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Patients with migraine and signs of leukoencephalopathy are frequently found to have cognitive impairment (CI), the pathogenesis of which is not entirely clear. The dynamics of CI in these patients during preventive therapy has been little studied.Patients and methods. A six-month follow-up study was conducted in 50 patients (8 men and 42 women; mean age, 41.9±11.9 years) with migraine (mainly chronic one) and signs of cerebral leukoencephalopathy according to magnetic resonance imaging (MRI). A control group consisted of 40 healthy individuals (13 males and 27 females) aged 20 to 64 years (mean age, 42.6±12.0 years). Neuropsychological examinations (the 12-word recall test; the test of literal and categorical associations; the Benton visual retention test, the Munsterberg test; the Montreal Cognitive Assessment (MoCA), the trail making test; the forward and backward digit recall test; the digit-symbol coding test; and the Stroop color test) and studies of emotional disorders (the Beck Depression Inventory (BDI), the Center for Epidemiological Studies Depression Scale (CES-D); the Hospital Anxiety and Depression Scale (HADS), and the Spielberger-Khanin Scale) were performed at baseline, and at 3 and 6 months of preventive therapy for migraine.Results and discussion. The patients with migraine versus the control group were observed to have lower scores of the MoCA (p=0.004), the 12- word recall test (p=0.0003), and the tests of literal (p=0.001) and categorical (p=0.0002) associations. No significant relationship was found between the volume of MRI cerebral white matter lesions and the severity of CI. There was a moderate inverse correlation (correlation coefficient R=-0.41) between the number of headache (HA) days per month and the MoCA score (p

Cognitive impairment (CI) is common in patients with migraine; its causes and pathogenesis continue to be discussed. Some authors consider that migraine proper does not lead to decreased cognitive functions, neuroimaging changes in the brain white matter are asymptomatic in migraine; and CI in patients with this condition is caused by comorbidities (depression, anxiety disorder) and/or concurrent cerebrovascular and neurodegenerative diseases. Other authors report the pathogenetic role of migraine in the development of CI and the importance of the frequency of headache attacks and neuroimaging changes in the brain matter in migraine. The paper reviews clinical trials dealing with the prevalence, causes, and pathogenesis of CI in patients with migraine. It sets forth the current principles of prevention and treatment of CI in patients with this condition.