Objective: To design an electrodiagnostic technique by which to accurately record the serratus anterior compound muscle action potential (CMAP).
Design: Observational study.
Setting: Academic electromyography laboratory.
Participants: Fifteen healthy volunteers.
Interventions: The long thoracic nerve was stimulated by using a standard bipolar surface electrode in the axilla, just anterior to the midaxillary line. The serratus anterior CMAP was recorded by using a self-adhesive, 8.0 x 0.5 cm, ring electrode as the E1 placed across the serratus anterior interdigitations starting at the nipple level. A self-adhesive, motor (1 x 1 cm) electrode was used as E2 and placed over the seventh rib. A standard self-adhesive ground electrode was placed over the inferior region of the latissimus dorsi.
Main Outcome Measures: Distal motor latency (DML), and CMAP amplitude and duration.
Results: After removing 2 outliers, the results are reported as the mean +/- 1.96 standard deviations. Right long thoracic DML was 2.2+/-1.0ms and the left was 2.3+/-0.9ms, with a side-to-side mean difference of 0.3+/-0.4ms. The right serratus CMAP amplitude was 3.8+/-3.9mV and the left was 3.9+/-3.7mV, with a side-to-side mean difference of 0.6+/-1.2mV. Statistical analysis did not reveal a significant side-to-side difference for DML or CMAP amplitude. Both sides were combined to form a single set of trials for DML and CMAP amplitude. The mean DML became 2.2+/-0.7ms, and the CMAP amplitude was 3.5+/-1.9mV. The CMAP duration was 14.5+/-4.3ms on the right and 14.5+/-4.1ms on the left. A significant, positive correlation existed between height and DML ( P <.02). The 95% confidence intervals for DML and CMAP amplitudes were 2.1 to 2.5ms and 1.5 to 3.1mV, respectively.
Conclusions: Our latency, side-to-side comparisons and amplitude data were consistent with other motor nerve conduction findings in the literature. Stimulating the long thoracic nerve in the axilla will provide a reliable technique to aid in the diagnosis and treatment of long thoracic neuropathy.
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http://dx.doi.org/10.1016/j.apmr.2004.04.050 | DOI Listing |
Brain Res
December 2024
Beijing Key Laboratory of Central Nervous System Injury, Beijing Neurosurgical Institute, Capital Medical University, Beijing 10070, China; Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 10070, China; U1195, Inserm et Universite Paris-Saclay, 94276 Le Kremlin-Bicetre, France. Electronic address:
Objective: Peripheral nerve injury results in functional alterations of the corresponding active brain areas, which are closely related to functional recovery. Whether such functional plasticity induces relative anatomical structural changes remains to be investigated.
Methods: In this study, we investigated the changes in brain cortical thickness in patients with facial paralysis following neurorrhaphy treatment at different follow-up times.
Front Neurol
December 2024
Department of Internal Medicine, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Background: Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of the presynaptic neuromuscular junction associated with antibody mediated dysfunction of voltage-gated calcium channels (VGCCs). LEMS can exist as a paraneoplastic syndrome, paraneoplastic-LEMS (P-LEMS), when associated with tumors, most commonly, small cell lung carcinoma (SCLC) or as a non-paraneoplastic condition (NP-LEMS) when no malignancies are detected.
Methods: A retrospective chart review was conducted in 3 tertiary hospitals in Saudi Arabia for patients diagnosed with LEMS between January 2010 and January 2020.
Neurol Sci
December 2024
Department of Neurology, Section of Clinical Neurophysiology, Faculty of Medicine, Gazi University, Ankara, Turkey.
Background: There is growing evidence that botulinum neurotoxin (BoNT) can mediate changes at the central level through peripheral mechanisms, leading to alterations in central sensorimotor integration. However, the effect of BoNT on brainstem excitability in patients with hemifacial spasm(HFS) is not yet fully understood, and its long-term effects remain unknown.
Objective: This study aims to investigate the impact of BoNT on the excitability of the facial nucleus in patients with idiopathic HFS.
J Cachexia Sarcopenia Muscle
February 2025
Department of Nanobiomedical Science & BK21 NBM Global Research Center for Regenerative Medicine, Dankook University, Cheonan, Korea.
Background: Muscle atrophy, including glucocorticoid-induced muscle wasting from treatments such as dexamethasone (DEX), results in significant reductions in muscle mass, strength and function. This study investigates the potential of lonafarnib, a farnesyltransferase inhibitor, to counteract DEX-induced muscle atrophy by targeting key signalling pathways.
Methods: We utilized in vitro models with C2C12 myotubes treated with DEX and in vivo models with Caenorhabditis elegans and DEX-treated Sprague-Dawley rats.
Muscle Nerve
December 2024
Referral Centre for Neuromuscular Diseases and ALS, La Timone University Hospital, Aix-Marseille University, ERN Neuro-NMD, Marseille, France.
Introduction/aims: It is imperative to screen asymptomatic carriers of transthyretin (TTR) mutations to initiate treatment early. The protocol for repeated electrodiagnostic (EDX) assessments over time lacks standardization. Our aim was to report the electrophysiological evolution of a cohort of asymptomatic carriers and to determine which biomarkers were most sensitive to change.
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