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Objectives: Proximal median nerve (PMN) neuropathies are caused by lesions proximal to the carpal tunnel, which include the forearm, elbow, upper arm, and brachial plexus. Differentiating between carpal tunnel syndrome and PMN neuropathies is important to guide management and is based on clinical, electrodiagnostic (EDX), and ultrasound (US) findings. This study describes the clinical, EDX, and US features in 62 patients with PMNs. Methods: All patients underwent EDX studies, and 52 (83.9%) had a US study. The patients were assigned to one of the following four localization zones of PMN neuropathies based on clinical and EDX criteria: Zone 1: extends from the fascicles in the brachial plexus contributing to the median nerve to the innervation of the pronator teres (PT); Zone 2: distal to the branch to the PT and proximal to the origin of the anterior interosseous nerve (AIN); Zone 3: involves the origin of the AIN; and Zone 4: distal to the origin of the AIN and proximal to the carpal tunnel. The localization was based on the pattern of muscle weakness, topography of EMG abnormalities, and US study findings. Results: The anatomical locations of the PMN neuropathies based on clinical, EDX, and US findings were as follows: Zone 1 in 38 patients (61.3%), Zone 2 in 6 patients (9.7%), Zone 3 in 7 patients (11.3%), and Zone 4 in 11 patients (17.7%). The most common etiology among all 62 patients was iatrogenic injury (30 [48.4%]), followed by non-iatrogenic trauma (20 [32.2%]). The following EDX findings were noted: prolonged distal motor latency (29 [46.8%]), decreased motor nerve conduction velocity in the forearm (22 [35.5%]), low amplitude or absent compound muscle action potentials (50 [80.6%]), and abnormal or absent sensory nerve action potentials (50 [80.6%]). Of the 52 (83.9%) patients who underwent US studies, a total of 22 (42.3%) patients showed an increased cross-sectional area of the median nerve. A neuroma was observed in 9 patients (17.4%). Conclusion: It is often possible to localize the site of the median nerve involvement and gain insight into the underlying cause based on clinical and EMG findings, but in certain cases, a US study may be necessary to confirm the location. [ABSTRACT FROM AUTHOR]

Background: The lateral antebrachial cutaneous nerve (LACN) is the terminal sensory branch of the musculocutaneous nerve and is rarely entrapped or injured. This study describes the electrodiagnostic (EDX) findings and etiologies of LACN neuropathy. Methods: This is a review of 49 patients with pain and/or paresthesia of the forearm who underwent EDX studies. The diagnosis of LACN neuropathy was based on clinical and sensory conduction abnormalities. Results: The most common etiology of LACN neuropathy was iatrogenic injury in 30 (61.2%) patients, primarily due to biceps tendon repair at the elbow (11 [36.7%]) and phlebotomy (5 [16.7%]). Fifteen (30.6%) patients sustained a non-iatrogenic injury at the proximal forearm/elbow, consisting of six (60%) laceration injuries and five (33.3%) stretch injuries. Four (8.2%) patients comprised the "other" etiology category, including two mass lesions causing LACN compression. Pain, paresthesia, and/or numbness in the LACN distribution were reported in 33 (67.3%), 27 (55.1%), and 23 (46.9%) patients, respectively. Hypoesthesia was detected in 45 (91.8%) patients, and dysesthesia in 7 (14.3%). The sensory nerve action potentials (SNAPs) of the LACN on the symptomatic side were absent in 44 (89.8%) patients. Of the five patients whose SNAPs of the LACN were detected, all had a decreased amplitude, and two had increased sensory latency. Conclusions: The most common etiology for LACN neuropathy in this series was iatrogenic injury; repair of biceps tendon at the elbow was the most frequent provoking cause. Protection of the LACN during surgical procedures at the elbow and forearm is vital to prevent iatrogenic injury. [ABSTRACT FROM AUTHOR]

Background: Osteopontin (OPN) is a proinflammatory cytokine that has been recently implicated in neuroinflammation and neurodegeneration. We hypothesized that an increase in plasma OPN is a deleterious neuroinflammatory marker in people with dementia and cerebral small vessel disease (CSVD). Methods: A pilot study was conducted on participants in the Northern Manhattan Study (NOMAS). Three groups were selected based on their dementia status and evidence of subclinical CSVD and chosen to be similar in age, sex, and education attainment: No dementia/No CSVD (n = 19), Dementia/No CSVD (n = 22), and Dementia + CSVD (n = 21). Dementia (any type) was diagnosed by consensus adjudication following a series of comprehensive neuropsychological assessments and a review of the medical history. CSVD was indicated by silent brain infarcts, enlarged perivascular spaces, cerebral microbleeds, and white matter hyperintensity volumes (WMHV) on MRI. Multinomial logistic regression was used to examine the difference in OPN levels across groups, adjusting for key determinants of CSVD and neurodegeneration. Results: Plasma OPN levels were elevated in the Dementia+CSVD group (mean = 70.69 ± 39.00 ng/mL) but not in the Dementia/No CSVD group (mean = 45.46 ± 19.11 ng/mL) compared to the No Dementia/No CSVD group (mean = 36.43 ± 15.72 ng/mL). OPN was associated with Dementia+CSVD (Odds Ratio [OR] per ng/mL = 1.06, 95% CI 1.02–1.11) after adjusting for covariates, including brain volume. OPN was strongly correlated with WMHV (Spearman's rank correlation ρ = 0.46, p = 0.0001) but not with other components of CSVD. Conclusion: In this pilot, greater levels of plasma OPN were associated with dementia with evidence of CSVD. This link was predominately driven by the contribution of OPN to dementia through the burden of white matter lesions. [ABSTRACT FROM AUTHOR]

Objectives: Gunshot wounds of the upper extremities may cause permanent neurovascular injuries, leading to significant morbidity, chronic pain, functional loss, and disability. While there are many reports on the incidence and intraoperative findings in gunshot-related nerve injuries (GSNI) sustained during wars, there is a paucity of details pertaining to GSNI of the upper extremities in civilians. The goal of this paper is to provide the clinical, electrodiagnostic (EDX), and ultrasound (US) findings in 22 patients with GSNI of the upper extremities. Methods: This is a retrospective study of patients referred for EDX studies to evaluate the presence of nerve injury after sustaining GSWs to the upper extremities. All patients underwent EDX studies, and 16 patients had US evaluations. Numerous metrics were documented including presenting symptoms, neurological abnormalities, EDX findings, and US features. Results: The forearm was the most frequent location of injury (8 [36%] patients). The ulnar nerve was the most common injured nerve (10 [45%] patients), followed by the brachial plexus (7 [32%] patients). All patients complained of muscle weakness; the most frequently affected muscles were the first dorsal interosseous (FDI) (14 [64%] patients) and abductor pollicis brevis (APB) (11 [50%] patients). Muscle atrophy was noted in 19 (86%) patients, 15 of whomhad atrophy of the FDI. Axonotmesis was the type of nerve injury in all patients based on EDX studies. Of the 16 patients who underwent US studies, a neuroma in continuity was noted in 4 (25%) patients and neurotmesis in 1 (6.2%) patient. Eleven (69%) patients had enlarged and/or hypoechoic nerves. Conclusions: Axonotmesis of the ulnar nerve was the most common finding among patients sustaining gunshot injuries to the upper extremities. EDX and US studies provide valuable insight into the underlying pathophysiology and guidance for management of patients with GSNI of the upper extremities. [ABSTRACT FROM AUTHOR]

Introduction: Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy and rarely develops after drug therapy. This study describes the clinical, electrodiagnostic (EDX), and ultrasound (US) findings in seven patients who experienced CTS due to anti-cancer therapeutic agents. Methods: All patients underwent EDX testing, and four patients had an US study. Results: CTS occurred in four patients with aromatase inhibitors, two with immune checkpoint inhibitors, and one with a selective estrogen receptor modulator. The mean duration between initiation of the anti-cancer therapeutic agents and symptom onset was 6 weeks (range: 2–12 weeks). Decreased digit sensation was noted in all patients; wasting and weakness of the abductor pollicis brevis (APB) was observed in three (42.8%) patients. The compound muscle action potentials (CMAP) of the APB and sensory nerve action potentials of the second or third digit could not be recorded in two (28.5%) and four (57.1%) patients, respectively. The needle EMG detected fibrillations and positive sharp waves in the APB in two patients. The motor unit potentials of the APB were decreased with large polyphasics in three (42.8%) patients. Of the four patients who underwent US testing, all had increased cross-sectional area of the median nerve at the carpal tunnel inlet, three (75%) had thenar muscle atrophy, and two (50%) had a loss of fascicular pattern. Three (42.8%) patients underwent a CTR. Conclusions: Physicians should be cognizant of the relationship between anti-cancer therapeutic agents and CTS. EDX studies and US play important roles in the diagnostic assessment of such patients. [ABSTRACT FROM AUTHOR]