Pharmacotherapy of Migraine

Pharmacotherapy of Migraine

1. Definition & overview

• Migraine is a common, recurrent, often disabling primary headache disorder characterised by attacks of pulsating (throbbing) head pain, usually unilateral, lasting 4–72 hours untreated, frequently accompanied by nausea/vomiting and sensitivity to light (photophobia), sound (phonophobia) and movement (DiPiro 12e Ch.80, pp.983–4).
• KDT frames migraine as a "mysterious disorder" of pulsating headache, usually restricted to one side, in attacks lasting 4–48 h, often with nausea, vomiting, photophobia/phonophobia, flashes of light, vertigo and loose motions (KDT 8e Ch.12, p.192).
• The immediate cause of pain is held to be pulsatile dilatation of certain large cranial vessels; the underlying pathogenic mechanisms remain incompletely understood (KDT 8e Ch.12, p.192).
• Migraine afflicts roughly 10–20% of the population; it is a specific neurological syndrome but its manifestations vary widely between and within patients (G&G 14e Ch.15, p.292).
• US epidemiology: ~20.7% of females and 9.7% of males experience ≥1 migraine/year; prevalence is highest in both sexes at ages 18–44 years, inversely related to income and education (DiPiro 12e Ch.80, p.981).
• Two major clinical subtypes (DiPiro 12e Ch.80, p.983; G&G 14e Ch.15, p.292):
  • Migraine without aura ("common migraine") — headache lacks the aura phase but is otherwise similar.
  • Migraine with aura ("classic migraine") — headache preceded/accompanied by a complex of reversible positive/negative focal neurological (most often visual) symptoms; subclasses include migraine with typical aura, with prolonged aura, aura without headache, hemiplegic, retinal, and brainstem aura.
• Therapy of migraine is complicated by variable responses among and within patients and by an incomplete understanding of pathophysiology; efficacy of antimigraine drugs varies with presence/absence of aura, headache duration, severity, intensity, and undefined environmental/genetic factors (G&G 14e Ch.15, p.292).
• Drug therapy must be individualised — severity and frequency of attacks plus the individual patient's prior response determine drug choice (KDT 8e Ch.12, p.192).