To clarify the mechanism of the development of cerebral infarcts in the internal carotid artery (ICA) dissection, the data of neuroimaging (localization of infarcts) and angiography have been analyzed in 49 patients (19 females 30 males, mean age 35,6 +/- 11,3 years). Four variants of infarct localization have been distinguished: 1 - the whole ICA territory (middle and anterior cerebral arteries - MCA, ACA) - 10%, 2 - the territory of superficial and deep branches of MCA- 37%, 3- the territory of superficial MCA branches and cortical-medullar arteries - 31% (the cortex and underlying white matter - 19%, the periventricular white matter and semiovale center - 6%, combined localization - 6%); 4 - the territory of deep (perforating) MCA branches (the basal ganglia and adjacent white matter) - 22%. In most of patients (92%) the dissection resulted in the occlusion or severe stenosis of intracranial ICA which in a half of cases extended to MCA and/or ACA. In 72% patients dissection involved the extracranial ICA. The marked obstructive process in the dissected ICA allows to assume that the hemodynamic, but not embolic, mechanism plays a key role in the development of infarcts. This is in line with the frequent infarct localization in the end or border zones (superficial and deep) of brain blood supply (31%) and the development of stroke during a sleep (49%). Arterio-arterial embolism as a mechanism of ischemic stroke development was found in 8% of patients with the isolated extracranial ICA dissection. It caused stenosis of the lumenand in 6% accompanied by the pseudoaneurism formation. Thrombi formed inside the aneurism could be the origin of the embolism.