A detailed analysis of the neurological disorders of «dysarthria–clumsy hand» syndrome (DCHS) is important for its earlier diagnosis.

The purpose of this study was to evaluate the incidence of DCHS and the range of its clinical signs, as well as the degree of hand/arm dysfunctions and its dynamics in patients with the acute lacunar stroke (LS).

Material and methods. 139 patients with acute LS were examined. Quantitative assessment of neurological deficits, such as paresis, cerebellar ataxia, and apraxia was performed using the relevant scales. The upper limb function was assessed by Action Research Arm Test and 9-Hole Peg Test. Barthel Index was used for disability evaluation.

Results. DCHS was diagnosed in 17% of LS patients (group1) and other clinical variants of LS was detected in 83% of patients (group 2). The cause of «clumsiness» in the hand/arm in DCHS was ataxia (83%), mild paresis (71%) and kinesthetic apraxia (29%), which were present independently or in combination. Hand/arm dysfunction and disability, while performing daily activities, were less severe in group 1 patients compared to group 2. The complete restoration of hand/arm function was observed in 63% of the patients with DCHS in 2 weeks after the onset of LS.

Conclusions. Mild paresis, cerebellar ataxia and apraxia are the main causes of «clumsiness» of the hand/arm in patients with DCHS. In general, DCHS has good functional outcomes.

Introduction. Craniocerebral trauma remains one of the most common forms of brain pathology. Its relevance is determined by both, high prevalence and significant financial costs associated with the treatment, and rehabilitation of injured. Mild forms predominate in the general structure of injury. Immune response is one of the manifestations characteristic for a complex of biochemical and pathophysiological reactions triggered in the brain in response to injury. At the same time, the subtle mechanisms of its functioning and their role in pathogenesis of diseases remain the subject of discussion. Our research was aimed to study the role of immune reactions in the pathogenesis of mild brain injury.

Materials and methods. 22 patients with concussion (aged from 20 to 45) were examined. The control group included 37 healthy individuals aged 20 to 46. The examination included the collection of complaints, medical history, assessment of somatic and neurological status, neuropsychological testing. The object of laboratory research was venous blood. Attention was mainly paid to the T-helpers of central (CM, CD45RA–CD62L+) and effector (EM, CD45RA–CD62L–) memory, which were evaluated using multicolored cytometric analysis.

Results. Patients presented complaints of general and cognitive nature upon admission to the hospital. Cerebellar lesion symptoms dominated while neurological status evaluation. Neuropsychological examination allowed us to detect neuro-dynamic and regulatory disorders predominance. While conducting the analysis of the main stages of cell maturation in the blood of patients with concussion, it was noted that there was a significant increase in both, relative and absolute content of central memory T-helpers compared to the control group. At the same time, the percentage of EM Th in those with injury was slightly reduced. Also, in patients with injured Th cells of central memory, the relative content of Th1 cells decreased and the relative content of Th17 cells increased. In addition, within the CM Th pool, there was an increase in the proportion of three types of Th17 — CCR6+DN Th17, Th17.1 and «classic» CCR4+CXCR3– Th17.

Conclusion. Changes in T-helpers of central memory and T-helpers of peripheral memory subpopulation among CD3+CD4+ cells can be considered as a predictor of the course of concussion in the acute period. However, T cells involved in autoimmunity, do not necessarily reflect the immune system disorders. It is possible that the basis for the decrease in the Th1 level in the circulatory bed in patients with brain injury is the recruitment of immune cells. An increase in the proportion of Th17 was also detected among T-helpers of central memory patrolling the lymphoid tissue the other day after the brain injury. This circumstance may indicate the fact that in the early stages after the nervous tissue damage, processes leading to the formation of «pro-inflammatory» cells are triggered. It allows us to consider these lymphocytes as one of the main populations of immunocompetent cells possessing a neuro-destructive effect.

Ischemic stroke (IS) and type 2 diabetes mellitus are factors that affect the homeostasis of low-molecularweight aminothiols (cysteine, homocysteine, glutathione etc.). It has already been shown that IS in the acute period led to a decrease a level of reduced forms of aminothiols, but it is not clear whether type 2 diabetes mellitus has a noticeable effect there.

Objective: to reveal the features of homeostasis of aminothiols in patients with type 2 diabetes mellitus in acute IS.

Material and methods. The study involved 76 patients with primary middle cerebral artery IS in the first 10–24 hours after development of neurological symptoms. Group 1 included 15 patients with IS and type 2 diabetes mellitus, group 2 — 61 patients with IS and stress hyperglycemia. Their total plasma levels of cysteine, homocysteine, and glutathione, their reduced forms, and redox status were determined at admission (in the first 24 hours after IS).

Results. There was a decrease in the level of total glutathione level (1.27 vs. 1.65 μM, p = 0.021), as well as its reduced form (0.03 vs. 0.04 μM, p = 0.007) in patients with IS and type 2 diabetes mellitus. Patients with type 2 diabetes mellitus who had a low redox status of homocysteine (0.65–1.2%) and glutathione (0.7–2.0%) were also characterized by a decrease in total glutathione level (p = 0.02; p = 0.03).

Conclusion. Thus, type 2 diabetes mellitus is associated with a decrease in the level of total glutathione in acute IS. Probably, type 2 diabetes mellitus is characterized by a particular relationship between the metabolism of homocysteine, glutathione and glucose. Therefore, the search for homocysteine-dependent approaches to correct glutathione metabolism in type 2 diabetes mellitus may be of interest as an adjuvant therapy for IS.

Introduction. White matter hyperintensity (WMH) is a neuroimaging age-related phenomenon associated with an increased cardiovascular risk in people with arterial hypertension (AH). The prevalence of WMH and its relationship with risk factors for cerebrovascular disease (CVD) in middle-age population requires clarification.

Aim: to assess the prevalence of the WMH phenomenon in people of working age (40–59 years) and to establish cerebrovascular risk factors associated with its development.

Material and methods. Study cohort (n = 376; 156 (41.5%) men and 220 (58.5%) women; mean age 49.7 ± 5.0 years) was formed by screening an open population (40–59 years of age). Using a questionnaire and clinical, laboratory and instrumental findings, including brain MRI (1T), the prevalence of cardiovascular and cerebrovascular risk factors was analyzed. The odds ratio (OR) of the event occurring and a 95% confidence interval were calculated.

Results. High prevalence of risk factors was revealed in the age group of 40–59 years, including AH in 46.7%, increased body mass index (BMI) in 60.6%, dyslipidemia (up to 39%), metabolic syndrome in 21.5%, thickening of the intima-media complex in 57.2%, atherosclerotic plaques in 49.7% of all cases. WMH was identified in 32% (120/376) of the subjects examined. An association between presence, severity of WMH and age, presence and severity of AH, as well as total burden of vascular risk factors was established. The most significant factors associated with the development of WMH in people aged 40–59 were found to be AH (OR 3.35), atherosclerosis of the brachiocephalic arteries (OR 1.79), and hyperglycemia (OR 1.36).

Conclusion. Thus, there is a high prevalence of risk factors for cardiovascular and cerebrovascular diseases in the working-age population of the megalopolis (Moscow) at the age of 40–59 years, which is associated with accelerated WMH formation. Significant factors that are associated with WMH are AH, atherosclerosis of the brachiocephalic arteries, hyperglycemia, as well as dyslipidemia and metabolic syndrome. Early detection and management of the listed modifiable risk factors are necessary to prevent the development and progression of cerebral injury.

The article represents the discussion of sarcoidosis involving the cranial nerves and meninges. It’s a rare disease difficult to diagnose. This form of the disease is a progressive lesion of the nervous system, characterized by granulomatous inflammation of the membranes and /or tissue of cerebrum or spinal cord, cranial and /or peripheral nerves. Clinical signs of the nervous system disorder found in sarcoidosis, are detected only in 5–15% of patients. They are often represented by symptoms of cranial nerve damage, meningeal syndrome and epileptic seizures. X-ray computed tomography and magnetic resonance imaging of the brain do not reveal specific changes, however, they allow to exclude other structural lesions of the central nervous system and to identify neuroimaging signs, most common in the course of this disease. Diagnosis of neurosarcoidosis is possible in the presence of neurological symptoms, signs of multisystem lesions, and histological confirmation of non-caseous granulomatous inflammation in one or more organs. The article also represents a clinical observation of a patient with neurosarcoidosis, manifested by acute bilateral neuropathy of the facial nerves, unilateral neuropathy of the trigeminal nerve and meningism syndrome. The neuroimaging signs, often found in this disease, were revealed: the accumulation of contrast agent by the membranes of the brain and the tissue of cavum Meckeli. The course of the disease and diagnostic search, which made it possible to detect signs of multisystem lesion, are described. The diagnosis was confirmed by histological examination of the biopsy material of the intrathoracic lymph node. The results of neurosarcoidosis anti-inflammatory therapy are presented. The peculiarities influencing the choice of this type of treatment terms, are indicated.

Rehabilitation and secondary prevention of ischemic stroke (IS) is the basis for the management of patients with ischemic stroke. The important role of non-drug methods of secondary prevention of IS should be noted: cessation of smoking and alcohol abuse, regular physical activity, proper nutrition, reduction of excess body weight. The normalization of blood pressure is one of the most effective areas of IS prevention. It is based on the regular intake of antihypertensive drugs in most cases. After noncardioembolic IS, antiplatelet agents are required: acetylsalicylic acid (ASA), clopidogrel, or a combination of dipyridamole and ASA. The possibility of taking a combination of clopidogrel and ASA for 21 days after IS with a subsequent switch to monotherapy with ASA or clopidogrel is discussed in patients with non-disabling IS. After cardiomoembolic IS, warfarin is required under the control of an international normalized ratio or with nonvalvular atrial fibrillation of new oral anticoagulants: apixaban, dabigatran or rivaroxaban. Most patients after IS require statins, and the doses are selected individually. Carotid endarterectomy is most effective in severe stenosis (narrowing of 70–99% of the diameter) of the internal carotid artery on the side of the involved hemisphere during the first 3–7 days after non-disabling IS. The data of multicenter placebo-controlled and open observational studies on the use of the metabolic drug Cytoflavin, which is widely used in our country in the rehabilitation of patients with IS, are presented.