Background: Patients with glenohumeral instability have proprioceptive deficits that are suggested to contribute to muscle activation alterations.
Hypothesis: Muscle activation alterations will be present in shoulders with anterior glenohumeral instability.
Study Design: Posttest-only control group design.
Methods: Eleven patients diagnosed with anterior glenohumeral instability were matched with 11 control subjects. Each subject received an external humeral rotation apprehension perturbation while reflexive muscle activation characteristics were measured with indwelling electromyography and surface electromyography.
Results: Patients with instability demonstrated suppressed pectoralis major and biceps brachii mean activation; increased peak activation of the subscapularis, supraspinatus, and infraspinatus; and a significantly slower biceps brachii reflex latency. Supraspinatus-subscapularis coactivation was significantly suppressed in the patients with instability as well.
Conclusions And Clinical Relevance: In addition to the capsuloligamentous deficiency and proprioceptive deficits present in anterior glenohumeral instability, muscle activation alterations are also present. The suppressed rotator cuff coactivation, slower biceps brachii activation, and decreased pectoralis major and biceps brachii mean activation may contribute to the recurrent instability episodes seen in this patient group. Clinicians can implement therapeutic exercises that address the suppressed muscles in patients opting for conservative management or rehabilitation before and after capsulorraphy procedures.
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http://dx.doi.org/10.1177/0363546503262190 | DOI Listing |
Ann Surg Oncol
January 2025
Department of Thoracic Surgery, Faculty of Medicine, Hacettepe University, Sihhiye, Ankara, Turkey.
Acta Neuropathol
January 2025
Department of Clinical Sciences, Lund Brain Injury Laboratory for Neurosurgical Research, Lund University, 222 20, Lund, Sweden.
Traumatic brain injury (TBI) often leads to impaired regulation of cerebral blood flow, which may be caused by pathological changes of the vascular smooth muscle cells (VSMCs) in the arterial wall. Moreover, these cerebrovascular changes may contribute to the development of various neurodegenerative disorders such as Alzheimer's-like pathologies that include amyloid beta aggregation. Despite its importance, the pathophysiological mechanisms responsible for VSMC dysfunction after TBI have rarely been evaluated.
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January 2025
Gene Expression Laboratory, Salk Institute, La Jolla, CA 92037-1002.
Nutritional status is a determining factor for growth during development and homeostatic maintenance in adulthood. In the context of muscle, growth hormone (GH) coordinates growth with nutritional status; however, the detailed mechanisms remain to be fully elucidated. Here, we show that the transcriptional repressor B cell lymphoma 6 (BCL6) maintains muscle mass by sustaining GH action.
View Article and Find Full Text PDFClin J Sport Med
January 2025
Memorial Care Long Beach Medical Center, Long Beach, California.
Objective: The exertional compartment syndrome (ECS) is often a delayed diagnosis. Compartment pressure measurements (CPM) confirm the diagnosis. Herein we present our algorithm for the evaluation and management (E&M) of ECS.
View Article and Find Full Text PDFFuture Sci OA
December 2025
Department of Gerontology, the First Affiliated Hospital, China Medical University, Shenyang, China.
Aim: The primary objective of this study is to investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), on the process of vascular smooth muscle cell (VSMC) senescence.
Methods: Rat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated.
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