Migraine treated by Shakespeare's son-in-law, Dr John Hall

Objectives: Migraine has been identified as an independent risk factor for ischemic stroke.Both neurogenic inflammation and platelet activation have been linked to the pathophysiology of migraine.Increased platelet activation results in up-regulation of specific binding to leukocytes which promotes proinflammatory leukocyte secretion and their tethering to endothelium, a mechanism that has been demonstrated in stroke and which could provide a link to migraine.We aimed to determine whether platelet-leukocyte aggregation is increased in migraine patients outside an acute attack.Methods: Seventy two patients with migraine according to IHS criteria were compared to a control group (n = 72).Whole blood flow cytometry was used to quantify the activation dependent P selectin on the platelet, and to assess the fraction of platelets bound to the different leukocyte subsets.Results: Migraine patients showed significantly more platelet-leukocyte aggregates compared to the control subjects (p = 0.003).This effect was driven by an increased polymorphonuclear cell-platelet aggregation (p = 0.003) whereas platelet aggregation with monocytes and lymphocytes was not.Platelet activation was also increased (p = 0.001).Conclusions: In migraine pro-inflammatory platelet adhesion to leukocytes occurs during the headache free interval similar to that seen in acute coronary and cerebrovascular syndromes.This may suggest a link between migraine and stroke on a cellular level.