Correction to: The role of virtual reality on outcomes in rehabilitation of Parkinson's disease: meta-analysis and systematic review in 1031 participants.

The originally published version of this article contained typesetting errors in Figure 4.

The role of virtual reality on outcomes in rehabilitation of Parkinson's disease: meta-analysis and systematic review in 1031 participants.

INTRODUCTION: Parkinson's disease (PD) is managed primarily by dopamine agonists and physiotherapy while virtual reality (VR) has emerged recently as a complementary method. The present study reviewed the effectiveness of VR in rehabilitation of patients with PD. METHODS: Literature search up to June 2019 identified ten studies (n = 343 participants) suitable for meta-analysis and 27 studies (n = 688 participants) for systematic review. Standard mean difference (SMD) and 95% confidence intervals (CI) were calculated using a random effects model. RESULTS: In meta-analysis, compared with active rehabilitation intervention, VR training led to greater improvement of stride length, SMD = 0.70 (95%CI = 0.32-1.08, p = 0.0003), and was as effective for gait speed, balance and co-ordination, cognitive function and mental health, quality of life and activities of daily living. Compared with passive rehabilitation intervention, VR had greater effects on balance: SMD = 1.02 (95%CI = 0.38-1.65, p = 0.002). Results from single randomised controlled trials showed that VR training was better than passive rehabilitation intervention for improving gait speed SMD = 1.43 (95%CI = 0.51-2.34, p = 0.002), stride length SMD = 1.27 (95%CI = 0.38-2.16, p = 0.005) and activities of daily living SMD = 0.96 (95%CI = 0.02-1.89). Systematic review showed that VR training significantly (p < 0.05) improved motor function, balance and co-ordination, cognitive function and mental health, and quality of life and activities of daily living. CONCLUSION: VR used in rehabilitation for patients with PD improves a number of outcomes and may be considered for routine use in rehabilitation.

Meta-analysis of changes in the levels of catecholamines and blood pressure with continuous positive airway pressure therapy in obstructive sleep apnea.

Stress from obstructive sleep apnea (OSA) stimulates catecholamine release consequently exacerbating hypertension. However, different studies have shown a conflicting impact of continuous positive airway pressure (CPAP) treatment in patients with OSA on catecholamine levels and blood pressure. We aimed to examine changes to catecholamine levels and blood pressure in response to CPAP treatment. We conducted a meta-analysis of data published up to May 2020. The quality of the studies was evaluated using standard tools for assessing the risk of bias. Meta-analysis was conducted using RevMan (v5.3) and expressed in standardized mean difference (SMD) for catecholamines and mean difference (MD) for systolic (SBP) and diastolic blood pressure (DBP). A total of 38 studies met our search criteria; they consisted of 14 randomized control trials (RCT) totaling 576 participants and 24 prospective cohort studies (PCS) of 547 participants. Mean age ranged between 41 and 62 year and body mass index between 27.2 and 35.1 kg/m2 . CPAP treatment reduced 24-hour urinary noradrenaline levels both in RCT (SMD = -1.1; 95% confidence interval (CI): -1.63 to - 0.56) and in PCS (SMD = 0.38 (CI: 0.24 to 0.53). SBP was also reduced by CPAP treatment in RCT (4.8 mmHg; CI: 2.0-7.7) and in PCS (7.5 mmHg; CI: 3.3-11.7). DBP was similarly reduced (3.0 mmHg; CI: 1.4-4.6) and in PCS (5.1 mmHg; CI: 2.3-8.0). In conclusion, CPAP treatment in patients with OSA reduces catecholamine levels and blood pressure. This suggests that sympathetic activity plays an intermediary role in hypertension associated with OSA-related stress.

Non-genetic and genetic risk factors for adult cerebral venous thrombosis.

INTRODUCTION: A wide variety of non-genetic and genetic factors have been shown to associate with increased risk for cerebral venous thrombosis (CVT). However, there is a paucity of risk factor data and conclusions about their impact are often conflicting. Herein, we quantified the associations of non-genetic and genetic risk factors for CVT in adults. MATERIALS AND METHODS: Electronic databases were searched up to January 2017. Meta-analyses were performed (RevMan v5.3) to determine pooled odds ratios (ORs and 95% CIs) for risk factors, interstudy heterogeneity and publication bias. RESULTS: Twenty non-genetic (n = 2314) and 33 genetic (n = 2117) studies up to January 2017 met the selection criteria. For non-genetic factors, CVT risk increased in the presence of glucocorticosteroid therapy by 18.3-fold (3.3-102.6), alcohol consumption 2.7-fold (1.8-3.9), infection 7.5-fold (2.6-21.6), surgery 9.6-fold (1.1-83.5), hypercholesterolaemia 2.4-fold (1.3-4.4), hyperhomocysteinaemia 3.1-fold (2.1-4.6), antiphospholipid antibodies 7.0-fold (2.1-23.6), autoimmune diseases 5.6-fold (2.3-13.6), anaemia 4.0-fold (2.1-7.9), malignancy 3.2-fold (1.4-7.1) and pregnancy/puerperium 11.4-fold (5.7-24.3). Smoking, hypertension and diabetes did not associate with CVT risk. For genetic factors, CVT risk increased in the presence of factor V Leiden (G1691A) by 2.5-fold (1.9-3.3), protein C deficiency 10.7-fold (3.1-37.7), protein S deficiency 5.7-fold (1.4-22.4), antithrombin deficiency 3.8-fold (1.0-13.8), prothrombin (G20210A) 5.5-fold (4.0-7.27) and TAFI gene variant (C1040T) 1.6-fold (1.0-2.4). Prothrombin G20210A and factor V Leiden polymorphisms tended to have higher ORs for CVT than for ischaemic stroke. CONCLUSIONS: We provide quantitative data supporting a strong basis for genetic and non-genetic risk factors in CVT. Its genetic liability seems higher when compared with sporadic ischaemic stroke.