Platelet-leukocyte interaction and platelet activation in migraine: a link to ischemic stroke?

Abstract

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.

Ischemic stroke subtypes and migraine with visual aura in the ARIC study

“…Taken together, it is possible that migraine with visual aura may promote vasospasm, activate platelet aggregation, [24][25][26] and increased concentration of procoagulant factors. [27][28][29][30] Directly or indirectly in the setting of PFO, these vasoactive substances could gain access to coronary artery as well as cerebral vasculature, Table 3 Hazard ratios (95% confidence intervals [CI]) for the association of migraine with visual aura compared to migraine without visual aura and risk of verified ischemic stroke (all types) where they induce visual aura symptoms, and subsequently may result in brain ischemic injury if larger emboli are formed. Our data suggest that migraine without visual aura is not an isolated risk factor for stroke, in our sample, when compared to healthy controls without any headache history; any association identified can be explained by the traditional stroke risk factors (it is also possible that the number of participants with migraine without visual aura is too low, and the study is underpowered to detect an association with stroke).…”

A Multidisciplinary Approach to a Complicated Acute Paradoxical Embolism via a Patent Foramen Ovale

“…Different pathophysiological mechanisms have been postulated like right-to-left shunting of small subclinical emboli and metabolites bypassing the pulmonary system and causing irritation of the trigeminal nerve or an increased platelet activation and aggregation in response to serotonin could possibly trigger migraine and aura (normally serotonin is metabolized in the pulmonary circulation by the lung monoamine oxidase) [11,12]. A 2010 meta-analysis concluded that closing the PFO could cure all the migraine symptoms in 46% of the patients and reduce the symptoms in about 83% of the patients [13].…”

Numerical Analysis on the Blood Flow Characteristic in the Arteriovenous Graft for Different Injection Method of Blood

“…Unsteady profile period 0.758 s Artery outlet 12.8% of Artery inlet Velocity profile Needle (suction) -400 mL/min Needle (injection) 400 mL/min Vein outlet Pressure-outlet Wall Rigid body [19][20][21][22]. 또 한 활성화된 백혈구는 항원반응 발현을 증가시키게 하여 내 피세포에 혈소판의 부착 및 염증작용을 야기하며, 혈전 형성 에 중요한 역할을 한다 [22].…”

“…또 한 활성화된 백혈구는 항원반응 발현을 증가시키게 하여 내 피세포에 혈소판의 부착 및 염증작용을 야기하며, 혈전 형성 에 중요한 역할을 한다 [22]. 따라서 정맥측 문합부의 1 Pa 이 하의 영역을 살펴보는 것은 중요하다.…”