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USMLE – Migraine

Clinical features
Patients may refer to any episodic paroxysmal headache as migraine. However, it is best to look upon migraine as a triad of paroxysmal headache, vomiting and focal neurological events (usually visual). Patients with all three of these features are said to have classical migraine. Those with just paroxysmal headache with or without vomiting but no classical focal events are said to have common migraine. It has been estimated that the lifetime prevalence of migraine is about 20% of females and 6% of males. Over 90% of migraine sufferers will have their first attack by the time they are 40 years old. Typically, a classical migraine attack starts with a non-specific prodrome of malaise and irritability followed by the ‘aura’ of a focal neurological event, a severe throbbing hemicranial headache, photophobia and vomiting. During the headache phase patients prefer to be in a quiet, darkened room and go to sleep. The headache may persist for several days.

The aura of migraine is most often in the form of ‘fortification spectra’, shimmering silvery zigzag lines which march across the visual fields over 20 minutes, sometimes leaving a trail of visual field loss. In some patients there is a spreading front of tingling followed by numbness which moves, over 20-30 minutes, from one part of the body to another, or even aphasia when the dominant side is involved. Weakness rather than sensory symptoms in migraine is distinctly unusual and ‘hemiplegic migraine’ should be diagnosed with extreme caution. In some patients the focal events may occur by themselves (‘migraine equivalent’) but other, structural disorders of the brain, or focal epilepsy, need then to be considered in the differential diagnosis.

Etiology and pathogenesis
The etiology of migraine is largely unknown. There is often a family history of migraine, suggesting a genetic predisposition. The great female preponderance and the tendency for some women to have migraine attacks at certain points in their menstrual cycle hint at hormonal influences. The relevance of the contraceptive pill in this context is difficult to establish. In some patients there are identifiable dietary precipitants such as cheese, chocolate or red wine. When psychological stress is involved, the migraine attack often occurs after the period of strain so that some patients tend to have attacks at weekends or at the beginning of a holiday.

The ‘aura’ of classical migraine probably represents a spreading front of excitation followed by a depression of activity of cortical cells. The cause of this is not understood but probably represents a paroxysmal alteration in cortical modulation pathways from the brain stem (especially serotoninergic projections). The headache is caused by vasodilatation of extracranial vessels and may, like the headache following an epileptic seizure, be a non-specific effect of intracranial metabolic disturbance.

Identification and avoidance of precipitants may prevent attacks. Treatment of an acute attack consists of simple analgesia with aspirin or paracetamol with an antiemetic such as metoclopramide. This is best in the form of effervescent combined preparations which enable better absorption. Severe attacks can be treated with sumatriptan, a 5-HT agonist which is a potent vasoconstrictor of the extracranial arteries, given either by subcutaneous injection or orally. Ergotamine preparations, whilst effective in some patients, should be avoided since they easily lead to a situation where headaches occur due to withdrawal of the ergotamine, establishing a vicious circle. This seems less likely to occur with sumatriptan. If attacks are frequent, prevention of migraine can be effected by propronolol (80-160 mg daily, preferably in a sustained-release preparation), pizotifen (a 5-HT antagonist, 1.5-3.0 mg daily) or a tricyclic such as amitriptyline (10-50 mg at night).

Lillian Thompson By Lillian Thompson

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