acute headache in the ed evidence-based evaluation and treatment options (2)
TRANSCRIPT
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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
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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)
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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)
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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.
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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
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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,
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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
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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
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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.)
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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.
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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
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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.
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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
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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.
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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.
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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 distri- bution 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.”
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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
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 distri- bution to promote any product or service is strictly prohibited.
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
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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
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 distri- bution to promote any product or service is strictly prohibited.
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