Migraine is an episodic headache disorder associated with autonomic symptoms with or without aura. Episodes of migraine could lead to loss of productivity in young professionals/individuals. Pathophysiological studies exhibit migraine to be a neurovascular headache. Migraine is caused by abnormal activation and modulation of trigeminocervical neurons. Impaired modulation of central nervous system aminergic pathways especially of the brainstem and activation of trigeminoparasympathetic system leads to vasodilation of meningeal arteries and dural venous sinuses.
Migraine was considered to be vascular headache until 2010. The aura phase of migraine has been demonstrated to be
a neuronal
event, with
electroencephalogram. A cortical wave showing cortical depression could be observed in electroencephalogram. So, physiologically
migraine is an heterogenous entity.
Migraine treatment comprises two
arms with an effort to address components of pathophysiology: (i) Strategy to
terminate acute attacks and (ii) Strategy to prevent further attacks.
Ergotamine was the earliest analgesic known to be effective in acute migraine since 1920s. Now large
number of ‘Nonsteroidal Anti-inflammatory Drugs’ (NSAID) and non-NSAID
analgesics have been used as rescue medications. The targeted treatment was launched
in 1990 with the advent of Triptans. Advances in preventive therapies have been very
few. Beta-blockers and tricyclic antidepressants remain the main component
of treatment of migraine,
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