Looking in the wrong place? The search for an ideal migraine preventative

Abstract

The cause of migraine headache is still unknown, although triggers for it are often apparent. There are, in consequence, no reliable migraine headache preventative drugs that act through an influence on known causal pathways. This review discusses the pathophysiology of migraine, the link between migraine triggers and the consequent headache and the putative mode of action of different classes of migraine drugs in the light of a number of pathophysiological models. It advances the idea that migraine triggers produce headache because they increase cortical excitability and discharge, which in turn reduces the inhibitory drive of the descending pain control system, selectively for trigeminovascular sensation. Supporting evidence for such a mechanism is presented and suggestions made as to the modes and sites of action of future improved migraine preventative agents. Drug Dev Res 68: 376-388, 2007.

The Mode of Action of Migraine Triggers: A Hypothesis

“…The antiepileptics and the β‐blockers may be the exceptions. A dismayingly large number of these preventative drugs have only been discovered to have migraine prophylactic effects by serendipity 224 – usually physicians have noted a decrease in migraine frequency after placing patients on a particular drug for other purposes. In at least one instance, the use of monoamine oxidase (MAO) inhibitors, the use of the drug for even the primary condition (in this case, hypertension) also had little basis in theory – a case of double serendipity.…”

Von Frey's hairs – a review of their technology and use – a novel automated von Frey device for improved testing for hyperalgesia

“…Migraine pain itself may be a consequence of centrally generated alterations in neurotransmission, in which innocuous sensory traffic becomes amplified and is perceived as noxious (Lambert, 2007;Yarnitsky et al, 2003). Migraine is frequently accompanied by allodynia in the trigeminal distribution (Lance and Goadsby, 1999;Mathew et al, 2004), probably due to altered responsiveness of the trigeminovascular system.…”