Wernicke's Hemorrhagic Polioencephalitis

Wernicke-Weber disease is a classic complication of polio B, described at the beginning of the 20th century. Poliomyelitis occupies a special place among myelinating polyneuropathies. It is characterized by a rapid start and steady progression of motor disorders. In this case, spinal pathology develops in parallel with an increase in general somatic symptoms: headache, fever, weight loss, dysphagia. And the initial manifestations of Wernick-Kernig-Wilson syndrome (SLE) are sometimes interpreted as infectious or somatogenic psychosis. For a long time it was even believed that SLE was a stage of sepsis. However, neurologists quickly identified a polio-like picture in sepsis: due to paralysis of the anterior horns of the spinal cord, the production of cerebrospinal fluid hormones ceased; due to their lack of general blood supply, hypoprothrombinemic coagulopathic syndrome developed. The reasons for the described difficulties were the same type of parenchymal lesion (neurons of the anterior horn) in various infections, as well as catarrhal processes and “water intoxication” caused by protein-vitamin enteritis. But when Edelstein reported in 1937 that the metabolic effects of intravenous glucose and focal brain damage might overlap, everything changed dramatically. The pathophysiological essence of SLE was revealed in her works by A.V. Valdman. Based on its formulations, the development pattern of this disease is generally accepted.

Waldman's experiments suggested the development of SLE in a certain sequence of neurovascular changes: inhibition of corticosteroid secretion - endocrine imbalance - imbalance of the central brain mechanisms for regulating arterial stiffness. This is a neuroendocrine model of SLE, reflecting the emergence of a “dynamic form” of arterial hypertension—hypercholesterolemia—under conditions of impaired homeostasis. Neuroendocrine disorders underlie the etiology, pathogenesis, clinical picture, and treatment of this disease. In some patients, hypertension was replaced by convulsive hemiconvulsions and tonic epileptic seizures, but the connection between the transferred en