Evaluation and Treatment of Primary Headache Syndromes

Headache can be a frustrating and worrisome disorder for the patient and physician alike. This review of diagnostic procedures and criteria will help you provide efficient and effective evaluation and treatment of primary headache syndromes.

By James Calabro, MD, and Kelly Anne Foley, MD

Dr. Calabro is a resident in emergency medicine and Dr. Foley is an assistant professor of emergency medicine at Eastern Virginia Medical School in Norfolk, Virginia.

For physicians, headaches can be among the most difficult disorders to treat. Afraid of missing an occult hemorrhage or being taken in by a patient reporting false symptoms in an attempt to obtain dangerous drugs, many clinicians approach management of headaches with trepidation. With proper understanding of the primary headache syndromes and firm criteria to determine which patients require further diagnostic testing, however, treatment of headaches can be efficient and effective. In this article, we will discuss proper diagnostic procedures and therapeutic methods of alleviating patient suffering.

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Major Public Health Problem

In our society, headaches are a major public health problem. According to Rasmussen and colleagues, the clinical prevalence of any type of headache in an industrial society is 69% among men and 88% among women (Journal of Clinical Epidemiology, vol. 44, p. 1147, 1991). As a socioeconomic burden in developed countries, headache ranks only behind dementia and stroke. The economic costs of headache can be attributed not only to lost days at work but also-and even to a greater degree-to decreased effectiveness while at work.

In 1988, the International Headache Society (IHS) published guidelines to classify headaches (Cephalalgia, vol. 8 [suppl. 7], p. 1, 1988). Similar to the classification protocol outlined in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM IV) for psychiatric diagnoses, the IHS guidelines provide a numbering system and criteria that must be met to declare a diagnosis of a specific type of headache. These criteria have helped eliminate the potential for confusion among researchers and clinicians, who often use different names for the same type of headache syndrome in their communications and in their research.

In practical terms, headache syndromes can be classified as either primary or secondary. Primary headaches can be classified as pure headache syndromes-that is, they are self-originating and are not triggered or produced by other disorders. They include tension, migraine, and cluster headaches. Secondary headaches, of which there are many types, occur as a symptom of other disorders, such as intracranial neoplasm, meningitis, or subarachnoid hemorrhage.

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Medical and Headache History

The information gained from physical examination of patients with headache symptoms is clearly inferior to that obtained in a thorough medical history. With few exceptions, the history will be the main determinant of diagnostic testing and the course of treatment.

Obtaining the history. The patient's medical history should be obtained with a focus on the headache history, which will often aid the practitioner more than any other part of the medical history. The history begins with a description of the headache, which includes the type of pain and its intensity, onset, location, duration, and progression. The diagnosis will be aided by a specific description, such as one that differentiates between a throbbing pain and a boring, excruciating pain.

Although nonspecific, the location of the pain may help narrow the diagnosis. Unilateral pain, for example, is associated mostly with cluster headaches, whereas bilateral pain is linked most often to tension headaches. Noting the severity of the pain during the initial examination is also essential, so that the results of treatment can be properly assessed in later examinations.

In the evaluation of a headache, stress is placed on its presentation, which, like its location, can narrow the diagnosis. A headache that begins and evolves slowly, for example, suggests a tension headache, whereas one that appears as a "thunderclap" points to a subarachnoid hemorrhage. The duration of a headache episode can indicate the severity of a presentation, thereby narrowing further the differential diagnosis. Short-lasting episodes of headache pain with acute onset may indicate cluster headache, for example, and chronic headache syndromes more often are associated with such structural disorders as tumors and slow subdural hemorrhage.

Common misconception regarding tumors. Traditionally, the progression of headache pain throughout the day has been emphasized, but it should not lead the physician to rule out certain diagnoses. A common misconception is that headaches associated with tumor are more common in the morning upon waking. In a recent study, however, headaches were associated with brain tumors in only 50% of patients, and of those patients, only 33% had a headache that was worse upon waking.

More beneficial to the diagnosis is a history of cephalalgia increasing in response to physical activity. The intensity of tension headaches, according to the IHS criteria, should not change during physical activity. In contrast, migraines can be exacerbated by activity. Headaches associated with tumor commonly worsen when a person bends over or performs the Valsalva maneuver. One third of patients who have a tumor have increasing pain when performing these maneuvers. The diagnosis of migraine headache can be suggested even further by a history of prodromal symptoms, such as yawning, malaise, or irritability; aura; or the symptoms that occur after an attack has passed (known as the postdrome), such as excessive sleep or emotional disturbance. Finally, a recent history of trauma is a key indicator in determining the necessity of imaging studies.

Additional signs and triggers. Associated symptoms are important in the headache history. Eye pain, loss of visual acuity, or blindness, for example, can suggest a secondary headache caused by temporal arteritis, pseudotumor cerebri, or acute angle-closure glaucoma. Neck pain, rash, or fever are alarming signs that warrant immediate testing and treatment for possible meningitis. Focal neurologic disorders such as numbness, weakness, dysarthria, or dysphagia suggest the occurrence of stroke. Seizures and loss of consciousness strongly suggest the presence of a structural lesion.

The dietary and medicinal history is also important. Caffeine, nicotine, alcohol, and foods containing tyramine are associated with migraine headaches. Many recreational drugs, such as cocaine, are also associated with headaches. Most patients with a history of migraine headaches are able to report the foods and substances that trigger their headache and may admit to a history of willingly ingesting them. In addition, because sleep disturbances or lack of sleep can cause headaches, an evaluation of a patient's sleep habits is important to the diagnosis.

The medicinal history should include the medications that have been both effective and ineffective in treating headache symptoms. The possibility that the headache is actually caused by withdrawal from medications taken for headache-referred to as medication rebound headache-should be included in the differential diagnosis of patients who have chronic headaches and take a heavy load of therapeutic pain medications. It is also important to note any previous neurologic examinations and imaging studies to avoid unnecessary repetition of these expensive tests.

The general history should note any previous episodes of seizure, neoplasm, psychiatric disturbance, hypertension, and stroke, and the patient's risk of diabetes should be assessed. A history of surgical procedures such as shunt placement or any neurosurgical procedure is also important.

It is highly probable that an accurate diagnosis could be derived from the medical history, but the ability to make such an assessment does not eliminate the necessity for an appropriate physical examination. For a patient reporting a headache, the basic focused physical examination should include evaluation of vital signs; a complete HEENT examination, including an evaluation of the fundi; and a neurologic examination. Of course, a more extensive evaluation may be necessary, depending on the findings.

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Diagnostic Testing

The pivotal question for most physicians during their evaluation of a patient's headache symptoms is knowing when more extensive diagnostic testing, such as lumbar puncture, computed tomography (CT), or magnetic resonance imaging (MRI), is necessary. Clearly, to employ these adjunctive diagnostic procedures for every patient presenting with a headache would be economically unfeasible and a poor use of resources. Indeed, as Evans has found, the chance of finding a brain tumor on a CT scan of a patient who presents with a headache and no neurologic findings is 0.8% (Neurologic Clinics, vol. 14, p. 1, 1996). As we have noted earlier, however, specific clues from the patient's medical and headache history can indicate when such an approach is appropriate and necessary and can therefore guide the direction of the clinical and physical examination (see table, below).

The diagnosis of subarachnoid hemorrhage, in particular, is a special situation. Usually, the most expedient testing method is the CT scan. It is only 92% sensitive, however, in detecting subarachnoid hemorrhage if the bleeding occurred within the 24 hours before presentation. This rate drops to 58% five days after the incident.

These results reveal the importance of lumbar puncture in the evaluation of all patients in whom a subarachnoid hemorrhage is suspected and for whom results of a CT scan of the head are negative. The sensitivity of lumbar puncture approaches 100% one to five days after the hemorrhage when photospectrometry is used to detect xanthochromia in the fluid sample. Because a lumbar puncture can precipitate brain herniation and death in the presence of increased intracranial pressure, a CT scan is warranted before the lumbar puncture is performed.

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Tension Headache

The tension headache is commonly called a muscle contraction headache or stress headache. The IHS has attempted to switch the name of this syndrome to tension-type headache because the actual cause of the disorder has not been confirmed.

In the past, muscle contraction was thought to cause inflammation that in turn led to headache pain, but studies have never been able to confirm this hypothesis. We do know, however, that the tension type of headache is the most common primary headache; lifetime prevalence is approximately 80% in the general population. The tension headache is more common in women, and its prevalence among a population is proportionately linked to that group's education and income.

Features of tension headache. Tension headaches are indicated by pain exhibiting at least two of the following characteristics: a pressing/tightening (nonpulsating) quality; mild or moderate intensity; bilateral location; and an absence of response to physical exertion or routine physical activity. Other diagnostic criteria include the absence of nausea and vomiting and evidence of either phonophobia or photophobia, but not both (see table, below).

Treatment. A caring approach to treatment will enhance a patient's satisfaction. The headache sufferer should be informed of the benefits that can be derived from reductions in stress and lifestyle changes that would decrease the frequency and intensity of headache episodes. Initial emergency treatment can begin with aspirin, acetaminophen, or nonsteroidal antiinflammatory drugs (NSAIDs). Some headache medications contain caffeine, which can increase the effectiveness of acetaminophen and aspirin. If overused, however, these drugs can produce caffeine withdrawal headaches. If symptoms still are not resolved after such therapy, an outpatient regimen may be tried, consisting of an analgesic/ sedative combination in very small amounts. If symptoms persist, an entire reassessment may be necessary, including further diagnostic studies or neurologic referral.

In treating tension headaches, physicians often prescribe narcotics, which in almost all cases are unnecessary. Strong narcotics in particular are an unacceptable choice, because tension headaches, by definition, produce only mild-to-moderate pain. In such situations, physicians should be suspicious when a patient asks for narcotic treatment; such a request suggests drug abuse. If narcotic therapy appears warranted in the treatment of what was thought to be a tension headache, then that diagnosis should be reassessed.

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Migraine Headaches

Migraine headaches have been extensively researched but the details of their pathogenesis remain enigmatic. Recent research points to both vascular and neurogenically mediated causes that can, in combination or individually, precipitate a migraine headache. The two most common types are migraine with aura (classic) and migraine without aura (common). The migraine with aura is actually more rare than a headache without aura. Roughly 80% of migraine headaches have no component of aura.

Stages of a migraine headache. The aura is actually only one of five possible phases that migraine sufferers describe. These phases consist of the prodrome, the aura, the headache itself, headache termination, and a postdromal phase. In some patients, not all of these phases may appear, and in others, stages may occur simultaneously.

The prodromal stage, which is often a term used by clinicians synonymously with aura, is actually a separate stage. The prodrome is a physical warning of a headache that will begin within hours or days. The symptoms that accompany this stage may be described as an emotional change, such as euphoria or a feeling of dread of an imminent headache. Other prodromal symptoms include photophobia or osmophobia. The prodromal presentation can be variable and is very specific to each person.

An aura, however, consists of focal neurologic symptoms that evolve quickly, usually in minutes. These can include changes in visual acuity, perception of auras or halos around light sources, or visual field deficits. The symptoms of an aura usually last less than one hour. It is classically a visual phenomenon but it can be a motor or sensory disturbance as well. The headache phase and headache termination phase are self-explanatory. The postdrome is similar to the prodrome in that it usually includes a nonspecific emotional or physical change, often associated with tiredness or weakness.

Migraine with aura. When an aura, which is a neurologic disturbance, is present, the diagnosis of a migraine becomes more involved. A typical migraine may produce homonymous visual disturbances-rainbow halos may appear around light sources, for example-and unilateral paresthesia, numbness, weakness, or aphasia. A migraine headache accompanied by an aura is indicated by at least three of the four following phenomena: one or more fully reversible symptoms of aura indicating cerebral or cortical brainstem dysfunction; aura symptoms developing gradually over a period of more than four minutes or two or more symptoms occurring in succession; all aura symptoms lasting less than 60 minutes; and a headache occurring at the same time as the aura or within 60 minutes of it.

When a true organic injury is suspected, diagnostic testing must focus first on that possibility and its causes before a diagnosis of migraine with aura can be made.

Migraine without aura. According to the IHS, a migraine headache without aura is defined by pain exhibiting two of the following qualities: unilateral location, pulsation, moderate-to-severe intensity, or susceptibility to aggravation by physical activity. Each episode must include nausea with or without vomiting or be accompanied by photophobia or phonophobia, but not both. The IHS guidelines also emphasize that before the diagnosis of migraine can be made, all types of secondary headache must be ruled out and the patient history should include at least five attacks that fulfill the criteria explained above. This last requirement is often not met when patients seek emergency treatment, but such an oversight should not prevent or limit appropriate therapy for patients with suspected migraine.

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Treatment of Migraine Headache

Treatment of symptoms begins with making the patient comfortable. The patient usually desires a darkened, quiet area. Warm or cool compresses may be applied as well. Intravenous fluid administration can be beneficial for patients who are dehydrated from nausea and vomiting. Antiemetic therapy is also beneficial and may even be the reason a patient seeks treatment. Approximately 80% of patients with migraine have nausea and vomiting at some point during their attack. Affording a patient these comforts can help engender a feeling of respect and trust for the physician.

Medications for treatment of migraine headache have been extensively studied. Medical therapy should follow a stepwise approach on the basis of each patient's medical history and results of physical examination. For example, the administration of over-the-counter medications such as NSAIDs and acetaminophen makes little sense if a patient has already tried them. Likewise, if a patient's symptoms include nausea or vomiting, a phenothiazine may be effective in treating both the gastrointestinal distress and the headache. Accordingly, if a patient knows of a successful treatment regimen that falls within reasonable treatment guidelines-that is, it does not include heavy doses of narcotics-you should attempt to accommodate him or her.

Of course, when prescribing or administering any drug, physicians must be fully aware of the possible adverse effects, which can certainly cause more harm than the headache itself.

Simple analgesics and NSAIDs. Simple analgesics such as acetaminophen and aspirin are commonly given for headache pain, but when they are administered after an emergency evaluation of a patient with migraine, it is important to determine the amount already taken by the patient at home to prevent iatrogenic overdose. The risk of liver injury and subsequent liver failure in patients who take excessive amounts of acetaminophen is widely known, as are the toxic effects associated with aspirin and NSAID overdose.

The IHS guidelines require the headache to be of moderate to severe intensity to qualify as a migraine headache. This criterion places the disorder beyond the scope of medications traditionally given for mild-to-moderate pain. Aspirin and acetaminophen can be more effective with the addition of caffeine or a mild sedative. This combination of medications has been relatively successful in reducing and even eliminating the pain of migraine. Recent research has shown that intravenous administration of 30 mg of ketorolac is an effective treatment for migraine (Academic and Emergency Medicine, vol. 5, p. 573, 1998).

Opioid agents. Results of studies by Lane and colleagues and Belgrade and colleagues, among others, indicated that opioids are relatively ineffective in treating migraine (Annals of Emergency Medicine, vol. 18, p. 360, 1989; Neurology, vol. 590, p. 39, 1989). Numerous other drugs are available that are specifically tailored to the pathogenesis of migraine headache and have a more favorable adverse effect profile. Opioids may be appropriate in situations in which their efficacy rate clearly exceeds that of less addictive medications. Narcotics are usually limited to a "rescue" role in circumstances in which other regimens have failed. Again, a specific request for narcotic agents should arouse the physician's suspicion for malingering and abuse.

Ergotamine and dihydroergotamine. Ergotamine and dihydroergotamine (DHE) are members of the ergot alkaloid family of drugs. The pharmacologic action of these medications is based on their 5-HT-receptor agonist ability. Although vasoconstriction was once thought to be the primary mechanism in effective migraine treatment, new research has shown that suppression of neurologic inflammatory responses and neuron conduction may play a more significant role.

Because of the risk of severe adverse effects, ergotamine and DHE should not be given to patients who are pregnant or who have uncontrolled hypertension, coronary or peripheral vascular disease, thyrotoxicosis, or sepsis. Ergotamine, while effective in treating migraine, produces significant adverse effects that include nausea and vomiting.

Since the 1940s DHE has been a favored option, because it produces fewer gastrointestinal effects and significantly less vasoconstriction and is a more potent alpha-blocker. The drug has a very favorable efficacy rate in reducing migraine headache pain. It also is associated with a very low frequency of rebound headaches, an effect that is probably linked to the long half-life of the ergotamines. The newer triptan class of antimigraine drugs has a shorter half-life and thus a higher frequency of administration and rebound effects.

Because DHE has a more favorable adverse effect profile, it should be the first choice of the ergot alkaloids. Dihydroergotamine can be given in numerous formulations but is most effective when administered in an intravenous dose. Because DHE can increase nausea and vomiting, antiemetic therapy, such as 10 mg of intravenous metoclopramide, and intravenous hydration are recommended before treatment with DHE.

Dihydroergotamine therapy should always begin with a 0.5-mg test dose given over two to three minutes. If no significant adverse events occur after 10 minutes, then a second dose of 0.5 mg may be given. A total dose of 1 mg is usually very effective for most patients with migraine. A nasal preparation of DHE is also effective and can completely resolve migraine headache in 50% of patients; it has a 24-hour headache relapse rate of 15%.

The triptans. Some of the adverse effects of ergotamine and its derivatives limit the number of patients who can use them safely. This profile has prompted a search for safer medications, which has produced a new class of drugs, the triptans. These drugs are serotonin-receptor agonists that abort the headache by producing cerebral vasoconstriction and exerting control over the neurohormonal milieu. Currently, naratriptan, rizatriptan, sumatriptan, and zolmitriptan are being heavily marketed specifically for the treatment of migraine. Although these medications are effective, they are associated with a higher rate of headache relapse than are the ergot alkaloids.

The efficacy rates associated with the triptans range from 60% (oral and nasal sumatriptan) to as high as 77% (rizatriptan), whereas those associated with placebo range from 26% to 40%. Although triptan agents are more effective than the ergot alkaloids, the rate of headache recurrence associated with them is 2.5 times higher. Dooley and Faulds found that 45% of those who received the drugs had a relapse within 24 hours, compared with 18% of those who received DHE (Drugs, vol. 58, p. 699, 1999). Such a response is a significant impediment to treatment, the goal of which is not only to provide symptomatic relief but also to eliminate the headache.

In addition, the triptans sometimes produce adverse effects that can interfere with expedient patient management, such as transient chest pain. Although usually insignificant, such pain must be taken seriously, because myocardial infarction has been caused by these drugs, albeit rarely. Triptan agents should not be administered to patients who have a cardiac history or significant cardiac risk, and they should not be taken within 24 hours of DHE administration. In patients taking selective serotonin reuptake inhibitors (SSRIs), triptans may trigger a serotonin interaction syndrome that includes flushing, weakness, and incoordination. As with other drugs, physicians find that only a limited number of patients can use these drugs safely.

Prochlorperazine. Recent studies have shown that the efficacy rate associated with prochlorperazine makes that drug an attractive alternative to the medications discussed so far. In the treatment of acute headaches including both tension and migraine, the rate can be as high as 74%. Prochlorperazine has not been studied extensively in the treatment of migraine headache, but preliminary trials show the rate at which complete relief of pain from migraine was attained was 32%, whereas the rate associated with placebo was 7%. With its low propensity to cause adverse effects, prochlorperazine, in a 10-mg intravenous dose, is a reasonable alternative, especially when contraindications rule out the triptans and the complications associated with the ergot alkaloids must be avoided. Dystonic reactions are occasionally produced, but occur at a rate of approximately 0.7%. Such reactions can be prevented by concomitant administration of an intravenous 25- to 50-mg dose of diphenhydramine.

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Cluster Headache

Cluster headaches occur rarely and are the most commonly misdiagnosed headaches. The cluster headache occurs in 0.4% of the population, and the ratio of men to women among affected persons is nine to one. These headaches usually occur in early adulthood, between 20 and 40 years of age. They tend to come in eerily regular cycles. A headache can occur daily for weeks or months, after which follows a period of relief that extends to months or years. The pain of a cluster headache is considered one of the worst ordeals that a person can experience. In fact, the cluster headache is sometimes referred to as the suicide headache.

Clinical signs of cluster headache.The pain of a cluster headache is most often unilateral and located behind the eye. Maximal pain intensity occurs within 10 to 15 minutes. The episode can last from 15 minutes to 2 hours and is often associated with physical findings ipsilateral to the location of the pain. Ipsilateral ptosis, edema, conjunctivitis, rhinorrhea, and lacrimation often occur. The headaches seem to correlate with the onset of the REM phase of sleep, and patients will often make attempts to stay awake for extended periods to avoid them. Patients with cluster headaches are often so agitated by the pain that they can not stay still and may be found standing or pacing in the examining room. The headaches can be triggered by alcohol (only during cluster periods), vasodilating medications, and sleep apnea-induced hypoxemia.

As with the other primary headache syndromes, diagnosis of cluster headache is made on the basis of clinical findings. The key difference between this headache syndrome and migraine is the short duration of each episode, the autonomic effects it causes, and the absence of nausea, vomiting, and photophobia.

Treatment of cluster headache. The acute nature and rapid resolution of the cluster headache does not make the disorder amenable to treatment with oral medications. The primary treatment for cluster headaches is oxygen therapy. Oxygen should be given at 7 L/min for 10 minutes. A response rate of 60% to 70% is expected with oxygen therapy alone.
Sumatriptan in a subcutaneous dose of 6 mg is also effective in the treatment of cluster headache. A therapeutic effect is seen in five minutes and is associated with a relief rate of 74%, compared with 26% for placebo. Topical intranasal lidocaine drops are also effective. With the patient's head tilted back, 1 cc of 4% lidocaine is placed in the ipsilateral nostril.

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Secondary Headaches: True Emergencies

The secondary headache syndromes are underlying disease states of which the headache is a symptom. There are only a few true emergencies in the treatment of headache. These are secondary headaches that are produced by a pathologic disorder that can cause rapid and irreversible effects, including permanent loss of function, such as sight, or even death. Such disorders include subarachnoid hemorrhage, temporal arteritis, and bacterial meningitis.

As mentioned earlier, a brief primary survey of a patient presenting with headache should be performed immediately to discern the presence of these three disorders. Once they have been ruled out, the physician can move toward the alleviation of pain and determine proper disposition for the patient.

Temporal arteritis. Also known as giant cell arteritis, temporal arteritis is seen most often in patients older than 50 years of age and frequently coexists with polymyalgia rheumatica. The disease is a systemic panarteritis that affects the medium and large vessels. The temporal artery is one of the most common arteries affected. Temporal arteritis can cause permanent blindness if not treated with steroids immediately. The blindness is caused by the occlusion of the posterior ciliary branch of the ophthalmic artery. The disease should be suspected when any patient presents with headache, scalp tenderness, visual symptoms, jaw claudication, or throat pain.

The temporal artery often appears normal on examination, including palpation, visual inspection, and auscultation for bruits. Often, funduscopic changes do not occur until 24 to 48 hours after onset of blindness. Again, steroid therapy must be given immediately; prednisone at a dosage of 40 to 60 mg a day is the usual choice. An immediate referral for temporal artery biopsy is also required.

Subarachnoid hemorrhage. Subarachnoid hemorrhage should be suspected in persons who present with a sudden onset of severe headache. Nausea, vomiting, and meningeal signs with progression to obtundation are also common. Immediate neurosurgical consultation is required, as is immediate treatment to reduce increased intracranial pressure.

Meningitis. Any patient who has a headache associated with a fever and meningeal signs should undergo a lumbar puncture to rule out meningitis, a secondary cause of headache. All physicians who provide emergency treatment should be readily prepared to perform and skilled in the technique of lumbar puncture. Symptoms of meningitis include nuchal rigidity and the presence of Kernig and Brudzinki signs. Antibiotic therapy is a priority for patients with these symptoms; however, even after rapid therapy is administered, the risk of death and further illness is still quite high.

Suggested Reading Forsyth P and Posner J: Headaches in patients with brain tumors: A study of 111 patients. Neurology 43:1678, 1993. Jensen R: Pathophysiological mechanisms of tension-type headache: A review of epidemiological and experimental studies. Cephalalgia 19:602, 1999. Lance JW: Current concepts of migraine pathogenesis. Neurology 43(Suppl 3):S11, 1993. Lipton R, et al.: Burden of migraine: Societal costs and therapeutic opportunities. Neurology 48(Suppl 3):S4, 1997. Lipton RB, et al. Efficacy and safety of acetaminophen, aspirin, and caffeine in alleviating migraine headache pain: Three double-blind, randomized, placebo-controlled trials. Arch Neuorol 55:210, 1998. Marks D and Rapoport A: Practical evaluation and diagnosis of headache. Semin Neurol 17:307, 1997. Mathew N: Cluster headache. Semin Neurol 17:313, 1997. Moskowitz MA and Cutrer FM: Attacking migraine headache from beginning to end. Neurology 49:1193, 1997. New "Triptans" and Other Drugs For Migraine. The Medical Letter On Drugs and Therapeutics. 40:97, 1998. Silberstein SD: Evaluation and emergency treatment of headache. Headache 32:396, 1992.

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