Vol 10, No 1 (2016)

Comparison of the results of investigation of the hemorheology and hemostasis system in patients with stroke of various types, localization, and severity who were treated at critical and intensive care units, with venous thromboembolic complications (VTECs) and without VTEC, demonstrated a high significance of impairments in the hemorheology and hemostasis system for VTEC pathogenesis in stroke patients. Despite ongoing anticoagulant therapy, aggravation of the prothrombogenic state was observed in VTEC patients. Ischemic stroke was associated with more severe changes compared to hemorrhagic stroke. Hemostasiological predictors of VTEC were identified. In patients without VTEC, both the coagulation and anticoagulation systems as well as the fibrinolysis system were preserved. The D-dimer and thrombophilia markers, such as hyperhomocysteinemia and antiphospholipid syndrome, were shown not to contribute to the development of VTEC in stroke patients.

Type 2 diabetes mellitus (T2DM) and metabolic syndrome (MS) facilitate the development of ischemic cerebrovascular diseases. This article presents the results of examination of patients with ischemic cerebrovascular diseases associated with T2DM and MS. We have found that T2DM adversely affects the progression of atherosclerosis in patients with cerebrovascular diseases, and activity of the atherosclerotic process in the great cerebral arteries directly depends on the duration of carbohydrate disorders.

The study purpose was to identify histological changes in the peripheral nerves and determine functional significance of subclinical neuropathy in experimental simulation of lower leg fractures. We simulated a tibial shaft fracture in 24 dogs under anesthesia and performed osteosynthesis using an Ilizarov apparatus. After 7, 14, 20, 35–37, and 50 days of fixation using the apparatus and 30, 60–90, and 120 days after removal of the apparatus, the dogs were euthanised. Electromyography was performed before fracture and within the main phases of the experiment. Samples of the sciatic, peroneal, and tibial nerves were studied histologically using computer morphometry of semithin araldite sections. After 37 days of fixation, the amplitude of M-responses of the tibialis anterior and gastrocnemius muscles decreased by 70% compared to the baseline value, increased after removal of the apparatus, but not restored. There were no sighs of nerve damage by bone fragments or wires. The fraction of degenerating myelinated fibers in the studied nerves was less than 13%. Reorganization of the Remak bundles led to a temporary increase in the number density of nerve fibers. Along with axonal atrophy, the peroneal nerve was characterized by demyelination-remyelination, and the tibial nerve was characterized by hypermyelination. The dynamics of numerical density of endoneurial blood vessels was also different. Despite minor sharp degenerative changes in myelinated fibers, persistent axonal atrophy, demyelination, and retrograde changes were not compensated for up to 120 days after removal of the apparatus. Correlations between the morphometric parameters of myelinated fibers and the M-response amplitude indicated a causal role of subclinical neurological changes in functional outcomes of fractures.

The article discusses the issues related to the personalization of preventive measures for ischemic stroke, in particular those associated with resistance to one of the most common antiplatelet drugs, aspirin. A brief historical note on investigation of acetylsalicylic acid is provided. The paper addresses the issue of etiological factors and epidemiology of aspirin resistance. Ananalysis and comparison of various techniques for evaluation of this phenomenon are performed. Separately, a molecular genetic aspect of the pathology is considered. In conclusion, the recommendations for overcoming tolerance to aspirin therapy are provided.

Intensive development of DNA analysis technologies and largescale genome-wide association studies have led to accumulation of a large array of data on the relationship between genetic factors and various phenotypic manifestations, including monogenic and polygenic hereditary diseases. This greatly has extended the capabilities of clinical diagnostics and predictive medicine in the field of socially significant diseases. For example, a role of a genetic component of the risk for such a multifactorial and polyetiologic disease as stroke is now actively explored. Large-scale studies have revealed both general and specific genetic markers associated only with a certain type and subtype of stroke. This review analyzes the current state of the problem of using genetic markers for diagnosis of stroke predisposition, complex issues associated with multiplicity of risk factors for stroke, and possible development in this area.

The article describes a clinical case of severe childhood epileptic syndrome, FIRES (DESC) syndrome, which is a form of epileptic encephalopathy in school-age children caused by hyperthermia. The emergence of this severe childhood condition leads to involvement of all diagnostic and human resources available at a pediatric critical care clinic to identify and treat this form of epileptic paroxysm. The described clinical case also had a severe course with a prolonged epileptic status, which was resistant to antiepileptic pharmacotherapy, and hyperthermia. The presented case is a modest contribution to the treasury of information about this syndrome in our country, with the aim to increase the doctors’ awareness of the problem.