Chapter 20. Headache

See Figure 20–1.

Has Head Trauma Occurred?

If recent head trauma has occurred, evaluation of this problem takes precedence (Chapter 22).

Have Seizures Occurred?

Patients may have headache following one or more grand mal seizures. However, because the seizures may themselves be due to serious underlying disease (eg, subdural hematoma), evaluation of this problem takes precedence (Chapter 19).

Are There Focal Neurologic Abnormalities?

The presence of new focal neurologic abnormalities with headache, especially if papilledema is present as well, is strongly suggestive of a mass lesion (tumor, hematoma, abscess). Computed tomography (CT) scan or magnetic resonance imaging (MRI) should be done as soon as possible to make the diagnosis. Further evaluation is discussed in Chapter 37.

Is Headache New or of Acute Onset?

The single most important item of information to obtain from a patient with headache is whether the headache is new or acute in onset. A new headache is one occurring in a patient without a history of headaches, or a novel pattern or quality of pain in a patient with a history of headaches. A headache that is acute in onset is far more likely to have underlying pathology that may be life-threatening requiring prompt investigation.

Is the Complaint Consistent with Meningitis or Meningeal Irritation?

If the headache is acute or subacute in onset, subarachnoid hemorrhage or meningitis must be suspected. The usual manifestations are signs of meningeal irritation (stiff neck; positive Kernig and Brudzinski signs) and fever. These findings may be minimal or even absent in very young or very old patients. Seizures, confusion, or coma may be present as well. Subarachnoid hemorrhage should be strongly suspected in a patient with abrupt onset of headache that is unique to the patient's experience, especially if meningeal irritation or focal neurologic findings are present. An emergency CT scan is the initial test of choice. However, as many as 2% of patients with subarachnoid hemorrhage can have a normal CT scan within the first 12 hours after the hemorrhage begins. If the diagnosis is unclear, lumbar puncture should be performed.

Meningitis should be strongly suspected in a patient who presents with headache accompanied by fever, especially if signs of meningeal irritation are present. Antibiotic therapy should be started as soon as possible (based on microorganisms most common for each age group) before the CT scan or lumbar punctures are performed (Chapter 42). However, if there are signs of focal neurologic findings in a patient with fever, a brain abscess should be suspected and the lumbar puncture (but not antibiotics) should be delayed until a CT scan is performed.

Is Headache Due to Hypertensive Encephalopathy or Preeclampsia-Eclampsia?

Moderate elevations of blood pressure alone seldom cause headache; however, severe hypertension as seen in hypertensive crises and eclampsia can be associated with headache. If hypertension is present and the patient is pregnant or has signs of cerebral dysfunction (confusion, obtundation, or coma) or other end-organ damage (retinitis; nephritis with proteinuria), a life-threatening emergency exists.

Note: In pregnancy, a slight increase in blood pressure may be more significant than in the nonpregnant patient. See Chapter 34 (see Hypertensive Crisis) or Chapter 38 (see Eclampsia).

Is This Temporal Arteritis?

Temporal arteritis is a rare but treatable disease with serious sequelae that must be considered in every elderly patient with new headache. The principal manifestations are headache with temporal artery tenderness (not found in every case) and a markedly elevated erythrocyte sedimentation rate. Sudden irreversible monocular blindness may occur. If this condition is suspected, immediate treatment with steroids is indicated and hospitalization should be considered to confirm the diagnosis by means of temporal artery biopsy.

Is Headache Due to Disease in Paracranial Structures?

New or acute headaches are often caused by disease in the eyes, ears, sinuses, or teeth. Look carefully for iritis or acute glaucoma (Chapter 31) or for sinusitis, otitis media, or dental caries or abscess (Chapter 32). Treatment should be focused on the primary condition.

Are There Multiple Patients from the Same Vicinity?

Multiple patients from the same vicinity with complaint of headache suggest carbon monoxide poisoning or other toxin exposure. Patients should be questioned specifically about heating sources (eg, gas heat or oven), burning materials (eg, charcoal) in poorly ventilated areas, use of household cleaners, or other chemical exposure. Specific treatment of carbon monoxide poisoning and other toxin exposure is discussed in Chapter 47.

Disposition

Even after careful initial history and physical examination, the diagnosis may not be apparent in the patient with new headache. Patients with recent onset of new headache should be hospitalized if there is any suspicion of a life-threatening process. Increasing severity of subacute headache over days or weeks, even without focal signs, suggests serious intracranial disease, and the patient should undergo appropriate diagnostic procedures. Subacute headaches without progressive symptoms and chronic headaches may be referred and evaluated on a nonemergency basis.

Pain-Sensitive Structures and Their Projections

Headache is caused by traction, displacement, inflammation, or distention of pain-sensitive structures in the head or neck. Disorders of the scalp, teeth, eyes, and ears and of the mucous membranes of the nose, sinuses, and oropharynx can produce pain. Pain-sensitive structures about the calvarium include the scalp and its blood vessels, the neck muscles, and the upper cervical nerves. The skull, brain, and most of the dura are not pain sensitive. In general, discrete intracranial lesions above the cerebellar tentorium produce pain in trigeminal distribution (anterior to ears), whereas lesions in the posterior fossa project pain to the second and third cervical dermatomes (posterior to ears).

History

Time of Onset

Chronic headache (duration of months or more) is usually not due to a serious disorder, but headache of acute onset or of a changing pain pattern demands prompt evaluation in the emergency department. If the patient has a chronic headache disorder, determine whether the present headache differs from or is identical to the patient's chronic problem. Headaches in the early morning or those causing waking may indicate an increase in intracranial pressure and prompt an evaluation for intracranial tumor.

Family History of Headaches

Primary headache disorders such as migraine and tension headaches commonly have a family history of headaches.

Location of Pain

Migraine or the Cluster Variant

Hemicranial or retroocular pain.

Tension Headache

Commonly diffuse, occipital, or bandlike pain.

Mass Lesion Headache

Often focal (“right here”).

Trigeminal Neuralgia

Stabbing pain localized to the second or third division of the trigeminal nerve.

Quality of Pain

Migraine or the Cluster Variant

Commonly described as throbbing and often preceded by prodromal symptoms or auras, for example, scintillating scotomas or other visual changes.

Tension Headache and Mass Lesion Headache

Usually steady pain.

Trigeminal Neuralgia

A shooting or stabbing character.

Timing

Mass Lesion Headache

Commonly maximal on awakening.

Cluster Variant of Migraine

Frequently awaken patients from sleep and often recur at the same time of day or night.

Tension Headache

May develop at regular intervals, especially with recurrent stressful situations.

Factors Influencing Severity

Migraine or the Cluster Variant

Frequently relieved by pressure on the ipsilateral temporal or carotid artery; by darkness, sleep, or vomiting; or during pregnancy.

Mass Lesion Headache

Often exacerbated by events such as coughing and sneezing that transiently raise intracranial pressure.

Precipitating Factors

Tension Headache

Tension, emotional stress, and fatigue.

Migraine

Hunger, nitrite-containing foods (hot dogs, salami, sausage), chocolate, aged cheeses, bright lights, menses, alcohol, caffeine, monosodium gluta-mate, aspartame, and insomnia.

Cluster Variant of Migraine

Alcohol.

Trigeminal Neuralgia and the Jaw Claudication of Temporal Arteritis

Chewing and eating.

Associated Symptoms

Nausea or vomiting is common with migraine and posttraumatic headache syndromes and may be seen late in the course of mass lesions. Photophobia is prominent with migraine headache but occurs also with meningitis, especially viral (aseptic) meningitis. Myalgias of pericranial muscles (eg, posterior neck muscles) often accompany tension headaches and viral syndromes. Rhinorrhea and lacrimation during headache typify the cluster variant of migraine and are ipsilateral to the pain.

Previous Diagnostic Tests

Has the headache that the patient is presenting with previously been evaluated, and what tests (CT scan, MRI, lumbar puncture, pertinent laboratory data) have been performed?

Response to Medication

Find out what medications have worked in the past for this patient and if the patient commonly takes medications for prevention of headache. Clinical response of decreased pain to a medication should no be used as a lone indicator of a benign etiology of the headache.

Physical Examination

Vital Signs

Fever

The presence of fever supports a diagnosis of meningitis, encephalitis, or headache associated with viral infection. A low-grade fever may also occur in temporal arteritis.

Blood Pressure

Hypertension per se rarely causes headache, but chronic hypertension is the major risk factor for stroke, especially intracerebral hemorrhage. Intracerebral hemorrhage may be associated with acute headache. Blood pressure may be markedly elevated during hypertensive encephalopathy or as a result of preeclampsia–eclampsia, subarachnoid hemorrhage, or brain-stem stroke.

Skin

Neurofibromas or café au lait spots of Recklinghausen disease may be associated with benign or malignant intracranial tumors.

Cutaneous angiomas sometimes accompany arteriovenous malformations of the central nervous system; rupture results in subarachnoid hemorrhage and acute headache.

Scalp and Head

Temporal Arteries

Note nodularity or tenderness compatible with temporal arteritis.

Sinuses

Note tenderness, erythema of overlying skin, or nasal discharge.

Temporomandibular Joints

Look for tenderness or limitation of motion.

Orbits

A bruit heard when the stethoscope is placed on the eyeball over closed eyelids may suggest intracranial arteriovenous malformation.

Neck and Back

Muscle Spasm

Cervical muscle spasm may be a sign of tension or may occur with migraine.

Meningeal Signs

Can the patient touch chin to sternum? If not, is the limitation of motion mainly in the anteroposterior direction, suggesting meningeal irritation, or in all directions, as is common with cervical spine disorders? Is there any discomfort, neck flexion, or contralateral knee flexion during straight leg raising (Kernig sign)? Most important, is there even slight flexion of the knee (Brudzinski sign) during passive neck flexion?

Meningeal signs may be absent or difficult to demonstrate in the early stages of subacute meningitis and may be very minimal in very young or older patients. Several hours may elapse before evidence of meningeal irritation develops after subarachnoid hemorrhage, and these signs disappear if the patient lapses into deep coma.

Neurologic Examination

Unilateral cranial nerve, cerebellar, motor, or reflex abnormalities suggest a diagnosis of intracranial mass lesion.

Miscellaneous Physical Findings

Papilledema, the hallmark of increased intracranial pressure, should always be sought. Acute confusion or altered consciousness is common after subarachnoid hemorrhage and with purulent meningitis.

Indications for Imaging in the ED

The following are indications to order no contrast CT scans in patients presenting to the ED with an acute headache:

1. Abnormal neurologic exam to include altered mental status, cognitive impairment, or a focal deficit.

2. Patients experience a new severe headache of sudden onset.

3. HIV positive patients with a presentation of a new headache.

Subarachnoid Hemorrhage

Essentials of Diagnosis

• Sudden onset of severe headache
• Nuchal rigidity is seen in most patients but can take hours to develop

Acute onset of severe headache with maximum intensity in just a few minutes, that is unlike any headache that the patient has experienced previously, is suspicious for subarachnoid hemorrhage. Subarachnoid hemorrhage usually results from rupture of an aneurysm or arterial venous malformation. The diagnostic test of choice is a noncontrast CT scan. However, 2% of patients with subarachnoid hemorrhage can have a normal CT scan within the first 12 hours after the hemorrhage begins. As a result, a lumbar puncture should be performed if the CT is normal and the diagnosis is still suspected. A detailed discussion of subarachnoid hemorrhage is found in Chapter 37.

Cerebrovascular Accident (Stroke)

See also Chapter 37.

Essentials of Diagnosis

• Sudden-onset focal neurologic deficit
• Symptoms related to vasculature involved

Clinical Findings

Thrombotic or embolic strokes may be associated with mild to moderate nonthrobbing headaches and are present in 14% of strokes. The headache may precede or accompany the stroke.

Treatment and Disposition

Treat stroke as described in Chapter 37. Hospitalize the patient for evaluation and treatment.

Meningitis and Meningoencephalitis

See also Chapter 42.

Essentials of Diagnosis

• Headache, fever
• Nuchal rigidity

Clinical Findings

Headache, confusion, and nuchal rigidity developing over hours to days are classic features of meningitis. However, in rapidly progressive pyogenic meningitis, fever and altered consciousness are the most prominent presenting signs. In patients with subacute meningitis, headache is an early symptom that may precede nuchal rigidity and other meningeal signs. The headache of meningitis is continuous and throbbing and, although generalized, usually most prominent over the occiput. The pain is increased by head shaking, jugular vein compression, or any other maneuver that increases intracranial pressure. Pain is not relieved by changes in posture. Neck stiffness and other signs of meningeal irritation must be sought with care, because they may not be obvious early.

If meningitis or meningoencephalitis is suspected, perform a lumbar puncture (Chapter 7) and obtain blood for culture. A neuroimaging study should be obtained prior to lumbar puncture if any of the following is present: (1) papilledema, (2) altered mental status, and (3) focal or lateralizing neurologic findings.

Treatment

Antimicrobials

Begin antibiotics immediately and do not delay awaiting blood draws or performance of a lumbar puncture. The choice of drug depends on the clinical circumstances and the age of the patient (see Chapter 42).

Supportive Care

General supportive care should be initiated in the emergency department. Protect the patient's airway and provide padded bed rails or restraints for agitated or delirious patients. If seizures have occurred, start anticonvulsant therapy. Concomitant corticosteroid treatment in bacterial meningitis has been shown in children to decrease the incidence of residual hearing impairment when caused by Haemophilus influenzae type B but not Streptococcus Pneumoniae or Neisseria meningitidis. Consider steroid therapy in children older than 1 month with suspected meningitis. There is also evidence to support steroid use in adults with meningitis.

Disposition

Immediate hospitalization is warranted except perhaps in the case of a patient with aseptic (viral) meningitis who appears well, can be observed at home by a third party, and has close follow-up within 24 hours for reexamination.

Postural (Postlumbar Puncture) Headache

Essentials of Diagnosis

• Follows lumbar puncture
• Headache exacerbated by the upright position
• Headache relieved by laying down

Clinical Findings

Postural headache may follow lumbar puncture, especially if a large gauge, medium bevel, cutting spinal needle is used. Studies have shown that the larger the needle diameter, the higher the incidence of postdural puncture headache. This type of headache is worse in the upright position and nearly absent in recumbency. The onset of headache is usually within the first 24–48 hours and rarely occurs later. The site of the headache may be bifrontal, occipital, or in the neck and upper shoulders.

Treatment and Disposition

Recumbency for 18–24 hours is often recommended but there is no evidence that it is beneficial. Adequate hydration and analgesics are usually sufficient management. For more persistent cases, IV caffeine can be tried. Referral to an anesthesiologist for an epidural blood patch may be of benefit.

Posttraumatic Headache

Essentials of Diagnosis

• History of head trauma
• May have associated dizziness, vertigo, insomnia

Clinical Findings

Headache caused by head injury may begin immediately or within weeks after trauma. Chronic posttraumatic headache is defined as a headache that continues for more than 3 months after the trauma occurs. The symptoms are not necessarily proportionate to the severity of the traumatic event. Associated dizziness, vertigo, insomnia, depression, and personality change may occur. This constellation of symptoms is referred to as posttraumatic syndrome. Posttraumatic headache usually presents no special diagnostic or distinguishing features, although it may be suggestive of tension headache or migraine. Pain usually remits after days to weeks but occasionally persists for years.

Treatment and Disposition

The character of the headache dictates the treatment of posttraumatic headache. The pharmacologic treatments for migraine and tension headache are appropriate for posttraumatic headache and should be chosen by the constellation of the patient's symptoms. Hospitalization is not indicated for posttraumatic headache, although referral for prophylactic therapy is indicated if symptoms persist.

Trigeminal Neuralgia

Essentials of Diagnosis

• Excruciating, stabbing, facial pain
• Pain in the distribution of the trigeminal nerve

Clinical Findings

Trigeminal neuralgia is distinguished by repetitive, brief unilateral facial pain confined to the distribution of the trigeminal nerve. Lightning-like stabs of excruciating pain characteristically recur over seconds to minutes and spontaneously abate. Occurrence during sleep is rare. Sensory stimulation (eg, touch, cold, wind, talking, chewing) of trigger zones about the cheek, nose, or mouth precipitates paroxysms of pain.

Trigeminal neuralgia usually develops after the fourth decade and is more common in women than men. Pain-free intervals may last minutes to weeks, but permanent spontaneous remission is rare. Pain is confined mainly to areas supplied by the second or third divisions of the trigeminal nerve (maxillary and mandibular areas of the face). Involvement of the first division of the trigeminal nerve (the forehead) or bilateral disease occurs in less than 5% of cases.

Treatment

Phenytoin, 250 mg IV over 5–10 minutes, may abort an acute attack. Remission of symptoms with carbamazepine occurs in so many patients that it has been used as a diagnostic test. Begin with 100 mg orally twice daily, and increase by 100 mg every other day until the patient is pain free or side effects develop.

Baclofen (Lioresal, others) is also beneficial and has synergistic effects when used with carbamazepine or phenytoin. Lamotrigine (Lamictal) has also been shown to be useful in the treatment of trigeminal neuralgia, with a starting dose of 25 mg daily with an increase of 25 mg each week until a maintenance dose is reached.

Narcotic therapy has been shown to be of little use because of the brief duration of the pain. Surgical referral may be indicated for patients who do not respond to conventional pharmaceutical intervention.

Disposition

Neurologic referral for evaluation and treatment is appropriate. Hospitalization is not usually indicated.

Intracranial Mass

Essentials of Diagnosis

• Mild to moderate headache increasing in frequency or duration
• Becomes associated with a focal neurologic deficit

Clinical Findings

Headache due to primary or metastatic intracranial tumor is usually mild to moderate in severity and described as deep, aching, and initially intermittent. Pain is maximal on awakening and during episodes of increased intracranial pressure (eg, coughing, sneezing, or straining at stool). Headaches increase in frequency and duration over weeks to months and become associated with focal neurologic signs. One-third to one-half of patients with brain tumor present with this classic history. A CT scan obtained with IV contrast will usually confirm the diagnosis. MRI, which is more sensitive, may be used as well.

Treatment and Disposition

If an intracranial mass lesion is found to be the cause of headache, urgent neurologic or neurosurgical consultation is indicated. Hospitalization may be required for initiation of treatment. The distinction between primary and metastatic tumor is essential.

Essentials of Diagnosis

• Papilledema
• Increased intracranial pressure
• Nonspecific brain imaging study

Clinical Findings

Idiopathic intracranial hypertension is a syndrome characterized by papilledema, increased intracranial pressure (with normal CSF), and a nonspecific brain imaging study demonstrating normal or small-sized ventricles. Women, specifically obese women, are affected much more commonly than men; the peak incidence occurs in the third decade. Diffuse headache is almost invariably a presenting symptom. Complaints of diplopia and blurred vision or transient visual obscuration occur in more than 60% of cases. Moderate to severe papilledema is seen in over 40% of affected persons. The diagnosis is made when the patient has symptoms of increased intracranial pressures, no localizing symptoms, a nonspecific or normal imaging study and CSF pressures are elevated over 250 mm of H2O with otherwise normal CSF findings.

The course in idiopathic cases is generally self-limited over several months, but visual loss may occur. Differentiation from space-occupying intracerebral mass lesions is critical and can be achieved by CT scan.

Treatment and Disposition

Hospitalization is necessary for evaluation and treatment in patients with newly diagnosed idiopathic intracranial hypertension in the emergency department. Appropriate treatments include repetitive lumbar punctures, carbonic anhydrate inhibitors (acetazolamide), thiazide diuretics, and corticosteroids for visual complaints. Surgical maneuvers, including lumbar-peritoneal shunting or optic nerve sheath decompression, may be required. Patients who present to the emergency department with a known diagnosis of pseudotumor cerebri should receive treatment in consultation with the patient's neurologist, neurosurgeon, or ophthalmologist.

Temporal Arteritis (Giant Cell Arteritis)

Essentials of Diagnosis

• Older than 50 years
• Unilateral headache
• Usually tender over the temporal artery
• Elevated erythrocyte sedimentation rate
• Unilateral vision loss if treatment is delayed

Clinical Findings

Temporal arteritis, although uncommon in the general population, is the most common form of systemic vasculitis. The disease preferentially involves large- to medium-sized arteries. It affects women twice as often as men and is rarely seen before the age of 50 years. Nonspecific signs and symptoms are typical: malaise, myalgia, weight loss, arthralgia, and fever. The headache is classically of rapid onset, unremitting, and located over the temporal arteries. It is often unilateral. Associated scalp tenderness may be a prominent complaint, especially when patients lie with their head on a pillow or brush their hair. Pain during chewing (jaw claudication) is strongly suggestive of temporal arteritis. Permanent unilateral blindness, usually sudden in onset, occurs in about half of patients if treatment is delayed; half of patients so affected go on to develop bilateral blindness.

The temporal arteries may be normal on examination, although focal tenderness, thickening, nodularity, or decreased pulsation may be found. The diagnosis should be suspected if the erythrocyte sedimentation rate is more than 50 mm/h.

The diagnosis can be established by demonstration of vasculitis in biopsy specimens of an affected artery. The biopsy specimens must be carefully examined (multiple sections) because involvement is segmental.

Treatment

Temporal arteritis responds dramatically to corticosteroid treatment. Begin prednisone, 40–60 mg/d orally, as soon as the diagnosis is suspected. Biopsy should be obtained within 2–3 days after beginning corticosteroids. Patients presenting with visual loss warrant immediate ophthalmology consult and should receive IV steroids in the emergency department.

Disposition

For patients with severe symptoms or visual loss, hospital admission is urgently indicated for evaluation and treatment with IV steroids. Patients with minimal symptoms may be discharged with oral prednisone but should make arrangements for close follow-up and biopsy within 3 days.

Tension Headache

Essentials of Diagnosis

• Gradual onset
• Bilateral pressure or tightening about the head
• No nausea or vomiting

Clinical Findings

Tension headache is the most prevalent form of headache. It has significant societal impact with lost workdays and reduced effectiveness when at work. Women are affected slightly more commonly than men. The age at onset is usually at age 25–30. Headaches are often associated with emotional stress and have no prodrome. The pain typically comes on gradually, is bilateral, occipital, or frontal in location, and is described as a tight band or pressure about the head. The pain is constant and nonthrobbing and persists for hours or for the entire day. Nausea and photophobia are frequent accompanying symptoms but are milder than that with migraine. Vomiting is not a feature of tension-type headache. Neurologic examinations are normal.

Treatment

The treatment approach for tension headaches in the emergency department is pharmacotherapy. Nonsteroidal antiinflammatory drugs remain the therapy of choice in abortive treatment of tension headache. Combination medications that contain caffeine, analgesics, and sedatives have been found to be effective. Muscle relaxants (cyclobenzaprine, methocarbamol) may be appropriate when muscle tension appears to play a strong role. Referral for prophylactic treatment with antidepressants (amitriptyline) and incorporation of a “wellness” component is appropriate for patients expressing depression or anxiety as precipitants to their headaches.

Disposition

If simple measures are not successful, neurologic referral may be necessary. Hospitalization is not indicated.

Migraine

Essentials of Diagnosis

• Throbbing-type pain
• Associated nausea, vomiting, and photophobia are common
• May have associated neurologic symptoms

General Considerations

Migraine headache is a primary brain disorder in which neural events result in vasodilation of blood vessels that causes pain and further nerve activation. Most cases occur in women, there is an inherited predisposition, and onset may be as early as the first decade. Recurrent vomiting during childhood may be the earliest manifestation of migraine. A family history of migraine is commonly present.

Clinical Findings

Migraine headaches are classified as being with aura (formerly called classic migraine) or without aura (formerly called common migraine).

In migraine without aura headache, pain is throbbing or pulsing, unilateral, and of moderate or severe intensity. Associated symptoms include nausea and vomiting, photophobia, or phonophobia. Continuing pain may cause cervical muscle contraction, leading to an erroneous diagnosis of tension headaches.

Migraine with aura is preceded by transient neurologic symptoms (the aura). The most common auras are visual disturbances: hemianopic field defects, scotomas, and scintillations that enlarge and spread peripherally. Other aura may include sensory symptoms or dysphasic speech disturbance. As the aura fades, vasodilatation occurs producing the headache that has identical characteristics as migraine without aura.

Attacks may be precipitated by certain foods such as tyramine-containing cheeses, wine, meats with nitrite preservatives, chocolate containing phenylethylamine, and monosodium glutamate (a flavor enhancer). Fasting, emotion, menses, drugs (especially oral contraceptive agents and vasodilators such as nitroglycerin), and bright lights may also trigger attacks.

Treatment

Analgesics and Analgesic Combinations

These drugs remain appropriate first-line therapy for acute migraine attacks. Commonly patient will have tried at least one or several analgesics prior to presentation to the emergency department. Appropriate analgesics include aspirin, nonsteroidal anti-inflammatory drugs, and combination medications that contain caffeine, analgesics, and sedatives. Opiates should be avoided because they can exacerbate gastrointestinal symptoms and have a high abuse potential.

Dopamine Antagonists (Antiemetics)

Several dopamine antagonists have been shown to be effective in aborting acute migraine headaches. Prochlorperazine and metoclopramide are most widely used. Prochlorperazine dosing is 10 mg IV. Side effects include hypotension and akathisia. Metoclopramide is also effective in doses of 10 mg IV.

Triptans

The triptans have an advantage of being selective pharmacologic agents for the treatment of migraine headaches. These compounds are serotonin 5-HT receptor agonists. All of these drugs have been shown to be effective in aborting acute migraine headaches. However, they have significant side effects including coronary artery constriction leading to myocardial infarction. These drugs cannot be used in patients with a history of ischemic heart disease, uncontrolled hypertension, or cerebrovascular disease. The following triptans can be used in the treatment of migraines in the emergency department:

• Sumatriptan—4–6 mg subcutaneously, which may be repeated after 1 hour; or 25–100 mg orally, which may be repeated after 2 hours.
• Naratriptan—1–2.5 mg orally, which may be repeated after 4 hours.
• Almotriptan—6.25–12.5 mg orally, which may be repeated after 2 hours.
• Rizatriptan—5–10 mg orally, which may be repeated after 2 hours.
• Zolmitriptan—1.25–2.5 mg orally, which may be repeated after 2 hours.

Ergot Derivatives

Ergot preparations have been used widely in the past for the acute treatment of migraine headaches. These drugs have complex pharmacology, and there is little evidence to support their use. With the effectiveness of dopamine antagonists and triptans, ergot preparations should be abandoned for abortive therapy in the emergency department.

Prophylactic Drugs

Prophylactic therapy may be useful in preventing migraine headaches, but it should not be initiated in the emergency department. Patients should be referred to a neurologist for evaluation for preventive treatment.

Disposition

Referral to a neurologist or primary care physician is indicated. Hospitalization (other than a brief stay in the emergency department for parenteral medication) is rarely needed.

Cluster Headache

Essentials of Diagnosis

• Clusters of daily attacks separated by week to months of pain-free intervals
• Attacks consist of severe unilateral headache
• Associated cranial autonomic symptoms include lacrimation, miosis, conjunctivalinjection, nasalcongestion, and rhinorrhea

Clinical Findings

Cluster headache is a syndrome of distinct attacks of severe, unilateral headache with ipsilateral cranial autonomic symptoms. The autonomic symptoms may include ptosis, lacrimation, miosis, conjunctival injection, nasal congestion, and rhinorrhea. It is more common in men than in women and begins later in life than migraine headaches.

Pain occurs in distribution of the trigeminal nerve and most commonly in the ocular, frontal, and temporal areas. Each attack builds in intensity over 10–15 minutes and may last up to 3 hours. Attacks recur one to three times daily, often at nearly the same time for periods of 2–12 weeks that may be separated by headache-free interval remission periods that average 6 months to 2 years. A subset of patients experience chronic cluster headaches without remission. These patients have attacks for more than 1 year without remission or with remissions lasting less than 14 days. Episodes may be precipitated by alcohol or vasodilator-type drugs. Nitroglycerin challenge can be diagnostic, producing a typical headache in 30–60 minutes.

Treatment

Standard treatment for acute attacks is oxygen (7 L/min for 15 min) delivered by face mask; this treatment has a reported 70% response rate. Sumatriptan subcutaneously or intranasally, although contraindicated in patients with known cardiovascular disease, has proved effective: more than 90% of patients experience complete or near complete relief. Less effective agents such as dihydroergotamine and ergotamine are also commonly used. Lidocaine, 20–60 mg given intranasally, provides some relief within 10 minutes in most patients, but complete relief is rare.

Due to the severity, reoccurrence, and chronicity of attacks, transitional therapy should follow treatment for the acute headache. Transitional treatment should be initiated at the first sign of an attack and continued for 2 weeks past the last attack. Agents for transitional therapy include corticosteroids (prednisone 60–80 mg/d tapered over 2 weeks), naratriptan 2.5 mg twice daily, and ergotamine 2 mg at bedtime or twice daily. Surgical interventions on the cranial parasympathetic system or on the trigeminal nerve have been recommended for intractable chronic cluster headaches that have become resistant to medical management.

Disposition

Neurologic referral is indicated.