Infarcts in the posterior circulation territory in migraine. The population-based MRI CAMERA study.
ABSTRACT In a previous study, migraine cases from the general population were found to be at significantly increased risk of silent infarct-like lesions in the posterior circulation (PC) territory of the brain, notably in the cerebellum. In this study we describe the clinical and neuroimaging characteristics of migraine cases with and without aura and controls with PC lesions. In total, 39 PC infarct-like lesions represented the majority (65%) of all 60 identified brain infarct-like lesions in the study sample (n = 435 subjects with and without migraine). Most lesions (n = 33) were located in the cerebellum, often multiple, and were round or oval-shaped, with a mean size of 7 mm. The majority (88%) of infratentorial infarct-like lesions had a vascular border zone location in the cerebellum. Prevalence of these border zone lesions differed between controls (0.7%), cases with migraine without aura (2.2%) and cases with migraine with aura (7.5%). Besides higher age, cardiovascular risk factors were not more prevalent in cases with migraine with PC lesions. Presence of these lesions was not associated with supratentorial brain changes, such as white matter lesions. The combination of vascular distribution, deep border zone location, shape, size and imaging characteristics on MRI makes it likely that the lesions have an infarct origin. Previous investigators attributed cases of similar 'very small' cerebellar infarcts in non-migraine patients to a number of different infarct mechanisms. The relevance and likelihood of the aetiological options are placed in the context of known migraine pathophysiology. In addition, the specific involvement of the cerebellum in migraine is discussed. The results suggest that a combination of (possibly migraine attack-related) hypoperfusion and embolism is the likeliest mechanism for PC infarction in migraine, and not atherosclerosis or small-vessel disease.
SourceAvailable from: Marcelo M ValençaFrontiers in Neurology 01/2014; 5:263. DOI:10.3389/fneur.2014.00263
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ABSTRACT: Migraine is a common disabling neurological disorder resulting from excessive cortical excitation and trigeminovascular afferent sensitization. In addition to aberrant neuronal processing, migraineurs are also at significant risk of vascular disease. Consequently, the impact of migraine extends well beyond the ictal headache and includes a well-documented association with acute ischemic stroke, particularly in young women with a history of migraine with aura. The association between migraine and stroke has been acknowledged for 40 years or more. However, examining the pathobiology of this association has become a more recent and critically important undertaking. The diversity of mechanisms underlying the association between migraine and stroke likely reflects the heterogenous nature of this disorder. Vasospasm, endothelial injury, platelet aggregation and prothrombotic states, cortical spreading depression, carotid dissection, genetic variants, and traditional vascular risk factors have been offered as putative mechanisms involved in migraine-related stroke risk. Assimilating these seemingly divergent pathomechanisms into a cogent understanding of migraine-related stroke will inform future studies and the development of new strategies for the prevention and treatment of migraine and stroke.Current Neurology and Neuroscience Reports 03/2015; 15(3):530. DOI:10.1007/s11910-015-0530-8 · 3.67 Impact Factor
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ABSTRACT: Migraine and epilepsy are disorders that are common, paroxysmal, and chronic. In many ways they are clearly different diseases, yet there are some pathophysiological overlaps, and overlaps in clinical symptomatology, particularly with regard to visual and other sensory disturbances, pain, and alterations of consciousness. Epidemiological studies have revealed that the two diseases are comorbid in a number of individuals. Both are now recognized as originating from electrical disturbances in the brain, although their wider manifestations involve the recruitment of multiple pathogenic mechanisms. An initial excess of neuronal activity in migraine leads to cortical spreading depression and aura, with the subsequent recruitment of the trigeminal nucleus leading to central sensitization and pain. In epilepsy, neuronal overactivity leads to the recruitment of larger populations of neurons firing in a rhythmic manner that constitutes an epileptic seizure. Migraine aura and headaches may act as a trigger for epileptic seizures. Epilepsy is not infrequently accompanied by preictal, ictal, and postictal headaches that often have migrainous features. Genetic links are also apparent between the two disorders, and are particularly evident in the familial hemiplegic migraine syndromes where different mutations can produce either migraine, epilepsy, or both. Also, various medications are found to be effective for both migraine and epilepsy, again pointing to a commonality and overlap between the two disorders. © 2015 American Headache Society.Headache The Journal of Head and Face Pain 04/2015; 55(3). DOI:10.1111/head.12536 · 3.19 Impact Factor