Irritable bowel syndrome associated with mitral valve prolapse and autonomic and haemostatic abnormalities in children, adolescents and adults with migraine

Dear Editor We read with considerable interest the paper by Termine et al. (1) regarding the high prevalence of mitral valve prolapse (MVP) and abnormalities of haemostasis in children and adolescents with migraine with aura (MA) compared with peers affected by other idiopathic headaches. Our published data (2) showed a high prevalence of MVP in patients (including young adults) with irritable bowel syndrome (IBS) reported to be associated with a higher prevalence of migraine; patients with IBS are more likely to have other disorders, mainly including migraine (3, 4). In particular, MVP occurred significantly more frequently in our 67 consecutive patients with IBS than in 32 control healthy members of the medical and laboratory staff [48% vs 2%; P = 0.00009 (two-tail Fisher s test)] associated with dysfunction of the autonomic nervous system and blood group A, thereby suggesting a genetic and clinical relationship between IBS and MVP syndrome (2). It is important to note that, apart from IBS, disturbance of the autonomic nervous system also appears to be a primary characteristic of migraine (5). Moreover, migraine carries a substantial genetic liability; linkage and genome-wide scans have disclosed numerous chromosomal liability loci in families with MA and migraine without aura, suggesting a genetic predisposition to migraines (6). The authors reported that abnormalities of haemostasis (positive anticardiolipin antibody titres) resulting in an increased thrombotic risk would provide a rational link between MA and ischaemic stroke. In this regard, they mentioned that Despite numerous studies of platelet hyperaggregability and activation in migraine, recent data do not provide strong support for a primary role of platelets in this condition (13) . However, more recent data indicate that platelets are activated during the migraine attack, thereby participating in the pathogenesis of the disorder. Platelets share many metabolic characteristics with serotonergic neurons and endothelial cells, and serotonin has long been implicated as a key neurotransmitter in migraine; migraine is the result of an inflammatory mechanism with serotonergic signalling, leucocyte and platelet functions, and intercellular communication between those cells is likely to be connected to the final pathway of the disorder (7–10). Specifically, the pathophysiology of migraine appears to be related with platelet hyper-aggregation caused by several stimulating agents including serotonin or 5-hydroxytryptamine (5-HT), collagen, thrombin, adenosine diphosphate and thromboxane A2. The blood levels of 5-HT 5, released from platelets, are elevated and the elevation of cerebral blood levels of 5-HT cause the aura of the first stage of migraine by contracting the cerebral blood vessels. Moreover, because the excessive 5-HT released is immediately metabolized, the second stage of migraine is caused by the relaxation of the cerebral blood vessels. While the underlying pathogenesis of 5-HT release has not been elucidated, it is generally thought to be related to the occurrence of migraine (11). On the other hand, studies have shown that selective serotonin reuptake inhibitors reduce platelet and whole-blood serotonin concentrations after repeated doses and could therefore exert an inhibitory effect on platelet activation, thereby possibly preventing migraine or acute coronary and cerebrovascular syndromes; trials on the efficacy of antiplatelet therapy in migraine patients will aid the understanding of underlying mechanisms and the deduction of possible prophylactic concepts (12, 13). Noticeably, goshuyuto, a traditional Competing interests: None declared. Acta Neurol Scand 2011: 123: 366–367 DOI: 10.1111/j.1600-0404.2010. 01456.x 2011 John Wiley & Sons A ⁄ S