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Associative brain-computer interface training increases wrist extensor corticospinal excitability in patients with subacute stroke.
J Neurophysiol
January 2025
Institute of Sport and Sport Science, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany.
Article Synopsis
- A new brain-computer interface (BCI) system uses electroencephalography to time stimulation with motor cortex activity, showing promise in helping stroke patients recover movement.
- A study with 24 subacute stroke patients tested this BCI on upper limb weakness, comparing an intervention group with a sham control group.
- Results showed that the intervention group had significantly increased muscle responses after training, demonstrating the potential for enhanced motor function in stroke recovery.
Motor Neuron Diseases and Central Nervous System Tractopathies: Clinical-Radiologic Correlation and Diagnostic Approach.
Radiographics
January 2025
From the Departments of Radiology (A.B.D., A.A., E.H.M., A.A.B., V.G.) and Neurology (A.S.M., K.H.M., S.L.C.), Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224; Department of Neurology, Mayo Clinic, Rochester, MN (N.K., E.S., E.P.F.); and Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy (E.S.).
Article Synopsis
- * Amyotrophic lateral sclerosis (ALS) is the most common acquired motor neuron disease, with multiple variants affecting different motor neuron types; characteristic MRI features include T2 hyperintensities along key areas of the brain.
- * Other conditions, including toxic, metabolic, genetic, and infectious diseases, can also damage corticospinal tracts, leading to upper motor neuron injury symptoms, which can be identified through MRI imaging.
The Lateral Corticospinal Tract Sign: An MRI Marker for Amyotrophic Lateral Sclerosis.
Radiology
September 2024
From the Translational Imaging in Neurology (ThINk), Department of Biomedical Engineering (M.J.W., E.K., L.S., M. Weigel, C.G., R.S.), Research Center for Clinical Neuroimmunology and Neuroscience Basel (RC2NB) (M.J.W., E.K., L.S., M. Weigel, C.G., R.S.), Department of Biomedical Engineering (M. Weigel, C.W., O.B.), Institute of Forensic Medicine, Department of Biomedical Engineering (D.N., E.S., C.L.), and Department of Biomedicine (M.S.), University of Basel, Basel, Switzerland; Neurology Clinic and Policlinic, Department of Clinical Research (E.K., L.S., M. Weigel, M.D., N.N., C.G., K.S., M.S., R.S.), Division of Radiological Physics, Department of Radiology (M. Weigel, C.W., T.H., P.M., O.B.), Department of Pathology, Institute of Medical Genetics and Pathology (N.D.), and Department of Theragnostics, Clinic of Radiology and Nuclear Medicine, Division of Diagnostic and Interventional Neuroradiology (J.L.), and Department of Neurology (R.S.), University Hospital Basel, University of Basel, Petersgraben 4, 4031 Basel, Switzerland; Institute of Neuropathology, Neurocenter, University Medical Center Freiburg, University of Freiburg, Freiburg, Germany (M.D.); Institute of Forensic Medicine, Health Department Basel-Stadt, Basel, Switzerland (D.N., E.S., C.L.); and Neuromuscular Diseases Unit/ALS Clinic, Kantonsspital St Gallen, St Gallen, Switzerland (C.N., N.B., M. Weber).
Background Radially sampled averaged magnetization inversion-recovery acquisition (rAMIRA) imaging shows hyperintensity in the lateral corticospinal tract (CST) in patients with motor neuron diseases. Purpose To systematically determine the accuracy of the lateral corticospinal tract sign for detecting patients with amyotrophic lateral sclerosis (ALS) at rAMIRA MRI. Materials and Methods This study included prospectively acquired data from participants in ALS and other motor neuron disease imaging studies at the University Hospital Basel, Switzerland.
View Article and Find Full Text PDFKv2 channels do not function as canonical delayed rectifiers in spinal motoneurons.
iScience
August 2024
Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.
The increased muscular force output required for some behaviors is achieved via amplification of motoneuron output via cholinergic C-bouton synapses. Work in neonatal mouse motoneurons suggested that modulation of currents mediated by post-synaptically clustered K2.1 channels is crucial to C-bouton amplification.
View Article and Find Full Text PDFMovement disorder phenotype in CTNNB1-syndrome: A complex but recognizable phenomenology.
Parkinsonism Relat Disord
September 2024
Neurology, Epilepsy and Movement Disorders Unit, Bambino Gesù Children's Hospital, IRCCS, Full Member of European Reference Network on Rare and Complex Epilepsies, EpiCARE, Rome, Italy.
Introduction: CTNNB1 gene loss-of-function variants cause Neurodevelopmental disorder with spastic diplegia and visual defects (NEDSDV, OMIM 615075). Although motor impairment represents a core feature of this condition, the motor phenotype remains poorly described. We systematically assessed a cohort of 14 patients with disease-causing CTNNB1 variants to better characterize the movement disorder phenotype.
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