Citations

ABSTRACT Training in electrodiagnostic (EDX) medicine is highly variable globally, with trainees receiving widely different levels of didactic education, skills training, and hands‐on experience. Global standardization of EDX training has the potential to improve diagnostic accuracy, promote equitable care, and strengthen international collaboration. Major barriers include limited resources, faculty shortages, and a lack of standardized curricula. To address these disparities, opportunities and strategies for international collaboration are proposed, including developing a uniform content curriculum, competency‐based evaluation frameworks, and integration of online and simulation‐based learning tools.

ABSTRACT Introduction/Aims In severe ulnar neuropathy at the elbow (UNE), occasionally surgeons will employ an end‐to‐side (ETS) nerve transfer of the anterior interosseous nerve (AIN) motor branch of pronator quadratus (PQ) to the ulnar motor component distally (AIN ETS). We used an ultrasound (US)‐guided near‐nerve monopolar needle stimulation of the AIN to determine the specific contribution of the transferred PQ motor branch to the ulnar‐innervated hand intrinsic muscles following AIN ETS in patients with UNE. Methods After inserting the monopolar needle under US guidance, direct stimulation of the AIN was performed while recording from the abductor digiti minimi (ADM), first dorsal interosseous (FDI), and flexor pollicis longus (FPL). The presence or absence of a compound muscle action potential (CMAP) was noted from each muscle. Results The technique was used in two patients with chronic UNE, one with a cubital tunnel decompression and AIN ETS and the other with a decompression alone. In the patient with decompression and AIN ETS, direct stimulation of the AIN revealed a low amplitude CMAP recorded from the FDI and FPL, suggesting AIN axonal contribution to FDI in the setting of prior AIN ETS. In the patient with decompression alone, near‐nerve stimulation generated an expected CMAP in the FPL but no response in the hand intrinsics. Discussion This study may demonstrate the utility of US‐guided near‐nerve monopolar needle AIN stimulation and suggests that it is a reliable technique to isolate the AIN contribution to hand intrinsic reinnervation following AIN ETS.

Abstract Vasculitic neuropathy is caused by inflammatory destruction of nerve blood vessels resulting in nerve ischaemia. Nerve vasculitis can be divided into two categories based on vessel size: large-arteriole vasculitis (≥75 µm) and microvasculitis (<75 µm). Herein, we characterize the clinical features of nerve large-arteriole vasculitis in comparison to nerve microvasculitis. This is a retrospective cohort study of patients evaluated and biopsied at Mayo sites between 2001 and 2020. We collected clinical and histopathological data from patients whose nerve biopsies were either diagnostic or highly suggestive of nerve vasculitis. Two hundred and seventy-eight cases were identified: 125 cases of large-arteriole vasculitis and 153 cases of microvasculitis. Nerve large-arteriole vasculitis presented with a more acute (50.4% versus 26.8%) versus chronic onset (33.6% versus 57.5%) than nerve microvasculitis (P = 0.0001). Nerve microvasculitis had longer mean time to diagnosis (10.5 versus 4.3 months; P < 0.0001) and longer time to plateau (8.9 versus 3.5 months; P < 0.0001). Nerve large-arteriole vasculitis typically presented as distal asymmetric polyneuropathy (48.0%), whereas nerve microvasculitis typically presented as radiculoplexus neuropathy/polyradiculoneuropathy (more proximal involvement of shoulder and thigh) (43.8%) (P < 0.0001). Systemic autoimmune disease was more common in nerve large-arteriole vasculitis (70.4% versus 22.9%, odds ratio, 8.0; 95% confidence interval, 4.7–13.7; P < 0.0001). Nerve microvasculitis was significantly related to non-systemic vasculitis (71% versus 23%, odds ratio, 7.9; 95% confidence interval, 4.6–13.6; P < 0.0001). Nerve microvasculitis had more autonomic involvement (24.2% versus 7.2%, odds ratio, 4.1; 95% confidence interval, 1.9–8.9; P = 0.0002). Nerve large-arteriole vasculitis and nerve microvasculitis have different but overlapping clinical features. Nerve large-arteriole vasculitis usually presents with acute onset, distal asymmetric polyneuropathy, associated with other autoimmune diseases and systemic involvement. In contrast, nerve microvasculitis usually presents with a subacute/chronic onset, as radiculoplexus neuropathy/polyradiculopathy (distal and proximal pattern) with autonomic involvement, and is more often a form of non-systemic vasculitis.

AbstractIntroduction/AimsRhabdomyolysis is an etiologically heterogeneous, acute necrosis of myofibers characterized by transient marked creatine kinase (CK) elevation associated with myalgia, muscle edema, and/or weakness. The study aimed to determine the role of electrodiagnostic (EDX) testing relative to genetic testing and muscle biopsy in patients with unprovoked rhabdomyolysis in identifying an underlying myopathy.MethodsEDX database was reviewed to identify unprovoked rhabdomyolysis patients who underwent EDX testing between January 2012 and January 2022. Each patient's clinical profile, EDX findings, muscle pathology, laboratory, and genetic testing results were analyzed.ResultsOf 66 patients identified, 32 had myopathic electromyography (EMG). Muscle biopsy and genetic testing were performed in 41 and 37 patients, respectively. A definitive diagnosis was achieved in 15 patients (11 myopathic EMG and 4 nonmyopathic EMG; p = .04) based on abnormal muscle biopsy (4/11 patients) or genetic testing (12/12 patients, encompassing 5 patients with normal muscle biopsy and 3 patients with nonmyopathic EMG). These included seven metabolic and eight nonmetabolic myopathies (five muscular dystrophies and three ryanodine receptor 1 [RYR1]‐myopathies). Patients were more likely to have baseline weakness (p < .01), elevated baseline CK (p < .01), and nonmetabolic myopathies (p = .03) when myopathic EMG was identified.DiscussionMyopathic EMG occurred in approximately half of patients with unprovoked rhabdomyolysis, more likely in patients with weakness and elevated CK at baseline. Although patients with myopathic EMG were more likely to have nonmetabolic myopathies, nonmyopathic EMG did not exclude myopathy, and genetic testing was primarily helpful to identify an underlying myopathy. Genetic testing should likely be first‐tier diagnostic testing following unprovoked rhabdomyolysis.