Background. Nitrous oxide abuse (“laughing gas”, N2O) is common among young people attending nightclubs. Contrary to popular belief about the safety of N2O, in some cases neurological complications develop due to a deficiency of vitamin B12, the activity of which is blocked by N2O. Purpose of the study – to determine the typology and course of neurological disorders in a group of patients who regularly use “laughing gas”. To note the key diagnostic markers that allow verification of vitamin B12 deficiency induced by nitrous oxide consumption. To describe pathogenetic therapy features and follow-up. Materials and methods. The study included 12 patients (10 men and 2 women) aged 18 to 45 years (average age 29 years) with a diagnosis of B12-deficient myelopolyneuropathy induced by regular use of nitrous oxide. Results. The most common neurological complication of nitrous oxide abuse for more than 1 month was a generalized lesion of the peripheral nerves with acute or subacute distal symmetric sensory or sensorimotor axonal polyneuropathy. In the clinical picture, sensory complaints and disorders prevailed. Paresis developed in half of the cases. A typical neuroimaging symptom characteristic of funicular myelosis was rarely detected (16.7 %). A decrease in B12 vitamin level could most reliably be diagnosed only indirectly, by the presence of hyperhomocysteinemia (91.7 % of cases). In all cases that were followed-up, prolonged therapy with cyanocobalamin led to partial (n = 5; 62.5 %) or complete (n = 3; 37.5 %) regression of neurological symptoms. Conclusion. Caution regarding the use of nitrous oxide should be in all cases of predominantly sensory polyneuropathy with acute or subacute development in young and middle-aged people. A thorough history taking (targeted survey on the fact of nitrous oxide consumption) and diagnostics (testing the level of homocysteine, if possible methylmalonic acid) allow you to not miss a deficiency of vitamin B12, the treatment of the consequences of which with timely verification and adequate correction is quite effective. It is recommended that the level of homocysteine in the blood to be regularly monitored during the treatment (in order to achieve its normalization).

Objective Glutathione (GSH) is a major intracellular thiol-containing antioxidant. We tried to determine whether blood plasma GSH level is a marker for the severity of the two subtypes of acute stroke (large-artery atherosclerosis, LA and cardioembolic, CE). Forty-three patients with LA and 36 patients with CE aged 65 (47–82) years were included in the study. Thirty-one patients with cerebral microangiopathy were included for comparison. Total (t) and reduced (r) GSH levels were determined at admission. Neurological deficit was assessed by the National Institutes of Health Stroke Scale (NIHSS) on the first day, functional outcome and independence were assessed by the modified Rankin scale (mRs) and Bartel index (BI), respectively, after 21 days. Results The tGSH and rGSH levels in acute stroke were significantly lower than cerebral microangiopathy patients. Low tGSH (≤ 1.45 μM) and rGSH (≤ 30 nM) levels were risk markers for stroke severity at admission (NIHSS > 10) in patients with LA: age and gender adjusted odds ratio (AOR) was 4.95, 95% coincidence interval (CI) 1.31–18.7, AOR = 9.141, CI 1.84–45.3 for t- and rGSH, respectively. A low level of rGSH (≤ 30 nM) was found as risk marker for functional independence (BI ≤ 60: AOR = 15.9, CI 2.22–114.2) in patients with LA. Low tGSH level (≤ 1.1 μM) was associated with the reduction of poor outcome risk (mRs > 2: AOR = 0.154, CI 0.029–0.809) in CE group. Conclusions Low t- and rGSH levels may be considered potential risk markers for severity and insufficient functional independence in LA. Conversely, low tGSH level reduce the risk of poor stroke outcome only for CE.

Hypertension (HT) and its cerebral complications are extremely vexing medical and social problems. Despite the obvious association between hypertension and the clinical and neuroimaging features of cerebral microangiopathy (CMA) (also known as cerebral small vessel disease), the causal links between them remain ambiguous. Besides, antihypertensive therapy as the only way to manage these patients does not always prevent brain damage. Knowledge about the key factors and mechanisms involved in HT and CMA development is important for predicting the risk of cerebral complications and developing new approaches to their prevention and treatment. At present, genome-wide association studies and other approaches are used to investigate the common hereditary mechanisms of HT and CMA development, which will explain a large number of CMA cases not associated with hypertension, lack of a correlation between HT severity and the degree of cerebral injury, and failure of antihypertensive therapy to prevent CMA progression. Epigenetic markers likely play a modulating role in the development of these diseases.

В обзоре, подготовленном по данным последних публикаций ведущих европейских специалистов в области постинсультных когнитивных нарушений, приведены краткие сведения о распространенности, механизмах развития и факторах риска этих состояний, которые представляют собой серьезную проблему в период восстановления после инсульта. Описаны общие под-ходы к профилактике постинсультной деменции и возможности нейропротективной терапии у этой категории пациентов. Post-stroke cognitive impairment and dementia are one of the major causes of the disability and quality of life deterioration following cerebrovascular accident. In this review we cover current views on the prevalence, mechanisms and risk factors of post-stroke cognitive deficit, according to recent publications of leading European opinion leaders in this area. We also focus on the approaches to the pharmacological treatment and the role of neuroprotective agents.

Objective: Acute brain ischemia is accompanied by a disruption of low-molecular-weight aminothiols (LMWTs) homeostasis, such as homocysteine (Hcy), cysteine (Cys), and glutathione (GSH). We investigated the redox balance of LMWTs in blood plasma and its influence on ischemic stroke severity and the functional outcome in patients with an acute period. Patients and methods: A total of 177 patients were examined. Total and reduced forms of LMWTs were determined in the first 10-24 h. Stroke severity and functional state were estimated using the National Institutes of Health Stroke Scale (NIHSS) and the modified Rankin Scale (mRs) at admission and after 21 days. Results: Patients with high levels of total Hcy (> 19 μM) showed significantly reduced redox statuses of all LMWTs. Patients with low total GSH levels (≤ 1.07 μM) were at an increased risk of higher stroke severity (NIHSS > 10) compared to patients with a total GSH level > 2.64 μM (age/gender-adjusted odds ratio: 4.69, 95% CI: 1.43-15.4). Discussion: (1) low total GSH level can be considered as a novel risk marker for the severity of acute stroke in conditions of low redox status of LMWTs and (2) high Hcy levels associated with low redox status of LMWTs.