Background. Severe disturbances of the cerebral circulation are considered to be among the most complicated disorders by the course and severity of damage to the central nervous system. In acute ischemia, brain tissue is initially subjected to reversible, and subsequently, irreversible damage. In brain hypoperfusion, penumbra may undergo necrosis or resume normal vital activity. Objective. of the research was to study peculiarities of pathomorphological changes of brain tissue in perifocal region in different periods from the onset of ischemic stroke. Methods. Material (autopsy) of 25 patients with ischemic stroke aged from 45 to 81 years has been analyzed. Case histories, clinical data, concomitant diseases and underlying conditions have been studied. The material has been grouped according to Mena H et al. classification of stages of cerebral infarction course in three phases: I – the phase of severe neuronal damage (1-3 days from the infarction development), II- the phase of acute organization (4-7 day from the onset of the disease), and III – the phase of chronic organization (in 7 days from the onset of the disease). Samples of brain tissue (1.5 х1.5 cm) were collected for histological analysis in the region adjacent to ischemic stroke. The materials were prepared by a standard technique and sections were stained with hematoxylin and eosin. Results. One, or more frequently a combination of several diseases in one patient influenced lethal outcome of the disease. Neurons with coagulation necrosis were observed in most cases in perifocal region in the most severe phase of the disease. Conclusion. In disease progression, in III phase, “red” neurons and “shadows” of neurons were frequently detected simultaneously in penumbra. In I phase, neutrophils and activated microglia appeared around the core of necrosis. Lymphocytes and macrophages were detected in the phase of severe and chronic organization. Initial organization with the presence of single hemistocytic astrocytes and thin-walled capillaries was primarily revealed in the region most adjacent to necrosis in I phase, and subsequently, spread into penumbra in II and III phases of cerebral infarction.