Edward Lichten, M.D.,PC
555 S. Old Woodward Avenue Suite 700
Birmingham, MI 48009 

Email: drlichten


INTRODUCTION:   Merle Diamond, M.D.
Diamond Headache Clinic, Chicago, Illinois

Headache is a frequent presenting complaint in the emergency department. The occurrence of headache as the chief complaint on admission is between 0.36% to 2.5% of patients[1]. The incidence of headache with significant morbid or fatal outcome is not frequent.[2] Determining differential diagnosis of the patient presenting with headache is essential in order to rule-out organic disease. Appropriate treatment regimens can be instituted once diagnosis has been established. In the Emergency Department (ED), relief of acute pain must usually be addressed. Referring the patient for follow-up care and preventing repeat ED visits and possible narcotic habituation are recurrent problems for the emergency physician.


In order to adequately treat the patient presenting to the ED with headache as the chief complaint, the emergency physician must be familiar with the various categories of headache. For simplicity, the division of headaches into three categories--- organic, vascular, and tension-type --- is very useful. Multiple disease processes are included in the category of organic headaches (Table I). In evaluating the headache patient, the emergency physician must be aggressive in diagnosing the patient in order to rule out life threatening illness. The emergency physician can be reassured that organic causes of headache occur rarely {<1%}.

Between 4.5% to 20% of headache patients visiting the ED will be suffering from vascular headaches.[3] Referral for follow-up is essential in order to prevent frequent repeat visits to the emergency department and dependence on habituating analgesics. At the ED, tension-type (muscle contraction) headache is the most prevalent diagnosis among these headache patients. Narcotic analgesics must be avoided in these patients.


History and Physical Examination

All patients presenting to the emergency department with the complaint of headache should be interviewed carefully regarding their headache history. This history is an essential tool in establishing the diagnosis. Patients presenting with recent onset headache or a change in the character of their headache should be thoroughly evaluated for possible organic disease. If the patient complains of the "worst headache of my life" with associated stiff neck, possible nausea and vomiting, and focal neurological symptoms, subarachnoid hemorrhage should be ruled-out. Conversely, the patient with an extensive history of headaches who presents at the ED with a typical acute headache that has been triggered by dietary indiscretion or is associated with menses, and is accompanied with nausea, vomiting, and photophobia, can probably be diagnosed with migraine.

During the history, certain factors should be identified. The time of onset of this particular headache, character of the pain, severity, duration, and any associated symptoms with this particular headache should be outlined. The interviewer should determine if the patient has a prior history of headache, and obtain information about the original onset of the headache, as well as any previous tests and treatment. The patient should also be questioned about a family history of headache, any exertional aspects to the acute attacks, and current therapeutic regimens.

A physical and neurological examination must be completed. If the patient relates a recent onset of headaches, or a change in character of the headaches, the emergency physician should be alert to possible organic pathology. The extent of the examination is dependent on the patient's current status. During the evaluation, the fundi, neck, throat, and nose should be examined.


Diagnostic testing will not usually establish the diagnosis in the majority of patients presenting to the ED with headache[4] The physical examination and the headache history will facilitate the choice of which diagnostic tests should be performed. In ordering diagnostic studies, the emergency physician should consider the possibility that the patient will not seek follow-up care.

A complete blood count should be performed if there is any suspicion of an infection, or if a marked anemia is suspected (which could cause a hypoxia-related vascular headache). Evaluation of renal function and electrolytes should be obtained in patients who appear to be dehydrated due to status migraine with associated vomiting. Blood chemistries should also be performed on those patients consuming excessive amounts of prescribed or over-the-counter analgesics.

CT scanning is particularly useful in patients with headache. Mill's group[5] have devised criteria for the indication of a high-yield CT scan (Table II). The CT scan can rule-out suspected organic cause, and if indicated, an M.R.I. should be obtained. Suspicion of elevated intracranial pressure due to focal lesions should indicate the need for obtaining a CT scan and a careful eye ground examination prior to performing a lumbar puncture, in order to prevent a possible cerebellar herniation. A CT scan should also be obtained on any hypertensive patient with a change in sensorium and focal neurological symptoms in order to rule-out increased intracranial pressure and intercerebral bleeding. In 75-90% of patients with subarachnoid hemorrhage (SAH), the CAT scan will demonstrate the abnormality, depending on the resolution of the scanner. The CT scan may also differentiate brain abscesses and some tumors.

A lumbar puncture is an important diagnostic tool in the ED. If the emergency physician suspects meningitis, a lumbar puncture should be performed. In the presence of an SAH, xanthochomia or red blood cells will be demonstrated in the spinal fluid expressed during the lumbar puncture. The fluid will also reveal white blood cells as well as bacteria in the patient with bacterial meningitis.. As previously stated, previously, the suspected presence of a focal lesion will contraindicate the performance of a lumbar puncture. Therefore, a CT scan must be obtained, prior to a lumbar puncture, on all patients with suspected increased intracranial pressure.

A sedimentation rate by the Westergen method should be obtained on all patients over the age of 50 who present with recent onset headache or a change in the character of the headache, in order to rule-out temporal arteritis. If the sedimentation rate is elevated, a temporal artery biopsy should be scheduled as soon as possible, and treatment with corticosteroids should be started promptly in order to prevent irreversible blindness.


At the ED, the most dramatic presentation is probably the patient with SAH. These patients typically present with a history absent of previous headache complaints.[6] The patient with a previous history of headaches will usually not report any unusual features of the headache nor describe difficulties with their therapeutic regimen. The emergency physician should be cognizant that thunderclap headache may occur in patients with migraine or with an SAH.[7] Approximately 10% of all cerebrovascular accidents are related to the presence of a SAH, and an approximately 50 percent mortality rate has been reporteD.[8]. It should be noted that 50 percent of those patients who survive the initial bleed but do not receive treatment, will die within the next two weeks.

The clinical picture of the patient with SAH is a terrible headache, usually described as "the worst ever", with a typically acute onset. Associated symptoms will often be reported related to increased intracranial pressure including nausea, vomiting, meningismus, and focal neurological signs. A transient loss of consciousness associated with the onset of bleeding may also be noted. Vital signs should be monitored as an elevated blood pressure may occur due to sympathetic hypersensitivity.[9]


The life threatening diagnosis of meningitis will more likely be confronted by the emergency physician than the office based clinician. This serious problem may occur in any age group. The diagnosis of meningitis is confirmed by examination of the cerebral spinal fluid, which may show cloudy fluid under raised pressure, white cells, elevated protein, decreased glucose, and positive cultures with elevated antigen levels. The purpose of the lumbar puncture is to determine which causative agent is responsible.[3] Hemophilus influenza is the most prevalent cause of meningitis in children, aged 2-5. Older children and adolescents with meninigitis are more frequently infected with Neisseria Meningitis. In older patients, the cause of their meningitis is usually due to Steptococcal pneumonia. Patients receiving immunosuppressive treatment are particularly susceptible to those as well as other organisms.

The clinical picture of the patient with meningitis is typically a severe global headache, throbbing in nature, and associated with nausea, vomiting, photophobia, and stiff neck. In some patients, an alteration in the level of consciousness may occur. Also, a rash may be manifested. A morbid outcome can be prevented with early diagnosis and treatment with the appropriate antibiotic.


In treating patients with temporal arteritis, early diagnosis and management are essential and the emergency physician should be conversant with the clinical picture of this disorder. Headache is the most common presenting complaint. The typical patient has been previously asymptomatic, is over age 50, with the headache being recent in onset. The female to male ratio is 2:1. Associated systemic symptoms include weight loss, night sweats, low grade fever, aching of joints, and jaw claudication.[9] Polymyalgia rheumaica is the medical terminology used to describe this cluster of symptoms.

The patient will complain of head pains or headache usually localized to the affected scalp vessels. Another characteristic symptom is pain in the jaw muscles on chewing. On examination, the area around the temporal artery is usually tender to touch and the skin may appear red.[10] The involved arteries will dictate which physical signs will be present.

The absolute necessity for early diagnosis and treatment should not be underestimated. Vision is lost in one or both eyes in 50 percent of untreated cases. This condition can be easily ruled-out through the use of the sedimentation rate. A sedimentation rate over 40 mm/hr indicates the need for a temporal artery biopsy. Corticosteroid treatment can be initiated during the interim while awaiting the temporal artery biopsy, if temporal arteritis is suspected. The corticosteroid therapy may need to be continued for several years, with follow-up sedimentation rates performed at regular intervals.


Inflammation, traction, and displacement or distention of the pain-sensitive structures of the cranium will cause the headache due to intracranial sources. The term "traction headache" describes the typical source of the displacement. A rapidly expanding lesion, which produces traction on the pain-sensitive areas of the head, will produce a headache which is a cardinal sign of a brain tumor. Headache is a frequent manifestation of increased intracranial pressure. If the tumor is slow growing, the headache is usually mild and transient. This headache is easily relieved by over-the-counter analgesics, and the patient will rarely visit an ED.

The morbid outcome of these traction headaches should alert the emergency physician to the generalizations regarding headache due to brain tumor. The patient with headache due to a brain tumor will often describe the pain as deep, aching, steady, dull and rarely throbbing. This headache can, at times, be severe, but is not typically as intense as migraine. Over-the-counter analgesics and ice packs often relieve the pain. Eventually, the headache may become progressive due to enlargement of the mass and resultant surrounding cerebral edema. Increases in intracranial pressure, due to Valsalva, exertion, or other maneuvers, may exacerbate the pain. Focal signs may occur in patients with a mass lesion, depending on which area of the brain is involved. Signs of increased elevation in blood pressure may also be demonstrated. CT Scanning, and possibly M.R.I., is indicated in those patients presenting with exertional aspects to their headaches. Other neurological signs, such as headache accompanied by fainting, should alert the emergency physician to the need for further testing and referral to the appropriate specialist.

Disease of adjacent nasal and aural structures will usually be the cause of the headache due to brain abscess. This pain will typically start at those sites prior to the involvement of the cerebral parenchyma. The development of papilledema and other signs of localized traction and generalize displacement of the brain will usually herald a brain abscess. These patients will also present with associated symptoms such as fever, leukocytosis, and pleocytosis. Ear infections will most often produce abscesses above or below the tantrum. Hiccoughing, vomiting, and occipital headache are typical of abscesses below the tentorium. Pain in the frontal region adjacent to the diseased frontal, ethmoid, and sphenoid sinus usually result from an epidural abscess due to a sinus infection.

The patient should be questioned about recent or concomitant ear infections or sinusitis. The presence of fever and purulent nasal drainage are indicative of the need for CT Scanning and possibly sinus x-rays. The possibility of a brain abscess should be suspected in a patient presenting with recent onset headache, and no other clinical signs except for an elevated white blood cell count. Referral to the appropriate specialist is indicated, and immediate antibiotic therapy should be instituted.


A frequently occurring presentation at the ED is the patient with hypertensive headache[3] Characteristically, the headache is worse upon awakening, and gradually improves throughout the day.[8] The diagnosis can only be confirmed with a diastolic blood pressure of 100 Hg or over. The degree of elevation in blood pressure may or may not affect the severity of the headache. Typically, the hypertensive headache is bilateral and usually occurs at the occiput. It can also involve the entire head. Patients will describe the pain as throbbing or "bursting" in nature and very severe. Tremors or palpitations or other symptoms of catecholamine release, may occur.

Essential hypertension does not usually cause headache. However, headache due to increased blood pressure may be a manifestation of another disorder. A sudden increase in blood pressure due to acute nephritis or acute pressor reactions may produce a similar headache.


Between 4.5 and 20 percent of patients presenting to the ED with headache will be suffering from migraine.3 Distinguishing migraine from an acute life-threatening medical emergency is simplified by an accurate history and physical examination. The patient with migraine will consistently report a prior history of this type of headache. Usually, patients will consult the emergency physician due to the severity of the headache as well as the associated gastrointestinal and neurological symptoms.

The neurological examination is typically negative. However, the blood pressure may be elevated during an acute attack. The patient presenting with status migraine may appear dehydrated due to prolonged vomiting. Laboratory evaluation of serum electrolytes is indicated. Hospitalization may be indicated in order to stabilize the patient, initiate IV fluid replacement, and provide analgesia.


The patient with complicated migraine may present at the ED because of the severity of the associated neurological symptoms. These symptoms are typified by hemiphegic migraine, manifested by hemipareses and opthalmoplegic migraine, with defects of the third and occasionally the fifth cranial nerve. Neurologic symptoms often persist after the resolution of the headache attack. A previous history of headaches may be a clue in identifying the complicated migraine. CT Scanning may be indicated, and a lumbar puncture may be considered if these symptoms persist.


Many patients with a specific form of complicated migraine, basilar artery migraine, are often misdiagnosed in the ED because basilar artery migraine is manifested by several neurological deficits. The headache is characteristically severe and paroxysmal[11], and occurs predominantly in females during adolescence and the third decade. The diagnosis can be established by the presence of any three of the following symptoms: 1)bioccipital headache; 2)impairment or loss in the temporal and nasal fields of both eyes; 3)Disturbed oculomotor function, such as diplopia or nystagmus; 4) Dysarthria; 5) Vertigo; 6)Tinnitus or impaired hearing 7)Ataxia of gait; 8)Bilateral paresis; 9)Bilateral paresthesia; or 10) Altered consciousness, such as amnesia, confusion, somnolence, stupor or syncope.

Due to the variety of symptoms, basilar artery migraine may be confused with a mental disorder, brain tumor or drug abuse. Differential diagnosis includes tumors of the posterior fossa, thrombosis of the basal artery or cerebral veins, cerebellar hemorrhage or infarction, drug intoxication, or metabolic disorders. It is essential that the emergency physician obtain a history of similar headaches in the patient or in the patient's family. Once the diagnosis is established, treatment with standard migraine prophylactic agents is recommended; and the patient should be referred for follow-up care.


Cluster headache is a form of vascular headache that is not as common as migraine. This type of headache is usually easy to differentiate from other headache conditions because of its characteristic presentation of severe, unilateral headache, typically localized around one eye. A male predominance prevails in cluster headaches, and the initial onset usually occurs between the third and fifth decades.

Cluster headache is personified by its episodic pattern, occurring in series usually lasting from three weeks to three months. During the series, the acute headache will occur several times per day, and often awakens the patient in the first few hours after falling asleep. Characteristically, the acute cluster headache has a very limited duration. The headache may been abated before the patient could arrive at the ED. However, the pain of cluster is extremely excruciating, and this headache sufferer may present in severe distress. The emergency physician should be aware that many cluster headache patients have contemplated suicide during a cluster series because of the severity and regularity of the pain.

The emergency physician may note an increase in the number of cluster headache patients visiting the ED during spring and fall. A previous history of cluster headaches will aid in the diagnosis. The associated symptoms of nasal congestion, rhinorrhea, ptossis, and conjunctival injection may confuse the picture, and acute sinusitis must be ruled out.


The patient with tension-type, muscle contraction, headaches will usually obtain relief with over-the-counter analgesics and simple relaxation methods. Most patients with this type of headache experience the pain on an episodic basis. However, some patients will report a daily, chronic headache. Because of the chronicity of these headaches, habituating analgesics must be avoided, particularly in the ED. Many patients with chronic tension-type headaches have an underlying depression, as evidenced by the presence of a sleep disturbance.[12] Narcotic analgesics, sedatives, and tranquilizers should be strictly avoided in all settings. Those patients with chronic tension-type headaches require an appropriate referral to a physician or clinic familiar with the treatment of such.


Although migraine has been a recognized entity for centuries, debate continues over its pathogenesis. Wolff described migraine as a self-limited, neurogenic sterile inflammation[2] He identified the occurrence of four dynamic events during a migraine attack: 1) initial cerebral vasoconstriction, which is correlated with the aura or warning of migraine; 2)the extracranial vasodilation (which Wolff considered the cause of migraine pain); 3)the sterile inflammation that increases the pain and prolongs the migraine attack; and 4)a secondary muscle contraction.

Wolff suggested that the vasoconstriction occurring during the aura involves either the retina (or the retinal or ophthalmic artery), or the occipital portion of the cerebral hemisphere. During his investigations, he attempted to determine if there was a causal relationship between the initial cerebral vasoconstriction to the cranial vasodilation of migraine. He observed that cerebral vasoconstriction had usually ended before the extracerebral vasodilatation had started. Wolff suggested that dilatation and the distention of large arteries, as well as an increase in pain-threshold-lowering substances, produce the headache. During a migraine attack, the pain usually radiates from the large subsurface cranial arteries and their branches. The patient will experience pain if the vessels are distended, pulled upon, or displaced.

Through further investigations, Wolff postulated that a sterile inflammation occurs in addition to the vasodilatation. A neurokinin and a proteolytic (neurokinin-forming) enzyme neurogenically induce the inflammatory reaction. Five groups of substances, and possibly more, have been implicated with the sterile inflammation. These substances include catecholamines, histamine and serotonin, peptikinins, prostaglandins, and the slow-reacting substances of anaphylaxis (SRSA), an acidic lipid. Contraction and relaxation of smooth muscle are caused by these substances, in addition to constriction or dilatation of arteries and veins, induction of water and sodium diuresis, fever, wheal and flare reactions, and triggering of pain, including headache. in his studies, Wolff noted that noxious stimulation of any part of the head triggers muscle contraction of the head and neck. Therefore, noxious stimulation triggered by vascular distention will also cause muscle contraction. Sustained muscle contraction of the muscles of the head and neck can be triggered by emotional tension. This sustained contraction may persist after the vascular aspects of the headache have diminished, and is considered a secondary feature of the migraine attack.

Wolff's theories have been disputed by several researchers, including Olesen's group.[3] In their investigations, they injected a radioactive isotope, xenon-133, into the carotid artery, and induced migraine after arteriography in a series of subjects. They described a "spreading oligemia" which usually starts in the occipital regions and radiates anteriorly, reaching a primary sensorimotor area after the symptoms from that region had started. After the focal symptoms ceased, the oligemia continued. The authors, using this regional blood flow method, suggested that the painless pre-headache phase of migraine with aura was possibly secondary to a reaction similar to the spreading depression described by Leao and not secondary to oligemia.

In an earlier study, Olesen's group noted that the striking oligemia did not occur in migraine without aura.[4] No significant change was demonstrated in cerebral or regional blood flow between the resting phase, the onset of migraine without aura, and the acute attack. Skyhoj Olsen reported on the limitations of these cerebral blood flow (CBF) studies[5] He proposed the "spreading oligemia" observed in CBF studies during migraine with aura may be an artifact that reflects a gradual decrease of CBF in an area of constant size. His theory suggests that migraine with aura and migraine without aura may be due to the same disease process but differ in the intensity of vasospasm and CBF reduction.

Local and systemic biochemical changes also occur during the headache phase. The preceding vasoconstriction phase causes local anoxia and acidosis. A systemic decrease in serotonin levels occurs as serotonin is transported by the blood vessels and the perivascular tissues. In response to local metabolic changes, the noninnervated parenchymal arteries dilate (a reaction also potentiated by the drop in blood serotonin), increasing cerebral blood flow and provoking local vasomotor changes in the innervated system of blood vessels, particularly marked dilation of the ipsilateral extracranial and intracranial arteries. Vasoactive substances, including serotonin, sensitized the pain receptors in the blood vessels and produces sterile inflammation around the vessels. These changes and the vasodilatation, cause the pain of migraine. This observation explains the hemicranial aspect of migraine.

In 1969, Heyck suggested that migraine is caused by the opening of    carotid arteriovenous anastomoses, shunts, in the head,[6] When open, direct oxygenated blood will be diverted wastefully to the veins. The tissues requiring oxygen will be bypassed. The shunt vessels may divert large volumes of blood and become distended and pulsating. Heyck's theory helps support the effectiveness of a new specific subtype-selective serotonin agonist which terminates established migraine with minimal side effects. Recent investigations have advanced our understanding of 5-hydroxytryptamine (5-HT) receptors. These receptors are membranal "trigger" proteins with which 5-HT must interact to produce its various actions. It is possible to selectively stimulate only one type of 5-HT receptor by producing a selective synthetic 5-HT-like molecule, and thus mimic some actions of 5-HT.

Age Distribution

For most migraine sufferers, the initial onset of their headaches occurred during adolescence or their twenties. Migraine does occur in childhood, as noted by Bille in this study of school children that the average age of onset was six years old.[7] The initial onset of migraine rarely occurs after age 40. During the fifth and sixth decade of life, migraine usually disappears, often with the onset of menopause. Some patients with migraine with aura will experience the prodromes long after the headaches have stopped.

Sex Distribution

The higher incidence of migraine in females has long been recognized. In an earlier study by Linet's group, the authors noted the prevalence of migraine in the general population was 7.4% for females and 3% for men.[8] In childhood migraine, there is an equal distribution between the sexes but after puberty, the predominance in females is obvious.

Family History

Migraine has long been considered a familial disorder. Selby and Lance reviewed the histories of 464 patients and noted a 55% family history of migraine.[9] Researchers have not concluded if migraine is a hereditary or familial disorder. In my own clinical experience of over 30 years, a family history of headache is reported by at least 70% of migraine sufferers.

Clinical Presentation

According to the definition established by the International Headache Society, migraine is "an idiopathic, recurring headache disorder manifesting in attacks lasting 4-72 hours. Typical characteristics of headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity, and association with nausea, photo- and phonophobia."[10] Migraine headaches do not occur on a daily basis, and the usual frequency is one to four per month. In some patients, the migraine may occur once yearly or as often as 15 to 20 times per month.

Characteristically, migraine affects one side of the head, and may switch sides. The headache can become generalized. Many patients indicated that the pain localizes around or behind the eyes, or in the front-temporal area. The pain may radiate towards the occiput or upper neck during an attack. The shoulder and lower portion of the neck may be involved. In some patients, the pain may radiate to the face.

The pain of migraine is often observed by the patient to start as a dull ache and develop into a throbbing and pulsating pain. Other patients will complain of a constant headache that is never pulsatile in nature. During the attack, the area over the dilated arteries may be tender, and this symptom may continue for several hours after the attack. The degree of severity is variable but migraine can be incapacitating. Migraine usually continues for 4 to 24 hours, although the attack may continue for one or more days. The patient may experience lethargy and fatigue for several days after an attack. Status migraine describes those attacks that are continuous for several days or weeks.

Migraine has often been described as a "sick" headache. Nausea and vomiting are frequent components of an acute attack. Other associated symptoms are anorexia, photophobia, phonophobia, constipation, diarrhea, dizziness, lightheadedness, blurred or double vision, chills, tremors, cold extremities, ataxia, and dysarthria. Difficulty in concentration and memory loss has been reported by some patients.

The prodromes occurring in patients with migraine with aura usually start one to two hours before the acute headache. The symptoms typically continue less than one hour. In order of frequency, the prodromes are: 1)scotoma (blind spots); 2) teichopsia (bright shimmering or wavy lines) or fortification spectra (a zigzag pattern resembling a fort); 3)flashing of lights (photopsia); 4)paresthesias; and 5)visual and auditory hallucinations (Alice in Wonderland Syndrome). The positive visual disturbances include photopsia, teichopsia, or the fortification spectra; the negative disturbances include scotomata; hemianopsia (partial visual field loss); or metamorphopsia (illusions of distorted size of shape). Other prodromal symptoms include paresthesias that occur as a "slow march" through the body.

Patients with migraine without aura may describe premonitions of an impending migraine attack. The vague symptoms may occur from two to 72 hours before an attack, and may occur four times as frequently as the prodromata of migraine with aura. These premonitions can occur in either type of migraine and include hunger, anorexia, drowsiness, depression, irritability, tension, restlessness, talkativeness, a surge of energy, and a feeling of well-being.

The Migraine Personality

The debate continues over the subject of "migraine personality." Wolff described migraine patients as ambitious, perfectionist, persistent, and unforgiving.[11] The children included in Bille's study were described as fearful, tense, sensitive, and easily frustrated.6 These findings confirmed the observations of Wolff. In 1976, however, Phillips reviewed several investigations and noted that evidence was limited to support the theory that migraine sufferers were more neurotic than age-matched controls [12] Ross and McNaughton reviewed the Rorschach records of migraine patients, and observed a tendency towards rigidity, perfectionism, intolerance, conventionality, obsessive-compulsive features, persistence towards success, and difficulty in sexual adjustment.[13] From my own clinical experience, I would agree with the findings of their study as well as that of Wolff.[14]

Precipitating Factors

Although many migraine patients will experience difficulty in identifying migraine triggers, the use of a headache diary will facilitate this process. On this diary, patients will be asked to record the frequency, duration, and severity of the migraine attack, as well as any provocative factors which may have triggered the headache. Migraine triggers can be divided into three categories: 1) external stimuli; 2)physiological; and 3)psychological.

Stress is probably the most readily identified trigger of an acute migraine attack. Curiously, many migraine patients will remain headache-free during a stressful period only to experience a severe headache when the stress has resolved. Many migraine patients will create an environment too great to handle, such as the working mother who attempts to go back to school, and juggle the demands of a career, raising a family, and pursuing a degree. An increase in migraine frequency is inevitable. Depression, fear, anger, anxiety, and repressed hostility have also been identified as migraine provocateurs. Although avoiding stress is difficult to achieve, instruction on coping methods may be beneficial for these patients.

The migraine sufferer is especially sensitive to any changes in sleep and eating patterns. Fasting or missing a meal is a known headache trigger. All migraine patients should be encouraged to maintain a strict meal schedule. Oversleeping or lack of sleep can also precipitate a migraine, although migraine rarely awakens a patient. The incidence of headaches occurring on weekends, holidays, or during vacations has been linked to oversleeping. Headache clinicians believe that the responsible mechanism is a relative hypoglycemia or an alteration in the level of carbon dioxide. In order to avoid these "weekend" headaches, patients should be instructed to maintain a regular sleeping schedule, and plan on arising at the same time each day. Lack of sleep and fatigue may also provoke an acute migraine attack.

The link between diet and migraine has long been a controversial subject. Most physicians who participated in a survey regarding "dietary migraine" believed that the acute attacks were triggered by certain foods that contain vasoactive substances. The term diet-precipitated migraine has been allotted to these headaches. The direct-acting vasoactive substances are the amines, including tyramine, nitrates, monosodium glutamate, and alcohol. Tyramine is found in aged cheese, pickled foods, fresh-baked yeast breads, and marinated foods. Another amine, phenylethylamine, is contained in chocolate. The nitrates, which cause migraine due to their vasodilating action, are found in cured meats. Monosodium glutamate is found in food additive and Chinese foods, and can cause a variety of symptoms, including pressure in both central and direct vasodilating properties. Migraine can be precipitated by a single glass of red wine.

Indirect-acting vasoactive substances include caffeine, nicotine, ergotamine, hypoglycemia, allergy, ingestion of ice cream, and monoamine oxidase inhibitors. Caffeine and nicotine are vasoconstrictors. However, rebound vasodilation may evolve from intemperate ingestion of these substances. Excessive consumption of caffeine-containing beverages, such as coffee, tea, or colas, can precipitate a migraine attack. Predictably, caffeine withdrawal, often associated with fasting, can trigger a severe headache.

Some migraine patients will describe a relationship between their headaches and weather. Rapid changes in barometric pressure as well as extreme variations in weather may provoke a migraine attack. During or subsequent to travel to areas of high altitude, a may report an increased frequency in their headaches. A diuretic, such as acetazolamide, used on the day of a flight may prevent these headaches.

A relationship between the menstrual cycle and migraine attacks is well documented. The increased incidence of migraine in women exemplifies this relationship. Of these female migraineurs, 60% to 70% will note a menstrual link to their migraine attacks, with severe headaches occurring immediately before, during, or after their period. Also, many of these women will note a remission in their headaches after the first trimester of pregnancy. Older patients will note a decrease or complete remission of their headaches after menopause. Oral contraceptives should be avoided in migraine patients as these drugs have been observed to increase the frequency, severity, duration, and complications of migraine. Also, estrogen replacement therapy should be avoiDed in post-menopausal migraineurs when giving these hormones exacerbates or restarts a migraine attack.


Drug therapy of migraine is difficult and will require frequent office visits and adequate lines of communication between the physician and the patient. Both the physician and the patient should have an adequate understanding of the complexities of treatment and the physician should be cognizant of drug interactions. Dependent on the patient's history, the physician must select the type of therapy indicated. If the patient is only experiencing occasional headaches, abortive treatment may be indicated. however, if the headaches are occurring two or more times per month, or if the attacks greatly impact on the patient daily life, due to absences from work or school, prophylactic therapy should be considered.

Abortive Therapy

Recently, a serotonin receptor agonist, sumatriptan, has demonstrated success in the abortive treatment of migraine. Sumatriptan acts as an agonist at the 5-HT(1D) receptor. The net effect of this action appears to be important in migraine as it causes the constriction of dilated arteries in the brain. Compared to serotonin itself, sumatriptan is safer and better tolerated by patients because its effect are highly specific are highly specific for this receptor. Also, sumatriptan may be advantageous over currently available agents for the treatment of migraine because of this specific effect on the 5-HT(1D) receptor as an agonist.

This agent, administered subcutaneously in doses of 6mg produced beneficial effects in treating migraine attacks.[14] This dose may be repeated after one hour if symptoms return. Side effects associated with this therapy included tingling, dizziness, warm-hot sensations, and injection-site reactions. Intravenous sumatriptan administration is contraindicated due to the potential of to cause coronary vasospasm. Sumatriptan should not be administered subcutaneously in patients with ischemic heart disease, prior history of myocardial infarction, documented silent ischemia, or patients with Prinzmetal's angina. Sumatriptan may cause increases in blood pressure and is therefore contraindicated in patients with uncontrolled hypertension. It should never be used concomitantly with ergotamine preparations. Studies are currently underway on the oral preparation of this drug in the treatment of acute migraine.

The ergotamine preparations have been used in migraine abortive therapy for several decades. These drugs are classified as vasoconstrictors that specifically counteract the dilation of some arteries and arterioles, primarily the branches of the external carotid artery. The success of ergot in a migraine attack impinges on early use of the drug during an attack or preferably during the prodromal phase. Ergotamine is available in preparations suitable for various routes of administration, including oral, sublingual, rectal, and parenteral. Selecting the route of administration is dependent on the following: 1)need for rapid action; 2)associated nausea and vomiting; 3)availability of the preparation; and 4)the patient's preference.

Nausea is a frequent side effect of ergot preparations and caffeine has been added to the oral and rectal preparations in order to facilitate absorption of the drug, and ergot and caffeine are believed to act synergistically. Sublingual preparations should be considered if the oral route is too slow or is not tolerated. The rectal suppository is the most effective of the non-parenteral preparations and is especially helpful for those patients with associated vomiting. However, its use may be awkward for the patient and should not be used in those migraineurs with associated diarrhea. The parenteral form of ergotamine is no longer available in the U.S. However, an ergotamine derivative, dihydroergotamine (DHE-45) may be used IV or IM.

In order to prevent ergotamine rebound phenomena, a four day hiatus must be maintained between days of use of these agents. Ergotamine should never be repeated on the second or third day of a migraine attack. If the drug is stopped abruptly, the patient will experience a severe rebound headache. Excessive consumption of the ergots may cause symptoms of vasoconstriction, such as cold, clammy extremities, and could lead to ergotism.

Patients with peripheral vascular disease, thrombophlebitis, severe hypertension, coronary ischemia, angina, renal or hepatic disease, or recent infection should not use an ergotamine preparation. These agents should not be used in the elderly, or during pregnancy because of the oxytocic effects of ergotamine. The us of a combination agent containing isometheptene mucate, dichloralphenazone, and acetaminophen (Midrin) may be indicated for those patients who cannot use the ergots. Isometheptene has cerebral vasoconstrictor action.

More Articles by Seymour Diamond:

  1. New Advances in Migraine Diagnosis and Treatment
  2. Biofeedback- Treatment for Migraine

    Revised: January 1, 2011