In a previous study, migraine cases from the general population were found to be at significantly increased risk of silent infarctlike 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 supra-tentorial brain changes, such as white matter lesions. The combination of vascular distribution, deep border zone location, shape, sizeand 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 attackrelated) hypoperfusion and embolism is the likeliest mechanism for PC infarction in migraine, and not atherosclerosis or smallvessel disease.u001a In a previous study, migraine cases from the general population were found to be at significantly increased risk of silent infarctlike lesions in the posterior (PC) territory of the brain, notably in the cerebellum. In this study we describe the clinical and neuroimaging characteristics of total migraine with 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 most of the 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%). not more prevalent in cases with migraine with PC lesions. Presence of these lesions was not associated with supra-tentorial 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 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 attackrelated) hypoperfusion and embolism is the likeliest mechanism for PC infarction in migraine, and not atherosclerrosis or smallvessel disease. u001a