Anti-cancer therapeutic agents and carpal tunnel syndrome: Clinical, electrodiagnostic, and ultrasound findings in seven patients.

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.

Osteopontin is associated with dementia in the presence of cerebral small vessel disease.

BACKGROUND: Osteopontin (OPN) is a proinflammatory cytokine that has been recently implicated in neuroinflammation and neurodegeneration. We hypothesized that an increase in plasma osteopontin 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 osteopontin 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). Osteopontin 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 =0.46, p=0.0001), but not with other components of CSVD. CONCLUSION: In this pilot, greater levels of plasma osteopontin 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.

Dynamic response of microglia/macrophage polarization following demyelination in mice.

BACKGROUND: The glial response in multiple sclerosis (MS), especially for recruitment and differentiation of oligodendrocyte progenitor cells (OPCs), predicts the success of remyelination of MS plaques and return of function. As a central player in neuroinflammation, activation and polarization of microglia/macrophages (M/M) that modulate the inflammatory niche and cytokine components in demyelination lesions may impact the OPC response and progression of demyelination and remyelination. However, the dynamic behaviors of M/M and OPCs during demyelination and spontaneous remyelination are poorly understood, and the complex role of neuroinflammation in the demyelination-remyelination process is not well known. In this study, we utilized two focal demyelination models with different dynamic patterns of M/M to investigate the correlation between M/M polarization and the demyelination-remyelination process. METHODS: The temporal and spatial features of M/M activation/polarization and OPC response in two focal demyelination models induced by lysolecithin (LPC) and lipopolysaccharide (LPS) were examined in mice. Detailed discrimination of morphology, sensorimotor function, diffusion tensor imaging (DTI), inflammation-relevant cytokines, and glial responses between these two models were analyzed at different phases. RESULTS: The results show that LPC and LPS induced distinctive temporal and spatial lesion patterns. LPS produced diffuse demyelination lesions, with a delayed peak of demyelination and functional decline compared to LPC. Oligodendrocytes, astrocytes, and M/M were scattered throughout the LPS-induced demyelination lesions but were distributed in a layer-like pattern throughout the LPC-induced lesion. The specific M/M polarization was tightly correlated to the lesion pattern associated with balance beam function. CONCLUSIONS: This study elaborated on the spatial and temporal features of neuroinflammation mediators and glial response during the demyelination-remyelination processes in two focal demyelination models. Specific M/M polarization is highly correlated to the demyelination-remyelination process probably via modulations of the inflammatory niche, cytokine components, and OPC response. These findings not only provide a basis for understanding the complex and dynamic glial phenotypes and behaviors but also reveal potential targets to promote/inhibit certain M/M phenotypes at the appropriate time for efficient remyelination.

A Hospital-Based Neuroscience Nursing Course Designed to Improve Competence and Confidence.

After experiencing growth in a neuroscience service line, nurse leaders identified a need for increased competencies among clinical staff. This hospital met the need by developing a unique multidisciplinary neuroscience nursing course to improve the clinical competence, confidence, and professional development of bedside nurses.

Cytosolic phospholipase A2 protein as a novel therapeutic target for spinal cord injury.

OBJECTIVE: The objective of this study was to investigate whether cytosolic phospholipase A2 (cPLA2 ), an important isoform of PLA2 that mediates the release of arachidonic acid, plays a role in the pathogenesis of spinal cord injury (SCI). METHODS: A combination of molecular, histological, immunohistochemical, and behavioral assessments were used to test whether blocking cPLA2 activation pharmacologically or genetically reduced cell death, protected spinal cord tissue, and improved behavioral recovery after a contusive SCI performed at the 10th thoracic level in adult mice. RESULTS: SCI significantly increased cPLA2 expression and activation. Activated cPLA2 was localized mainly in neurons and oligodendrocytes. Notably, the SCI-induced cPLA2 activation was mediated by the extracellular signal-regulated kinase signaling pathway. In vitro, activation of cPLA2 by ceramide-1-phosphate or A23187 induced spinal neuronal death, which was substantially reversed by arachidonyl trifluoromethyl ketone, a cPLA2 inhibitor. Remarkably, blocking cPLA2 pharmacologically at 30 minutes postinjury or genetically deleting cPLA2 in mice ameliorated motor deficits, and reduced cell loss and tissue damage after SCI. INTERPRETATION: cPLA2 may play a key role in the pathogenesis of SCI, at least in the C57BL/6 mouse, and as such could be an attractive therapeutic target for ameliorating secondary tissue damage and promoting recovery of function after SCI.

Krüppel-like Factor 7 engineered for transcriptional activation promotes axon regeneration in the adult corticospinal tract.

Axon regeneration in the central nervous system normally fails, in part because of a developmental decline in the intrinsic ability of CNS projection neurons to extend axons. Members of the KLF family of transcription factors regulate regenerative potential in developing CNS neurons. Expression of one family member, KLF7, is down-regulated developmentally, and overexpression of KLF7 in cortical neurons in vitro promotes axonal growth. To circumvent difficulties in achieving high neuronal expression of exogenous KLF7, we created a chimera with the VP16 transactivation domain, which displayed enhanced neuronal expression compared with the native protein while maintaining transcriptional activation and growth promotion in vitro. Overexpression of VP16-KLF7 overcame the developmental loss of regenerative ability in cortical slice cultures. Adult corticospinal tract (CST) neurons failed to up-regulate KLF7 in response to axon injury, and overexpression of VP16-KLF7 in vivo promoted both sprouting and regenerative axon growth in the CST of adult mice. These findings identify a unique means of promoting CST axon regeneration in vivo by reengineering a developmentally down-regulated, growth-promoting transcription factor.

Unilateral Calf Atrophy: A Case Series of Clinical and Electrodiagnostic Findings With a Review of the Literature.

Unilateral calf atrophy may result from several medical conditions, such as lumbar radiculopathy, asymmetric myopathy/dystrophy, a Baker's (popliteal) cyst leading to tibial nerve compression, and disuse atrophy. We present a case series of four patients with unilateral calf atrophy, including chronic neurogenic atrophy (benign focal amyotrophy, one patient), tibial nerve compression at the popliteal fossa by a Baker's cyst (one patient), and disuse atrophy (two patients). All four patients underwent electrodiagnostic (EDX) studies, and two of them had denervation changes of the gastrocnemius. One patient underwent an ultrasound (US), which revealed a large cyst in the popliteal fossa causing compression of the tibial nerve. The differential diagnosis of unilateral calf atrophy as well as diagnostic techniques to confirm the underlying pathology are described. EDX and US studies are useful in differentiating between the varied conditions that may cause asymmetric calf muscle wasting.

Clinical, Electrodiagnostic, and Ultrasound Findings in 87 Patients With Finger Drop.

BACKGROUND: The inability to extend the fingers at the metacarpophalangeal and interphalangeal joints leads to finger drop. While wrist drop and foot drop are well recognized, the causes of finger drop are poorly understood. AIMS: This study describes the clinical, electrodiagnostic (EDX), and ultrasound (US) features in patients with finger drop. MATERIALS AND METHODS: This is a retrospective study of 87 patients presenting with finger drop and referred for EDX studies during the past 10 years. We analyzed the clinical picture, EDX data, and US findings. The patients were categorized into global (all five digits) or partial (limited to 1-4 digits) finger drop. RESULTS: Fifty-six (64%) patients had global finger drop, while 31 (36%) had partial finger drop. The frequent cause of finger drop was Parsonage-Turner syndrome (PTS) (29 [33%]), followed by trauma (23 [26%]), cervical radiculopathy (16 [18%]), extensor tendon rupture (four [4%]), and compression/entrapment (two [2%]). In 13 (15%) patients, no cause was identified. A total of 13/16 (81%) patients with cervical radiculopathy and four of the patients with tendon rupture had partial finger drop, while 52/64 (81%) with posterior interosseous nerve (PIN) neuropathy had global finger drop. Of the 16 patients who experienced cervical radiculopathy as the cause of the finger drop, 15 patients had C7 and C8 radiculopathy and one patient had C7 radiculopathy. EDX studies of patients with PTS revealed partial axon loss in 18 (62%) patients, conduction block in eight (28%), and total axon loss in four (14%). Enlarged fascicles were observed by US in 40% of patients with PTS. EDX studies of patients who sustained iatrogenic nerve injury causing finger drop demonstrated total axon loss in six (46%) patients, partial axon loss in four (31%), demyelination in two (15%), and conduction block in two (15%). CONCLUSIONS: PIN neuropathy is the most common cause of finger drop, however, lesser-known causes such as cervical radiculopathy and extensor tendon rupture should also be considered. Global finger drop is suggestive of PIN neuropathy, while partial finger drop occurs more often in cervical radiculopathy and tendon rupture. EDX and US studies provide valuable information for localizing the lesion site and may reveal the cause of the finger drop.

A Retrospective Study of Lateral Antebrachial Cutaneous Nerve Neuropathy: Electrodiagnostic Findings and Etiologies in 49 Cases.

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.

Age-associated temporal decline in butyrate-producing bacteria plays a key pathogenic role in the onset and progression of neuropathology and memory deficits in 3×Tg-AD mice.

Alterations in the gut-microbiome-brain axis are increasingly being recognized to be involved in Alzheimer's disease (AD) pathogenesis. However, the functional consequences of enteric dysbiosis linking gut microbiota and brain pathology in AD progression remain largely undetermined. The present work investigated the causal role of age-associated temporal decline in butyrate-producing bacteria and butyrate in the etiopathogenesis of AD. Longitudinal metagenomics, neuropathological, and memory analyses were performed in the 3×Tg-AD mouse model. Metataxonomic analyses showed a significant temporal decline in the alpha diversity marked by a decrease in butyrate-producing bacterial communities and a concurrent reduction in cecal butyrate production. Inferred metagenomics analysis identified the bacterial acetyl-CoA pathway as the main butyrate synthesis pathway impacted. Concomitantly, there was an age-associated decline in the transcriptionally permissive acetylation of histone 3 at lysines 9 and 14 (H3K9/K14-Ac) in hippocampal neurons. Importantly, these microbiome-gut-brain changes preceded AD-related neuropathology, including oxidative stress, tau hyperphosphorylation, memory deficits, and neuromuscular dysfunction, which manifest by 17-18 months. Initiation of oral administration of tributyrin, a butyrate prodrug, at 6 months of age mitigated the age-related decline in butyrate-producing bacteria, protected the H3K9/K14-Ac status, and attenuated the development of neuropathological and cognitive changes associated with AD pathogenesis. These data causally implicate age-associated decline in butyrate-producing bacteria as a key pathogenic feature of the microbiome-gut-brain axis affecting the onset and progression of AD. Importantly, the regulation of butyrate-producing bacteria and consequent butyrate synthesis could be a significant therapeutic strategy in the prevention and treatment of AD.

Mouse intermittent hypoxia mimicking apnoea of prematurity: effects on myelinogenesis and axonal maturation.

Premature babies are at high risk for both infantile apnoea and long-term neurobehavioural deficits. Recent studies suggest that diffuse structural changes in brain white matter are a positive predictor of poor cognitive outcomes. Since oligodendrocyte maturation, myelination, axon development, and synapse formation mainly occur in the third trimester of gestation and first postnatal year, infantile apnoea could lead to and/or exaggerate white matter impairments in preterm neonates. Therefore, we investigated oligodendroglia and axon development in a neonatal mouse model of intermittent hypoxia between postnatal days 2 and 10. During critical phases of central nervous system development, intermittent hypoxia induced hypomyelination in the corpus callosum, striatum, fornix, and cerebellum, but not in the pons or spinal cord. Intermittent hypoxia-elicited alterations in myelin-forming processes were reflected by decreased expression of myelin proteins, including MBP, PLP, MAG, and CNPase, possibly due to arrested maturation of oligodendrocytes. Ultrastructural abnormalities were apparent in the myelin sheath and axon. Immature oligodendrocytes were more vulnerable to neonatal intermittent hypoxia exposures than developing axons, suggesting that hypomyelination may contribute, at least partially, to axonal deficits. Insufficient neurofilament synthesis with anomalous components of neurofilament subunits, ß-tubulin, and MAP2 isoforms indicated immaturity of axons in intermittent hypoxia-exposed mouse brains. In addition, down-regulation of synapsin I, synaptophysin, and Gap-43 phosphorylation suggested a potential stunt in axonogenesis and synaptogenesis. The region-selective and complex impairment in brain white matter induced by intermittent hypoxia was further associated with electrophysiological changes that may underlie long-term neurobehavioural sequelae.

Intrathecal treatment of cerebral vasospasm.

Treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) remains a major therapeutic challenge. Systemic drug administration is the current treatment of choice, but patients often do not respond beneficially to this approach. Intrathecal (IT) drug administration has several anatomic and pharmacodynamic advantages over conventional systemic treatment of cerebral vasospasm. We reviewed the most recent literature describing IT administration of several drugs to treat aneurysm-induced SAH and cerebral vasospasm, including 16 clinical trials using IT fibrinolytic agents and 10 trials using several IT vasodilators. We evaluated the safety and effectiveness of these trials but made no attempt to perform a meta-analysis using these data. IT drug administration of fibrinolytic agents and vasodilators caused lysis of the subarachnoid clot burden and diminished cerebral vasospasm, respectively. The studies reviewed reported a wide range of drug doses, intervals between aneurysm hemorrhage and initiation of treatment, success of clot dissolution, and degree of vasodilation of vessels in vasospasm. Treatment of vasospasm by IT drug administration is safe and largely effective after the aneurysm has been secured. Our findings indicate that IT treatment effectively delivers a higher drug concentration to vessels in vasospasm with minimal systemic effects. Drugs administered by this route are reported to lyse subarachnoid clots, attenuate cerebral vasospasm, improve clinical outcomes, and decrease the incidence of hydrocephalus. With greater understanding of drug pharmacodynamics, the IT route of drug administration may provide a rational, alternative approach to treating aneurysm-induced cerebral vasospasm.

Clinical Features of a Newly Described Mutation of Myelin Protein Zero in a Family.

Charcot-Marie-Tooth (CMT) disease is the most common hereditary neuropathy. Duplication of the peripheral myelin protein-22 (PMP22) gene is the most frequent genetic abnormality in CMT disease. Although rare compared to PMP22 gene mutations, many different myelin protein zero (MPZ) gene mutations have been described in patients with CMT disease. MPZ gene mutations are known to cause hereditary neuropathies with heterogenous phenotypes ranging from early-onset severe demyelinating to adult-onset axonal forms. MPZ, the major protein component of peripheral nerve myelin, is important for myelin compaction. We report a family in which a mother and her son, both with adult-onset CMT disease, showed a newly described mutation p.Glu37Lys of the MPZ gene. The clinical features of the mother provided insight into the progression of the disease over decades, while features in the early stage of the disease could be studied in the son. Clinical, electrodiagnostic, and sonographic findings are described in the early and late stages of the disease. The MPZ gene mutation p.Glu37Lys is associated with clinical features of a progressive axonal type of adult-onset CMT disease.

Clinical Spectrum of Postsurgical Parsonage-Turner Syndrome: A Perspective From an Electrodiagnostic Laboratory.

BACKGROUND: Parsonage-Turner syndrome (PTS) is an underdiagnosed disorder characterized by the acute onset of severe pain in the shoulder/scapula/arm followed by muscle weakness/numbness in the distribution of nerves derived from the brachial plexus (BP). Surgical procedures are one of several antecedent events of PTS. This study describes the clinical spectrum of postsurgical Parsonage-Turner syndrome (PSPTS) in a large cohort of patients. MATERIALS AND METHODS: Charts of patients diagnosed with PTS during a 16-year (2006-2022) retrospective review were analyzed to identify cases of PSPTS. The clinical criteria for PSPTS included the new onset of severe pain two days to four weeks after a surgical procedure followed by weakness of muscles innervated by one or more nerves arising from the BP. EDX criteria consist of denervation localized to branches of the BP. PSPTS cases were subdivided into two categories: definite PSPTS (surgery at a remote site) and probable PSPTS (surgery of the ipsilateral upper extremity or the cervical spine). RESULTS: Of 202 patients (204 episodes) diagnosed with PTS, 111 (54%) were idiopathic and 61 (30%) were PSPTS. Of the 61 PSPTS episodes, 26 were definite and 35 were probable PSPTS. The anterior interosseous nerve (AIN) was most affected, followed by the posterior interosseous (PIN), and suprascapular nerve. CONCLUSION: In this series, surgery was the most commonly recognized antecedent event for PTS, and the AIN and PIN were the most frequent nerves affected. Surgeons should consider PTS in patients who develop postoperative severe shoulder pain and weakness of muscles innervated by the BP.

Causes of Dorsal Cutaneous Branch of the Ulnar Nerve Neuropathy Among Patients Undergoing Electrodiagnostic Studies: A Series of 14 Patients.

BACKGROUND: Isolated neuropathy of the dorsal cutaneous branch of the ulnar nerve (DCBUN) is rare and most cases are secondary to trauma, often iatrogenic. The topography of sensory abnormalities and abnormal electrodiagnostic (EDX) findings are crucial in confirming DCBUN neuropathy.  Materials and methods: This is a retrospective study of patients with isolated involvement of the DCBUN from among patients referred for EDX studies for upper extremity symptoms. All patients underwent a focused neurological examination followed by EDX studies. Ultrasound (US) studies were performed in two patients.  Results: Of the 14 patients with DCBUN neuropathy, decreased pinprick sensation in the distribution of the DCBUN was noted in 11 (78%) patients. DCBUN sensory nerve action potential (SNAP) was not recordable in 13 (92%) patients. In one patient who had a recordable SNAP, the latency was prolonged, and the amplitude was decreased. Four (28%) patients had incidental EDX abnormalities suggestive of entrapment of the median nerve at the carpal tunnel. The most common cause of DCBUN neuropathy was trauma in 13 (92%) patients, of which eight were iatrogenic. No specific etiology was detected in one patient (7%). Of the two patients who underwent US studies, one had increased cross-sectional area (CSA) at the wrist with prominent fascicles and hyperechoic scar tissue, while the CSA was normal in the other patient. CONCLUSIONS: Although rare, DCBUN neuropathy can be readily confirmed by typical clinical features and EDX findings. Surgeons should be aware of the anatomy and clinical features of DCBUN neuropathy and avoid injuring the nerve during surgical procedures at the wrist and forearm.

Iatrogenic Ulnar Nerve Neuropathy Following Reverse Total Shoulder Arthroplasty: Electrodiagnostic Findings in 18 Patients.

Background A reverse total shoulder arthroplasty (RTSA) is often recommended for rotator cuff pathology and may be associated with a myriad of complications, including prosthetic instability, infection, humeral problems, and glenoid loosening. Neurological injuries following an RTSA are infrequent and are usually related to brachial plexus or proximal nerve injury in the affected arm. Iatrogenic ulnar nerve neuropathy is exceedingly rare. Aims This study describes the clinical and electrodiagnostic (EDX) features of 18 patients with ulnar nerve neuropathy complicating RTSA. Materials and methods All patients underwent EDX studies, and 14 had an ultrasound (US) study. Results All patients complained of numbness, tingling, hyperalgesia, and/or allodynia in the distribution of the ulnar nerve. Eight (44%) patients reported hand weakness, and one (6%) noted wasting of the intrinsic hand muscles. Decreased pinprick sensation in the ulnar nerve distribution was detected in all patients. Seventeen (94%) patients had weakness of the ulnar nerve-innervated intrinsic hand muscles. All patients had focal slowing of the motor conduction of the ulnar nerve across the elbow. Sensory potentials were either absent or of a low amplitude over the digital and/or dorsal cutaneous branch of the ulnar nerve in all patients. Twelve (86%) patients showed an increase in the cross-sectional area (CSA) of the ulnar nerve at the elbow; six (43%) had a hypoechoic ulnar nerve. Ulnar nerve neuropathy was confirmed at the elbow in all 18 patients. Of the 14 (78%) patients who underwent surgical intervention for ulnar nerve neuropathy following an RTSA, only four had complete symptom resolution. Conclusions Surgeons should be cognizant of ulnar nerve neuropathy as a potential complication of an RTSA and take precautions to avoid damage to the ulnar nerve intraoperatively. EDX and US studies should be performed to confirm and assess the site and severity of the injury.

Iatrogenic median and ulnar nerve injuries during carpal tunnel release: clinical, electrodiagnostic, and ultrasound features in 12 patients. Patient series.

BACKGROUND: Nerve injuries during carpal tunnel release (CTR) are rare. Electrodiagnostic (EDX) and ultrasound (US) studies may be helpful in evaluating iatrogenic nerve injuries during CTR. OBSERVATIONS: Nine patients sustained a median nerve injury, and 3 patients experienced ulnar nerve damage. Decreased sensation occurred in 11 patients, and dysesthesia occurred in 1 patient. Abductor pollicis brevis (APB) weakness occurred in all patients with median nerve injury. Of the 9 patients with median nerve injury, the compound muscle action potentials (CMAPs) of the APB and sensory nerve action potentials (SNAPs) of the 2nd or 3rd digit were not recordable in 6 and 5 patients, respectively. Of the 3 patients sustaining ulnar nerve injuries, the CMAPs of the abductor digiti minimi (ADM) and SNAPs of the 5th digit were not recordable in 1 patient; 2 patients showed prolonged latency and decreased amplitude of CMAPs/SNAPs. US studies of 8 patients with a median nerve injury showed a neuroma within the carpal tunnel. One patient underwent surgical repair urgently, and 6 did so after variable intervals. LESSONS: Surgeons should be cognizant of nerve injuries during CTR. EDX and US studies are useful in evaluating iatrogenic nerve injuries during CTR.

Etiological study of superficial radial nerve neuropathy: series of 34 patients.

Objectives: Superficial radial nerve (SRN) neuropathy is a rare focal neuropathy leading to pain and paresthesia of the dorsolateral aspect of the hand. Reported causes include trauma, extrinsic compression, or it may be idiopathic. We describe the clinical and electrodiagnostic (EDX) features of 34 patients with SRN neuropathy of varied etiology. Methods: This is a retrospective study of patients with upper limb neuropathy referred for EDX studies who were found to have SRN neuropathy based on clinical and EDX findings. Twelve patients also had ultrasound (US) evaluations. Results: Decreased pinprick sensation was noted in the distribution of the SRN in 31 (91%) patients, and a positive Tinel's sign was observed in 9 (26%). Sensory nerve action potentials (SNAPs) were not recordable in 11 (32%) patients. Of the patients who had a recordable SNAP, the latency was delayed, and the amplitude was decreased in all cases. Of the 12 patients who underwent US studies, 6 (50%) had an increased cross-sectional area of the SRN at or immediately proximal to the site of injury/compression. A cyst was located adjacent to the SRN in 2 patients. The most common cause of SRN neuropathy was trauma in 19 (56%) patients, of which 15 were iatrogenic. A compressive etiology was identified in 6 patients (18%). No specific etiology was detected in 10 patients (29%). Conclusion: This study is aimed at raising the awareness among surgeons about the clinical features and varied causes of SRN neuropathy; such knowledge may potentially lessen iatrogenic causes of injury.

Etiology of spastic foot drop among 16 patients undergoing electrodiagnostic studies: patient series.

BACKGROUND: Differentiating foot drop due to upper motor neuron (UMN) lesions from that due to lower motor neuron lesions is crucial to avoid unnecessary surgery or surgery at the wrong location. Electrodiagnostic (EDX) studies are useful in evaluating patients with spastic foot drop (SFD). OBSERVATIONS: Among 16 patients with SFD, the cause was cervical myelopathy in 5 patients (31%), cerebrovascular accident in 3 (18%), hereditary spastic paraplegia in 2 (12%), multiple sclerosis in 2 (12%), chronic cerebral small vessel disease in 2 (12%), intracranial meningioma in 1 (6%), and diffuse brain injury in 1 (6%). Twelve patients (75%) had weakness of a single leg, whereas 2 others (12%) had bilateral weakness. Eleven patients (69%) had difficulty walking. The deep tendon reflexes of the legs were hyperactive in 15 patients (94%), with an extensor plantar response in 9 patients (56%). Twelve patients (75%) had normal motor and sensory conduction, 11 of whom had no denervation changes of the legs. LESSONS: This study is intended to raise awareness among surgeons about the clinical features of SFD. EDX studies are valuable in ruling out peripheral causes of foot drop, which encourages diagnostic investigation into a UMN source for the foot drop.

Impact of Occupations and Hobbies on the Severity of Carpal Tunnel Syndrome: An Electrodiagnostic Perspective.

OBJECTIVE: This study describes the clinical and electrodiagnostic (EDX) findings as well as occupations and hobbies in 613 patients diagnosed with carpal tunnel syndrome (CTS). METHODS: Patients with moderate, moderately severe, or severe CTS based on EDX criteria were included. RESULTS: The most common occupations included workers in offices, construction/maintenance, and assembly lines. The occupation severity scores were greatest in garment workers, musicians, and landscapers. Regardless of occupation, patient age and occupation duration were significantly correlated ( P < 0.001). Gardeners had the highest average severity score of the hobbies, followed by painters, those who sew, and individuals who perform house chores. CONCLUSIONS: Physicians should be aware of particular occupations and hobbies associated with a greater risk of severe CTS and offer modifications to their patients' work duties and hobbies to minimize the likelihood of developing severe CTS.