Background: brain-derived neurotrophic factor (BDNF) may play a role during neurorehabilitation following ischemic stroke. This study aimed to elucidate the possible role of BDNF during early recovery from ischemic stroke assisted by motor training. Methods: fifty patients were included after acute recovery from ischemic stroke: 21 first received classical rehabilitation followed by ‘motor rehabilitation using motion sensors and augmented reality’ (AR-rehabilitation), 14 only received AR-rehabilitation, and 15 were only observed. Serum BDNF levels were measured on the first day of stroke, on the 14th day, before AR-based rehabilitation (median, 45th day), and after the AR-based rehabilitation (median, 82nd day). Motor impairment was quantified clinically using the Fugl–Meyer scale (FMA); functional disability and activities of daily living (ADL) were measured using the Modified Rankin Scale (mRS). For comparison, serum BDNF was measured in 50 healthy individuals. Results: BDNF levels were found to significantly increase during the phase with AR-based rehabilitation. The pattern of the sequentially measured BDNF levels was similar in the treated patients. Untreated patients had significantly lower BDNF levels at the endpoint. Conclusions: the fluctuations of BDNF levels are not consistently related to motor improvement but seem to react to active treatment. Without active rehabilitation treatment, BDNF tends to decrease.

Background: Motor recovery after stroke is based on neuronal plasticity and the structural reorganization of the brain. Questions are debated about the proper moment to start rehabilitation in the acute period of stroke, the significance of rehabilitation interventions during the so-called “plastic window”, and the advantages of modern and traditional programs. The aims of this study were to evaluate the role of different rehabilitation strategies and their combinations for motor recovery and the impact on functional disability by way of neurological and functional outcomes 3 months after ischemic stroke. Methods: We used three rehabilitation approaches: early rehabilitation from the first day of stroke (Phase I), traditional exercise programs (Phase II), and an author’s new method of biofeedback rehabilitation using motion sensors and augmented reality (AR) rehabilitation (Phase III). Clinical and functional outcomes were measured on the 90th day after stroke. We developed algorithms for quantifying the quality of movements during the execution of tasks in the motor domains of the AR rehabilitation program. Results: Phase I of rehabilitation led to an improvement in functional independence, and the recovery of motor functions of the extremities with an absence of mortality and clinical deterioration. AR rehabilitation led to significant improvement both with respect to clinical and functional scores on scales and to variables reflecting the quality of movements. Patients who were actively treated during Phases II and III achieved the same final level of motor recovery and functional outcomes as that of participants who had only received AR rehabilitation during Phase III. Patients who underwent outpatient observation after Phase I showed a deficit of spontaneous motor recovery on the 90th day after stroke. Conclusions: Early rehabilitation was successful but was not enough; rehabilitation programs should be carried out throughout the entire “sensitive period” of poststroke plasticity. The newly developed AR biofeedback motion training is effective and safe as a separate rehabilitation method in the early recovery period of moderately severe, hemiparalytic, and ischemic stroke. These two rehabilitation approaches must be applied together or after each other, not instead of each other, as shown in clinical practice.

This literature review is devoted to the study of recent advances in the field of neurorehabilitation using robotic technologies. Objective: to study best practices of applying robotic rehabilitation technologies in stroke patients, its clinical efficacy and influence on the molecular mechanisms of neuroplasticity. Keywords were searched in the Web of Science, Core Collection, Scopus and PubMed databases.Results.Robotic neurorehabilitation occupies a certain place in the comprehensive rehabilitation of patients with motor deficiency after stroke. An interdisciplinary patient-oriented approach and consistency at all stages of medical rehabilitation are especially important when using rehabilitation methods that implement advances in robotics and information technologies in patients after stroke. Rehabilitation with the use of high-tech computerized rehabilitation systems operating in the biofeedback mode is one of the promising areas and requires further neurophysiological and laboratory studies to create scientifically based methodological approaches. It will have great social significance and tangible economic effects from improving the quality of neurorehabilitation and reducing its duration.

OBJECTIVE To evaluate the clinical features and the level of serum brain-derived neurotrophic factor (BDNF) in groups of patients with Parkinson’s disease (PD) differentiated by the genotypes of BDNF polymorphism (rs6265). MATERIAL AND METHODS The level of serum BDNF in the biomarkers’ multiplex panel of neurodegenerative diseases (HNDG3MAG-36K) was assessed in 134 PD patients. Allele discrimination was carried out by real-time PCR using TaqMan probes for the analysis of BDNF rs6265 polymorphism in groups of patients and controls (n=192) matched for sex, age and ethnicity. RESULTS Comparing the distribution of rs6265 genotypes and alleles between groups of patients and controls no significant differences were found (p>0.05). Serum BDNF levels varied significantly by genotype (rs6265) among PD patients. Minimum mean serum BDNF level (320.1±164.6 pg/ml) was noted for individuals with the AA genotype, which significantly differs from the corresponding indicator among individuals with GA (2944.2±1590.6 pg/ml; p=0.0001) and GG genotypes (2949.4±1620.6 pg/ml; p=3.9×10^–5). The concentration of BDNF significantly differed between patients with different forms of PD (p=0.0007) and increased as the stage of the disease progressed according to Hoehn and Yahr staging scale (p=1.0×10^–6). CONCLUSION The BDNF rs6265 polymorphism was not associated with the development of PD in the studied population. The variability of the mean serum BDNF level was established depending on the genotype of the BDNF polymorphism in PD patients and a number of clinical features.

Паранеопластическая мозжечковая дегенерация представляет собой поражение клеток Пуркинье мозжечка антителами anti-Yo, синтезируемыми иммунной системой в ответ на выработку нейрональных белков злокачественными клетками аденокарциномы простаты в 25% случаев. Неврологические симптомы поражения мозжечка опережают манифестацию рака в среднем на два года у 70% пациентов. Уже на ранних стадиях заболевания, когда опухоль еще не визуализируется и клинически себя не проявляет, отмечается высокий титр антител anti-Yo в спинномозговой жидкости больных. У 90–98% больных с мозжечковой атаксией и наличием антител anti-Yo обнаруживают рак простаты с клинически скрытым течением. Онконевральные аутоантитела класса IgG хорошо детектируются в сыворотке крови методами иммуноблоттинга и непрямой иммунофлуоресценции. Гибель клеток Пуркинье зернистого и молекулярного слоев коры мозжечка, умеренная периваскулярная лимфоцитарная инфильтрация, дальнейшая пролиферация микроглии приводят к атрофии. Воспалительные инфильтраты могут также быть в стволе и коре головного мозга, хотя их значительно меньше, чем в мозжечке. Этим объясняется наличие дополнительных неврологических симптомов. Результаты томографии головного мозга на начальных стадиях паранеопластической мозжечковой дегенерации мало информативны и только через несколько месяцев по мере нарастания неврологического дефицита обнаруживаются дегенеративные изменения мозжечка. Удаление злокачественной опухоли приводит к регрессу неврологической симптоматики в 80% случаев. Это свидетельствует о целесообразности проведения направленного онкологического поиска у пациентов с симптомами паранеопластической мозжечковой дегенерации и обнаруженными в крови онконевральными антителами. Иммуномодулирующая терапия, включающая применение внутривенных иммуноглобулинов, плазмафереза, гормонотерапии, также эффективна в лечении неврологических нарушений. В статье описан клинический случай паранеопластической мозжечковой дегенерации у мужчины 65 лет с возникновением неврологических симптомов за 5 мес до диагностики аденокарциномы простаты. Обсуждены трудности дифференциальной диагностики неврологического расстройства и течение неврологического заболевания на фоне удаления опухоли и проводимой иммунотерапии.

OBJECTIVE To evaluate the clinical and laboratory correlation of biomarkers with anti- and pro-apoptotic activity with the severity of motor and non-motor symptoms depending on the progression rate of Parkinson’s disease (PD). MATERIAL AND METHODS A wide range of non-motor symptoms (emotional-affective, cognitive, psychotic and behavioral disorders, fatigue, sleep disorders and autonomic disorders) was evaluated using validated scales and a number of serum neuromarkers responsible for neuroplasticity and neuronal survival processes (BDNF, PDGF, cathepsin D) in 71 patients with PD (mean age 65 (55; 70) years, disease duration 7 (4; 9) years, age of onset 57 (49; 62) years). RESULTS The concentration of biomarkers (BDNF, PDGF and cathepsin D) was the lowest in the group of patients with a rapid PD progression rate (p<0.001, p=0.001 and p=0.031, respectively), the severity of motor and most non—motor symptoms was higher (p=0.023 and p=0.001, respectively) compared to middle and slow progression rate. There were correlations between BDNF concentration and the severity of depression (r=–0.63, p<0.001), apathy (r=–0.48, p<0.001), impulsive behavioral disorders (r=0.500, p<0.001), level of cognitive functions (r=0.54, p<0.001), motor symptoms (r=–0.43, p<0.001); between PDGF level and the severity of motor manifestations of PD (r=–0.30, p=0.011), depression (r=–0.70, p<0.001), apathy (r=–0.460, p<0.001), the degree of severity of behavioral disorders (r=0.742, p<0.001). No significant correlations were observed between the level of cathepsin D and the severity of clinical manifestations of PD, which indicates the connection of cathepsin D with the general pathogenesis of PD. CONCLUSION The possibility of using serum proteins of the neurotrophin subfamily and the protein associated with autophagy, cathepsin D, as biomarkers that determine the prognosis of PD, is considered.