Acute Headache in the ED Evidence-Based Evaluation and Treatment Options (2)

8/17/2019 Acute Headache in the ED Evidence-Based Evaluation and Treatment Options (2)

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June 2001Volume 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.

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

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 im-

munocompetent and immunosuppressed patients;

5. describe treatment options, including identifying

the medications considered to be first-line

agents; and6. list specific circumstances in the evaluation

of the headache that should be treated with

special considerations.

Dat e of origin al release: Jun e 7, 2001.

Dat e of m ost recent review: Jun e 5, 2001.

See “Physician CME Inform atio n” on b ack pa ge.

EMERGENCY MEDICINE PRACTICEAN EVIDENCE-BASED A PPROACH T O EMERGENCY MEDI CINE

Editor-in-Chief

Stephen A. Colucciello, MD, FACEP,Assistant Chair, Director of Clinical Services, Department of Emergency Medicine, CarolinasMedical Center, Charlotte, NC;

Associate Clinical Professor,Department of EmergencyMedicine, University of NorthCarolina at Chapel Hill, ChapelHill, NC.

Associate Editor

Andy Jagoda, MD, FACEP, Professorof Emergency Medicine; Director,International Studies Program,Mount Sinai School of Medicine,New York, NY.

Editorial Board

Judith C. Brillman, MD,ResidencyDirector, Associate Professor,Department of Emergency

Medicine, The University of New Mexico Health SciencesCenter School of Medicine,Albuquerque, NM.

W. Richard Bukata, MD,AssistantClinical Professor, EmergencyMedicine, Los Angeles County/

USC Medical Center, Los Angeles,CA; Medical Director, EmergencyDepartment, San Gabriel ValleyMedical Center, San Gabriel, CA.

Francis M. Fesmire, MD, FACEP,Director, Chest Pain—StrokeCenter, Erlanger Medical Center;Assistant Professor of Medicine,UT College of Medicine,Chattanooga, TN.

Valerio Gai, MD,Professor and Chair,Department of EmergencyMedicine, University of Turin, Italy.

Michael J . Gerardi, MD, FACEP,Clinical Assistant Professor,Medicine, University of Medicineand Dentistry of New Jersey;Director, Pediatric EmergencyMedicine, Children’s Medical

Center, Atlantic Health System;Vice-Chairman, Department of Emergency Medicine, MorristownMemorial Hospital.

Michael A. Gibbs, MD, FACEP,Residency Program Director;Medical Director, MedCenter Air,

Department of EmergencyMedicine, Carolinas MedicalCenter; Associate Professor of Emergency Medicine, Universityof North Carolina at Chapel Hill,Chapel Hill, NC.

Gregory L. Henry, MD, FACEP,CEO, Medical Practice RiskAssessment, Inc., Ann Arbor,MI; Clinical Professor, Departmentof Emergency Medicine, Universityof Michigan Medical School, AnnArbor, MI;President, AmericanPhysicians Assurance Society, Ltd.,Bridgetown, Barbados, West Indies;Past President, ACEP.

Jerome R. Hoffman, MA, MD, FACEP,Professor of Medicine/Emergency Medicine, UCLA

School of Medicine; AttendingPhysician, UCLA EmergencyMedicine Center; Co-Director, The Doctoring Program,UCLA School of Medicine,Los Angeles, CA.

John A. Marx, MD,Chair and Chief,

Department of EmergencyMedicine, Carolinas MedicalCenter, Charlotte, NC; ClinicalProfessor, Department of Emergency Medicine, Universityof North Carolina at Chapel Hill,Chapel Hill, NC.

Michael S. Radeos, MD, MPH, FACEP,Attending Physician inEmergency Medicine, LincolnHospital, Bronx, NY; ResearchFellow in Emergency Medicine,Massachusetts General Hospital,Boston, MA; Research Fellow inRespiratory Epidemiology,Channing Lab, Boston, MA.

Steven G. Rothrock, MD, FACEP,FAAP, Associate Professorof Emergency Medicine,

University of Florida; OrlandoRegional Medical Center; MedicalDirector of Orange CountyEmergency Medical Service,Orlando, FL.

Alfred Sacchetti , MD, FACEP,Research Director, Our Lady of

Lourdes Medical Center, Camden,NJ; Assistant Clinical Professorof Emergency Medicine, Thomas Jefferson University,Philadelphia, PA.

Corey M. Slovis, MD, FACP, FACEP,Department of EmergencyMedicine, Vanderbilt UniversityHospital, Nashville, TN.

Mark Smith, MD,Chairman,Department of EmergencyMedicine, Washington HospitalCenter, Washington, DC.

Thomas E. Terndrup, MD, Professorand Chair, Department of Emergency Medicine, Universityof Alabama at Birmingham,Birmingham, AL.

Acute Headache In The ED:

Evidence-Based EvaluationAnd Treatment OptionsIt’s 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. It’s decision time—

CT? LP? Some IM pain meds and discharge? Or should I turn her over to the

next doc coming on?

“When your head did but ache, I knit a handkercher about my brows.”

—William Shakespeare (1554-1616), King John, IV, I, 41

THE majority of patients who come to the ED with a headache do nothave a life-threatening problem. The challenge is to identify thesmall but significant percent that do. The differential diagnosis of

headache is huge—by the time some work-ups are complete, the emer-

gency 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 managementof 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


2/32Emergency Medicine Practice 2 June 2001

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

prospective, randomized trials regarding the clinical

evaluation of patients, there are no consistent stan-

dards for assessing the headache patient.

Discrepancies in study methodology are a recur-

ring 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 andpromethazine, in particular).

Additional confusion arises due to the phenom-

enon of spectrum bias. This “glitch” in the evidence-

based 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 andthe American College of Emergency Physicians.6

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 categoriz-

ing 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 forthe majority of all cases. Secondary headaches are far

less common and include headaches associated with

diverse underlying pathology such as tumor, aneu-

rysm, meningitis, or giant cell arteritis.8,13

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 Fortu-

nately, few of these patients will have life-threatening

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 head-

aches 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

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, coldstimulus, benign cough, benign exertional, associatedwith sexual activity)

Secondary causes

• Head trauma• Vascular disorders (CVA, intracranial hematoma, SAH,

unruptured vascular malformation, arteritis, venous

thrombosis, arterial hypertension)• Nonvascular intracranial disorder (high or low cerebrospi-

nal 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 orcranial structures)

• Neuralgias (persistent pain of cranial nerve origin, nervusintermedius neuralgia, superior laryngeal neuralgia,occipital neuralgia)


3/323 Emergency Medicine Practice June 2001

underlying etiology. A variety of mechanisms may be

responsible, including:10

• distention or traction of intra- or extra-

cranial 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 inflamma-

tory 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 manage-

ment.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

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

Migraine HeadachesMigraines 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 orpounding. 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, con-

sider 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)

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, drowsi-

ness, 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 patient’s 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.

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 distur-

bances (usually a lateral field deficit).

• Hemiplegic migraines: accompanied by

unilateral weakness.

Tension HeadachesTension 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

Table 2. Aura Symptoms Frequently AssociatedWith 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

Cluster HeadachesOver 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 HeadachesHeadache 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, neckstiffness, 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.

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 distur-

bances, 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 animportant cause of headache that is more common

than once thought.37 CVT may present with a sudden-

onset 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 usuallypresent 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 character-

ized 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 onsetof head and neck pain.42

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

Table 3. Hunt And Hess Classification Of Subarachnoid Hemorrhage.

• Grade 1: Asymptomatic, or minimal headache; slightnuchal 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.

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.



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 ad-

vanced 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 perfu-

sion. 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 Association’s Stroke Council

has published consensus-based guidelines for bloodpressure 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.

ED Evaluation

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 theED 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.)

HistoryThough the presentations of ominous headaches vary,

most authors agree that the most important factors

include severity, onset and quality of pain, and associ-

ated symptoms.2,45 (See Table 5.)

Worst Heada che In clinical practice, the chief complaint of the worst

headache of one’s 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 orsevere, 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.)

Time To Ma xima l Onset Some data suggest that the suddenness of a headache

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

Table 4. Pearls In The Clinical Evaluation Of ThePatient With Headache.

Finding Consideration

Thunderclap headache Subarachnoid hemorrhage

Worst headache SAH, cerebral venous

thrombosis

Use of space heater Carbon monoxide

Pregnancy Eclampsia, cerebral venousthrombosis

Change in vision Glaucoma, optic neuritis

Pain with eye movement Optic neuritis

Fever Infection (CNS vs systemic)

Double vision Intracranial mass, idiopathicintracranial 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



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

Conflicting Da ta Other studies suggest little correlation between worstor sudden headache and final diagnosis.15,51,52 However,

each of these studies suffers from a variety of method-

ological flaws.

Although neither sensitive nor specific, there is

some evidence that the “worst headache” and espe-

cially “sudden-onset” headache are important histori-

cal findings. When present, the physician should

consider further diagnostic evaluation.

Heada che Qua lity And Location Headache quality and location are at times helpful, but

rarely diagnostic. Throbbing quality suggests vascularetiologies 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 occipito-

nuchal region has been associated with increased

intracranial pathology—especially 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. Glossopharyn-

geal neuralgia is characterized by pain in the pharynx,

tonsils, and ear and is usually precipitated by swallow-

ing, yawning, or eating.

Associated Sympt oms Determine whether the patient has other symptoms.

Neurologic complaints are especially important. Visual

field deficits, double vision, or seizures may be

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 vomit-

ing is often seen with an intracranial bleed. Jaw

claudication and pain in the shoulder muscles are

associated with temporal arteritis.

Additional Aspects Of The H istory Of Present Illness Additional components of the history focus on exacer-

bating 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 patientsover 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 tempo-

ral arteritis.54

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 foundthat 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.

History Of Intracranial Pathology Or M alignancy Patients with history of previous neurosurgery—

including shunt, arteriovenous malformation or

aneurysm, and non-CNS malignancy—are at increased

risk for serious underlying pathology with the com-

plaint of headache.6,56

Likewise, a history of malignancy should raiseconcern 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

Immunocompromise HIV infection and other immunocompromised states,



such as alcoholism and transplants, raise additional

concerns. Such patients may suffer from lesions such as

toxoplasmosis or progressive multifocal leukoencepha-

lopathy as well as being more susceptible to a variety

of meningeal infections.

Trauma A history of trauma introduces the possibility of

chronic subdural hematoma or post-traumatic head-

ache 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 patient’s home is heated. Head-

ache and dizziness are the two most common com-

plaints in occult carbon monoxide poisoning and areseen in 90% and 82% of patients, respectively. 59 Expo-

sure 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

M edicat ion 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 Starbuck’s tattoo or finding a photo

of Juan Valdez in the patient’s wallet.)

Miscellaneous SAH may be associated with polycystic kidney disease,

fibromuscular dysplasia, or a family history of SAH.2

Physical ExamThe physical examination provides important clues to

the underlying pathology. The “first impression” of the

patient may demonstrate toxicity or signs of physi-

ologic stress, such as diaphoresis.

Vita l 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,

can occur in a variety of infections, ranging from the

benign to the lethal. I t can also occur with SAH.2

Hea d 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 (Tinel’s sign). Those with temporal arteritis

may demonstrate induration or tenderness of the

temporal artery. Other patients with headache may show

signs of trauma, including Battle’s sign.

Eyes

While the eyes may or may not be the windowto 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 patient’s lids. Ptosis may occur with

cluster headaches as well as with more serious pathol-

ogy such as Horner’s syndrome (droopy lid, small

pupil, and an absence of facial sweating on the in-

volved side). The presence of Horner ’s syndrome in

conjunction with a headache may represent a carotid

dissection.65 Periorbital ecchymosis (raccoon’s eyes)

suggests basilar skull fracture.

Test the patient’s visual fields by confrontation; afield 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 nerve—often 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. Adilated, 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



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 headpain. However, of all physical findings, studies show

that purulent nasal secretion and abnormal sinus

transillumination are the best clinical predictors

of sinusitis.68

Neck 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.

Neurologic Exam

The neurologic exam has special significance in thepatient with headache, because a new neurologic

deficit mandates imaging and/or LP.

One of the first assessments should be the patient’s

mental status. What is the patient ’s 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 meningococce-

mia, vasculitis, or Rocky Mountain spotted fever. The

presence of skin tracks should raise concern for HIV.

Physical Examination ManeuversThe most familiar maneuvers in the evaluation of

headache involve testing for Brudzinski’s and Kernig’s

signs. Brudzinski’s sign is positive when the supine

patient bends both knees in response to flexion of his

or her neck. Kernig’s 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 Brudzinski’s and

Kernig’s 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 study’s 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 aheadache with the Valsalva maneuver increases the

likelihood of a positive finding on cranial CT. 72

Diagnostic Testing

“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

Blood tests rarely reveal the cause of a headache.

In older patients with any combination of jaw

claudication, proximal muscle pain, visualcomplaints, 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 menin-

gitis; 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 hypoglycemiain 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



emergency physician, the most valuable is

analysis of the CSF. In patients suspected of

meningitis, a cell count, Gram’s stain, protein,

and glucose evaluation of the spinal fluid are

essential for diagnosis. The typical pattern in

bacterial meningit is may show a positive Gram’s

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 cmH2O

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.

The Role Of NeuroimagingThe non-contrast CT scan is the most widely available

and useful neuroimaging test available to the emer-

gency 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 physi-

cians. In addition, CT is generally able to demonstrateany 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 Neuroima ging? 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 variouscriteria guide the need for urgent neuroimaging and/

or LP.78-80 However, no large , prospective tr ials 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

• 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

With the possible exception of detecting SAH,

neuroimaging in patients who have a normal neuro-

logic 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 emergentneuroimaging. 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 evalua-

tion 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 presentwith 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.

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 classi-

fied as either a rule or guideline. The authors recom-mended CT as a “rule” for patients with severe,

sudden-onset headache, suspected intracranial infec-

tion, 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 patient’s 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.)



CT And SAH The accuracy of a CT scan in SAH depends on a

number of factors—not 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

Do es A Pat ient Suspected Of SAH N eed An LP After A Nega tive CT? 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 litera-

ture 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 subse-

quent LP.86 The counter-argument is that it is the well-appearing patient with a negative scan who needs the

subsequent LP.2 They argue that because of spectrum

bias, patients with minor symptoms are l ikely to have

less blood on CT and therefore are more likely to be

missed on neuroimaging.

What is the correct answer? Clearly, numerous

small series and case reports document the phenom-

enon 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 patient’s sensorium was clear

when he or she signs out against medical advice.

Can LP Be Used Before Or In stea d Of CT To Eva lua te SAH? 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.

LP And Spinal Fluid Evalua tion: Wha t Do You Do W ith 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 contami-

nates 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 compared to tube #1, while RBCs may

remain constant in face of a traumatic bleed.81,89 Theclinical 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 xantho-

chromia as determined by spectrophotometry (and not

by visual examination) is the pr imary criterion for

diagnosis of SAH.2,90 Xanthochromia suggests that

blood has been present in the spinal fluid for at least 1-2 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 ForNeuroimaging In Patients With Non-acute Headache.

• Neuroimaging should be considered in patients withnon-acute headache and an unexplained abnormality onneurologic examination.

• There is insufficient evidence to make neuroimagingrecommendations based on the presence or absence of

neurological symptoms (note that this guideline ad-dresses chronic headache, not acute).

• Neuroimaging is usually not warranted in patients

presenting with a typical migraine headache with noneurologic deficits.

• There are insufficient data for an evidence-basedrecommendation on the use of neuroimaging fortension-type headaches.

• There are insufficient data for evidence-based recom-mendations regarding CT vs. MRI in the evaluation of non-acute headache.



Is A CT Necessa ry Prior To Ob ta ining An LP? 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.

Thunderclap Hea dache With A Negat ive CT/LP: Is Angiograp hy Indicat ed? A history of thunderclap headaches should trigger

the emergency physician to consider SAH. But

what if such a patient has a negative CT and anegative LP—does 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 42-

year-old woman who presented with three thunderclap

headaches within one week.99 The patient’s evaluation

revealed a negative CT and bloodless CSF. Angiogra-

phy 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 patient’s headaches. This case report led some toargue that a normal CT scan and LP are not sufficiently

sensitive to exclude aneurysm in thunderclap head-

ache. 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 con-

cluded from the study that angiography is not recom-

mended 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

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.

Pharmacotherapy

The pharmacotherapy of headaches is an extraordinar-ily 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.

Migraine HeadacheMany 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 intrave-

nously, but they may also be administered intramuscu-

larly, 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 otherposturing). 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,111metoclopramide, 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 signifi-

cantly better than placebo in controlling migraine

pain.113 However, the IV route may be more appropri-

ate 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



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

effective in migraineurs.121

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 treat-

ment of migraine headaches.129 Furthermore, barbitu-

Cost-Effective Strategies In Headache Management1. Minimize laboratory tests.

Most patients with headache need no laboratory tests. They

will require only a targeted history and physical examination.Risk-Mana gem ent 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.

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 notinclude 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”

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-Man agem ent 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.

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-Man agem ent Caveat: Patients who are vomiting

or those suffering severe migrainous attacks will likely

benefit from subcutaneous, intramuscular, or

intravenous medications.

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.



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

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.

Non-Steroidal Anti-Inflamm atory D rugs Oral non-steroidal anti-inflammatory drugs (NSAIDs)

are effective in relieving acute migraines, particularly

Ten Excuses That Don’t Work In Court1. “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.

2. “The CT was negative, so I figured he didn’t 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.

3. “I thought the chest pain was just a side effect

of the medication; I didn’t 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.

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 patient’s

“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 patient’s narcotic dependence/addiction?”

Although narcotics continue to be used by many as first-

line therapy for migraine headaches, they are best reserved

for rescue therapy.

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

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.

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.

8. “I didn’t 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, Behçet’s disease, oral contraceptive use,

pregnancy, or lupus).

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.

10. “I didn’t 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.

Cont inued on page 20



Table 7. Treatment Of The Acute Migraine Headache In The Emergency Department.

Drug Adverse effects Class of Drug cost and caution Comments evidenceAntiemetics Metoclopramide IM $$ Mild; extrapyramidal side effects Role in pregnancy (Category III

(e.g., dystonia) and sedation B). Special role with nauseaand vomiting.

Metoclopramide IV $$ Moderate; extrapyramidal side Role in pregnancy. Special III

effects (e.g., dystonia) and role with nausea andsedation vomiting.

Prochlorperazine PR $ Occasional Good for use in mild/ Indeterminate IM $ Occasional moderate/severe headache. III IV $ Moderate; Rectal route had modest II

occasional extrapyramidal clinical effects. Special roleside effects and sedation with nausea and vomiting

and as adjunct with othermedications.

Promethazine IM $ Occasional Special role as adjunct with Indeterminate IV $ Extrapyramidal side effects other medications. Indeterminate

and sedation

IV serotonergic antagonists $$$ Infrequent (constipation Expensive. Special role Indeterminate (granisetron, zatosetron, and common side effect when patient has and ondansetron) with granisetron) phenothiazine intolerance.

Droperidol IM $ Moderate; mostly sedation Very few studies. Rapid IM IIIand akathisia onset of action.

Antipsychotics Haloperidol IV $ Infrequent Rapid onset of action. Indeterminate

Few studies available.

Chlorpromazine IV $ Frequent and severe; most Good clinical effect, but IIIstudies give IV fluids with orthostatic hypotensionthe medication may limit its usefulness.

Barbiturate/Hypnotics Butalbital PO $ Moderate; sedation common Risk of headache rebound Indeterminate Fiorinal, Fioricet $$$ with both and overuse. Indeterminate

Dihydroergotamine (DHE) and ergot alkaloids DHE SC $$ Moderate SC route may have delayed II DHE IM $$ Moderate onset of action. Not for use III DHE IV $$ Frequent; nausea, vomiting, in patients at risk for III

dysphoria, flushing, and ischemic heart disease.restlessness most common Treatment associated with

low recurrence rates.

NSAIDs Acetaminophen PO $ Infrequent; very well tolerated Special use in pediatrics III

or pregnancy. Modestclinical effect.

Ketorolac IM $ Infrequent nausea and Good clinical effect. III IV $ drowsiness; not for patients III

with renal and GI diseases

NSAIDs PO $ Occasional nausea and vomiting Very good clinical effect. II for tensionFor use in mild/moderate headache;migraine only. III for migraine

Opiate analgesics Butorphanol $$$ Frequent; dizziness, drowsiness, Good clinical effect but III nasal spray nausea, vertigo high risk of rebound and

abuse potential.

Narcotics—oral combinations $ Occasional; dizziness, fatigue, Good clinical effect but III (acetaminophen + hydrocodone nausea, and drowsiness high risk of rebound or oxycodone) and abuse potential.



Meperidine Modest clinical effect, but IM $ Occasional rebound headache and III IV $ Frequent; sedation, nausea, addiction potential limit use. III

and dizziness common Special use as rescue therapy.

“ Triptans”(serotonin agonists) Sumatriptan nasal spray $$ Frequent, unpleasant taste and Useful when non-oral route II-III

flushing. Avoid with coronary of administration needed.artery disease/uncontrolled For moderate/severe migraine.hypertension and ergot drugs Good clinical effect. Frequent(this is true for all“triptans,”for rebound headaches.all routes).

Sumatriptan SC $$ Frequent chest pain and Useful when non-oral route II-IIIflushing. Chest pain is common, of administration needed.but true ischemic events are rare. For moderate/severeShould not be used in basilar migraine. Frequent reboundor hemiplegic migraine. headaches.

Others Nitrous oxide (inhaled) $$ Infrequent Obviates the need for Indeterminate

intravenous access.

100% oxygen (inhaled) $ Infrequent No significant clinical effects. Unadvised

IV corticosteroids $$ Infrequent Rescue therapy in status IIImigrainosus.

Isometheptene-containing $ Infrequent; drowsiness, dizziness, Good clinical effect. For III combinations PO and nausea mild/moderate headache.

Special consideration tooutpatient therapy.

Lidocaine IN $ Frequent; nasal discomfort Short duration of action Indeterminateand very frequentheadache recurrence.

Lidocaine IV $ Moderate Minimal clinical effects. UnadvisedPoor efficacy.

Magnesium IV $ Moderate Few studies available. Indeterminate

Table 7. Treatment Of The Acute Migraine Headache In The Emergency Department(continued).

Drug Adverse effects Class of Drug cost and caution Comments evidence

Drug costs:Drug cost guidelines are based solely on the cost of themedication and do not take into consideration theadditional costs of intravenous line placement and/ornursing/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 ormore prospective studies that yield consistently

positive results.

• Class II: Acceptable and useful. Very good evidence

provides support. Considered treatments of choice. Basedon higher levels of evidence and results that consistentlyyield positive results.

• Class III: Acceptable and useful. Fair to goodevidence provides support. Considered excellentoptional or alternative treatments. Based onintermediate levels of evidence not always yieldingpositive results.

• Indeterminate: Continuing area of research; results not

compelling or contradictory. Higher studies may be inprogress and no recommendations until further research.

• Unadvised: Not acceptable, not useful, or may even beharmful. Based on studies that yield no consistent

positive data.



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?

Yes No

→

→

Theevidence for recommendations 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 cl inical pat hwa y is intended to supplement, rather th an subst i tute, professional judg ment and m ay be changed depending u pon a

pat ient ’ s individual needs. Fai lure to com ply w i th t his pathw ay does not represent a breach of th e stand ard of care.

Copyright © 2001 Pinnacle Publishing, Inc. Pinnacle Publishing (1-800-788-1900) grants each subscriberlimited copying privileges for educational distribution within your facility or program. Commercial distribution to promote any product or service is strictly prohibited.

Suspect primary headache: migraine,tension, cluster. Go to“Clinical Pathway:Assessment And Management Of Patients

With Primary Headaches.”

Yes No →

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

Yes No → →

Evidence of infection, such as fever or shaking chills?

→

Go to“Clinical Pathway: Assessment And Management Of

Headache In Patients With Fever Or Immunosuppression.”



Clinical Pathway: Assessment And Management Of HeadacheIn Patients With Fever Or Immunosuppression

Theevidence for recommendations 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 cl inical pathw ay is intended to supplement, rather th an subst i tute, professional judg m ent and may be changed depending u pon a



Suspected immune suppression?• History of HIV with CD4 < 200 or unknown

• Prior history of opportunistic infection• Significant HIV risk factors

• Oral thrush

Possible mass lesion or increasedintracranial pressure?

• Papilledema or unable to visualize fundi

• Focal neurologic deficit• New-onset seizures• Headache present for days or weeks• Ventriculoperitoneal shunt• Recent head trauma

Signs of meningitis?

• Positive jolt test• Stiff neck

• Kernig’s orBrudzinski’s sign

• Altered mental status

CT results

• CT of head (Class II)• Give intravenous

ceftriaxone or similardrug effective againstbacterial meningitisbefo re CT if patient has

fever, stiff neck, oraltered mental status(Class II)

→ No

Yes →

→

→ No

Consider other causes of headache and fever

• Systemic infections• Rocky Mountain spotted fever• Temporal arteritis

• Sinusitis• Pharyngitis (especially in children)

(Class II)

Perform lumbar puncture

(Class I-II)• Measure opening

pressure (Class III)• CSF: cell count, Gram’s

stain, protein, glucose(Class I-II)

If suspected HIV, order:• CSF cryptococcal

antigen (Class II)

• CSF VDRL (Class III)• India ink stain

(Class II)

→ No

→

Yes

→

Yes: Option 1

Yes: Option 2 →

From “Clinical Pathw ay: Initial Assessment And M ana gement O f Imm unocompetent Pat ients With N on-Trauma tic Head aches”

Treat as indicated

→ → Negative Positive



Clinical Pathway: Assessment And Management Of PatientsWith Headaches And No Evidence Of Infection

From “ Clinical Pathw ay: In itial Assessment And M ana gemen t Of Imm unocompetent Patient s With N on-Trauma tic Heada ches ”

Theevidence for recommendations 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 cl inical pat hwa y is intended to supplement, rather th an subst i tute, professional judg ment and m ay be changed depending u pon a



Headache was“sudden-onset, worst-ever, or different than ever before”

Yes No → →

Non-contrast cranial CT (Class II) →

Subarachnoid hemorrhage present?

→ Yes 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)

Intracerebral hemorrhage?

Performlumbarpunc-

ture(Class II)

→

Bloodor

xantho-chromiapresent?

→ Yes No

→

Check for other causes• Consider discharge

home if patient’s painis well controlled andthe patient is tolerat-

ing oral hydration(Class III)

Ag

Documents

Acute Headache in the ED Evidence-Based Evaluation and Treatment Options (2)