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EVALUATION AND MANAGEMENT OF HEADACHE IN THE EMERGENCY DEPARTMENT
0025-7125/01 $15.00
HEADACHE
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EVALUATION AND MANAGEMENT OF HEADACHE IN THE EMERGENCY DEPARTMENT Thomas N. Ward, MD, Morris Levin, MD, and Joseph M. Phillips, MD
Patients presenting to the emergency department (ED) with a chief complaint of headache are common, representing 2% or more of all ED visits.' Headache as a symptom in ED patients is more common because headache accompanies many systemic illnesses. Although there are perhaps several hundred illnesses that may occur with headache as a significant feature, the presence of this symptom may be considered as a useful clue to the underlying problems. In the evaluation of these patients, there is no substitute for a thorough, efficient approach, especially because most such patients are not known to the ED personnel. Using a systematic approach enables the physician to arrive at the diagnosis reliably and to alleviate suffering more rapidly. APPROACH TO THE HEADACHE PATIENT IN THE EMERGENCY DEPARTMENT
When a patient presents to the ED with headache, despite technologic advances, the performance of a thorough history and an appropriate general medical and neurologic examination is essential. The
From the Department of Medicine, Dartmouth Medical School (TNW, ML); Section of Neurology, Dartmouth-Hitchcock Medical Center (TNW, ML); and Upper Valley Neurology/Neurosurgery WP),Lebanon, New Hampshire
MEDICAL CLINICS OF NORTH AMERICA VOLUME 85 * NUMBER 4 * JULY 2001
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selection of testing, if any, is based on the clinical impression derived from the clinical evaluation. The threshold for obtaining testing is generally lower in the ED than otherwise, given time constraints and the usual lack of physician familiarity with the patient. The history of the headache is the most useful part of the evaluation. All available resources should be used, including direct interview of the patient if possible, reports of family members, emergency transport personnel, and hospital records. In the case of children presenting to the ED with headache, sometimes family members may provide much of the relevant history, although a skilled interviewer may be able to tease out significant useful details from very young children. In documenting the headache history, it is essential to inventory properly salient features of the headache presentation to determine whether there are worrisome features that might point toward a diagnosis of a serious underlying cause. Essential questions for headache patients in the ED include the following: 1. Has the patient ever had a headache similar to this one before? 2. Has the patient experienced recent head trauma? 3. What was the patient doing at the onset of the headache? 4. Was the headache sudden in onset? 5. What other medical conditions are present (e.g., acquired immunodeficiency syndrome [AIDS])? 6. Is this a new, progressive headache?
Worrisome aspects (or red flags) in headache patients include the following: 1. Sudden onset or onset during exertion 2. Any abnormality on the neurologic examination (including mental status) 3. Age greater than 50 years 4. Worsening under observation 5. Abnormal vital signs, especially fever or Cushing’s reflex 6. New-onset headaches in patients with cancer or AIDS 7. Firstlworst (severe) headache 8. Seizures The goal is to sort out whether the headache type is primary (and not due to a serious underlying cause) or secondary (due to potentially threatening pathologic condition) or whether the patient has more than one type of headache. Primary headaches seen in the ED include the following: 1. Migraine with and without aura and status migrainosus (migraine with duration >72 hours) 2. Tension-type headache 3. Cluster headache
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There are other primary headache types, but the most common one to present to the ED is migraine. Secondary headaches seen in the ED include the following: 1. Mass lesions, including primary and metastatic tumors, epidural and subdural hematomas, and brain abscess 2. Subarachnoid hemorrhage (SAH) (also consider thunderclap headache) 3. Meningitis (bacterial, fungal, viral, parasitic, and carcinomatous) 4. Stroke or transient ischemic attack 5. Giant cell arteritis 6. Neuralgia (trigeminal) 7. Toximetabolic-remote infections, drug abuse, carbon monoxide 8. Primary ocular, dental, and sinus disease After the diagnosis is made, therapy is directed against any underlying causes, and pain relief is addressed. Analgesic therapy should not be instituted until a diagnosis is made because important physical clues may be Given the presence of suffering, all due haste is appropriate. Useful questions to ask patients include why precisely have they come to the ED, and how did they arrive? Some patients present because even though they are long-standing headache sufferers this particular episode is associated with new or unusual symptoms causing them concern, whereas others have tried all their usual remedies without relief and their pain has plagued them for too long. Some patients seek relief in the ED because they have no primary care provider, and the ED is their point of access to the system. In one study, it was suggested that the mode of arrival (ambulatory versus emergency transport) may be revealing.22The time course of events is crucial information. Was the headache sudden or explosive in onset, or did it develop gradually? What was the patient doing when the headache began? Is the patient improving or worsening under observation? Does the patient have any underlying medical conditions that might put them at risk for particular serious causes of headaches, such as HIV or other immunosuppressed states? Although most patients with HIV in the ED turn out to have a primary headache such as migraine, secondary headache resulting from opportunistic infection or central nervous system lymphoma must be considered.I6Questions regarding coexisting medical conditions, recent head or neck trauma, and medication history (including illicit drug or alcohol use) must be asked. An occupational history should be taken considering the possibility of toxic exposure. Family history may reveal the presence of migraine, which may present in the ED as a severe first attack or an atypical attack with unusual features, especially in pediatric patients.31 After the history has been obtained, general medical (including vital signs) and neurologic examinations are performed. Vital signs are particularly important. Fever (reliably measured) is not expected in primary headache disorders such as migraine and suggests a secondary
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process, such as infection or bleeding in the central nervous system (resulting from subarachnoid or intraparenchymal hemorrhage). Acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), and steroids may mask fever, and it may be absent in immunosuppressed patients. Mild elevations of blood pressure, as in essential hypertension, are not associated typically with headache; however, severely elevated readings, as occur in malignant hypertension (diastolic pressures >120 to 130 mm Hg with papilledema), are associated with headache.38Paroxysmal elevations of blood pressure, as occur with pheochromocytoma or the tyramine reaction in patients taking monoamine oxidase inhibitors, are associated with intermittent headache. Serial observations of vital signs in the ED are mandatory. A rising blood pressure with a falling pulse rate (Cushing’s reflex) is a sign of rising intracranial pressure (e.g., due to an expanding intracranial mass lesion) and may be a harbinger of impending herniation and neurologic deterioration. A neurologic examination is necessary and should include examination of the head and neck (after fracture has been ruled out) as well as a mental status examination. Signs of local cranial pathology, such as dental abscess, sinusitis, otitis, and pharyngitis, should be sought specifically. Battle’s sign, raccoon eyes, hemotympanum or otorrhea, and cerebrospinal fluid (CSF) rhinorrhea all suggest significant head trauma with likely skull fracture. Papilledema suggests increased intracranial pressure (although its absence does not rule it out), and although subhyaloid (preretinal) hemorrhages are found rarely, their presence on funduscopic examination suggests the occurrence of a sudden severe increase in intracranial pressure (as seen in ruptured aneurysm). The use of mydriatics during the funduscopic examination should be avoided. Performing the examination in a darkened room usually is sufficient. Pupillodilating agents may obscure crucial neurologic signs, such as the blown pupil seen with impending transtentorial h e r n i a t i ~ n . ~ ~ When historical information is gathered, and the examinations have been performed, tentative diagnoses are made. The selection of testing, if any, is based on the clinical impression. Certain aspects of the clinical information make it more likely that testing will be abnormal. Older patients (>55 years old), patients with an acute or sudden onset of headache, patients manifesting an occipitonuchal location of pain, and patients with any abnormality on the neurologic examination (including the mental status examination) are more likely to have a relevant abnormality on neuroimaging studies such as computed tomography (CT) scan or magnetic resonance (MR) imagingz6 If a primary headache type (see previous list) is diagnosed, attention turns immediately to pain relief (see later).39Otherwise, for patients believed to have a secondary headache, test selection is the next order of business (Table 1).Neuroimaging is most appropriate when there is suspicion of mass lesion or bleeding. CSF examination by lumbar puncture is used to search for SAH (missed in perhaps 10% of CT scans), infection, or increased or decreased intracranial pressure. Potentially enlightening laboratory tests include erythrocyte sedimentation rate
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Table 1. TESTING USEFUL IN THE EMERGENCY DEPARTMENT EVALUATION OF THE HEADACHE PATIENT Test
CT scan MR imaging, MR angiography, MR venography Lumbar puncture Angiography Laboratory
Indication
Suspected mass lesion, SAH, stroke Suspected mass lesion, vascular anomaly such as arterial dissection, AVM, aneurysm, venous thrombosis, stroke Suspected meningitis, SAH, intracranial hypertension, intracranial hypotension Suspected aneurysm, AVM, vasculitis, venous thrombosis, arterial dissection Giant cell arteritis (ESR), infection (WBC, cultures), hypoxemia/hypercarbia (arterial blood gas), thyroid function tests, Lyme disease testing, drug screens, alcohol level, serum glucose, calcium, BUN/creatinine, electrolytes, PT/PTT
SAH = subarachnoid hemorrhage; AVM = arteriovenous malformation; ESR = erythrocyte sedimentation rate; WBC = white blood cell count; BUN = blood urea nitrogen; PT/PTT = prothrombin time/partial thromboplastin time.
(NSAIDs and steroids may suppress the value), complete blood count, electrolytes, serum glucose, blood urea nitrogren and creatinine, prothrombin time and partial thromboplastin time, thyroid function tests, toxicology and alcohol level, and serum calcium. Arterial blood gas measurements may detect hypercarbia or hypoxemia. Other studies, such as carbon monoxide level, may be appropriate. Results of testing for Lyme disease, lupus, and certain other conditions may not be available for several days after being drawn but may be useful in certain scenarios. Imaging of the paranasal sinuses and cervical spine may be necessary. Treatment of secondary headaches is directed against the underlying pathologic condition and may necessitate consultation and admission from the ED. Discussion of the long-term management of such conditions is beyond the scope of this article. SECONDARYHEADACHEINTHEEMERGENCY DEPARTMENT
In evaluating ED patients with headaches, the fundamental task is to avoid missing serious pathology as a cause. Because of time constraints and the need for the ED to function efficiently as well as the general lack of physician familiarity with this patient population, there is generally a lower threshold for obtaining testing. Causes of secondary headache include infections (meningitis or encephalitis, parameningeal, and systemic or remote); vasculitis (especially giant cell or temporal arteritis); vascular dissection; intracranial hypertension or hypotension;
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mass lesion (abscess, tumor, hematoma); SAH (resulting from aneurysm or arteriovenous malformation); systemic illnesses; extreme hypertension; head trauma; so-called thunderclap headache; transient ischemic attack or stroke; and diseases of the head, eyes, ears, nose, and throat (such as acute narrow-angle glaucoma). Appropriate and timely consultation may clarify difficult diagnostic questions. The time course of the headache may suggest a diagnosis. Vascular conditions often are sudden or explosive in onset. SAH from a ruptured aneurysm or arteriovenous malformation may be one of the most impressive clinical presentations seen by physicians. Some presentations of SAH may be less dramatic, with a warning (sentineI) hemorrhage occurring in 30% or more of patients.15,35 In the situation in which a sentinel bleed has occurred, there may be improvement (or not) followed by rebleeding that can be catastrophic. The warning leak sometimes is unreported by the patient or is dismissed as a migraine. Headache is a nearly universal symptom of SAH and usually is associated with nausea and vomiting that may be severe and persistent. Onset is sudden, and this diagnosis always should be considered if the headache was triggered by exertion, including sexual activity. The headache itself typically is severe and holocranial (although it may begin briefly unilaterally). As the subarachnoid blood spreads, pain becomes occipitonuchal with ensuing neck stiffness (80%), and eventually (hours later), low back pain may develop. At the ictus, there may be a loss of consciousness, a seizure, or both. In this situation, an oculomotor nerve palsy suggests the possibility of a posterior communicating artery aneurysm, whereas a lower extremity monoplegia should hint at the possibility of an anterior communicating artery aneurysm. Many features may confound the history. The initial presentation may be subtle, instead of dramatic, and be mistaken for a migraine attack. Arteriovenous malformations may be migraine mimics, eluding detection for years unless an intracranial bruit is heard by an astute examiner or even the patient. A seizure may signal a problem. Frequently the diagnosis finally may become obvious only after a hemorrhage. The clinical entity of thunderclap headache may cause serious diagnostic dilemmas5,12,27, 42 These are severe headaches of sudden onset, sometimes occurring in the setting of exertion. The history triggers an evaluation for SAH, resulting in a negative CT scan and lumbar puncture. Although most patients actually have a rapid-onset (crash) migraine, a few patients have been found by MR angiography or conventional pancerebral angiography to harbor unruptured aneurysms, which are postulated to have generated headache by sudden expansion, thrombosis, or hemorrhage .into their walls without frank SAH.43Whether these aneurysms represent incidental findings ( 2 1 %to 2% of the general population may have intracranial aneurysms) or whether they are related to the genesis of these headaches is controversial. In all cases of thunderclap headache, a high index of suspicion for a secondary cause is appropriate. If SAH is suspected after the clinical evaluation, a CT scan of the
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brain is performed. If the CT scan is negative, a lumbar puncture is performed. This study should include opening pressure, xanthochromia and spectrophotometry, protein, glucose, and cell counts and differentials in tubes 1 and 3. If the lumbar puncture is performed too early (within 2 hours of the ictus), blood may not have had sufficient time to reach the lumbar levels. Some authors advise that if the initial lumbar puncture is negative, the patient should be monitored clinically and the If clinical suspicion is high or the patient study repeated at 12 is deteriorating, prompt pancerebral angiography and neurosurgical consultation are indicated. If CT scan and lumbar puncture are truly negative but clinical suspicion is high for unruptured aneurysm, MR imaging or MR angiography within 24 hours is reasonable. Vascular dissection occurs when there is a hemorrhage into the vessel wall with resultant narrowing of the lumen. When vascular dissection occurs in the internal carotid or vertebral arteries, headache often results.38In the case of the carotid artery, there may be pain emanating from the vessel itself, and ipsilateral headache often occurs in the cheek, eye, and forehead. A partial Horner’s syndrome (ptosis, miosis) may be manifest, and there may be a vascular bruit. With vertebral artery dissection, there is usually posterior neck pain as well as occipital pain sometimes radiating forward to the ipsilateral frontotemporal region. Vascular dissection may be spontaneous or idiopathic or associated with trauma, fibromuscular dysplasia, cystic medial necrosis, or Marfan’s syndrome. With dissection of either artery, transient ischemic attack or stroke may occur distal to the site of injury. Diagnosis of arterial dissection can be confirmed by MR imaging or MR angiography (preferred), ultrasound, or conventional angiography. Treatment is controversial but may include aspirin, heparin, or warfarin (Coumadin). Headache may occur in the setting of transient ischemic attack or 38 A history of transient neurologic deficit with headache in an older individual should prompt consideration of this possibility because a subsequent stroke might be prevented. Headache is less frequent in bland or ischemic events including lacunar strokes, but much more common and prominent (often with nausea and vomiting) in hemorrhagic strokes. The location of the headache may be misleading, but with events in the carotid distribution they tend to be anterior, and with posterior circulation events, they tend to be parieto-occiptal. Cerebral venous thrombosis is an often elusive diagnosis to make in a patient with headache. The most typical site for the thrombosis is the superior sagittal sinus, although when the transverse sinus is involved, intracranial hypertension and pulsatile tinnitus (pseudoturnor cerebri) may result. The past medical history may suggest this diagnostic possibility because causes include trauma, postoperative status, dehydration, the puerperium, parameningeal infections, cancer, sepsis, and any other hypercoagulable state. The headache associated with superior sagittal sinus thrombosis often is bilateral and severe, sometimes with nausea and vomiting, photophobia, and focal neurologic There may be signs of raised intracranial pressure (papilledema, sixth cranial nerve
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palsies, loss of upward gaze) and seizures. Cerebral venous thrombosis may be detected by MR imaging, MR venography, or conventional angiography. A history of trauma in a patient with headache should prompt consideration of the presence of a subdural or epidural hematoma. An epidural hematoma is a rapid arterial bleed with a collection forming between the calvaria and dura (there is no space there normally). The usual history is one of a head injury severe enough to cause a loss of consciousness or concussion, sometimes followed by a lucid interval during which consciousness is regained, followed by a second neurologic deterioration as the epidural hematoma grows in volume. An unconscious patient in the ED after head trauma requires an emergency brain CT scan. If examined during the lucid interval, the patient may complain of headache. Emergency CT scan and neurosurgical consultation are obtained if this entity is suspected on clinical grounds. Subdural hematomas (venous bleeding into the [potential] subdural space) may be either chronic or acute. In chronic subdural hematomas, there may be a history of trauma days to weeks before the presentation to the ED, although such a history may not be proffered, especially by the elderly. With the slower venous bleeding, progressive headache occurs, and neurologic deficits may appear.zoAcute subdural hematomas (as seen in pugilists) are less common, the rapid accumulation of blood causing rapid neurologic decline. Management of these lesions involves neuroimaging and neurosurgical consultation. A discussion of chronic posttraumatic headaches is outside the scope of this article, and these conditions generally should not be managed in the ED. Head trauma in children, especially children with a family history of migraine, may precipitate mental status changes and transient neurologic deficits.31 Although migraine turns out to be the culprit in many cases, a careful approach that rules out secondary headaches is necessary. One diagnostic entity that may be dramatic in presentation is pituitary apoplexyz8Patients hemorrhaging into a pituitary tumor may develop sudden severe headache with nausea and vomiting and sometimes progressive visual loss. Symptoms of endocrinopathy, such as loss of libido, may have preceded the event, and further signs of pituitary insufficiency may evolve subsequently. The scout film on the brain CT scan may reveal an enlarged sella on careful inspection, but coronal views of the pituitary are best to delineate the lesion fully. Neurosurgical consultation is indicated promptly for possible transsphenoidal evacuation of the hematoma, especially if compression of the optic chiasm and surrounding structures is leading to progessive visual loss. Patients presenting with a chief complaint of headache often fear they harbor a brain tumor. Although this generally is not the case, mass lesions may be associated with some headaches.z4The history is usually subacute or chronic and progressive. Fever and signs of a parameningeal focus may suggest brain abscess, as may a history of immunosuppression. The possibility of metastatic tumor (or carcinomatous meningitis) is suggested by the presence of a primary malignancy. Primary brain
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tumor may present with headache, although often not as the primary ~omplaint.~ With mass lesions, neurologic deficits tend to appear and accrue in addition to the headache. Seizures may be seen, and eventually signs of raised intracranial pressure develop. Headaches associated with mass lesions often worsen with Valsalva maneuvers and may be worse with recumbency and alleviated with sitting or standing. Projectile (without nausea) vomiting may occur. Nocturnal awakening with headaches classically is taught as a sign of mass lesions, but also commonly is found with migraine and cluster atta~ks.2~ In the case of suspected mass lesion, neuroimaging is indicated, with gadolinium-enhanced MR imaging generally preferred. Meningitis or encephalitis (cerebritis) can generate headaches, but in that the mental status typically deteriorates, an accurate description of the headache often is unavailable. There almost always is fever, with a holocranial progressive headache. The headache may be dull or throbbing with nausea and vomiting, evolving neurologic deficits, and signs of rising intracranial pressure. Clinical progression may be extremely rapid, and the work-up for these entities needs to be expeditious. With meningitis, meningismus often is present, although this sign disappears as coma ensues. Abnormal mental status, fever, and headache may be the most typical early presentation of these problems, and prompt diagnosis is essential so that appropriate therapy may be initiated to prevent further neurologic compromise. Neuroimaging is obtained to rule out a mass lesion (MR imaging is preferred if encephalitis is suspected); if imaging negative, CSF is obtained to look for infectious causes.3oPolymerase chain reaction studies are being used increasingly. Herpes simplex encephalitis is the most common form of sporadic encephalitis. Because it is a necrotizing, hemorrhagic illness resulting in brain destruction, yet treatable with acyclovir, early diagnosis and treatment are vital to prevent substantial irreversible brain damage. Gadolinium-enhanced MR imaging may be the most sensitive test showing the early abnormalities in the frontal and medial temporal lobes. Electroencephalography may be useful, and CSF studies (including polymerase chain reaction) may make the specific diagnosis. Brain biopsy sometimes is advocated in equivocal cases. Therapy with acyclovir should not be withheld pending test results but instead should be initiated immediately when the diagnosis is suspected and continued for 14 to 21 days 32, 41 or until an alternative diagnosis is e~tablished.~, Headaches may be due to high or low intracranial pressure. Idiopathic intracranial hypertension, formerly known as pseudoturnor cerebri or benign intrucrunial hypertension (a misnomer because the possibility of blindness is not at all benign), occurs usually with headaches and papilledema. Given this history, neuroimaging is performed to rule out a mass lesion. When none is found, the subsequent lumbar puncture reveals an elevated CSF opening pressure with normal CSF laboratory analysis. Obese young women seem to be particularly at risk. The headaches may be constant or intermittent and may have features of tension-type headache, migraine, or both.32,36 Transient visual phenom-
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ena and pulsatile tinnitus are common. Untreated, there is a risk of visual loss. Sixth nerve palsies sometimes are seen as well as worsening visual acuity, papilledema, and an enlarging blind spot with constricting visual fields. The lumbar puncture may be diagnostic and therapeutic. Treatment may consist of serial lumbar punctures and ophthalmologic examinations, carbonic anhydrase inhibitors such as acetazolamide, and diuretics such as furosemide. Weight loss is advised but seldom achieved. Optic nerve sheath fenestration is indicated in refractory cases with threatened or actual visual loss. Diagnostic confusion arises because of the related diagnostic entity of idiopathic intracranial hypertension without papilledema (these patients do not seem to be at risk for visual loss, however).17 Headaches resulting from CSF hypotension most often are seen after a lumbar puncture but may occur after trauma, surgery, or exertion or spontaneously. These headaches vary in severity and typically are dull or throbbing, with a posterior or holocranial location. A diagnostic clue is that headaches worsen with assumption of the upright posture and improve with recumbency, but the change in severity may not always be rapid and dramatic, and improvement may be incomplete, with a less severe headache persisting. Patients manifesting either otorrhea or rhinorrhea after head trauma may show this condition. When suspected, the diagnosis may be confirmed by gadolinium-enhanced MR imaging (revealing meningeal enhancement in 90% of cases), followed by lumbar puncture (CSF pressure generally <50 mm H,O).,I If there is no obvious source of a CSF leak, such as a recent lumbar puncture, the source may be detected by an indium radionuclide scan. Trauma may cause a dural root sleeve tear, leading to a persistent CSF leak. General medical treatment includes bed rest, abdominal binders, and sometimes intravenous caffeine sodium ben~oate.~ Specific therapy usually involves an epidural blood patch for post-lumbar puncture headaches or neurosurgical repair of damaged dural root sleeves. Giant cell arteritis (temporal arteritis) is a worrisome cause of headache in older patients. The patient usually is older than 50 years of age, and the erythrocyte sedimentation rate usually is greater than 50 mm/h. The headache may be located at the temple (with a tender superficial temporal artery), be hemicranial, be holocranial, or be anywhere in the head. Its character may be intermittent or constant, dull or throbbing, or sharp. Patients may report jaw claudication or symptoms of polymyalgia r h e ~ m a t i c a Untreated, .~~ approximately 50% of patients may go blind permanently in one or both eyes, with a smaller number having strokes, usually in the posterior circulation.lo,38 When this diagnosis is considered, the patient is placed immediately on 60 to 80 mg/d of prednisone, and superficial temporal artery biopsy is arranged promptly (if an adequate sample of one artery is negative, a biopsy sample of the other side should be obtained).22Fewer than 10% of patients with giant cell arteritis have negative bilateral biopsies.'l, 14,34 For ED patients with pain localized to the eye, the possibility of local ocular pathology should be considered. Acute (narrow-angle) closure
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glaucoma is usually straightforward to diagnose with severe headache localized to the orbit, redness, corneal clouding, and the appearance of halos around objects. Tonometry is diagnostic, revealing elevated intraocular pressures (>21 mm Hg). Emergency ophthalmologic consultation is appropriate. Local ocular pathology should be considered in all cases of visual loss whether transient or progressive, and a low threshold for consultation should be maintained. One uncommon clinical entity that may cause focal eye pain with few physical findings is posterior s~leritis.'~ An exudative retinal detachment may be present. A clue by history is that posterior scleritis frequently is associated with various autoimmune conditions, including lupus, polyarteritis nodosa, and rheumatoid arthritis. MANAGEMENT OF PRIMARY HEADACHES IN THE EMERGENCY DEPARTMENT
When secondary headaches have been ruled out, primary headaches remain as the diagnostic possibilities. Most such patients (65%)prove to have migraine.26Tension-type headache and cluster headaches are not seen commonly in the ED. The appropriate management of these individuals consists of rapid pain relief and arranging for ongoing followup to avoid repeat visits to the ED.39 There are many potential reasons for a migraineur to report to the ED. The headache may have had a sudden and severe onset (crash migraine) or be associated with intractable vomiting and dehydration. The headache may have begun in unusual circumstances, such as during sexual intercourse, or be more intense than usual, or simply be refractory to all the measures the patient has tried to terminate it. The attack may have unusual features causing concern to the patient or family members, as occur during basilar migraine, hemiplegic migraine, or ophthalmoplegic migraine.23Some patients present during their first attack or because they have no access to health care other than the ED. Other patients have intractable chronic daily headache secondary to analgesic rebound, caused by misuse or overuse of acute medication^.^^ For the primary headache sufferer in the ED, the main goals should be to eradicate headache and associated symptoms rapidly and to arrange proper long-term management. Constraints on ED resources make it a suboptimal location to provide long-term headache care. It also is not the ideal place to try to sort out complicated long-standing headache problems.6 Referral to a competent physician interested in managing primary headaches is desirable. The diagnostic criteria for primary headaches have been published and are discussed elsewhere in this issue.I3 For migraine patients, placement in a quiet, darkened room complements other therapeutic maneuvers. Dehydration is addressed with intravenous fluids. Antiemetics often are indicated, although some headache remedies, such as the triptans (see later), may relieve the entire symptom complex. Many remedies may be initiated, although most
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clinicians avoid vasoactive agents in hemiplegic, basilar, or ophthalmoplegic migraine. Although narcotics often are employed, this represents a suboptimal strategy and should not be first-line therapy. Meperidine (Demerol) has a short duration of action of 3 to 4 hours and often fails (owing to recurrence) in migraine, which typically lasts 4 to 72 The use of narcotics may attract drug-seeking patients, and there is excellent evidence for the superiority of other agents with fewer side effects.2,39 The use of 10 mg of metoclopramide (Reglan) intravenously may alleviate migraine. When insufficient, intravenous dihydroergotamine (D.H.E. 45) titrated to the effective subnauseating dose (0.5 to 1.0 mg) has extremely high efficacy. Prochlorperazine, 10 mg intravenously, may be successf~l.~~ Side effects such as akathisia (motor restlessness, jitteriness) and acute dystonic reactions can be managed with intravenous diphenhydramine (Benadryl),25 to 50 mg, or benztropine mesylate ( C ~ g e n t i n )Ketorolac .~~ (Toradol), 60 mg intramuscularly or 30 mg intravenously, is effective in some patients. Intravenous valproate (Depacon) has been reported as efficacious in some patients in doses of 300 to 500 mgs, Triptans, such as sumatriptan (Imitrex), may be highly effective. The usual 6-mg subcutaneous dose works rapidly and can be used if the patient is vomiting. Triptans and ergot derivatives such as dihydroergotamine, being vasoconstrictors, should be avoided in patients with possible underlying coronary artery disease. For patients unresponsive to therapy in the ED, chronic daily headache sufferers (analgesic rebound), or patients with status migrainosus (migraine duration >72 hours), steroids, inpatient admission, or both should be considered. Response to therapy is not diagnostic; there have been reports of patients with secondary headaches caused by SAH who have responded transiently to dihydroergotamine or sumatriptan only to deteriorate subseA proper diagnosis must be made first; only then is specific q~ently.*~ therapy initiated. Complete relief of migraine pain in the ED should be the goal because incomplete relief seems to be associated with headache recurrence and prolonged di~ability.~ Patients with tension-type headache usually are not seen in the ED. If these headaches are frequent and severe, drugs that are prophylactic in migraine often also help relieve tension-type headache.40NSAIDs or acetaminophen may be effective acutely. Referral for follow-up is important. Cluster headache, being an uncommon condition, is not seen commonly in the ED. These patients experience recurrent episodes of extremely severe, but relatively brief, headache multiple times a day.I3 Patients may be agitated and have difficulty remaining still. This unilateral headache is usually in or near the eye and has associated autonomic symptoms, such as an ipsilateral partial Homer’s syndrome (ptosis and miosis), lacrimation, nasal stuffiness, and rhinorrhea. There are several effective acute remedies, including inhaled oxygen 100% by mask at 7 L/min or more; intravenous metoclopramide and dihydroergotamine as for migraine (see earlier); sumatriptan, 6 mg subcutaneously; and transnasal butorphanol (Stadol NS), 1 puff (1 mg).39, Many cluster
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headache sufferers have risk factors for coronary artery disease, and the use of sumatriptan and dihydroergotamine may be contraindicated. When the acute attack has subsided, consultation with a physician skilled in the management of cluster headaches is appropriate, and prophylactic therapy or steroids (or both) may be initiated.4O Follow-up is vital because the pain is recurrent and severe, and suicide risk is a concern. Occasionally, patients with neuralgias may present to the ED. These patients usually appear because of new-onset severe repetitive lancinating pain. Between episodes, there may be a milder, dull baseline discomfort. The lancinating pain generally has a sharp or electric quality, is maximal at onset, and brief (seconds). The second and third divisions (less often the first) of the trigeminal nerve are involved most often (trigeminal neuralgia or tic douloureux). Often a trigger point can be discovered that elicits paroxysms of pain, and the patient may resist examination for fear of provoking a paroxysm. Neuralgias may be either primary (actually often due to vascular compression of the fifth cranial nerve) or secondary (e.g., resulting from a tumor or multiple sclerosis). Evaluation usually is nonemergent and is accomplished in part by MR imaging with contrast enhancement. Acute therapy is paramount and may be achieved by intravenous phenytoin (Dilantin) or fosphenytoin (Cerebyx), 500 mg intravenously (or the equivalent) at 50 mg/min or slower, monitoring pulse and blood pressure. This maneuver may provide temporary relief for 1 or more days while long-term prophylactic therapy (such as carbamazepine [Tegretol]) is initiated.37 Uncommon headache types, such as chronic paroxysmal hemicrania, are encountered rarely in the ED.23,26 Diagnosis and management often require the assistance of a headache expert. In this situation, however, because of their rarity, a high index of suspicion for secondary headache causes must be maintained. SUMMARY
In the ED, correct diagnosis is the necessary foundation on which specific therapy is based. There is no substitute for obtaining a thorough history and examining the patient competently. Patients with a past history of primary headaches, such as migraine, also may be afflicted with (new) secondary headaches. Although efficiency is desirable from the perspective of ED management, a thoughtful approach complemented by the judicious selection of tests is compatible with that goal as well as achieving the desired outcome of accurate diagnosis and relief of pain. Arrangements for long-term follow-up are important. References 1. Barton CW: Evaluation and treatment of headache in the emergency department A survey. Headache 34:91, 1994
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2. Belgrade MJ, Ling LJ, Schleevogt MB, et al: Comparison of single dose meperidine,
butorphanol and dihydroergotamine in the treatment of vascular headache. Neurology 39:590, 1989 3. Camann WR, Murray RS, Mushlin PS, et al: Effects of oral caffeine on postdural puncture headache: A double-blind, placebo-controlled trial. Anesth Analg 70181,1990 4. Davis LE: Acute viral meningitis and encephalitis. In Kennedy PGE, Johnson RT (eds): Infections of the Nervous System. London, Buttenuorths, 1985, pp 155-176 5. Day JW, R a s h NH: Thunderclap headache: Symptom of unruptured cerebral aneurysm. Lancet 21247,1986 6. Dodick DW The patient in the emergency room: Case 1. In Rapoport AM, Sheftell FD, Purdy RA (eds): Advanced Therapy of Headache. Hamilton, Toronto, BC Decker, 1999, pp 79-87 7. Ducharme J, Beveridge RC, Lee JS, et al: Emergency Management of Migraine: Is the Headache Really Over? Acad Emerg Med 5:899, 1998 8. Edwards K, Santarcangelo V, Shea P, et al: Intravenous valproate for acute treatment of migraine headaches [abstr]. Cephalalgia 19:356, 1999 9. Forsyth PA, Posner JB: Headaches in patients with brain tumors: A study of 111 patients. Neurology 43:1678, 1993 10. Goodman BW Temporal arteritis. Am J Med 67839, 1979 11. Hall S, Lie JT, Kurland LT, et al: The therapeutic impact of temporal artery biopsy. Lancet 21212, 1983 12. Harling DW, Peatfield RC, Van HiUe PT, et al: Thunderclap headache: Is it migraine? Cephalalgia 9:87, 1989 13. Headache Classification Committee of the International Headache Society: Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia S(supp17):1, 1988 14. Hedges TR, Gieger GL, Albert D M The clinical value of negative temporal artery biopsy specimens. Arch Ophthalmol 101:1251, 1983 15. Leblanc R The minor leak preceding subarachnoid hemorrhage. J Neurosurg 66:35, 1987 16. Lipton RB, Pfeffer D, Newman LC, et al: Headache and HIV-1 related disorders. Headache 31:518,1991 17. Mathew NT, Ravishankar K, Sanin LC: Coexistence of migraine and idiopathic intracranial hypertension without papilledema. Neurology 46:1226, 1996 18. Mathew NT, Kailasam J, Meadors L, et al: Intravenous valproate sodium (Depacon) aborts migraine rapidly: A preliminary report [abstr]. Cephalalgia 19:373, 1999 19. McCluskey PJ, Watson PG, Lightman S, et al: Posterior scleritis: Clinical features, systemic associations, and outcome in a large series of patients. Ophthalmology 106:2380, 1999 20. McKissock W Subdural hematoma: A review of 389 cases. Lancet 1:1365, 1960 21. Mokri B, Krueger BR, Miller GM, et al: Meningeal gadolinium enhancement in lowpressure headaches. J Neuroimaging 3:11, 1993 22. Nemer JA, Tallick SA, OConnor RE, et al: Emergency medical services transport of patients with headache: Mode of arrival may indicate serious etiology. Prehosp Emerg Care 2304, 1998 23. Newman LC, Lipton RB: Emergency department evaluation of headache. Neurol Clin North Am 16285, 1998 24. Pfund Z, Szapary L, Jaszberenyi 0, et al: Headache in intracranial tumors. Cephalalgia 19:787, 1999 25. Portenoy RK, Abissi CJ, Lipton RB, et al: Headache in cerebrovascular disease. Stroke 15:1009, 1984 26. Ramirez-LassepasM, Espinosa CE, Cicero JJ, et al: Predictors of intracranial pathologic findings in patients who seek emergency care because of headache. Arch Neurol 541506, 1997 27. Raps EC, Rogers JD, Galetta SL, et al: The clinical spectrum of unruptured intracranial aneurysms. Arch Neurol50:265, 1993 28. Reid R, Quigley M, Yen S Pituitary apoplexy: A review. Arch Neurol 42712, 1985
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29. Seymour JJ: Response of headaches to nonnarcotic analgesics resulting in missed intracranial hemorrhage. Am J Emerg Med 13:43, 1995 30. Silberstein SD, Lipton RB, Goadsby PJ: Headache in Clinical Practice. Oxford, Isis Medical Media, 1998, pp 183-190 31. Soriani S, Cavaliere B, Faggioli R, et al: Confusional migraine precipitated by mild head trauma. Arch Adolesc Med 154:90, 2000 32. Sztajnkrycer M, Jauch EC: Unusual headaches. Emerg Med Clin North Am 16:741,1998 33. Vermeulen M, van Gijn J: The diagnosis of subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry 53:365, 1990 34. Vilaseca J, Gonzalez A, Cid MC, et al: Clinical usefulness of temporal artery biopsy. Ann Rheum Dis 46:282. 1987 35. Waga S, Ohtsubo K, Handa H: Warning signs in intracranial aneurysms. Surg Neurol 3:15, 1975 36. Wall M: The headache profile of idiopathic intracranial hypertension. Cephalalgia 10:331, 1990 37. Ward TN: Facial pain. In Warfield C, Bajwa Z (eds): Principles and Practice of Pain Medicine, ed 2. New York, McGraw-Hill, in press 38. Ward TN: Headache in cerebrovascular disease. In Samuels MA, Feske S (eds): Office Practice of Neurology. New York, Churchill Livingstone, 1996, pp 1141-1144 39. Ward TN: Management of an acute primary headache. Clin Neurosci 5:50, 1998 40. Ward TN: Providing relief from headache pain: Current options for acute and prophylactic therapy. Postgrad Med 108:121, 2000 41. Whitley RJ, Lakeman F: Herpes simplex virus infections of the central nervous system: Therapeutic and diagnostic considerations. Clin Infect Dis 20:414, 1995 42. Wijdicks EFM, Kerkhoff H, Van Gijn J: Long-term follow-up of 71 patients with thunderclap headache mimicking subarachnoid hemorrhage. Lancet 268,1988 43. Witham TF, Kaufmann AM: Unruptured cerebral aneurysm producing a thunderclap headache. Am J Emerg Med 18:88, 2000
Address reprint requests to Thomas N. Ward, MD Section of Neurology Dartmouth-Hitchcock Medical Center 1 Medical Center Drive Lebanon, NH 03756 e-mail: Thomas.N.WardOhitchcock.org
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EVALUATION AND MANAGEMENT OF HEADACHE IN THE EMERGENCY DEPARTMENT Thomas N. Ward, MD, Morris Levin, MD, and Joseph M. Phillips, MD
Patients presenting to the emergency department (ED) with a chief complaint of headache are common, representing 2% or more of all ED visits.' Headache as a symptom in ED patients is more common because headache accompanies many systemic illnesses. Although there are perhaps several hundred illnesses that may occur with headache as a significant feature, the presence of this symptom may be considered as a useful clue to the underlying problems. In the evaluation of these patients, there is no substitute for a thorough, efficient approach, especially because most such patients are not known to the ED personnel. Using a systematic approach enables the physician to arrive at the diagnosis reliably and to alleviate suffering more rapidly. APPROACH TO THE HEADACHE PATIENT IN THE EMERGENCY DEPARTMENT
When a patient presents to the ED with headache, despite technologic advances, the performance of a thorough history and an appropriate general medical and neurologic examination is essential. The
From the Department of Medicine, Dartmouth Medical School (TNW, ML); Section of Neurology, Dartmouth-Hitchcock Medical Center (TNW, ML); and Upper Valley Neurology/Neurosurgery WP),Lebanon, New Hampshire
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selection of testing, if any, is based on the clinical impression derived from the clinical evaluation. The threshold for obtaining testing is generally lower in the ED than otherwise, given time constraints and the usual lack of physician familiarity with the patient. The history of the headache is the most useful part of the evaluation. All available resources should be used, including direct interview of the patient if possible, reports of family members, emergency transport personnel, and hospital records. In the case of children presenting to the ED with headache, sometimes family members may provide much of the relevant history, although a skilled interviewer may be able to tease out significant useful details from very young children. In documenting the headache history, it is essential to inventory properly salient features of the headache presentation to determine whether there are worrisome features that might point toward a diagnosis of a serious underlying cause. Essential questions for headache patients in the ED include the following: 1. Has the patient ever had a headache similar to this one before? 2. Has the patient experienced recent head trauma? 3. What was the patient doing at the onset of the headache? 4. Was the headache sudden in onset? 5. What other medical conditions are present (e.g., acquired immunodeficiency syndrome [AIDS])? 6. Is this a new, progressive headache?
Worrisome aspects (or red flags) in headache patients include the following: 1. Sudden onset or onset during exertion 2. Any abnormality on the neurologic examination (including mental status) 3. Age greater than 50 years 4. Worsening under observation 5. Abnormal vital signs, especially fever or Cushing’s reflex 6. New-onset headaches in patients with cancer or AIDS 7. Firstlworst (severe) headache 8. Seizures The goal is to sort out whether the headache type is primary (and not due to a serious underlying cause) or secondary (due to potentially threatening pathologic condition) or whether the patient has more than one type of headache. Primary headaches seen in the ED include the following: 1. Migraine with and without aura and status migrainosus (migraine with duration >72 hours) 2. Tension-type headache 3. Cluster headache
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There are other primary headache types, but the most common one to present to the ED is migraine. Secondary headaches seen in the ED include the following: 1. Mass lesions, including primary and metastatic tumors, epidural and subdural hematomas, and brain abscess 2. Subarachnoid hemorrhage (SAH) (also consider thunderclap headache) 3. Meningitis (bacterial, fungal, viral, parasitic, and carcinomatous) 4. Stroke or transient ischemic attack 5. Giant cell arteritis 6. Neuralgia (trigeminal) 7. Toximetabolic-remote infections, drug abuse, carbon monoxide 8. Primary ocular, dental, and sinus disease After the diagnosis is made, therapy is directed against any underlying causes, and pain relief is addressed. Analgesic therapy should not be instituted until a diagnosis is made because important physical clues may be Given the presence of suffering, all due haste is appropriate. Useful questions to ask patients include why precisely have they come to the ED, and how did they arrive? Some patients present because even though they are long-standing headache sufferers this particular episode is associated with new or unusual symptoms causing them concern, whereas others have tried all their usual remedies without relief and their pain has plagued them for too long. Some patients seek relief in the ED because they have no primary care provider, and the ED is their point of access to the system. In one study, it was suggested that the mode of arrival (ambulatory versus emergency transport) may be revealing.22The time course of events is crucial information. Was the headache sudden or explosive in onset, or did it develop gradually? What was the patient doing when the headache began? Is the patient improving or worsening under observation? Does the patient have any underlying medical conditions that might put them at risk for particular serious causes of headaches, such as HIV or other immunosuppressed states? Although most patients with HIV in the ED turn out to have a primary headache such as migraine, secondary headache resulting from opportunistic infection or central nervous system lymphoma must be considered.I6Questions regarding coexisting medical conditions, recent head or neck trauma, and medication history (including illicit drug or alcohol use) must be asked. An occupational history should be taken considering the possibility of toxic exposure. Family history may reveal the presence of migraine, which may present in the ED as a severe first attack or an atypical attack with unusual features, especially in pediatric patients.31 After the history has been obtained, general medical (including vital signs) and neurologic examinations are performed. Vital signs are particularly important. Fever (reliably measured) is not expected in primary headache disorders such as migraine and suggests a secondary
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process, such as infection or bleeding in the central nervous system (resulting from subarachnoid or intraparenchymal hemorrhage). Acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), and steroids may mask fever, and it may be absent in immunosuppressed patients. Mild elevations of blood pressure, as in essential hypertension, are not associated typically with headache; however, severely elevated readings, as occur in malignant hypertension (diastolic pressures >120 to 130 mm Hg with papilledema), are associated with headache.38Paroxysmal elevations of blood pressure, as occur with pheochromocytoma or the tyramine reaction in patients taking monoamine oxidase inhibitors, are associated with intermittent headache. Serial observations of vital signs in the ED are mandatory. A rising blood pressure with a falling pulse rate (Cushing’s reflex) is a sign of rising intracranial pressure (e.g., due to an expanding intracranial mass lesion) and may be a harbinger of impending herniation and neurologic deterioration. A neurologic examination is necessary and should include examination of the head and neck (after fracture has been ruled out) as well as a mental status examination. Signs of local cranial pathology, such as dental abscess, sinusitis, otitis, and pharyngitis, should be sought specifically. Battle’s sign, raccoon eyes, hemotympanum or otorrhea, and cerebrospinal fluid (CSF) rhinorrhea all suggest significant head trauma with likely skull fracture. Papilledema suggests increased intracranial pressure (although its absence does not rule it out), and although subhyaloid (preretinal) hemorrhages are found rarely, their presence on funduscopic examination suggests the occurrence of a sudden severe increase in intracranial pressure (as seen in ruptured aneurysm). The use of mydriatics during the funduscopic examination should be avoided. Performing the examination in a darkened room usually is sufficient. Pupillodilating agents may obscure crucial neurologic signs, such as the blown pupil seen with impending transtentorial h e r n i a t i ~ n . ~ ~ When historical information is gathered, and the examinations have been performed, tentative diagnoses are made. The selection of testing, if any, is based on the clinical impression. Certain aspects of the clinical information make it more likely that testing will be abnormal. Older patients (>55 years old), patients with an acute or sudden onset of headache, patients manifesting an occipitonuchal location of pain, and patients with any abnormality on the neurologic examination (including the mental status examination) are more likely to have a relevant abnormality on neuroimaging studies such as computed tomography (CT) scan or magnetic resonance (MR) imagingz6 If a primary headache type (see previous list) is diagnosed, attention turns immediately to pain relief (see later).39Otherwise, for patients believed to have a secondary headache, test selection is the next order of business (Table 1).Neuroimaging is most appropriate when there is suspicion of mass lesion or bleeding. CSF examination by lumbar puncture is used to search for SAH (missed in perhaps 10% of CT scans), infection, or increased or decreased intracranial pressure. Potentially enlightening laboratory tests include erythrocyte sedimentation rate
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Table 1. TESTING USEFUL IN THE EMERGENCY DEPARTMENT EVALUATION OF THE HEADACHE PATIENT Test
CT scan MR imaging, MR angiography, MR venography Lumbar puncture Angiography Laboratory
Indication
Suspected mass lesion, SAH, stroke Suspected mass lesion, vascular anomaly such as arterial dissection, AVM, aneurysm, venous thrombosis, stroke Suspected meningitis, SAH, intracranial hypertension, intracranial hypotension Suspected aneurysm, AVM, vasculitis, venous thrombosis, arterial dissection Giant cell arteritis (ESR), infection (WBC, cultures), hypoxemia/hypercarbia (arterial blood gas), thyroid function tests, Lyme disease testing, drug screens, alcohol level, serum glucose, calcium, BUN/creatinine, electrolytes, PT/PTT
SAH = subarachnoid hemorrhage; AVM = arteriovenous malformation; ESR = erythrocyte sedimentation rate; WBC = white blood cell count; BUN = blood urea nitrogen; PT/PTT = prothrombin time/partial thromboplastin time.
(NSAIDs and steroids may suppress the value), complete blood count, electrolytes, serum glucose, blood urea nitrogren and creatinine, prothrombin time and partial thromboplastin time, thyroid function tests, toxicology and alcohol level, and serum calcium. Arterial blood gas measurements may detect hypercarbia or hypoxemia. Other studies, such as carbon monoxide level, may be appropriate. Results of testing for Lyme disease, lupus, and certain other conditions may not be available for several days after being drawn but may be useful in certain scenarios. Imaging of the paranasal sinuses and cervical spine may be necessary. Treatment of secondary headaches is directed against the underlying pathologic condition and may necessitate consultation and admission from the ED. Discussion of the long-term management of such conditions is beyond the scope of this article. SECONDARYHEADACHEINTHEEMERGENCY DEPARTMENT
In evaluating ED patients with headaches, the fundamental task is to avoid missing serious pathology as a cause. Because of time constraints and the need for the ED to function efficiently as well as the general lack of physician familiarity with this patient population, there is generally a lower threshold for obtaining testing. Causes of secondary headache include infections (meningitis or encephalitis, parameningeal, and systemic or remote); vasculitis (especially giant cell or temporal arteritis); vascular dissection; intracranial hypertension or hypotension;
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mass lesion (abscess, tumor, hematoma); SAH (resulting from aneurysm or arteriovenous malformation); systemic illnesses; extreme hypertension; head trauma; so-called thunderclap headache; transient ischemic attack or stroke; and diseases of the head, eyes, ears, nose, and throat (such as acute narrow-angle glaucoma). Appropriate and timely consultation may clarify difficult diagnostic questions. The time course of the headache may suggest a diagnosis. Vascular conditions often are sudden or explosive in onset. SAH from a ruptured aneurysm or arteriovenous malformation may be one of the most impressive clinical presentations seen by physicians. Some presentations of SAH may be less dramatic, with a warning (sentineI) hemorrhage occurring in 30% or more of patients.15,35 In the situation in which a sentinel bleed has occurred, there may be improvement (or not) followed by rebleeding that can be catastrophic. The warning leak sometimes is unreported by the patient or is dismissed as a migraine. Headache is a nearly universal symptom of SAH and usually is associated with nausea and vomiting that may be severe and persistent. Onset is sudden, and this diagnosis always should be considered if the headache was triggered by exertion, including sexual activity. The headache itself typically is severe and holocranial (although it may begin briefly unilaterally). As the subarachnoid blood spreads, pain becomes occipitonuchal with ensuing neck stiffness (80%), and eventually (hours later), low back pain may develop. At the ictus, there may be a loss of consciousness, a seizure, or both. In this situation, an oculomotor nerve palsy suggests the possibility of a posterior communicating artery aneurysm, whereas a lower extremity monoplegia should hint at the possibility of an anterior communicating artery aneurysm. Many features may confound the history. The initial presentation may be subtle, instead of dramatic, and be mistaken for a migraine attack. Arteriovenous malformations may be migraine mimics, eluding detection for years unless an intracranial bruit is heard by an astute examiner or even the patient. A seizure may signal a problem. Frequently the diagnosis finally may become obvious only after a hemorrhage. The clinical entity of thunderclap headache may cause serious diagnostic dilemmas5,12,27, 42 These are severe headaches of sudden onset, sometimes occurring in the setting of exertion. The history triggers an evaluation for SAH, resulting in a negative CT scan and lumbar puncture. Although most patients actually have a rapid-onset (crash) migraine, a few patients have been found by MR angiography or conventional pancerebral angiography to harbor unruptured aneurysms, which are postulated to have generated headache by sudden expansion, thrombosis, or hemorrhage .into their walls without frank SAH.43Whether these aneurysms represent incidental findings ( 2 1 %to 2% of the general population may have intracranial aneurysms) or whether they are related to the genesis of these headaches is controversial. In all cases of thunderclap headache, a high index of suspicion for a secondary cause is appropriate. If SAH is suspected after the clinical evaluation, a CT scan of the
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brain is performed. If the CT scan is negative, a lumbar puncture is performed. This study should include opening pressure, xanthochromia and spectrophotometry, protein, glucose, and cell counts and differentials in tubes 1 and 3. If the lumbar puncture is performed too early (within 2 hours of the ictus), blood may not have had sufficient time to reach the lumbar levels. Some authors advise that if the initial lumbar puncture is negative, the patient should be monitored clinically and the If clinical suspicion is high or the patient study repeated at 12 is deteriorating, prompt pancerebral angiography and neurosurgical consultation are indicated. If CT scan and lumbar puncture are truly negative but clinical suspicion is high for unruptured aneurysm, MR imaging or MR angiography within 24 hours is reasonable. Vascular dissection occurs when there is a hemorrhage into the vessel wall with resultant narrowing of the lumen. When vascular dissection occurs in the internal carotid or vertebral arteries, headache often results.38In the case of the carotid artery, there may be pain emanating from the vessel itself, and ipsilateral headache often occurs in the cheek, eye, and forehead. A partial Horner’s syndrome (ptosis, miosis) may be manifest, and there may be a vascular bruit. With vertebral artery dissection, there is usually posterior neck pain as well as occipital pain sometimes radiating forward to the ipsilateral frontotemporal region. Vascular dissection may be spontaneous or idiopathic or associated with trauma, fibromuscular dysplasia, cystic medial necrosis, or Marfan’s syndrome. With dissection of either artery, transient ischemic attack or stroke may occur distal to the site of injury. Diagnosis of arterial dissection can be confirmed by MR imaging or MR angiography (preferred), ultrasound, or conventional angiography. Treatment is controversial but may include aspirin, heparin, or warfarin (Coumadin). Headache may occur in the setting of transient ischemic attack or 38 A history of transient neurologic deficit with headache in an older individual should prompt consideration of this possibility because a subsequent stroke might be prevented. Headache is less frequent in bland or ischemic events including lacunar strokes, but much more common and prominent (often with nausea and vomiting) in hemorrhagic strokes. The location of the headache may be misleading, but with events in the carotid distribution they tend to be anterior, and with posterior circulation events, they tend to be parieto-occiptal. Cerebral venous thrombosis is an often elusive diagnosis to make in a patient with headache. The most typical site for the thrombosis is the superior sagittal sinus, although when the transverse sinus is involved, intracranial hypertension and pulsatile tinnitus (pseudoturnor cerebri) may result. The past medical history may suggest this diagnostic possibility because causes include trauma, postoperative status, dehydration, the puerperium, parameningeal infections, cancer, sepsis, and any other hypercoagulable state. The headache associated with superior sagittal sinus thrombosis often is bilateral and severe, sometimes with nausea and vomiting, photophobia, and focal neurologic There may be signs of raised intracranial pressure (papilledema, sixth cranial nerve
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palsies, loss of upward gaze) and seizures. Cerebral venous thrombosis may be detected by MR imaging, MR venography, or conventional angiography. A history of trauma in a patient with headache should prompt consideration of the presence of a subdural or epidural hematoma. An epidural hematoma is a rapid arterial bleed with a collection forming between the calvaria and dura (there is no space there normally). The usual history is one of a head injury severe enough to cause a loss of consciousness or concussion, sometimes followed by a lucid interval during which consciousness is regained, followed by a second neurologic deterioration as the epidural hematoma grows in volume. An unconscious patient in the ED after head trauma requires an emergency brain CT scan. If examined during the lucid interval, the patient may complain of headache. Emergency CT scan and neurosurgical consultation are obtained if this entity is suspected on clinical grounds. Subdural hematomas (venous bleeding into the [potential] subdural space) may be either chronic or acute. In chronic subdural hematomas, there may be a history of trauma days to weeks before the presentation to the ED, although such a history may not be proffered, especially by the elderly. With the slower venous bleeding, progressive headache occurs, and neurologic deficits may appear.zoAcute subdural hematomas (as seen in pugilists) are less common, the rapid accumulation of blood causing rapid neurologic decline. Management of these lesions involves neuroimaging and neurosurgical consultation. A discussion of chronic posttraumatic headaches is outside the scope of this article, and these conditions generally should not be managed in the ED. Head trauma in children, especially children with a family history of migraine, may precipitate mental status changes and transient neurologic deficits.31 Although migraine turns out to be the culprit in many cases, a careful approach that rules out secondary headaches is necessary. One diagnostic entity that may be dramatic in presentation is pituitary apoplexyz8Patients hemorrhaging into a pituitary tumor may develop sudden severe headache with nausea and vomiting and sometimes progressive visual loss. Symptoms of endocrinopathy, such as loss of libido, may have preceded the event, and further signs of pituitary insufficiency may evolve subsequently. The scout film on the brain CT scan may reveal an enlarged sella on careful inspection, but coronal views of the pituitary are best to delineate the lesion fully. Neurosurgical consultation is indicated promptly for possible transsphenoidal evacuation of the hematoma, especially if compression of the optic chiasm and surrounding structures is leading to progessive visual loss. Patients presenting with a chief complaint of headache often fear they harbor a brain tumor. Although this generally is not the case, mass lesions may be associated with some headaches.z4The history is usually subacute or chronic and progressive. Fever and signs of a parameningeal focus may suggest brain abscess, as may a history of immunosuppression. The possibility of metastatic tumor (or carcinomatous meningitis) is suggested by the presence of a primary malignancy. Primary brain
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tumor may present with headache, although often not as the primary ~omplaint.~ With mass lesions, neurologic deficits tend to appear and accrue in addition to the headache. Seizures may be seen, and eventually signs of raised intracranial pressure develop. Headaches associated with mass lesions often worsen with Valsalva maneuvers and may be worse with recumbency and alleviated with sitting or standing. Projectile (without nausea) vomiting may occur. Nocturnal awakening with headaches classically is taught as a sign of mass lesions, but also commonly is found with migraine and cluster atta~ks.2~ In the case of suspected mass lesion, neuroimaging is indicated, with gadolinium-enhanced MR imaging generally preferred. Meningitis or encephalitis (cerebritis) can generate headaches, but in that the mental status typically deteriorates, an accurate description of the headache often is unavailable. There almost always is fever, with a holocranial progressive headache. The headache may be dull or throbbing with nausea and vomiting, evolving neurologic deficits, and signs of rising intracranial pressure. Clinical progression may be extremely rapid, and the work-up for these entities needs to be expeditious. With meningitis, meningismus often is present, although this sign disappears as coma ensues. Abnormal mental status, fever, and headache may be the most typical early presentation of these problems, and prompt diagnosis is essential so that appropriate therapy may be initiated to prevent further neurologic compromise. Neuroimaging is obtained to rule out a mass lesion (MR imaging is preferred if encephalitis is suspected); if imaging negative, CSF is obtained to look for infectious causes.3oPolymerase chain reaction studies are being used increasingly. Herpes simplex encephalitis is the most common form of sporadic encephalitis. Because it is a necrotizing, hemorrhagic illness resulting in brain destruction, yet treatable with acyclovir, early diagnosis and treatment are vital to prevent substantial irreversible brain damage. Gadolinium-enhanced MR imaging may be the most sensitive test showing the early abnormalities in the frontal and medial temporal lobes. Electroencephalography may be useful, and CSF studies (including polymerase chain reaction) may make the specific diagnosis. Brain biopsy sometimes is advocated in equivocal cases. Therapy with acyclovir should not be withheld pending test results but instead should be initiated immediately when the diagnosis is suspected and continued for 14 to 21 days 32, 41 or until an alternative diagnosis is e~tablished.~, Headaches may be due to high or low intracranial pressure. Idiopathic intracranial hypertension, formerly known as pseudoturnor cerebri or benign intrucrunial hypertension (a misnomer because the possibility of blindness is not at all benign), occurs usually with headaches and papilledema. Given this history, neuroimaging is performed to rule out a mass lesion. When none is found, the subsequent lumbar puncture reveals an elevated CSF opening pressure with normal CSF laboratory analysis. Obese young women seem to be particularly at risk. The headaches may be constant or intermittent and may have features of tension-type headache, migraine, or both.32,36 Transient visual phenom-
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ena and pulsatile tinnitus are common. Untreated, there is a risk of visual loss. Sixth nerve palsies sometimes are seen as well as worsening visual acuity, papilledema, and an enlarging blind spot with constricting visual fields. The lumbar puncture may be diagnostic and therapeutic. Treatment may consist of serial lumbar punctures and ophthalmologic examinations, carbonic anhydrase inhibitors such as acetazolamide, and diuretics such as furosemide. Weight loss is advised but seldom achieved. Optic nerve sheath fenestration is indicated in refractory cases with threatened or actual visual loss. Diagnostic confusion arises because of the related diagnostic entity of idiopathic intracranial hypertension without papilledema (these patients do not seem to be at risk for visual loss, however).17 Headaches resulting from CSF hypotension most often are seen after a lumbar puncture but may occur after trauma, surgery, or exertion or spontaneously. These headaches vary in severity and typically are dull or throbbing, with a posterior or holocranial location. A diagnostic clue is that headaches worsen with assumption of the upright posture and improve with recumbency, but the change in severity may not always be rapid and dramatic, and improvement may be incomplete, with a less severe headache persisting. Patients manifesting either otorrhea or rhinorrhea after head trauma may show this condition. When suspected, the diagnosis may be confirmed by gadolinium-enhanced MR imaging (revealing meningeal enhancement in 90% of cases), followed by lumbar puncture (CSF pressure generally <50 mm H,O).,I If there is no obvious source of a CSF leak, such as a recent lumbar puncture, the source may be detected by an indium radionuclide scan. Trauma may cause a dural root sleeve tear, leading to a persistent CSF leak. General medical treatment includes bed rest, abdominal binders, and sometimes intravenous caffeine sodium ben~oate.~ Specific therapy usually involves an epidural blood patch for post-lumbar puncture headaches or neurosurgical repair of damaged dural root sleeves. Giant cell arteritis (temporal arteritis) is a worrisome cause of headache in older patients. The patient usually is older than 50 years of age, and the erythrocyte sedimentation rate usually is greater than 50 mm/h. The headache may be located at the temple (with a tender superficial temporal artery), be hemicranial, be holocranial, or be anywhere in the head. Its character may be intermittent or constant, dull or throbbing, or sharp. Patients may report jaw claudication or symptoms of polymyalgia r h e ~ m a t i c a Untreated, .~~ approximately 50% of patients may go blind permanently in one or both eyes, with a smaller number having strokes, usually in the posterior circulation.lo,38 When this diagnosis is considered, the patient is placed immediately on 60 to 80 mg/d of prednisone, and superficial temporal artery biopsy is arranged promptly (if an adequate sample of one artery is negative, a biopsy sample of the other side should be obtained).22Fewer than 10% of patients with giant cell arteritis have negative bilateral biopsies.'l, 14,34 For ED patients with pain localized to the eye, the possibility of local ocular pathology should be considered. Acute (narrow-angle) closure
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glaucoma is usually straightforward to diagnose with severe headache localized to the orbit, redness, corneal clouding, and the appearance of halos around objects. Tonometry is diagnostic, revealing elevated intraocular pressures (>21 mm Hg). Emergency ophthalmologic consultation is appropriate. Local ocular pathology should be considered in all cases of visual loss whether transient or progressive, and a low threshold for consultation should be maintained. One uncommon clinical entity that may cause focal eye pain with few physical findings is posterior s~leritis.'~ An exudative retinal detachment may be present. A clue by history is that posterior scleritis frequently is associated with various autoimmune conditions, including lupus, polyarteritis nodosa, and rheumatoid arthritis. MANAGEMENT OF PRIMARY HEADACHES IN THE EMERGENCY DEPARTMENT
When secondary headaches have been ruled out, primary headaches remain as the diagnostic possibilities. Most such patients (65%)prove to have migraine.26Tension-type headache and cluster headaches are not seen commonly in the ED. The appropriate management of these individuals consists of rapid pain relief and arranging for ongoing followup to avoid repeat visits to the ED.39 There are many potential reasons for a migraineur to report to the ED. The headache may have had a sudden and severe onset (crash migraine) or be associated with intractable vomiting and dehydration. The headache may have begun in unusual circumstances, such as during sexual intercourse, or be more intense than usual, or simply be refractory to all the measures the patient has tried to terminate it. The attack may have unusual features causing concern to the patient or family members, as occur during basilar migraine, hemiplegic migraine, or ophthalmoplegic migraine.23Some patients present during their first attack or because they have no access to health care other than the ED. Other patients have intractable chronic daily headache secondary to analgesic rebound, caused by misuse or overuse of acute medication^.^^ For the primary headache sufferer in the ED, the main goals should be to eradicate headache and associated symptoms rapidly and to arrange proper long-term management. Constraints on ED resources make it a suboptimal location to provide long-term headache care. It also is not the ideal place to try to sort out complicated long-standing headache problems.6 Referral to a competent physician interested in managing primary headaches is desirable. The diagnostic criteria for primary headaches have been published and are discussed elsewhere in this issue.I3 For migraine patients, placement in a quiet, darkened room complements other therapeutic maneuvers. Dehydration is addressed with intravenous fluids. Antiemetics often are indicated, although some headache remedies, such as the triptans (see later), may relieve the entire symptom complex. Many remedies may be initiated, although most
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clinicians avoid vasoactive agents in hemiplegic, basilar, or ophthalmoplegic migraine. Although narcotics often are employed, this represents a suboptimal strategy and should not be first-line therapy. Meperidine (Demerol) has a short duration of action of 3 to 4 hours and often fails (owing to recurrence) in migraine, which typically lasts 4 to 72 The use of narcotics may attract drug-seeking patients, and there is excellent evidence for the superiority of other agents with fewer side effects.2,39 The use of 10 mg of metoclopramide (Reglan) intravenously may alleviate migraine. When insufficient, intravenous dihydroergotamine (D.H.E. 45) titrated to the effective subnauseating dose (0.5 to 1.0 mg) has extremely high efficacy. Prochlorperazine, 10 mg intravenously, may be successf~l.~~ Side effects such as akathisia (motor restlessness, jitteriness) and acute dystonic reactions can be managed with intravenous diphenhydramine (Benadryl),25 to 50 mg, or benztropine mesylate ( C ~ g e n t i n )Ketorolac .~~ (Toradol), 60 mg intramuscularly or 30 mg intravenously, is effective in some patients. Intravenous valproate (Depacon) has been reported as efficacious in some patients in doses of 300 to 500 mgs, Triptans, such as sumatriptan (Imitrex), may be highly effective. The usual 6-mg subcutaneous dose works rapidly and can be used if the patient is vomiting. Triptans and ergot derivatives such as dihydroergotamine, being vasoconstrictors, should be avoided in patients with possible underlying coronary artery disease. For patients unresponsive to therapy in the ED, chronic daily headache sufferers (analgesic rebound), or patients with status migrainosus (migraine duration >72 hours), steroids, inpatient admission, or both should be considered. Response to therapy is not diagnostic; there have been reports of patients with secondary headaches caused by SAH who have responded transiently to dihydroergotamine or sumatriptan only to deteriorate subseA proper diagnosis must be made first; only then is specific q~ently.*~ therapy initiated. Complete relief of migraine pain in the ED should be the goal because incomplete relief seems to be associated with headache recurrence and prolonged di~ability.~ Patients with tension-type headache usually are not seen in the ED. If these headaches are frequent and severe, drugs that are prophylactic in migraine often also help relieve tension-type headache.40NSAIDs or acetaminophen may be effective acutely. Referral for follow-up is important. Cluster headache, being an uncommon condition, is not seen commonly in the ED. These patients experience recurrent episodes of extremely severe, but relatively brief, headache multiple times a day.I3 Patients may be agitated and have difficulty remaining still. This unilateral headache is usually in or near the eye and has associated autonomic symptoms, such as an ipsilateral partial Homer’s syndrome (ptosis and miosis), lacrimation, nasal stuffiness, and rhinorrhea. There are several effective acute remedies, including inhaled oxygen 100% by mask at 7 L/min or more; intravenous metoclopramide and dihydroergotamine as for migraine (see earlier); sumatriptan, 6 mg subcutaneously; and transnasal butorphanol (Stadol NS), 1 puff (1 mg).39, Many cluster
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headache sufferers have risk factors for coronary artery disease, and the use of sumatriptan and dihydroergotamine may be contraindicated. When the acute attack has subsided, consultation with a physician skilled in the management of cluster headaches is appropriate, and prophylactic therapy or steroids (or both) may be initiated.4O Follow-up is vital because the pain is recurrent and severe, and suicide risk is a concern. Occasionally, patients with neuralgias may present to the ED. These patients usually appear because of new-onset severe repetitive lancinating pain. Between episodes, there may be a milder, dull baseline discomfort. The lancinating pain generally has a sharp or electric quality, is maximal at onset, and brief (seconds). The second and third divisions (less often the first) of the trigeminal nerve are involved most often (trigeminal neuralgia or tic douloureux). Often a trigger point can be discovered that elicits paroxysms of pain, and the patient may resist examination for fear of provoking a paroxysm. Neuralgias may be either primary (actually often due to vascular compression of the fifth cranial nerve) or secondary (e.g., resulting from a tumor or multiple sclerosis). Evaluation usually is nonemergent and is accomplished in part by MR imaging with contrast enhancement. Acute therapy is paramount and may be achieved by intravenous phenytoin (Dilantin) or fosphenytoin (Cerebyx), 500 mg intravenously (or the equivalent) at 50 mg/min or slower, monitoring pulse and blood pressure. This maneuver may provide temporary relief for 1 or more days while long-term prophylactic therapy (such as carbamazepine [Tegretol]) is initiated.37 Uncommon headache types, such as chronic paroxysmal hemicrania, are encountered rarely in the ED.23,26 Diagnosis and management often require the assistance of a headache expert. In this situation, however, because of their rarity, a high index of suspicion for secondary headache causes must be maintained. SUMMARY
In the ED, correct diagnosis is the necessary foundation on which specific therapy is based. There is no substitute for obtaining a thorough history and examining the patient competently. Patients with a past history of primary headaches, such as migraine, also may be afflicted with (new) secondary headaches. Although efficiency is desirable from the perspective of ED management, a thoughtful approach complemented by the judicious selection of tests is compatible with that goal as well as achieving the desired outcome of accurate diagnosis and relief of pain. Arrangements for long-term follow-up are important. References 1. Barton CW: Evaluation and treatment of headache in the emergency department A survey. Headache 34:91, 1994
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2. Belgrade MJ, Ling LJ, Schleevogt MB, et al: Comparison of single dose meperidine,
butorphanol and dihydroergotamine in the treatment of vascular headache. Neurology 39:590, 1989 3. Camann WR, Murray RS, Mushlin PS, et al: Effects of oral caffeine on postdural puncture headache: A double-blind, placebo-controlled trial. Anesth Analg 70181,1990 4. Davis LE: Acute viral meningitis and encephalitis. In Kennedy PGE, Johnson RT (eds): Infections of the Nervous System. London, Buttenuorths, 1985, pp 155-176 5. Day JW, R a s h NH: Thunderclap headache: Symptom of unruptured cerebral aneurysm. Lancet 21247,1986 6. Dodick DW The patient in the emergency room: Case 1. In Rapoport AM, Sheftell FD, Purdy RA (eds): Advanced Therapy of Headache. Hamilton, Toronto, BC Decker, 1999, pp 79-87 7. Ducharme J, Beveridge RC, Lee JS, et al: Emergency Management of Migraine: Is the Headache Really Over? Acad Emerg Med 5:899, 1998 8. Edwards K, Santarcangelo V, Shea P, et al: Intravenous valproate for acute treatment of migraine headaches [abstr]. Cephalalgia 19:356, 1999 9. Forsyth PA, Posner JB: Headaches in patients with brain tumors: A study of 111 patients. Neurology 43:1678, 1993 10. Goodman BW Temporal arteritis. Am J Med 67839, 1979 11. Hall S, Lie JT, Kurland LT, et al: The therapeutic impact of temporal artery biopsy. Lancet 21212, 1983 12. Harling DW, Peatfield RC, Van HiUe PT, et al: Thunderclap headache: Is it migraine? Cephalalgia 9:87, 1989 13. Headache Classification Committee of the International Headache Society: Classification and diagnostic criteria for headache disorders, cranial neuralgias, and facial pain. Cephalalgia S(supp17):1, 1988 14. Hedges TR, Gieger GL, Albert D M The clinical value of negative temporal artery biopsy specimens. Arch Ophthalmol 101:1251, 1983 15. Leblanc R The minor leak preceding subarachnoid hemorrhage. J Neurosurg 66:35, 1987 16. Lipton RB, Pfeffer D, Newman LC, et al: Headache and HIV-1 related disorders. Headache 31:518,1991 17. Mathew NT, Ravishankar K, Sanin LC: Coexistence of migraine and idiopathic intracranial hypertension without papilledema. Neurology 46:1226, 1996 18. Mathew NT, Kailasam J, Meadors L, et al: Intravenous valproate sodium (Depacon) aborts migraine rapidly: A preliminary report [abstr]. Cephalalgia 19:373, 1999 19. McCluskey PJ, Watson PG, Lightman S, et al: Posterior scleritis: Clinical features, systemic associations, and outcome in a large series of patients. Ophthalmology 106:2380, 1999 20. McKissock W Subdural hematoma: A review of 389 cases. Lancet 1:1365, 1960 21. Mokri B, Krueger BR, Miller GM, et al: Meningeal gadolinium enhancement in lowpressure headaches. J Neuroimaging 3:11, 1993 22. Nemer JA, Tallick SA, OConnor RE, et al: Emergency medical services transport of patients with headache: Mode of arrival may indicate serious etiology. Prehosp Emerg Care 2304, 1998 23. Newman LC, Lipton RB: Emergency department evaluation of headache. Neurol Clin North Am 16285, 1998 24. Pfund Z, Szapary L, Jaszberenyi 0, et al: Headache in intracranial tumors. Cephalalgia 19:787, 1999 25. Portenoy RK, Abissi CJ, Lipton RB, et al: Headache in cerebrovascular disease. Stroke 15:1009, 1984 26. Ramirez-LassepasM, Espinosa CE, Cicero JJ, et al: Predictors of intracranial pathologic findings in patients who seek emergency care because of headache. Arch Neurol 541506, 1997 27. Raps EC, Rogers JD, Galetta SL, et al: The clinical spectrum of unruptured intracranial aneurysms. Arch Neurol50:265, 1993 28. Reid R, Quigley M, Yen S Pituitary apoplexy: A review. Arch Neurol 42712, 1985
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29. Seymour JJ: Response of headaches to nonnarcotic analgesics resulting in missed intracranial hemorrhage. Am J Emerg Med 13:43, 1995 30. Silberstein SD, Lipton RB, Goadsby PJ: Headache in Clinical Practice. Oxford, Isis Medical Media, 1998, pp 183-190 31. Soriani S, Cavaliere B, Faggioli R, et al: Confusional migraine precipitated by mild head trauma. Arch Adolesc Med 154:90, 2000 32. Sztajnkrycer M, Jauch EC: Unusual headaches. Emerg Med Clin North Am 16:741,1998 33. Vermeulen M, van Gijn J: The diagnosis of subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry 53:365, 1990 34. Vilaseca J, Gonzalez A, Cid MC, et al: Clinical usefulness of temporal artery biopsy. Ann Rheum Dis 46:282. 1987 35. Waga S, Ohtsubo K, Handa H: Warning signs in intracranial aneurysms. Surg Neurol 3:15, 1975 36. Wall M: The headache profile of idiopathic intracranial hypertension. Cephalalgia 10:331, 1990 37. Ward TN: Facial pain. In Warfield C, Bajwa Z (eds): Principles and Practice of Pain Medicine, ed 2. New York, McGraw-Hill, in press 38. Ward TN: Headache in cerebrovascular disease. In Samuels MA, Feske S (eds): Office Practice of Neurology. New York, Churchill Livingstone, 1996, pp 1141-1144 39. Ward TN: Management of an acute primary headache. Clin Neurosci 5:50, 1998 40. Ward TN: Providing relief from headache pain: Current options for acute and prophylactic therapy. Postgrad Med 108:121, 2000 41. Whitley RJ, Lakeman F: Herpes simplex virus infections of the central nervous system: Therapeutic and diagnostic considerations. Clin Infect Dis 20:414, 1995 42. Wijdicks EFM, Kerkhoff H, Van Gijn J: Long-term follow-up of 71 patients with thunderclap headache mimicking subarachnoid hemorrhage. Lancet 268,1988 43. Witham TF, Kaufmann AM: Unruptured cerebral aneurysm producing a thunderclap headache. Am J Emerg Med 18:88, 2000
Address reprint requests to Thomas N. Ward, MD Section of Neurology Dartmouth-Hitchcock Medical Center 1 Medical Center Drive Lebanon, NH 03756 e-mail: Thomas.N.WardOhitchcock.org