Pharmacotherapeutics of migraine and the blood-brain barrier: serendipity, empiricism, hope, and hype
Abstract
Bigal and Krymchantowski[1] review the role of new and potential pharmacologic agents for the preventive treatment of migraine.[1] Whereas cortical spreading depression and brainstem involvement are presumed pathogenetic concepts, a substantial body of clinical, experimental, and pharmacologic evidence challenges the traditional view that migraine is the outcome of a brain neuronal aberration.[2–5]
In direct contrast to attack-aborting agents, migraine-preventing agents unambiguously affect the primary pathogenetic processes (afferent limb of migraine) rather than influencing events of the trigeminovascular system (efferent limb of migraine).[3] To critically influence brain neuronal function, it cannot be argued that migraine prophylactic agents must readily or freely cross the intact blood-brain barrier (BBB).[2–4] First, atenolol, a first-line migraine preventive agent that – like propranolol – prevents both migraine with aura and migraine without aura but – unlike propranolol – does not readily cross the BBB or critically influence brain neuronal function.[2,3] Second, drugs that abort the aura of migraine, such as nifedipine, nitrates, and isoproterenol, do not significantly cross the BBB and, therefore, cannot directly influence the visual or other cortical functions.[3,4] Third, as reviewed, the migraine preventive effect of topiramate is unpredictable, not dose-related; does not prevent migraine aura; and is not superior to propranolol while being found effective for…
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