[Clinical aspects of pathophysiological mechanisms in migraine.]

Migraine is more than the pain involved in the "migraine attack." Before the onset of pain many clinical symptoms can be observed. These symptoms may be classified as vegetative, affective, and vascular. Brain perfusion is altered during migraine attacks as well as during the intervals between attacks. These "more recent" findings are important because brain perfusion is controlled by metabolic and by neurotransmission mediated pathways: 750 ml blood/min is available in brain perfusion. The skull, on the other hand, limits the volume of blood in the brain to 130 ml. Control of the shift of blood inside the brain, with a chance of maximal blood flow or strictly limited blood volume, may be one of the most important problems in neurotransmission mediated cerebral perfusion control. The most important neurotransmission systems of cerebral perfusion control are those that are believed to be involved in affective and vegetative symptoms. It must be assumed that platelets are involved in migraine. Platelet reactivity is enhanced in migraine patients during the interval between attacks. When a migraine attack occurs a release of platelet serotonin and a further increase of platelet reactivity can be observed. Platelet activation in these cases is comparable to the situation in transient ischemic attacks. During transient ischemic attacks, platelet serotonin has been found to be enhanced in the area of transient ischemia. Serotonin is a neurotransmitter, low concentrations of which induce vasodilation, while higher concentrations induce vasoconstriction. It may be assumed that platelet serotonin is a potent vasoregulating substance that may interact in the brain vessels with the neurotransmission controlled perfusion. The hypothesis of an (inborn) instability of the interaction of cerebral neurotransmission systems in patients suffering from migraine is in accordance with the vegetative and affective symptoms in migraine, the observed imbalance of neurotransmission mediated cerebrovascular autoregulation and the irritation of platelets in migraine attacks, as well as in the interval between attacks. The "modern" treatments of migraine with acetylsalicylic acid, ergotamin and/or beta blockers are discussed in relation to this proposed hypothesis of a migraine pathophysiology.