Background Isolated hand motor nerve injuries, specifically those affecting the recurrent motor branch of the median nerve and the deep motor branch of the ulnar nerve, are rarely reported in medical literature. Diagnosing and quantifying these injuries pose significant challenges due to their uncommon nature and the variety of mechanisms that can cause them. Methodology This study reviews six unusual cases of isolated damage to the recurrent motor branch of the median nerve and the deep motor branch of the ulnar nerve, including cases with combined injuries. The etiologies include various traumatic and compressive mechanisms, such as a blow from the thenar to the back of a knife blade, long-distance cycling, impact from a broken shovel handle, knife injury, and damage from a screw while using a cordless screwdriver. In one case, the cause was indeterminate. Diagnostic methods involved clinical evaluation, electrophysiological testing (nerve conduction studies and electromyography), and high-resolution ultrasound imaging. A thorough medical history was also crucial in understanding the injury mechanisms. Results The cases demonstrated a range of causes for isolated hand motor nerve injuries, with both traumatic and compressive mechanisms identified. The diagnostic process highlighted the value of integrating clinical assessments, electrophysiological data, and ultrasound imaging to accurately diagnose and understand the extent and nature of the injuries. Conclusions Isolated motor nerve injuries in the hand can arise from diverse and often unexpected causes. Comprehensive clinical evaluation, supported by electrophysiological testing and ultrasound imaging, is essential for accurate diagnosis and management. A detailed medical history is invaluable in identifying the mechanism of injury, which is critical for developing an appropriate treatment plan. The study underscores the importance of a multidisciplinary approach in diagnosing and treating these rare neuropathies.

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Peripheral neuropathy and radiculopathy often result in skeletal muscle disorders, typically leading to muscle atrophy. Concurrent muscle hypertrophy or persistently elevated creatine kinase (CK) is rare. While muscle hypertrophy is commonly observed in myogenic diseases, such as muscular dystrophy, acromegaly, inflammatory myopathies, and hypothyroidism, reports of muscle hypertrophy caused by neuropathy are infrequent. We encountered a patient with persistently elevated CK levels and unilateral lower leg muscle hypertrophy associated with neuropathy. The patient had cauda equina syndrome symptoms and pain in the left lower leg. Lumbar spine magnetic resonance imaging (MRI) revealed central spinal stenosis, which was believed to be the cause of the symptoms. Lower-limb MRI revealed high signal intensity in the gastrocnemius muscle on fat-suppressed T2-weighted imaging. Surgical treatment improved the radiculopathy, hypertrophy, and pain in the left lower leg. During the one-year follow-up, improvement was confirmed with both MRI and nerve conduction studies. Calf muscle hypertrophy associated with neuropathy has been reported; however, no reports have demonstrated pre- and postoperative changes with MRI and nerve conduction studies. We report a patient with lower leg muscle hypertrophy and persistent CK elevation associated with neuropathy, along with a literature review.

This study investigates the impact of the anatomical separation point of the dorsal ulnar cutaneous nerve (DUCN) on nerve conduction studies (NCS). Involving 25 subjects with DUCN NCS findings, it utilizes ultrasound to mark the DUCN\'s divergence from the ulnar nerve. NCS was performed at four points relative to the separation point. The findings indicate the maximal amplitudes occurred 2 cm distal to the separation point. The study suggests it is ideal when the stimulation is performed between the seperation point and 2 cm distal to it.

OBJECTIVE: To establish the reference standard of the median nerve conduction study (NCS) in Korea.
METHODS: A total of 648 median motor and 602 median sensory NCSs from 349 Korean healthy volunteers were tested and analyzed prospectively. Equipment calibration, assessment of intraand inter-rater reliability, and the NCSs per se were conducted according to a predetermined protocol. A reference standard was established from uncertainty components for the following parameters: the onset and peak latencies; the baseline-to-peak and peak-to-peak amplitudes; the area and duration of the negative wave; and the nerve conduction velocity. The effects of sex, age and stimulation intensity were analyzed.
RESULTS: Each measured value of 648 median motor and 602 median sensory nerves were obtained and presented with both mean and expanded uncertainties, as well as mean and standard deviations. The cut-off values with expanded uncertainty were determined for different age and sex groups. After adjusting for anthropometric covariates, all parameters except duration were affected by age, and sex appeared to influence both duration and area. While stimulation intensity significantly affected some parameters including latencies, the effect sizes were negligible.
CONCLUSIONS: We propose the median NCS reference standard using the largest Korean dataset ever available. The use of the traceable and reliable reference standard is anticipated to promote more accurate and dependable diagnosis and appropriate management of median neuropathies in Korea.

OBJECTIVE: Nerve enlargement has been described in autoimmune nodopathy and chronic inflammatory demyelinating polyneuropathy (CIDP). However, comparisons of the distribution of enlargement between autoimmune nodopathy and CIDP have not been well characterized. To fill this gap, we explored differences in the ultrasonographic and electrophysiological features between autoimmune nodopathy and CIDP.
METHODS: Between March 2015 and June 2023, patients fulfilling diagnostic criteria for CIDP were enrolled; among them, those with positive antibodies against nodal-paranodal cell-adhesion molecules were distinguished as autoimmune nodopathy. Nerve ultrasound and nerve conduction studies (NCS) were performed.
RESULTS: Overall, 114 CIDP patients and 13 patients with autoimmune nodopathy were recruited. Cross-sectional areas (CSA) at all sites were larger in patients with CIDP and autoimmune nodopathy than in healthy controls. CSAs at the roots and trunks of the brachial plexus were significantly larger in patients with anti-neurofascin-155 (NF155), anti-contactin-1 (CNTN1), and anti-contactin-associated protein 1 (CASPR1) antibodies than in CIDP patients. The patients with anti-NF186 antibody did not have enlargement in the brachial plexus. NCS showed more frequent probable conduction block at Erb\'s point in autoimmune nodopathy than in CIDP (61.9% vs. 36.6% for median nerve, 52.4% vs. 39.5% for ulnar nerve). Markedly prolonged distal motor latencies were also present in autoimmune nodopathy.
CONCLUSIONS: Patients with autoimmune nodopathies had distinct distributions of peripheral nerve enlargement revealed by ultrasound, as well as distinct NCS patterns, which were different from CIDP. This suggests the potential utility of nerve ultrasound and NCS to supplement clinical characteristics for distinguishing nodopathies from CIDP.

OBJECTIVE: Leprosy is a chronic infectious disease caused by Mycobacterium leprae (M. leprae), an intracellular bacillus that systematically invades the peripheral nerves. Diagnosing leprosy neuropathy is still a defying skill, and late diagnosis and treatment are still a reality. Based on the biological characteristics of M. leprae, particularly its preference for invading the Schwann cells localized at the coldest areas of human body, we hypothesized that these areas have focal demyelination that may escape detection through standard nerve conduction studies (NCSs) protocols.
METHODS: Twenty-five patients with confirmed multibacillary leprosy and 14 controls were accessed. A multisegmented NCS protocol (MP) was performed, targeting short segments through the coldest areas, to identify focal areas of slowed conduction velocity. The effectiveness of this multisegmented protocol was compared to the standard protocol (SP) to detect abnormalities.
RESULTS: All leprosy patients presented an abnormal study with the MP, contrasting to 19 with the SP. The most frequent NCS pattern was an asymmetric neuropathy with focal slowing of conduction velocity, found in 23 out of 25 leprosy patients. Significant differences favoring the proposed method were observed when comparing the MP with the SP. Notably, the MP increased the sensitivity to detect abnormalities by 122%, 133%, and 257% for the median, peroneal, and tibial nerves, respectively. MP also increases sensitivity to detect focal abnormalities in the ulnar nerve.
CONCLUSIONS: The MP protocol significantly increases the sensitivity of NCSs to detect neurophysiological abnormalities in leprosy neuropathy.

OBJECTIVE: Superior laryngeal nerve (SLN) function is critical to laryngeal sensation. Sensory dysfunction in the larynx, mediated through the internal branch of the superior laryngeal nerve (iSLN), is thought to occur with aging and neurodegenerative disease. However, objective analysis of iSLN neurophysiology is difficult due to its anatomic location and small diameter. This study measures sensory nerve action potentials (SNAP) from the iSLN in a rat model.
METHODS: SNAP data were obtained from two adult rat strains (Sprague-Dawley, SD and Fischer 344 × Brown Norway F1 Hybrid rats, FBN). Evoked responses were obtained by stimulating the main trunk of the SLN and recording the response using a 160-μm cuff electrode placed around the iSLN. SNAP were averaged from 10 stimulations. Laryngeal adductor reflex (LAR) threshold measurements were obtained with stimulation of the iSLN and direct laryngoscopy. The sections of the iSLN were obtained for histologic analysis.
RESULTS: SLN-evoked responses were successfully obtained in 18 hemi-laryngeal preparations (SD n = 13 and FBN n = 5) with corresponding LAR threshold measurements. Mean(±SD) SNAP latency, total duration, amplitude, negative durations, and intensity were 2.28 ms (±0.56), 2.13 ms (±0.70), 879 μV (±535), and 0.69 mA (±0.25), respectively. SLN stimulation threshold to elicit an LAR was of 0.84 mA (±0.31).
CONCLUSIONS: It is feasible to record evoked SLN responses in two adult rat strains. This work may lead to a tractable animal model for objective measurements of SLN neurophysiology with various disease states.
METHODS: N/A Laryngoscope, 2024.

OBJECTIVE: Various electrodiagnostic criteria have been developed in Guillain-Barré syndrome (GBS). Their performance in a broad representation of GBS patients has not been evaluated. Motor conduction data from the International GBS Outcome Study (IGOS) cohort were used to compare two widely used criterion sets and relate these to diagnostic amyotrophic lateral sclerosis criteria.
METHODS: From the first 1500 patients in IGOS, nerve conduction studies from 1137 (75.8%) were available for the current study. These patients were classified according to nerve conduction studies criteria proposed by Hadden and Rajabally.
RESULTS: Of the 1137 studies, 68.3% (N = 777) were classified identically according to criteria by Hadden and Rajabally: 111 (9.8%) axonal, 366 (32.2%) demyelinating, 195 (17.2%) equivocal, 35 (3.1%) inexcitable and 70 (6.2%) normal. Thus, 360 studies (31.7%) were classified differently. The areas of differences were as follows: 155 studies (13.6%) classified as demyelinating by Hadden and axonal by Rajabally; 122 studies (10.7%) classified as demyelinating by Hadden and equivocal by Rajabally; and 75 studies (6.6%) classified as equivocal by Hadden and axonal by Rajabally. Due to more strictly defined cutoffs fewer patients fulfilled demyelinating criteria by Rajabally than by Hadden, making more patients eligible for axonal or equivocal classification by Rajabally. In 234 (68.6%) axonal studies by Rajabally the revised El Escorial (amyotrophic lateral sclerosis) criteria were fulfilled; in axonal cases by Hadden this was 1.8%.
CONCLUSIONS: This study shows that electrodiagnosis in GBS is dependent on the criterion set utilized, both of which are based on expert opinion. Reappraisal of electrodiagnostic subtyping in GBS is warranted.

Neuropathies secondary to tophus compression in gout patients are well known; however, limited data exist on other types of peripheral neuropathies (PN). Our aim was to describe PN frequency, characteristics, distribution, patterns, and associated factors in gout patients through clinical evaluation, a PN questionnaire, and nerve conduction studies (NCS). This cross-sectional descriptive study included consecutive gout patients (ACR/EULAR 2015 criteria) from our clinic. All underwent evaluation by Rheumatology and Rehabilitation departments, with IRB approval. Based on NCS, patients were categorized as PN + (presence) or PN- (absence). PN + patients were further classified as local peripheral neuropathy (LPN) or generalized somatic peripheral neuropathy (GPN). We enrolled 162 patients, 98% male (72% tophaceous gout). Mean age (SD): 49.4 (12) years; mean BMI: 27.9 (6.0) kg/m2. Comorbidities included dyslipidemia (53%), hypertension (28%), and obesity (23.5%). Abnormal NCS: 65% (n = 106); 52% LPN, 48% GPN. PN + patients were older, had lower education, and severe tophaceous gout. GPN patients were older, had lower education, and higher DN4 scores compared to LPN or PN- groups (p = 0.05); other risk factors were not significant. Over half of gout patients experienced neuropathy, with 48% having multiplex mononeuropathy or polyneuropathy. This was associated with joint damage and functional impairment. Mechanisms and risk factors remain unclear. Early recognition and management are crucial for optimizing clinical outcomes and quality of life in these patients. Key Points Peripheral neuropathies in gout patients had been scarcely reported and studied. This paper report that: • PN in gout is more frequent and more diverse than previously reported. • Mononeuropathies are frequent, median but also ulnar, peroneal and tibial nerves could be injured. • Unexpected, generalized neuropathies (polyneuropathy and multiplex mononeuropathy) are frequent and associated to severe gout. • The direct role of hyperuricemia /or gout in peripheral nerves require further studies.