They did not, however, order a CT scan on every
patient who had headache accompanied by nausea or
vomiting.) These criteria identified all those with significant
intracranial pathology and reduced the utilization of head
CTs by 28%. This study was repeated by a group in England.221
These authors argued that age could be eliminated as a
variable and suggested that the altered mental status
4. Prevent rebound.
Patients who develop rebound headaches may return for
further treatment, driving up costs. One prospective study
showed that parenteral dexamethasone significantly
decreased the incidence of rebound headache.
12
June 2001
suggest that DHE is more effective than meperidine,130

less effective than chlorpromazine, 125 and as effective
as sumatriptan.131 Because of their vasoconstrictive
properties, ergots should not be used in those who are
pregnant, at risk for ischemic heart disease, or in those
with peripheral vascular disease.
rate-containing compounds are associated with a very

high rate of rebound headache.129
Dihydroergotamine And Ergot Alkaloids

Ergot alkaloids have long been used in the
treatment of migraines. Because of their tendency
to cause nausea, most studies have combined the
ergots with an antiemetic.
DHE is the best studied of these medications. It
can be given subcutaneously, intramuscularly, or
intravenously; 1 mg is the typical dose. Various studies
Non-Steroidal Anti-Inflammatory Drugs

Oral non-steroidal anti-inflammatory drugs (NSAIDs)
are effective in relieving acute migraines, particularly
Continued on page 20
Ten Excuses That Dont Work In Court

other NSAIDs, it should be avoided in patients with active
bleeding/peptic ulcer disease. Furthermore, it should not
be used if you are considering the diagnosis of SAH or
intracerebral bleeds.
1. Well, I gave him prochlorperazine and his

pain completely resolved, so I thought it was a
migraine headache.
Prochlorperazine and other migraine medicines can
decrease and at times eliminate the pain associated with
other types of headaches, such as SAH.9 Pain relief should
not terminate the search for a dangerous etiology.
7. She had a history of TIAs, so I thought that she had

another TIA and discharged her home on warfarin.
Always consider temporal arteritis in patients with
monocular visual loss, particularly if the patient is
over 50 and has a tender temporal artery. Order an
ESR in these patients and give steroids if the level is
significantly elevated.
2. The CT was negative, so I figured he didnt have an SAH.

CT scans are not 100% sensitive for the detection of
subarachnoid blood, especially when performed more than
12 hours after the ictus. When evaluating for SAH, an LP
should be done if the CT scan is negative.
8. I didnt know that CVT could present with headaches.

Although rare, CVT is one of the important secondary
causes of headaches. It is more likely if the patient has
papilledema and is predisposed to a hypercoagulable state
(i.e., cancer, Behets disease, oral contraceptive use,
pregnancy, or lupus).
3. I thought the chest pain was just a side effect

of the medication; I didnt think that patient could
have a heart attack!
Sumatriptan (and the other triptans) as well as the ergots
are contraindicated in patients with coronary artery
disease, severe hypertension, ischemia, or myocardial
infarction. Always ask about coronary artery disease or
hypertension before administering these drugs.
9. I thought that you never gave antibiotics in suspected

meningitis until after the LP.
Afraid the antibiotics will mess up the cultures? If an LP is to
be delayed in a febrile patient with signs of meningitis due
to a CT or other reasons, give antibiotics before the patient
leaves the ED. Cultures will remain positive for at least six
hours after the administration of antibiotics.223,224 Besides,
having a patient survive meningitis intact is more
important than a pristine culture on any day of the week.
4. But she had a history of migraines!

Keep in mind the long list of secondary causes of
headache, especially if this is a change from the patients
usual pattern. Any significant deviation from the usual
warrants an investigation for SAH, meningitis, possible toxic
exposures, and the like.
5. Why would his attorney state that I was partially to
blame for the patients narcotic dependence/addiction?
Although narcotics continue to be used by many as firstline therapy for migraine headaches, they are best reserved
for rescue therapy.
10. I didnt think that her headache could even be related

to a possible pregnancy!
Postictal women who seize as a result of eclampsia are
unlikely to tell you that they are pregnant. If the patient
is obese, the gravid uterus may not be obvious. Listen for
fetal heart tones or obtain a pregnancy test in such
situations. Consider the diagnosis of preeclampsia in
women who present with headache during the second
half of pregnancy.
6. He only had a tension headache. How was I supposed to

know that he had a history of peptic ulcer disease?
Ketorolac is a potent prostaglandin inhibitor; thus, like the
June 2001
13
Table 7. Treatment Of The Acute Migraine Headache In The Emergency Department.

Drug
cost
Adverse effects
and caution
$$
Mild; extrapyramidal side effects

(e.g., dystonia) and sedation
Role in pregnancy (Category

B). Special role with nausea
and vomiting.
III
Metoclopramide IV
$$
Moderate; extrapyramidal side

effects (e.g., dystonia) and
sedation
Role in pregnancy. Special

role with nausea and
vomiting.
III
Prochlorperazine
PR
IM
IV
$
$
$
Occasional
Occasional
Moderate;
occasional extrapyramidal
side effects and sedation
Good for use in mild/

moderate/severe headache.
Rectal route had modest
clinical effects. Special role
with nausea and vomiting
and as adjunct with other
medications.
Indeterminate
III
II
Promethazine
IM
IV
$
$
Occasional
Extrapyramidal side effects
and sedation
Special role as adjunct with

other medications.
Indeterminate
Indeterminate
IV serotonergic antagonists
(granisetron, zatosetron, and
and ondansetron)
$$$
Infrequent (constipation
common side effect
with granisetron)
Expensive. Special role

when patient has
phenothiazine intolerance.
Indeterminate
Droperidol IM
Moderate; mostly sedation

and akathisia
Very few studies. Rapid IM

onset of action.
III
Antipsychotics
Haloperidol IV
Infrequent
Rapid onset of action.

Few studies available.
Indeterminate
Frequent and severe; most

studies give IV fluids with
the medication
Good clinical effect, but

orthostatic hypotension
may limit its usefulness.
III
$
$$$
Moderate; sedation common

with both
Risk of headache rebound

and overuse.
Indeterminate
Indeterminate
Moderate
Moderate
Frequent; nausea, vomiting,
dysphoria, flushing, and
restlessness most common
SC route may have delayed

onset of action. Not for use
in patients at risk for
ischemic heart disease.
Treatment associated with
low recurrence rates.
II
III
III
Infrequent; very well tolerated
Special use in pediatrics

or pregnancy. Modest
clinical effect.
III
Ketorolac
IM
IV
$
$
Infrequent nausea and

drowsiness; not for patients
with renal and GI diseases
Good clinical effect.
III
III
NSAIDs PO
Occasional nausea and vomiting
Very good clinical effect.

For use in mild/moderate
migraine only.
II for tension
headache;
III for migraine
$$$
Frequent; dizziness, drowsiness,

nausea, vertigo
Good clinical effect but

high risk of rebound and
abuse potential.
III
Occasional; dizziness, fatigue,

nausea, and drowsiness
Good clinical effect but

high risk of rebound
and abuse potential.
III
Drug
Antiemetics
Metoclopramide IM
Chlorpromazine IV
Barbiturate/Hypnotics
Butalbital PO
Fiorinal, Fioricet
Dihydroergotamine (DHE) and ergot alkaloids

DHE SC
$$
DHE IM
$$
DHE IV
$$
NSAIDs
Acetaminophen PO
Opiate analgesics
Butorphanol
nasal spray
Narcoticsoral combinations
(acetaminophen + hydrocodone
or oxycodone)
Comments
14
Class of
evidence
June 2001
Table 7. Treatment Of The Acute Migraine Headache In The Emergency Department (continued).
Drug
Meperidine
IM
IV
Triptans (serotonin agonists)
Sumatriptan nasal spray
Sumatriptan SC
Others
Nitrous oxide (inhaled)
Drug
cost
Adverse effects
and caution
Comments
Class of
evidence
$
$
Occasional
Frequent; sedation, nausea,
and dizziness common
Modest clinical effect, but

rebound headache and
addiction potential limit use.
Special use as rescue therapy.
$$
Frequent, unpleasant taste and

flushing. Avoid with coronary
artery disease/uncontrolled
hypertension and ergot drugs
(this is true for all triptans, for
all routes).
Useful when non-oral route

II-III
of administration needed.
For moderate/severe migraine.
Good clinical effect. Frequent
rebound headaches.
$$
Frequent chest pain and

flushing. Chest pain is common,
but true ischemic events are rare.
Should not be used in basilar
or hemiplegic migraine.
Useful when non-oral route

of administration needed.
For moderate/severe
migraine. Frequent rebound
headaches.
II-III
$$
Infrequent
Obviates the need for

intravenous access.
Indeterminate
III
III
100% oxygen (inhaled)
Infrequent
No significant clinical effects.
Unadvised
IV corticosteroids
$$
Infrequent
Rescue therapy in status

migrainosus.
III
Isometheptene-containing
combinations PO
Infrequent; drowsiness, dizziness,

and nausea
Good clinical effect. For

mild/moderate headache.
Special consideration to
outpatient therapy.
III
Lidocaine IN
Frequent; nasal discomfort
Short duration of action

and very frequent
headache recurrence.
Indeterminate
Lidocaine IV
Moderate
Minimal clinical effects.

Poor efficacy.
Unadvised
Magnesium IV
Moderate
Few studies available.
Indeterminate
Drug costs:
Class II: Acceptable and useful. Very good evidence

provides support. Considered treatments of choice. Based
on higher levels of evidence and results that consistently
yield positive results.
Class III: Acceptable and useful. Fair to good
evidence provides support. Considered excellent
optional or alternative treatments. Based on
intermediate levels of evidence not always yielding
positive results.
Indeterminate: Continuing area of research; results not
compelling or contradictory. Higher studies may be in
progress and no recommendations until further research.
Unadvised: Not acceptable, not useful, or may even be
harmful. Based on studies that yield no consistent
positive data.
Drug cost guidelines are based solely on the cost of the

medication and do not take into consideration the
additional costs of intravenous line placement and/or
nursing/monitoring costs.
$: least expensive (< $25)

$$: $25-$49
$$$: $50-$99
$$$$: $100-$199
Class of evidence:
Class I: Definitely recommended. Definitive, excellent
evidence provides support. Based on one or
more prospective studies that yield consistently
positive results.
June 2001
15
Clinical Pathway: Initial Assessment And Management Of

Immunocompetent Patients With Non-Traumatic Headaches
Headache
Targeted, focused history and physical examination (Class I)
History of headaches?
Change from their usual pattern?
No
Yes
No
Yes
Suspect primary headache: migraine,

tension, cluster. Go to Clinical Pathway:
Assessment And Management Of Patients
With Primary Headaches.
Evidence of infection, such as fever or shaking chills?
No
Yes
Go to Clinical Pathway: Assessment And Management Of

Patients With Headaches And No Evidence Of Infection.
Go to Clinical Pathway: Assessment And Management Of

Headache In Patients With Fever Or Immunosuppression.
The evidenc e for recommenda tions is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute, professional judgment and may be changed depending upon a
patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriber
limited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited.
16
June 2001
Clinical Pathway: Assessment And Management Of Headache

In Patients With Fever Or Immunosuppression
From Clinical Pathway: Initial Assessment And Management Of Immunocompetent Patients With Non-Traumatic Headaches
Suspected immune suppression?

History of HIV with CD4 < 200 or unknown
Prior history of opportunistic infection
Significant HIV risk factors
Oral thrush
CT of head (Class II)

Give intravenous
ceftriaxone or similar
drug effective against
bacterial meningitis
before CT if patient has
fever, stiff neck, or
altered mental status
(Class II)
Yes
No
Possible mass lesion or increased

intracranial pressure?
Papilledema or unable to visualize fundi
Focal neurologic deficit
Yes
New-onset seizures
Headache present for days or weeks
Ventriculoperitoneal shunt
Recent head trauma
CT results
Perform lumbar puncture

(Class I-II)
Measure opening
pressure (Class III)
CSF: cell count, Grams
stain, protein, glucose
(Class I-II)
No
Yes: Option 1
Yes: Option 2
Positive
Treat as indicated
If suspected HIV, order:

CSF cryptococcal
antigen (Class II)
CSF VDRL (Class III)
India ink stain
(Class II)
Signs of meningitis?
Positive jolt test
Stiff neck
Kernigs or
Brudzinskis sign
Altered mental status
No
Negative
Consider other causes of headache and fever

Systemic infections
Rocky Mountain spotted fever
Temporal arteritis
Sinusitis
Pharyngitis (especially in children)
(Class II)
June 2001
17
Clinical Pathway: Assessment And Management Of Patients

With Headaches And No Evidence Of Infection
Headache was sudden-onset, worst-ever, or different than ever before
No
Yes
Age greater than 50?
Non-contrast cranial CT (Class II)
No
Yes
LP (Class
I-II)
Rule out other secondary causes:

dehydration, CO toxicity, post-herpetic
neuralgia, post-LP headache, glaucoma,
pseudotumor cerebri, cerebral venous
thrombosis (Class III)
Blood
or
xanthochromia
present?
CT (Class
III)
Administer
steroids
(Class III)
No
No
Temporal
arteritis
Stiff neck,
meningeal
signs, or jolt
headache?
Yes
Perform
lumbar
puncture
(Class II)
Stat neurosurgical consult, admit (Class II)

Manage airway as necessary (Class I)
Avoid hypotension or unnecessary
lowering of blood pressure (Class II)
Administer nimodipine 60 mg PO if
SAH Hunt/Hess grade I-III (Class I)
Administer phenytoin IV (Class
indeterminate)
Yes
No
Intracerebral hemorrhage?
Yes
Normal neurological exam?
Consider CT if patient
does not have a long
history of similar
headaches in the past
(Class III)
ESR > 50?*
No
Yes
If cerebral thrombosis, obtain stat neurologic consult (Class II)
No
Stat neurosurgical
consult, admit (Class II)
Manage airway as
necessary (Class I)
Avoid hypotension or
unnecessary lowering
of blood pressure
(Class II)
Administer
nimodipine 60 mg PO
if SAH Hunt/Hess
grade I-III (Class I)
Administer phenytoin
IV (Class indeterminate)
Subarachnoid hemorrhage present?
Yes
No
Yes
Check for other causes

Consider discharge
home if patients pain
is well controlled and
the patient is tolerating oral hydration
(Class III)
Once all of the above have been ruled out,

consider primary headache (Class II)
* ESR most likely to be useful in patients with visual complaints,
jaw claudication, low-grade fever, myalgias, or in those with
abnormal palpation of temporal arteries. In very rare cases, the
ESR may be normal.
The evidenc e for recommenda tions is graded using the following scale. For complete definitions, see back page.
Class I: Definitely recommended. Definitive, excellent evidence provides support. Class II: Acceptable and useful.
Good evidence provides support. Class III: May be acceptable, possibly useful. Fair-to-good evidence provides
support. Indeterminate: Continuing area of research.
18
June 2001
Clinical Pathway: Assessment And Management Of Patients

With Primary Headaches
Duration and course of headache
Episodic
Constant
Onset unilateral?
Unilateral?
Yes
Analgesic
abuse?
No
Ergotamine
dependency?
Stop analgesics (Class II)
Yes
Stop ergotamines (Class II)
No
Likely
tension headache
* If eye is
red,
evaluate for
glaucoma:
steamy
cornea,
fixed pupil,
increased
intraocular
pressure
Abortive treatment:
Prochlorperazine 10 mg IV (Class II)
DHE 1 mg SC (often used in conjunction with antiemetic) (Class II)
Sumatriptan 6 mg SQ (Class II)
Consider parenteral steroids to prevent
rebound headache (Class II)
Order ESR;
consider
referral
for
temporal
artery
biopsy
(Class
II-III)
Migraine with or without aura
Further medication history (Class II)
100% oxygen (at least 6 L/min via

non-rebreather mask) (Class II)
Sumatriptan 6 mg SQ (Class II)
DHE IV (Class III)
Age > 50,

tender
temporal
artery
CT (Class III) and further

neurological workup
Consider
trigger
point
injection
(Class III)
Neurological exam normal?
No
Consider migraine
(Class II)
Cluster
headache*
Trigger point
Yes
Lacrimation, rhinorrhea, or retro/

periorbital pain
Clinical and/or laboratory

evaluation for temporal
arteritis (Class II-III)
Other
symptoms?
Consider:
Tension headache
(Class II-III)
Migraine (Class II-III)
Cervical arteritis
(Class II-III)
No
Yes
Throbbing?
No
Yes
No
Yes
NSAIDs IM/PO (Class II)

Acetaminophen (Class
III)
Prochlorperazine IV
(Class III)
Opiates (Class III)
June 2001
19
Continued from page 13
results in some studies63%-78% pain relief. 147,148

However, the nasal spray is considered unpalatable by
many users.
Several new triptans are available in oral form. A
recent meta-analysis found rizatriptan (10 mg) to be
15%-20% more effective than oral sumatriptan (100 mg)
for the management of acute migraine.149
Triptans should be avoided in patients with
coronary artery disease or uncontrolled hypertension.
They are also contraindicated in cases of hemiplegic or
basilar migraines. Because of their vasoconstrictive
effect, they should not be administered in conjunction
with ergotamines. 150
132-134
mild attacks.
IM ketorolac (Toradol) is an effective
abortive agent, even in moderate to severe headaches.128,135,136 Studies show that ketorolac (60 mg IM) is
equivalent to meperidine, 135,136 but less effective than
prochlorperazine,112 for the treatment of migraines. In
other studies, ketorolac was no better than placebo.1
At least one study (in children) showed that
ibuprofen is more efficacious than acetaminophen in
relieving migraine pain.137
A randomized, double-blind, placebo-controlled
study concluded that acetaminophen is more effective
than placebo in reducing migraine headache. 138 (However, the migraineur who presents to the ED in distress
is unlikely to be swayed by such data.)
Other Interventions
IV Corticosteroids: Intravenous dexamethasone may be a
useful adjunct in patients treated for migraines in the ED.
In a prospective Canadian study, migraine patients
given 24 mg of IV dexamethasone in addition to
standard therapy had significantly fewer relapses. 151
Twenty-two percent of patients not given steroids
returned to the ED for rebound headache, compared
to none in the dexamethasone group.151 Two other
studies report that steroids are useful in the treatment
of status migrainosus.24,152
Oral Isometheptene: Two studies show that
isometheptene-containing compounds (Duradrin,
Midrin) are superior to placebo and have few side
effects.153,154 However, because of their oral route, slow
onset of action, and modest clinical efficacy, this class
of medication is typically reserved for mild-to-moderate headaches.
Lidocaine: Lidocaine has had limited success in
migraine therapy. One study showed that intranasal
lidocaine was superior to placebo, but the recurrence
rate of headache within one hour was high.155 Other
studies show that IV lidocaine is less effective than
either DHE or chlorpromazine 125 and merely equivalent
to placebo.28
Opiate Analgesics
Despite their well-documented limitations for this
indication, opiates continue to be overused in the
treatment of migraines.113 Patients may become habituated or even addicted from frequent use, and rebound
headaches are common.
Meperidine
While there are no prospective, double-blind, placebocontrolled studies on the effectiveness of meperidine
for the relief of migraine headache, comparison trials
show mixed results. In one study, meperidine 75 mg
IM was superior to 30 mg ketorolac IM.139 However,
another trial found meperidine and hydroxyzine to be
equivalent to IM DHE and hydroxyzine.140 When
combined with dimenhydrinate, prochlorperazine was
more efficacious than meperidine (91% vs 50%).141
Butorphanol Nasal Spray

Butorphanol nasal spray has frequent side effects and
limited efficacy in the treatment of migraine. Although
superior to placebo in a multicenter study,142 only 53%
of patients treated with butorphanol nasal spray were
pain-free at 48 hours. The majority of the participants
rated the drug as poor, likely because of unwanted
side effects. Other studies have shown higher efficacy
and fewer side effects. 143
Cluster Headache
Inhaled oxygen has been shown in double-blind
studies to be effective in the treatment of cluster
headaches. 156,157 It can be given via non-rebreathing
facemask with a flow rate of at least 6 L/min for 15
minutes or less.
Oral triptans such as zolmitriptan (5 mg or 10 mg)
effectively abort cluster headaches with few side
effects.158 While 6 mg of subcutaneous sumatriptan
successfully treats cluster headaches,157,159-163 62% of
patients complained of adverse events in one study.159
Triptans often cause abnormal feelings, such as
heaviness, tingling, burning, or other paresthesias.
Sumatriptan nasal spray appears less useful than
subcutaneous sumatriptan in cluster headache.
Several studies show that IV DHE is also effective
in the acute treatment of cluster headaches.29,164
If the patient is having numerous attacks, a variety
The TriptansSerotonin Agonists

Although most studies confirm good clinical efficacy of
these drugs, they are associated with a high incidence
of rebound headache. The 24-hour recurrence rate is as
high as 45%. 5
Subcutaneous sumatriptan (Imitrex; 6 mg SQ as
the initial dose) is perhaps the best studied of its class,
demonstrating therapeutic success rates of between
70% and 80%.144-146 When comparing IV DHE with IV
sumatriptan, the rates of relief at 3-4 hours were
statistically similar.131 Sumatriptan is therapeutically
equivalent to chlorpromazine,126 but it is less effective
than prochlorperazine. 111
Sumatriptan nasal spray has recently shown good
20
June 2001
tions in the literature vary, the most consistent recommendation for early therapy remains corticosteroids.
Most authorities suggest oral steroids, usually in
the range of 20-100 mg of prednisone per day.178 Some
postulate that parenteral steroids may be more efficacious than oral steroids, usually in the range of 125-250
mg of methylprednisolone IV. However, one prospective trial of 164 patients found no therapeutic advantage to IV methylprednisolone. 179
Because the results of a temporal biopsy are
unlikely to be available to the emergency physician,
initial treatment must be based on clinical suspicion
for example, in an older patient with a suggestive
history or physical exam and an elevated ESR.
of medications such as corticosteroids or verapamil

may decrease their frequency.165
Tension Headache
Although the scientific data are limited, NSAIDs
remain the most frequently used drugs in the treatment
of acute tension headache. In a multi-center, placebocontrolled, randomized trial, the authors found that
worthwhile effect or total relief was obtained in 36%
of those given placebo, 70% of those on ketoprofen,
and 61% of those given acetaminophen.166 Another
study found ibuprofen, naproxen, and ketoprofen more
efficacious than aspirin or acetaminophen.167
NSAIDs may be given by a variety of routes. For
patients who want an injection, one study showed that
ketorolac 60 mg IM was more effective than meperidine and promethazine.168 Even solubilized ibuprofen
was found to be useful in the acute treatment of
tension headaches 169 (although why one would nebulize ibuprofen remains a mystery).
The addition of caffeine may enhance the
therapeutic effect of NSAIDs. Ibuprofen plus
caffeine is more successful than either ibuprofen
or caffeine alone.170
NSAIDs may cause gastritis and renal insufficiency and should generally be avoided in pregnancy.
Some authors recommend muscle relaxants for the
treatment of tension headache,171,172 although no
randomized, double-blind studies address this issue.
Cerebral Venous Thrombosis:

Unique And Often Missed
Treatment modalities for CVT include anticoagulation,
thrombolytics, and careful observation. Antibiotics
may be given if an infectious triggering event is
suspected. Although anticoagulation may prevent
further thrombus formation, it could theoretically
cause further intracerebral hemorrhage, leading some
to advocate heparin only when patients deteriorate
despite symptomatic treatment.37 However, several
trials support the safety and efficacy of IV heparin,
even in patients with preexisting hemorrhage.180-183 The
use of low molecular weight heparin results in a
slightly more favorable outcome than unfractionated
heparin. 184 IV thrombolytic therapy has been efficacious in several studies,185-187 but its use is best left to
the consultant.
Subarachnoid Hemorrhage
Although definitive treatment continues to be surgical,
multiple adjunctive modalities for SAH have been
described, including calcium-channel blockers, hyperdynamic therapy, hyperventilation, anti-epileptics, and
mannitol. The calcium-channel blocker nimodipine can
prevent delayed vasospasm. Several prospective,
controlled studies document its utility.173-176 Consider
giving nimodipine (60 mg PO) in the ED once the
diagnosis of SAH has been established (most studies
support its use in Hunt/Hess grades I-III only).
Hyperdynamic therapy involves maintaining the
mean arterial pressure and cerebral perfusion pressure
above a certain limit. This is usually achieved through
a triple-H treatmenthypertension, hypervolemia,
and hemodilution. However, no prospective, randomized, controlled trials show any improvement in the
long- or short-term neurologic outcome using this
approach. 177 Although several anecdotal series claim
efficacy for the triple-H treatment, no strict guidelines, blood-pressure parameters, or consensus exist. 90
Similarly, no good data refute or support the
empiric use of hyperventilation, anti-epileptics, or
mannitol in SAH.
Special Circumstances
Pediatric Patients
The assessment and stabilization of children with
headaches is generally the same as for adults.
Pediatric headache is often the result of systemic
infections or dehydration. While headache can be an
expression of psychosocial stress, consider organic
etiologies first.
One large study regarding children who came to
the ED with headache revealed that most children had
a viral illness (39.2%). Other frequent diagnoses
included sinusitis (16.0%), migraine (15.6%), posttraumatic headache (6.6%), streptococcal pharyngitis
(4.9%), and tension headache (4.5%). No cases of brain
tumor or bacterial meningitis were identified during
the ED visit. Serious neurologic conditions were rare
and included 15 cases of viral meningitis (5.2%), one
shunt malfunction, one newly diagnosed hydrocephalus, one Burkitts lymphoma, and one post-traumatic
punctate hemorrhage.188
Another prospective ED study of children with
headaches confirmed that upper respiratory infection
was the most common cause of acute cephalgia. In this
study, objective neurologic signs, including papille-
Temporal Arteritis
Visual loss is one of the most feared complications of
temporal arteritis. Although treatment recommenda-
June 2001
21
dema, ataxia, and hemiparesis (with or without

abnormal eye movements), occurred in all of the
children with significant underlying conditions.67
Determine whether the child has a
ventriculoperitoneal (VP) shunt. The presence of a
shunt in a child with headache should prompt
neuroimaging to detect shunt malfunction.189
Carefully assess the child who presents with an
apparent migraine for vascular and infectious etiologies. If the child has a history of similar events,
especially in conjunction with a classic prodrome, then
an emergent CT is not indicated, assuming the child
has a normal neurologic exam.
Several variants of childhood migraine warrant
discussion. There is a correlation between motion
sickness and migraine, though whether motion
sickness itself is a migraine variant remains undetermined. Cyclic vomiting may be associated with
migraine events, as is cyclic abdominal pain.
In the periodic syndrome of Wyllie and Schlesinger,
the child has recurrent headaches in association with
dizziness, vomiting, abdominal pain, or fever. Such
obscure diagnoses, however, are in the purview of
the consultant.
Familial hemiplegic migraine presents in a
dramatic fashion. The child develops progressive
unilateral sensory or motor symptoms, often associated
with dysarthria, aphasia, or altered mental status.
When receptive aphasias are present, the child can
appear confused or even psychotic. The headache is
usually contralateral to the neurologic deficit. These
events can last up to a week. 190 The diagnosis of
familial hemiplegic migraine should be made only
after neuroimaging and consultation; any child with
such an exam must be presumed to have a mass lesion
until proven otherwise.
While CNS tumors in children are rare, certain
clinical findings may be useful guides for
neuroimaging. In one review from a tertiary medical
center that focused on children referred for MRI, the
authors identified several independent predictors of a
surgical space-occupying lesion. These included a
headache that woke the child from sleep or was
present on waking (odds ratio [OR], 25.8); no family
history of migraine (OR, 20.3); associated vomiting
(OR, 19.5); lack of visual symptoms (OR, 16.4); headache duration of less than six months (OR, 15.2);
confusion (OR, 12.4); and abnormal neurologic exam
(OR, 8.0). All children with surgical lesions had at least
three or more of these findings.191
DHE is age-dependent.
Idiopathic Intracranial Hypertension

Patients presenting with symptoms of headache, visual
disturbances, vomiting, and papilledema may have
idiopathic ICH (pseudotumor cerebri). The diagnosis is
confirmed after a normal neuroimaging study and by
an LP that shows high CSF pressure but an otherwise
normal analysis. Initial treatment is limited to a
therapeutic LP that relieves the intracranial pressure;
the neurologist will determine later care.
While most cases are idiopathic, associated causes
may include the mundane, such as the extravagant use
of penicillin, or the exotic, such as ingestion of polar
bear liver. (So if you happen see a blind, vomiting,
Arctic explorer who complains of a headache in your
ED, youll know what to do.)
Post-LP Headache
Headache after LP is common, and there are several
effective treatments. Symptomatic relief is often
obtained with hydration, keeping the patient flat, and
using NSAIDs or opioid analgesics. Caffeine (either
oral or intravenous) is useful. Administer 500 mg of
caffeine sodium benzoate in one liter normal saline
over one hour.193 If these measures fail, consider an
epidural blood patch.194
Chronic Headache
The most important issue facing the emergency
physician when dealing with a patient who has chronic
headaches is the question Is this the same chronic
pain, or is it something new? (That is, could this
episode be due to SAH or meningitis?) If the patients
headache truly is chronic, consider the possibility of
analgesic overuse or medication rebound. One study
reported that 72% of 300 patients with chronic headache suffered from analgesic rebound.195 In such cases,
the primary care provider can help coordinate a
detoxification program.
History Of HIV Infection

A patient history of HIV poses additional complications in the evaluation of headache. Those with
advanced disease may have space-occupying lesions or
meningitis (due to either traditional or opportunistic
organisms). In this situation, the neurological examination is less likely to identify intracranial pathology
than it is in immunocompetent patients.
In one retrospective study that looked at 169
cranial CTs performed on HIV patients, the majority of
patients who had lesions on CT had a normal neurological examination.78 Other trials show that 24%-35%
of all HIV-infected patients who present to the ED with
a headache may harbor a mass lesion.196,197
Clinical factors that predict a positive CT include
a new seizure, focal motor deficit, depressed or
altered mental status, or headache that is different in
Management Of Pediatric Headache

Many of the treatments used in adults have
been employed in children as well. Sumatriptan
and DHE, however, have not been tested extensively
in children younger than 12. In one study, adolescents
12-18 were treated with a 90% success rate with IV
DHE and metoclopramide.192 Note that dosing for
22
June 2001
However, there are few to no data to support this

contention (although it is certainly possible that
getting a headache may cause a rise in blood pressure
as opposed to the other way around). A recent study
used ambulatory blood pressure monitoring in adults
and correlated the pressure with symptoms. There was
no relationship between elevations in blood pressure
(up to 180/110 mmHg) and the occurrence of headache
in patients with mild-to-moderate hypertension.204
This study does not obviate the fact that hypertensive emergencies exist. Headache, encephalopathy, and
visual symptoms can occur with very elevated pressures, usually in those with a diastolic pressure greater
than 140 mmHg. In a patient with a headache and
extremely high blood pressure, it is crucial to look for
the sine qua non of a hypertensive emergency: papilledema or encephalopathy or confusion.
Because a severe headache may also cause mild-tomoderate increases in blood pressure, adequate pain
control in a dark, quiet room may be all that is needed
to control the headache and hypertension simultaneously. In one study, 27% of patients with an initial
diastolic blood pressure greater than 130 mmHg fell
below critical levels after relaxation and no specific
pharmacological intervention.205
character than usual or that has lasted for more than

three days. 197-199
If the CT scan is normal, further evaluation
entails an LP even in the absence of meningeal signs.
The immunosuppressive effects of the disease may
prevent the development of classical meningeal signs
despite a CNS infection.200 As the India ink test is
positive in only half of cryptococcal meningitis cases,201
order a cryptococcal antigen test as well. When
performing the LP, measure the CSF pressure, as
an elevated pressure may be both the only early
clue and a prognostic indicator in cases of
cryptococcal meningitis.202
If available, the patients CD4 count may help
estimate the probability of opportunistic disease. If the
CD4 count is greater than 200, leukodystrophy,
toxoplasmosis, and cryptococcal meningitis become
unlikely diagnoses.203
Headache And Hypertension

A headache in a patient with a significantly elevated
blood pressure does not automatically equal a hypertensive crisis. Many patients (and occasionally their ED
physicians) maintain the unshakable belief that their
headaches are due to elevations in blood pressure.
Tool 1. Sample Discharge Instructions For The Patient With Headache.

Preventive measures
Try to reduce stress
Drink at least one gallon of water per day
Activity
Exercise regularly
Rest in a dark, quiet room while you have a headache
Do not drive, swim, or operate heavy machinery during the headache
Keep a record of what triggers the headache
Diet
Do not skip meals
Avoid alcohol and tobacco
Avoid triggers of the headache (for example, red wine, foods that may contain nitrites,
and certain cheeses)
Keep a record of food eaten prior to the onset of the headache
Medications
Take all medications as prescribed
Return to the emergency department if you have:
A headache that persists, becomes worse, or if you have any change in vision
Numbness or weakness of your arms or legs
Neck stiffness, sensitivity to light, or any fever greater than 100.3F
Drowsiness, lethargy, abdominal pain, or continued nausea and vomiting
June 2001
23
Headache And Stroke
Patient With Headache on page 23.)

Although admission criteria vary with the specific
diagnosis, intractable pain, suicidal ideation, persistent
vomiting, electrolyte imbalance, and inability to take
oral hydration are all valid reasons to admit. 218,219
Patients with bacterial meningitis, SAH, hypertensive
emergencies, or dangerous carbon monoxide levels
require additional treatment and admission.
In one study of more than 3000 patients with TIA or

ischemic stroke, headache occurred in nearly 20%.206
Headache was most frequent in those whose infarcts
were in the cortex or posterior circulation. Patients
with hemorrhagic stroke are even more likely to
suffer cephalagia.207,208 While stroke patients may
complain of headache, they will also present with focal
neurologic findings.
Summary
Headache And Associated Pain Syndromes
While the vast majority of patients with headache have

benign conditions, hidden among the multitudes are
those with a potentially fatal disease. While these
pathologies may be easily detected with neuroimaging
or LP, the challenge is knowing when to order these
tests. The answer lies in a focused clinical examinationasking the right questions and performing the
correct physical maneuvers. Ask how quickly the
headache came on and whether it is different from any
headache the patient has had before. Look for fever,
pay close attention to the eye and neuro exam, flex the
neck, and use the jolt test. Once serious etiologies are
ruled out, the rest of headache management is easy.
Temporomandibular joint (TMJ) pain may be referred

to the head and can lead to agonizing headaches. The
treatment is generally supportive, with massage, moist
heat, NSAIDs, and muscle relaxants.
Trigeminal neuralgia also causes debilitating
cephalgia. As many as 25%-50% of patients eventually
stop responding to drug therapy, typically
carbamazepine (Tegretol), and require some form of
alternative treatment. 209 Such patients may need
referral to a neurosurgeon, particularly if they develop
trigeminal neuralgia prior to the age of 60 or have
failed aggressive medical therapy.
Patients with occipital neuralgia may be treated in
the ED. A lidocaine or bupivacaine injection at the
trigger point can be both diagnostic and therapeutic (at
least temporarily). 210,211
References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a
case report.
To help the reader judge the strength of each
reference, pertinent information about the study, such
as the type of study and the number of patients in the
study, will be included in bold type following the
reference, where available. In addition, the most
informative references cited in the paper, as determined by the authors, will be noted by an asterisk (*)
next to the number of the reference.
Controversies/Cutting Edge
The emergency management of headaches remains in
flux. New drugs come to the market, and old drugs are
used in novel ways. Several studies show that oral
valproic acid is effective in the treatment of chronic
headaches, 212,213 including those with post-traumatic
headaches. 214 More recently, IV valproate relieved acute
migraine in 73% of 61 patients studied.215 More radical
steps in the treatment of migraine headache, such as
surgery on the frontalis muscle, have been proposed.216
Other areas of research include the designer
triptans, biofeedback, and holistic/alternative approaches. A meta-analysis of 22 trials suggests that
acupuncture has a role in the treatment of recurrent
headaches. The authors concluded, however, that the
quality of the evidence is not fully convincing. 217
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Most patients who present to the ED with headache will

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27
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88. Which of the following items obtained in the

history of the headache patient should be
considered most important?
a. Nausea and vomiting
b. Thunderclap headache, worst headache, or
change in the usual pattern of headache
c. First onset of headache before 40 years of age
d. Flashing lights prior to the onset of
the headache
Physician CME Questions

81. Which of the following courses of action is
appropriate in individuals with a negative CT
and thunderclap headache?
a. No further workup; discharge home and
recheck in 24 hours
b. Lumbar puncture
c. CBC, ESR; discharge home if results of both
are normal
d. Intravenous compazine; no further workup if
headache resolves
89. The major complication of temporal arteritis is:

a. unilateral blindness.
b. acute hemiplegia.
c. acute cranial nerve VI palsy.
d. subarachnoid hemorrhage.
90. Which of the following statements regarding
SAH is true?
a. The sensitivity of CT is about 98%
at 24 hours.
b. Lumbar puncture is always the initial
choice for detecting the bleed.
c. ECG changes may resemble those produced
by cardiac ischemia.
d. The physician must always do a CT prior to
performing the LP.
82. The chances that a headache will return within 24

hours after a single injection of sumatriptan is:
a. almost 0%.
b. less than 10%.
c. about 30%-40%.
d. greater than 75%.
83. Which agent should not be considered as a firstline agent in the treatment of acute cephalgia?
a. Prochlorperazine 10 mg IV
b. DHE 1 mg SC
c. Ibuprofen 800 mg PO
d. Meperidine 50 mg IV
91. The least common cause of headache presenting

to the ED is:
a. brain tumor.
b. subarachnoid hemorrhage.
c. migraine headache.
d. sinusitis.
84. The most common intracranial hemorrhage

associated with closed-head injury is:
a. subarachnoid.
b. epidural.
c. subdural.
d. cerebellar.
92. The emergency workup for the immunosuppressed patient presenting with a severe headache is identical to the workup for the immunocompetent patient.
a. True
b. False
85. The percentage of SAH secondary to rupture of

berry aneurism that will be missed on initial CT
scan is about:
a. 1%-2%.
b. 5%-15%.
c. 15%-25%.
d. 25%-35%.
93. The assessment and stabilization of children

with headaches is the same as that for the adult.
a. True
b. False
94. The triptans are commonly associated with:
a. rebound headache.
b. fever and chills.
c. numbness and weakness.
d. shortness of breath.
86. Meperidine has consistently been shown to be a

more effective pain reliever in migraine headaches than chlorpromazine.
a. True
b. False
95. Papilledema is most consistent with which

clinical finding?
a. Mass lesions, optic neuritis, or pseudotumor
b. Carbon monoxide poisoning
c. Subarachnoid hemorrhage
d. CNS infection
87. Most patients who present to the ED will have a

headache that is benign in etiology.
a. True
b. False
June 2001
31
Physician CME Information
96. The most effective acute therapy for a 30-year-old

white male with severe, stabbing unilateral
headache that wakes him up from sleep and is
associated with flushing, rhinorrhea, and lacrimation on the affected side is:
a. beta-blockers.
b. calcium-channel blockers.
c. 100% oxygen.
d. metoclopramide IV.
This CME enduring material is sponsored by Mount Sinai School of

Medicine and has been planned and implemented in accordance with
the Essentials and Standards of the Accreditation Council for Continuing
Medical Education. Credit may be obtained by reading each issue and
completing the post-tests administered in December and June.
Target Audienc e: This enduring material is designed for emergency
medicine physicians.
Needs A ssessmen t: The need for this educational activity was
determined by a survey of medical staff, including the editorial board
of this publication; review of morbidity and mortality data from the
CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for
emergency physicians.
Date of O riginal R elease: This issue of Emergency Medicine
Practice was published June 7, 2001. This activity is eligible for
CME credit through June 7, 2004. The latest review of this material
was June 5, 2001.
Discussion of I nvestiga tional I nformation: As part of the
newsletter, faculty may be presenting investigational information
about pharmaceutical products that is outside Food and Drug
Administration approved labeling. Information presented as part of
this activity is intended solely as continuing medical education and is
not intended to promote off-label use of any pharmaceutical product.
Disclosure of Off-Label Usage: Many standard treatments for migraine
headaches discussed in this issue of Emergency Medicine Practice are
considered off-label. These include the antiemetics and neuroleptic
medications, among others.
This test concludes the January through June semester

testing period of Emergency Medicine Practice. The
answer form for this semester and a postage-paid return
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customer number printed on the outer envelope to submit
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the answer form.
Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency
Medicine Practice receives an alpha-numerical score based on
the following definitions.
Class I
Always acceptable, safe
Definitely useful
Proven in both efficacy and
effectiveness
Level of Evidence:
One or more large prospective
studies are present (with
rare exceptions)
High-quality meta-analyses
Study results consistently
positive and compelling
Class II
Safe, acceptable
Probably useful
Level of Evidence:
Generally higher levels
of evidence
Non-randomized or retrospective studies: historic, cohort, or
case-control studies
Less robust RCTs
Results consistently positive
Class III
May be acceptable
Possibly useful
Considered optional or
alternative treatments
Level of Evidence:
Generally lower or intermediate levels of evidence
Facult y Disclosur e: In compliance with all ACCME Essentials, Standards,

and Guidelines, all faculty for this CME activity were asked to complete
a full disclosure statement. The information received is as follows: Dr.
Godwin, Dr. Villa, Dr. Lukens, and Dr. Burke report no significant
financial interest or other relationship with the manufacturer(s) of any
commercial product(s) discussed in this educational presentation.
Accreditation: Mount Sinai School of Medicine is accredited by the
Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credit D esigna tion: Mount Sinai School of Medicine designates this
educational activity for up to 4 hours of Category 1 credit toward the
AMA Physicians Recognition Award. Each physician should claim only
those hours of credit actually spent in the educational activity.
Emergency Medicine Practice is approved by the American College of
Emergency Physicians for 48 hours of ACEP Category 1 credit (per
annual subscription).
Earning C redit: Physicians with current and valid licenses in the United
States, who read all CME articles during each Emergency Medicine
Practice six-month testing period, complete the CME Evaluation Form
distributed with the December and June issues, and return it
according to the published instructions are eligible for up to 4 hours
of Category 1 credit toward the AMA Physicians Recognition Award
(PRA) for each issue. You must complete both the post-test and CME
Evaluation Form to receive credit. Results will be kept confidential.
CME certificates will be mailed to each participant scoring higher than
70% at the end of the calendar year.
Case series, animal studies,

consensus panels
Occasionally positive results
Indeterminate
Continuing area of research
No recommendations until
further research
Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent,
contradictory
Results not compelling
Significantly modified from: The

Emergency Cardiovascular Care
Committees of the American Heart
Association and representatives
from the resuscitation councils of
ILCOR: How to Develop EvidenceBased Guidelines for Emergency
Cardiac Care: Quality of Evidence
and Classes of Recommendations;
also: Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring
effectiveness of community-wide
emergency cardiac care. JAMA
1992;268(16):2289-2295.
Publisher : Robert Williford. Vice Presiden t/General Manager : Connie Austin.

Executiv e Editor: Heidi Frost.
Direct all editorial or subscription-related questions to Pinnacle

Publishing, Inc.: 1-800-788-1900 or 770-992-9401
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Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year)
by Pinnacle Publishing, Inc., 1000 Holcomb Woods Parkway, Building 200, Suite 280,
Roswell, GA 30076-2587. Opinions expressed are not necessarily those of this
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32
June 2001

Acute Headache in The ED Evidence-Based Evaluation and Treatment Options

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Acute Headache in The ED Evidence-Based Evaluation and Treatment Options

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EMERGENCY MEDICINE PRACTICE

Acute Headache In The ED:

HE majority of patients who come to the ED with a headache do not

Clinical Practice Guidelines And Systematic Reviews

Medicine, The University of

Center, Atlantic Health System;

Upon completing this article, you should be able to:

Date of original release: June 7, 2001.

School of Medicine; Attending

University of Florida; Orlando

pathology. In one series, only 3.8% of patients who

should be used to make decisions. Due to the lack of

Table 1. Major Categories Of Headache Disorders.

Emergency Medicine Practice

The headache in migraine without an aura is

underlying etiology. A variety of mechanisms may be

Atypical migraines may present with a variety of

Table 2. Aura Symptoms Frequently Associated

Scotoma (blind spots)

Emergency Medicine Practice

key in classifying this form of headache.24,28

Meningitis is another life-threatening cause of

Table 3. Hunt And Hess Classification Of

Emergency Medicine Practice

A basic unit can transport patients with stable vital

When confronted by the headache patient, the wary

Table 4. Pearls In The Clinical Evaluation Of The

SAH, cerebral venous

Use of space heater

Time To Maximal Onset

Eclampsia, cerebral venous

Some data suggest that the suddenness of a headache

Glaucoma, optic neuritis

Pain with eye movement

Infection (CNS vs systemic)

Intracranial mass, idiopathic

Carotid artery dissection

Mass lesion, optic neuritis,

Age greater than 50 years

Temporal arteritis, mass

Table 5. Danger Signals In Headache.

Emergency Medicine Practice

associated with SAH. 50 As many as half of all patients

is an even more important factor than severity. The

Additional Aspects Of The History Of Present Illness

Past Medical History

Headache Quality And Location

History Of Intracranial Pathology Or Malignancy

Emergency Medicine Practice

such as alcoholism and transplants, raise additional

can occur in a variety of infections, ranging from the

Head And Scalp

Emergency Medicine Practice

or her neck. Kernigs sign is produced by flexing one

retina) just where it emerges from the disc. One study

Lord, how my head aches! What a head have I!

Perhaps the most important aspect of the neck exam is

Blood tests rarely reveal the cause of a headache.

Physical Examination Maneuvers

Emergency Medicine Practice

New-onset headache in patients older than

emergency physician, the most valuable is