Migraine

Migraine

Essentials of Diagnosis

• Headache, usually pulsatile.
• Pain is typically, but not always, unilateral.
• Nausea, vomiting, photophobia, and phonophobia are common accompaniments.
• May be transient neurologic symptoms (commonly visual) preceding headache of classic migraine.
• No preceding aura is common.

General Considerations

The pathophysiology of migraine probably relates to neurovascular dysfunction. Headache results from the dilatation of blood vessels innervated by the trigeminal nerve caused by release of neuropeptides from parasympathetic nerve fibers approximating these vessels. The probable underlying mechanism is activation of the trigeminal nucleus caudalis, nucleus tractus solitarius, and dorsal raphe nucleus. Imaging studies have revealed changes in brainstem regions involved in sensory modulation, suggesting that migraine relates to a failure of normal sensory processing. Before or simultaneous with symptom onset, regional cerebral blood flow is decreased in the cortex corresponding to the clinically affected area; after one to several hours, hyperemia occurs in this same region. Cortical spreading depression of Leão has been implicated.

Clinical Findings

Classic migrainous headache is a lateralized throbbing headache that occurs episodically following its onset in adolescence or early adult life. In many cases, however, the headaches do not conform to this pattern, although their associated features and response to antimigrainous preparations nevertheless suggest that they have a similar basis. In this broader sense, migrainous headaches may be lateralized or generalized, may be dull or throbbing, and are sometimes associated with anorexia, nausea, vomiting, photophobia, phonophobia, osmophobia, cognitive impairment, and blurring of vision. They usually build up gradually and may last for several hours or longer. Focal disturbances of neurologic function may precede or accompany the headaches and have been attributed to constriction of branches of the internal carotid artery. Visual disturbances occur commonly and may consist of field defects; of luminous visual hallucinations such as stars, sparks, unformed light flashes (photopsia), geometric patterns, or zigzags of light; or of some combination of field defects and luminous hallucinations (scintillating scotomas). Other focal disturbances such as aphasia or numbness, paresthesias, clumsiness, dysarthria, dysequilibrium, or weakness in a circumscribed distribution may also occur.

In rare instances, the neurologic or somatic disturbance accompanying typical migrainous headaches becomes the sole manifestation of an attack ("migraine equivalent"). Very rarely, the patient may be left with a permanent neurologic deficit following a migrainous attack.

Patients often give a family history of migraine. Attacks may be triggered by emotional or physical stress, lack or excess of sleep, missed meals, specific foods (eg, chocolate), alcoholic beverages, bright lights, loud noise, menstruation, or use of oral contraceptives.

An uncommon variant is basilar artery migraine, in which blindness or visual disturbances throughout both visual fields are initially accompanied or followed by dysarthria, dysequilibrium, tinnitus, and perioral and distal paresthesias and are sometimes followed by transient loss or impairment of consciousness or by a confusional state. This, in turn, is followed by a throbbing (usually occipital) headache, often with nausea and vomiting.

In ophthalmoplegic migraine, lateralized pain—often about the eye—is accompanied by nausea, vomiting, and diplopia due to transient external ophthalmoplegia. The ophthalmoplegia is due to third nerve palsy, sometimes with accompanying sixth nerve involvement, and may outlast the orbital pain by several days or even weeks. The ophthalmic division of the fifth nerve has also been affected in some patients. Ophthalmoplegic migraine is rare; more common causes of a painful ophthalmoplegia are internal carotid artery aneurysms and diabetes.

Familial hemiplegic migraine (FHM) designates the occurrence of migraine with aura including weakness when at least one first- or second-degree relative has a similar disorder. Specific genetic subtypes are recognized: in FHM1, mutations occur in the CACN1A gene on chromosome 19, and in FHM2, mutations occur in the ATP1A2 gene on chromosome 1. In sporadic hemiplegic migraine, no other family members are affected.

Treatment

Management of migraine consists of avoidance of any precipitating factors, together with prophylactic or symptomatic pharmacologic treatment if necessary.

Symptomatic Therapy

During acute attacks, many patients find it helpful to rest in a quiet, darkened room until symptoms subside. A simple analgesic (eg, aspirin, acetaminophen, ibuprofen, or naproxen) taken right away often provides relief, but treatment with prescription therapy is sometimes necessary. To prevent medication overuse, use of simple analgesics should be limited to 15 days or less per month, and combination analgesics should be limited to < 10 days per month.

Cafergot, a combination of ergotamine tartrate (1 mg) and caffeine (100 mg), is often particularly helpful; one or two tablets are taken at the onset of headache or warning symptoms, followed by one tablet every 30 minutes, if necessary, up to six tablets per attack and no more than 10 days per month. Because of impaired absorption or vomiting during acute attacks, oral medication sometimes fails to help. Cafergot given rectally as suppositories (one-half to one suppository containing 2 mg of ergotamine) or dihydroergotamine mesylate (0.5–1 mg intravenously or 1–2 mg subcutaneously or intramuscularly) may be useful in such cases. Alternatively, prochlorperazine administered rectally (25 mg suppository) or intravenously (10 mg) may be prescribed. Ergotamine-containing preparations may affect the gravid uterus and thus should be avoided during pregnancy.

Sumatriptan, which has a high affinity for serotonin₁ receptors, is a rapidly effective agent for aborting attacks when given subcutaneously by an autoinjection device (4–6 mg once subcutaneously, may repeat once after 2 hours if needed; maximum dose 12 mg/24 h). It can also be taken in a nasal form, but absorption is limited, and an oral preparation is available. Zolmitriptan, another selective serotonin₁ receptor agonist, has high bioavailability after oral administration and is also effective for the immediate treatment of migraine. The optimal initial oral dose is 5 mg, and relief usually occurs within 1 hour; may repeat once after 2 hours. It is also available in a nasal formulation, which has a rapid onset of action; the dose is 5 mg in one nostril once and it may be repeated once after 2 hours. The maximum dose for both formulations is 10 mg/24 h. A number of other triptans are available, including rizatriptan (5–10 mg orally at onset; may repeat every 2 hours twice [maximum dose 30 mg/24 h]), naratriptan (1–2.5 mg orally at onset; may repeat once after 4 hours [maximum dose 5 mg/24 h]), almotriptan (6.25–12.5 mg orally at onset; may repeat dose once after 2 hours [maximum dose 25 mg/24 h]), frovatriptan (2.5 mg orally at onset; may repeat after 2 hours once [maximum dose 7.5 mg/24]), and eletriptan (20–40 mg orally at onset; may repeat after 2 hours once [maximum dose 80 mg/24 h]).

Eletriptan is useful for immediate therapy and frovatriptan, which has a longer half-life, may be worthwhile for patients with prolonged attacks. Triptans may cause nausea and vomiting. They should probably be avoided in women who are pregnant, in patients with hemiplegic or basilar migraine, and in patients with risk factors for stroke (such as hypertension, prior stroke or transient ischemic attack, diabetes mellitus, hypercholesterolemia, obesity). Triptans are contraindicated in patients with coronary or peripheral vascular disease. Patients often experience greater benefit when the triptan is combined with naproxen (500 mg).

The neuroleptic droperidol is also helpful in aborting acute attacks. Metoclopramide given intravenously may be helpful and is being studied. Opioid analgesics are needed in rare instances, as when patients are unable to use vasoactive agents or nonsteroidal medications; options include meperidine (100 mg intramuscularly) or butorphanol tartrate by nasal spray (1 mg/spray in one nostril, repeated after 3 or 4 hours if necessary). Intravenous propofol in subanesthetic doses may help in intractable cases.

Preventive Therapy

Preventive treatment may be necessary if migrainous headaches occur more frequently than two or three times a month or significant disability is associated with attacks. Some of the more common drugs used for this purpose are listed in Table 24–1. Their mode of action is unclear but may involve alteration of central neurotransmission. Several drugs may have to be tried in turn before the headaches are brought under control. Once a drug has been found to help, it should be continued for several months. If the patient remains headache-free, the dose can then be tapered and the drug eventually withdrawn. Botulinum toxin type A may be effective for migraine prevention in some patients; it has few systemic side effects and need only be given at intervals of several months. However, no statistically significant between-group differences were found in frequency of migraine episodes per 30-day period in a randomized, double-blind, placebo-controlled exploratory study. Although acupuncture has been widely used in the prophylaxis of migraine, a randomized controlled trial failed to show any difference between it and sham acupuncture.

Posted in: Headache,Migraine