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Stroke continues to be the main cause of motor disability worldwide. While rehabilitation has been promised to improve recovery after stroke, efficacy in clinical trials has been mixed. We need to understand the cortical recombination framework to understand how biomarkers for neurophysiological reorganized neurotechnologies alter network activity. Here, we summarize the principles of the movement network, including the current evidence of changes in the connections and function of encephalic regions, recovery from stroke and the therapeutic effects of rehabilitation. Overall, improvements or therapeutic effects in limb motor control following stroke are correlated with the effects of interhemispheric competition or compensatory models of the motor supplementary cortex. This review suggests that future research should focus on cross-regional communication and provide fundamental insights into further treatment and rehabilitation for post-stroke patients.
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http://dx.doi.org/10.2174/0118715249277597231226064144 | DOI Listing |
Stroke
September 2025
Brain Language Laboratory, Freie Universität Berlin, Germany (A.-T.P.J., M.R.O., A.S., F.P.).
Background: Intensive language-action therapy treats language deficits and depressive symptoms in chronic poststroke aphasia, yet the underlying neural mechanisms remain underexplored. Long-range temporal correlations (LRTCs) in blood oxygenation level-dependent signals indicate persistence in brain activity patterns and may relate to learning and levels of depression. This observational study investigates blood oxygenation level-dependent LRTC changes alongside therapy-induced language and mood improvements in perisylvian and domain-general brain areas.
View Article and Find Full Text PDFFront Neurol
August 2025
Division of Neurology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Introduction: A subset of patients with homonymous hemianopia can consciously perceive motion within their blind visual fields-a phenomenon known as the Riddoch phenomenon. However, the factors predicting this residual motion perception remain poorly understood. This study aims to identify clinical and neuroanatomical predictors of the Riddoch phenomenon in stroke patients.
View Article and Find Full Text PDFAppl Neuropsychol Adult
September 2025
Psychiatry Department, Mashhad University of Medical Sciences Mashhad, Iran.
Ischemic stroke survivors often experience persistent cognitive and psychosocial deficits not fully addressed by conventional rehabilitation. This study compared the effectiveness of Mindfulness-Based Stress Reduction (MBSR) and Cognitive Rehabilitation Therapy (CRT) on Stroke Impact Scale (SIS) outcomes. In a quasi-experimental design with a control group and follow-up, 45 eligible patients were purposively sampled and randomly assigned to MBSR, CRT, or control groups.
View Article and Find Full Text PDFArch Phys Med Rehabil
September 2025
Department of Rehabilitation Medicine, Wuxi Central Rehabilitation Hospital, The Affiliated Mental Health Center of Jiangnan University, Wuxi, Jiangsu, China. Electronic address:
Objective: To identify baseline factors linked to a positive response to intermittent theta-burst stimulation (iTBS) in individuals with stroke.
Design: Secondary analysis of a randomized controlled trial.
Setting: A single rehabilitation hospital.
Chem Biodivers
September 2025
School of Pharmaceutical Science, Yunnan Key Laboratory of Pharmacology for Natural Products/College of Modern Biomedical Industry, NHC Key Laboratory of Drug Addiction Medicine, Kunming Medical University, Kunming, P. R. China.
20(R)-ginsenoside Rg3 can reduce the effects of oxidative stress and cell death in cerebral ischemia‒reperfusion injury (CIRI). Neuroinflammation is crucial post-CIRI, but how 20(R)-Rg3 affects ischemia‒reperfusion-induced neuroinflammation is unclear. To study 20(R)-Rg3's effects on neuroinflammation and neuronal preservation in stroke models and explore toll-like receptor 4/myeloid differentiation factor-88/nuclear factor kappa B (TLR4/MyD88/NF-κB) pathway mechanisms.
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