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Objective: To study the follow-up of adult patients with status epilepticus or a history of serial seizures, assessing the likelihood of achieving long-term remission and identifying predictors of treatment effectiveness., Material and Methods: The study included 280 patients divided into 137 patients with epilepsy with a series of seizures or a history of status epilepticus (group 1) and 143 patients, who had not previously received therapy and did not have a series of seizures or a history of status epilepticus (group 2). A clinical and neurological examination, analysis of medical documentation data, electroencephalography, and MRI were performed., Results: After correction of therapy, remission in patients in group 1 was achieved in 21.9%, improvement in 30%, no effect was observed in 48.1%; in group 2 the indicators were 51%, 28.7%, 20.3%, respectively. The onset of epilepsy in childhood, frequent seizures, and regional epileptiform activity were associated with the lack of treatment effect., Conclusion: The results confirm the main role of the clinical examination in determining the prognosis of epilepsy in a particular patient. Currently available instrumental techniques have limited predictive value.

The paper addresses genetic causes of stroke: MELAS, antiphospholipid syndrome, CADASIL, Fabry disease. The etiology and pathogenesis, symptoms, diagnosis, treatment methods of these diseases are described.

Marburg's variant of multiple sclerosis, first described by the Austrian neurologist Otto Marburg in 1906, is a rare demyelinating disease that usually leads to severe disability or death within weeks to months. Our case report describes a young 24-year old woman with Marburg's variant of multiple sclerosis who became totally disabled over a period of some months. Clinical features and MRI-characteristics of two demyelinating diseases: acute disseminated encephalomyelitis (ADEM) and Marburg's variant of multiple sclerosis are discussed. The use of intense immunosuppression in the case described is considered.

Fabry disease (Anderson-Fabry disease) is an X-linked recessive lysosomal storage disorder resulting from deficient activity of lysosomal hydrolase, alpha-galactosidase A (alpha-Gal A), which leads to progressive accumulation of globotriaosylceramide (Gb3) in various cells, predominantly endothelial and vascular smooth muscle cells, with clinical manifestations affecting major organs including the central nervous system. Manifestations of Fabry disease include progressive renal and cardiac insufficiency, neuropathic pain, stroke and cerebral disease, skin and gastrointestinal symptoms. Clinical onset usually occurs in childhood, but many severe patients are diagnosed in adulthood. Females may be severely affected as males and both may die prematurely due to stroke, heart disease and renal failure. Early recognition of symptoms, enzyme activity levels, concentration of Gb3 levels in the blood, urine and skin biopsies, as well as genetic testing (GLA gene) enable establishment of early diagnosis and therapeutic intervention with enzyme replacement therapy. Enzyme replacement therapy can stabilize or reduce the progression of the disease. Early therapy may prevent complications of the disease.