Background: Upper limb (UL) impairment in stroke survivors is both multifactorial and heterogeneous. Stratification of motor function helps identify the most sensitive and appropriate assessments, which in turn aids the design of effective and individualized rehabilitation strategies. We previously developed a stratification method combining the Grooved Pegboard Test (GPT) and Box and Block Test (BBT) to stratify poststroke UL motor function.
Objective: To investigate the resilience of the stratification method in a larger cohort and establish its appropriateness for clinical practice by investigating limitations of the GPT completion time.
Methods: Post hoc analysis of motor function for 96 community-dwelling participants with stroke (n = 68 male, 28 female, age 60.8 ± 14 years, 24.4 ± 36.6 months poststroke) was performed using the Wolf Motor Function Test (WMFT), Fugl-Meyer Assessment (F-M), BBT, and GPT. Hypothesis-free and hypothesis-based hierarchical cluster analyses were conducted to determine the resilience of the stratification method.
Results: The hypothesis-based analysis identified the same functional groupings as the hypothesis-free analysis: low (n = 32), moderate (n = 26), and high motor function (n = 38), with 3 exceptions. Thirty-three of the 38 participants with fine manual dexterity completed the GPT in ≤5 minutes. The remaining 5 participants took 6 to 25 minutes to place all 25 pegs but used alternative movement strategies to complete the test. The GPT time restriction changed the functional profile of the moderate and high motor function groups leading to more misclassifications.
Conclusion: The stratification method unambiguously classifies participants by UL motor function. While the inclusion of a 5-minute cutoff time for the GPT is preferred for clinical practice, it is not recommended for stratification purposes.
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http://dx.doi.org/10.1177/1545968321992048 | DOI Listing |
Sci Rep
January 2025
Department of Neurology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave, Chicago, IL, 60611, USA.
Corticospinal motor neurons (CSMN), located in the motor cortex of the brain, are one of the key components of the motor neuron circuitry. They are in part responsible for the initiation and modulation of voluntary movement, and their degeneration is the hallmark for numerous diseases, such as amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegia, and primary lateral sclerosis. Cortical hyperexcitation followed by in-excitability suggests the early involvement of cortical dysfunction in ALS pathology.
View Article and Find Full Text PDFNPJ Parkinsons Dis
January 2025
Brain Electrophysiology and Epilepsy Lab (BEE-L), Epilepsy and EEG Unit, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
We aimed to study the effect of Parkinson's disease (PD) and motor-cognitive load on the interplay between activation level and spatial complexity. To that end, 68 PD patients and 30 controls underwent electroencephalography (EEG) recording while executing visual single- and dual- Go/No-go tasks. The EEG underwent source localization, followed by parcellation of the neural activity into 116 regions of interest.
View Article and Find Full Text PDFBMJ Open
January 2025
Department of Rehabilitation, Daping Hospital, Army Medical University, Chongqing, China
Introduction: Spasticity is a common complication of stroke, which is related to poor motor recovery and limitations in the performance of activities. Both transcranial magnetic stimulation (TMS) and extracorporeal shockwave therapy (ESWT) are effective treatment methods for poststroke spasticity (PSS). However, there is no existing study exploring the safety and effectiveness of TMS combined with ESWT for PSS.
View Article and Find Full Text PDFIntroduction: Dual-task (DT) exercises combine both physical and cognitive activities and have the potential to efficiently enhance both physical and cognitive function.
Background/objectives: This study aimed to determine if, compared with exercise-only (EO) and control (C) groups, adults in a DT training program improved measures of cognitive and/or physical functioning.
Methods: Thirty-five participants (Mage = 65.
Am J Hum Genet
January 2025
Institute of Medical Genetics and Applied Genomics, University of Tübingen, 72076 Tübingen, Germany; Center for Rare Disease, University of Tübingen, 72076 Tübingen, Germany; Genomics for Health in Africa (GHA), Africa-Europe Cluster of Research Excellence (CoRE).
Inborn errors of selenoprotein expression arise from deleterious variants in genes encoding selenoproteins or selenoprotein biosynthetic factors, some of which are associated with neurodegenerative disorders. This study shows that bi-allelic selenocysteine tRNA-specific eukaryotic elongation factor (EEFSEC) variants cause selenoprotein deficiency, leading to progressive neurodegeneration. EEFSEC deficiency, an autosomal recessive disorder, manifests with global developmental delay, progressive spasticity, ataxia, and seizures.
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