There is increasing attention to sprint interval exercise (SIE) training as a time-efficient exercise regime. Recent studies, including our own (Kujach et al., 2018), have shown that acute high-intensity intermittent exercise can improve cognitive function; however, the neurobiological mechanisms underlying the effect still remain unknown. We thus examined the effects of acute SIE on cognitive function by monitoring the peripheral levels of growth and neurotrophic factors as well as blood lactate (LA) as potential mechanisms. Thirty-six young males participated in the current study and were divided into two groups: SIE (n = 20; mean age: 21.0 ± 0.9 years) and resting control (CTR) (n = 16; mean age: 21.7 ± 1.3 years). The SIE session consisted of 5 min of warm-up exercise and six sets of 30 s of all-out cycling exercise followed by 4.5 min of rest on a cycling-ergometer. Blood samples to evaluate the changes of serum concentrations of brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), vascular endothelial growth factor (VEGF), and blood LA were obtained at three time points: before, immediately after, and 60 min after each session. A Stroop task (ST) and trail making test (TMT) parts A and B were used to assess cognitive functions. Acute SIE shortened response times for both the ST and TMT A and B. Meanwhile, the peripheral levels of BDNF, IGF-1, and VEGF were significantly increased after an acute bout of SIE compared to those in CTR. In response to acute SIE, blood LA levels significantly increased and correlated with increased levels of BDNF, IGF-1, and VEGF. Furthermore, cognitive function and BDNF are found to be correlated. The current results suggest that SIE could have beneficial effects on cognitive functions with increased neuroprotective factors along with peripheral LA concentration in humans.

People with Huntington's disease (HD) may show reduced awareness of physical and mental changes in themselves. This article reviews the evidence for loss of awareness (anosognosia) in an attempt to elucidate its characteristics and possible underlying mechanisms. It is shown that defective awareness occurs across domains. People with HD may under-report the presence or severity of involuntary movements, under-estimate cognitive impairment and deny behavioural change. Nevertheless, awareness is not all or none. Moreover, it may be affected differentially for different symptom domains and emerge at different stages of disease, raising the possibility of distinct contributory mechanisms. Findings of an inverse relationship between insight and severity of disease suggest that cognitive impairment, in particular executive dysfunction, may be an important contributory factor. Evidence has accrued to support this argument. However, cognitive impairment cannot fully account for patients' lack of awareness of involuntary movements. Findings that patients accurately report consequences but not the experience of involuntary movements, and better acknowledge their presence when watching videotapes of themselves suggests that physiological factors play an important role. The putative role of denial as a coping mechanism is discussed. Recognition by clinicians of deficient self-awareness is crucial because of its implications for diagnosis and optimal clinical management of HD.

Background and aims. The present study aimed to assess the frequency of spasticity in a single-centre cohort of stroke patients in a one-year follow-up, its predictors, and its impact on the activities of daily living (ADL) and health-related quality of life (HRQoL). Material and methods. A group of 121 consecutive patients with hemiparesis (aged 73 ± 11 years) was selected for further observation, out of 381 Stroke Department patients during one year. At three follow-up assessments three, six and 12 months after stroke, muscle tone and muscle weakness were rated using Modified Ashworth Scale (MAS) and Medical Research Council (MRC); Activities of Daily Living (ADL) and Health Related Quality of Life (HRQoL) were evaluated using the Barthel Index (BI), Modified Rankin Scale (mRS) and an SF-36 questionnaire. Results. Fifty five of 121 (45%) patients after three months had developed spasticity (MAS ≥ 1), and in 19 of the 121 (15%) this spasticity was severe. After one year, 33/94 (35%) patients showed spasticity, and in 19/94 (20%) it was severe. Baseline muscle weakness (MRC), stroke severity as measured by the National Institutes of Health Stroke Scale (NIHSS), and greater disability (BI), were the most significant predictors of persistent post-stroke spasticity. Patients with spasticity had worse HRQoL in terms of their physical functioning, role limitations, physical pain, and vitality. Conclusion. Spasticity, which affects a significant proportion of stroke survivors, was present in 35% of our patients at 12 months after stroke. It has a major impact on both ADL and HRQoL. Severe disability and muscle weakness are the most important predictors of persistent post-stroke spasticity. Background and aims. The present study aimed to assess the frequency of spasticity in a single-centre cohort of stroke patients in a one-year follow-up, its predictors, and its impact on the activities of daily living (ADL) and health-related quality of life (HRQoL). Material and methods. A group of 121 consecutive patients with hemiparesis (aged 73 ± 11 years) was selected for further observation, out of 381 Stroke Department patients during one year. At three follow-up assessments three, six and 12 months after stroke, muscle tone and muscle weakness were rated using Modified Ashworth Scale (MAS) and Medical Research Council (MRC); Activities of Daily Living (ADL) and Health Related Quality of Life (HRQoL) were evaluated using the Barthel Index (BI), Modified Rankin Scale (mRS) and an SF-36 questionnaire. Results. Fifty five of 121 (45%) patients after three months had developed spasticity (MAS ≥ 1), and in 19 of the 121 (15%) this spasticity was severe. After one year, 33/94 (35%) patients showed spasticity, and in 19/94 (20%) it was severe. Baseline muscle weakness (MRC), stroke severity as measured by the National Institutes of Health Stroke Scale (NIHSS), and greater disability (BI), were the most significant predictors of persistent post-stroke spasticity. Patients with spasticity had worse HRQoL in terms of their physical functioning, role limitations, physical pain, and vitality. Conclusion. Spasticity, which affects a significant proportion of stroke survivors, was present in 35% of our patients at 12 months after stroke. It has a major impact on both ADL and HRQoL. Severe disability and muscle weakness are the most important predictors of persistent post-stroke spasticity.

The aim of this study was to identify determinants of functional disability, patient’s quality of life (QoL) and caregivers’ burden in Huntington’s disease (HD). Eighty HD patients participated in the study. Motor and behavioral disturbances as well as cognitive impairment were assessed using motor, behavioral and cognitive parts of the Unified Huntington Disease Rating Scale (UHDRS); Hamilton Depression Rating Scale was used to assess depression. Disability, health-related QoL and the impact of the disease on the caregivers were assessed using the following methods: UHDRS Functional Assessment Score, SF-36 Scale and Caregiver Burden Inventory. Multiple regression analysis showed that motor disturbances, cognitive impairment, apathy and disease duration were the independent predictors of disability. Depression and cognitive disturbances were the determinants of patient’s QoL, while motor disturbances and depression were the predictors of the caregiver burden. Patient’s disability and QoL as well as caregivers’ burden should be taken into consideration while planning treatment strategy and the results of the present study show that the predictors of those treatment targets are different.

Introduction Elevated plasma homocysteine (Hcy) concentration is an independent risk factor for cardiovascular disease, and its involvement in endothelial cell dysfunction is well established. However, the role of Hcy and folate in the pathogenesis of Parkinson’s disease (PD) remains controversial. Objectives The study was aimed at evaluating the relationships between Hcy, vitamin B12, and folic acid levels in the blood and cognitive status in PD patients with the genetic polymorphisms of MTHFR (rs1801133: C>T-677C>T, rs1801131: A>C-1298A>C), COMT (rs4680: A>G-Val158Met, rs6269: A>G, rs4633: C>T, rs4818: C>G), or SLC19A1 (rs1051266: G>A-80G>A). Methods A total of 502 participants (248 with PD and 254 age-matched and sex-matched controls) were included in the study. The Unified Parkinson’s Disease Rating Scale score, Hoehn–Yahr staging, and the Schwab–England scale were used to assess motor abilities and activity during daily life. Complex psychological examination with a battery of tests was used to classify patients into groups with (PDD) and without (nPDD) dementia. Blood samples were examined for Hcy, vitamin B12, and folic acid levels, as well as polymorphisms in genes related to Hcy metabolism, such as COMT, MTHFR, and SLC19A1(RFC-1). Results The frequency of homozygous COMT rs4680G and rs4633C allele carriers was significantly decreased in PD patients in comparison with the controls (P=0.015; odds ratio=0.60; 95% confidence interval 0.41–0.90 and P=0.020; odds ratio=0.619; 95% confidence interval 0.42–0.92, respectively). No significant differences in the distribution of MTHFR 677C>T, 1298A>C, and SLC19A1 80G>A alleles and genotypes between PD patients and the controls were found. Hcy levels were significantly increased in PD patients (18±7.8 μmol/l) as compared with the controls (14.0±9.6 μmol/l, P=10^–8) and were significantly associated with the MTHFR 677C>T polymorphism both in PD patients and controls, in which T allele carriers were characterized by markedly elevated Hcy plasma concentrations. No association was observed between Hcy plasma level and COMT and SLC19A polymorphisms. The results of multivariate logistic regression analysis revealed age (P=0.0003) and Hcy plasma levels (P=0.07) as independent risk factors predisposing individuals to PD dementia. The studied polymorphisms were not associated with cognitive status in PD patients. Conclusion The genetic factors studied were not associated with cognitive status in PD patients. Only age and Hcy plasma levels were found to be independent risk factors predisposing individuals to PD dementia. However, COMT: rs4680: A>G and rs4633: C>T polymorphisms were found to significantly affect PD risk, and the MTHFR 677C>T polymorphism helped determine plasma Hcy concentrations.