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.

UNASSIGNED: To inquire into the relationship between diabetic peripheral neuropathy (DPN) and serum levels of growth differentiation factor-15 (GDF-15) in individuals with type 2 diabetes mellitus (T2DM).
UNASSIGNED: Out of 162 T2DM patients classified according to the diagnostic criteria of DPN, 75 were allocated to the non-DPN group and 87 to the DPN group. In turn, based on serum GDF-15 quartiles, all patients were additionally divided (GDF-15 low to high) into group A (40 cases), group B (41 cases), group C (41 cases), and group D (40 cases). General data and laboratory indexes of patients were collected, and enzyme-linked immunosorbent assay (ELISA) was used to determine serum GDF-15 levels.
UNASSIGNED: Compared to the non-DPN group, in the DPN group GDF-15 levels were noticeably greater (P < 0.001). Using serum GDF-15 as a grouping variable, DPN prevalence and body mass index were gradually increased, motor and sensory nerve latencies were gradually lengthened, and amplitude (Amp) and nerve conduction velocity (NCV) were gradually decreased with increasing GDF-15 levels (P < 0.05). Linear regression modeling revealed that GDF-15 levels correlated positively with the latencies of sensory and motor nerves, and negatively with their corresponding NCV (P < 0.05). Binary logistic regression results indicated GDF-15 as an independent predictor for DPN (P < 0.05), whereas restricted cubic spline analysis indicated a dose-response, nonlinear relationship between GDF-15 and DPN.
UNASSIGNED: Serum GDF-15 level strongly correlates with DPN, and may represent an independent predictor and a biological marker for the disease.

Background Nerve conduction studies ease the understanding of the various pathologies of the peripheral nervous system. It helps physicians to delineate between the two principal types of peripheral etiologies: axonal degeneration and demyelination. An increase in weight in the form of excessive fat deposition or obesity could have a worrisome effect on nerve conduction. So, to find the association of various anthropometric parameters (age, gender, height, weight, waist-hip ratio and body mass index) with motor and sensory median nerve conduction parameters (latency, amplitude and velocity) this cross-sectional study was conducted. Materials and method A total of 87 subjects were taken and their height, weight, waist-hip ratio and body mass index were measured using standard techniques. Motor and sensory nerve conduction parameters were measured on an electromyography machine. Data was stored, tabulated and analyzed. Results The average height of male and female subjects ± SD was 1.699 ± 0.072 m and 1.589 ± 0.067 m respectively. The average weight of male and female subjects ± SD was 64.089 ± 11.497 kg and 52.949 ± 8.404 kg, respectively. The average BMI of normal, underweight and overweight subjects ± SD was 21.668 ± 2.048 kg/m2, 17.074 ± 0.794 kg/m2 and 26.595 ± 0.915 kg/m2 respectively. Weight showed a significant (p = 0.0025) correlation with the latency of motor median nerve conduction. Waist-hip ratio showed a significant (p = 0.042 and p = 0.036) correlation with motor median nerve conduction velocity in both male and female subjects, respectively. BMI in the overweight category showed a significant (p = 0.0156 and p = 0.0290) correlation with latency and amplitude of motor median nerve conduction study, respectively. Conclusions This study exemplifies that an increase in BMI of our body can affect nerve conduction. This could serve as a preliminary study to assess the effect of obesity on peripheral nerve conduction, especially in the Indian population.

BACKGROUND: Increasing evidence indicates a higher prevalence of polyneuropathy (PNP) in Parkinson\'s disease (PD). However, the involvement of large fiber neuropathy in PD still remains poorly understood. Given the lack of longitudinal data, we investigated the course of PNP associated with PD.
METHODS: In total, 41 PD patients underwent comprehensive clinical evaluation including motor and non-motor assessments as well as nerve conduction studies at baseline and at 2 years of follow-up. The definition of PNP was based on electrophysiological standard criteria. Common causes of PNP were excluded.
RESULTS: At baseline, PNP was diagnosed in 65.85% of PD patients via electroneurography. Patients with PNP presented with higher age (p = 0.019) and PD motor symptom severity (UPDRS III; p < 0.001). Over the course of 2 years, PNP deteriorated in 21.95% of cases, and 26.83% remained without PNP. Deterioration of nerve amplitude was most prevalent in the median sensory nerve affecting 57.58% of all PD cases with an overall reduction of median sensory nerve amplitude of 45.0%. With regard to PD phenotype, PNP progression was observed in 33.33% of the tremor dominant and 23.81% of the postural instability/gait difficulties subtype. Decrease of sural nerve amplitude correlated with lower quality of life (PDQ-39, p = 0.037) and worse cognitive status at baseline (MoCA, p = 0.042).
CONCLUSIONS: The study confirms the high PNP rate in PD, and demonstrates a significant electrophysiological progression also involving nerves of the upper extremities. Longitudinal studies with larger cohorts are urgently needed and should elucidate the link between PD and PNP with the underlying pathomechanisms.

UNASSIGNED: Subclinical involvement of nerves may sometimes be present much before the overt clinical manifestations become apparent. Protein gene product (PGP) 9.5, a ubiquitin-C-terminal hydrolase, has been widely used as a marker to study the involvement of peripheral nerve fibers in many diseases.
UNASSIGNED: To evaluate the change in cutaneous nerve fiber staining and distribution from pre-treatment and post completion of multidrug therapy through the expression of PGP9.5 and to assess PGP9.5 as a marker of treatment response.
UNASSIGNED: In this prospective single-center observational study, skin biopsy was taken in patients with leprosy, having areas of nerve function impairment (NFI), based on findings of nerve conduction studies (NCSs), but not having lesions or impaired tactile or thermal impairment clinically. The thin nerve fiber density in the clinically normal skin in areas supplied by nerve showing changes of sensory neuropathy was evaluated to study the density of the fibers. A second biopsy was taken at the end of treatment from a site near the previous site to assess the changes in intra-epidermal nerve fiber staining and distribution.
UNASSIGNED: Thirty-three patients were recruited in the present study (24 males and 9 females). Pre-treatment, 27 patients had abnormal NCSs, while six patients did not have any evidence of neuropathy on NCSs. Staining for nerve fibers using PGP9.5; in the epidermis was positive in five patients pre-treatment and 11 patients post treatment (P = 0.181). Staining in the dermis revealed positivity in 14 pre-treatment, which increased to 18 post treatment (P = 0.342). Adnexae showed positivity in five patients pre-treatment and increased to 17 post treatment (P = 0.005).
UNASSIGNED: A reduced PGP9.5 staining in the epidermal, dermal, and adnexal regions was seen in leprosy patients, which improved post treatment. Thus, PGP9.5 may serve as a marker of NFI and treatment response.

Traumatic peripheral nerve injuries (PNI), present with symptoms ranging from pain to loss of motor and sensory function. Difficulties in intraoperative visual assessment of nerve functional status necessitate intraoperative nerve conduction studies (INCSs) by neurosurgeons and neurologists to determine the presence of functioning axons in the zone of a PNI. This process, also referred to as nerve \"inching\", uses a set of stimulating and recording electrode hooks to lift the injured nerve from the surrounding surgical field and to determine whether an electrical stimulus can travel through the zone of injury. However, confounding electrical signal artifacts can arise from the current workflow and electrode design, particularly from the mandatory lifting of the nerve, complicating the definitive assessment of nerve function and neurosurgical treatment decision-making. The objective of this study is to describe the design process and verification testing of our group\'s newly designed stimulating and recording electrodes that do not require the lifting or displacement of the injured nerve during INCSs. Ergonomic in vivo analysis of the device within a porcine model demonstrated successful intraoperative manipulation of the device, while quantitative nerve action potential (NAP) signal analysis with an ex vivo simulated \"inching\" procedure on healthy non-human primate nerve tissue demonstrated excellent reproducible recorded NAP fidelity and the absence of NAP signal artifacts at all points of recording. Lastly, electrode pullout force testing determined maximum forces of 0.43 N, 1.57 N, and 3.61 N required to remove the device from 2 mm, 5 mm, and 1 cm nerve models, respectively, which are well within established thresholds for nerve safety. These results suggest that these new electrodes can safely and successfully perform accurate PNI assessment without the presence of artifacts, with the potential to improve the INCS standard of care while remaining compatible with currently used neurosurgical technology, infrastructure, and clinical workflows.

Neuronal intranuclear inclusion disease is a neurodegenerative disorder with a wide phenotypic spectrum, including peripheral neuropathy. This study aims to characterize the nerve conduction features and proposes an electrophysiological criterion to assist the diagnosis of neuronal intranuclear inclusion disease. In this study, nerve conduction studies were performed in 50 genetically confirmed neuronal intranuclear inclusion disease patients, 200 age- and sex-matched healthy controls and 40 patients with genetically unsolved leukoencephalopathy. Abnormal electrophysiological parameters were defined as mean values plus or minus two standardized deviations of the healthy controls or failure to evoke a response on the examined nerves. Compared to controls, neuronal intranuclear inclusion disease patients had significantly slower motor and sensory nerve conduction velocities, as well as lower amplitudes of compound motor action potentials and sensory nerve action potentials in all tested nerves (P < 0.05). Forty-eight of the 50 neuronal intranuclear inclusion disease patients (96%) had at least one abnormal electrophysiological parameter, with slowing of motor nerve conduction velocities being the most prevalent characteristic. The motor nerve conduction velocities of median, ulnar, peroneal and tibial nerves were 44.2 ± 5.5, 45.3 ± 6.1, 37.3 ± 5.3 and 35.6 ± 5.1 m/s, respectively, which were 12.4-13.6 m/s slower than those of the controls. The electrophysiological features were similar between neuronal intranuclear inclusion disease patients manifesting with CNS symptoms and those with PNS-predominant presentations. Thirteen of the 14 patients (93%) who underwent nerve conduction study within the first year of symptom onset exhibited abnormal findings, indicating that clinical or subclinical peripheral neuropathy is an early disease marker of neuronal intranuclear inclusion disease. We then assessed the feasibility of using motor nerve conduction velocity as a diagnostic tool of neuronal intranuclear inclusion disease and evaluated the diagnostic performance of various combinations of nerve conduction parameters using receiver operating characteristic curve analysis. The criterion of having at least two nerves with motor nerve conduction velocity ranging from 35 to 50 m/s in median/ulnar nerves and 30-40 m/s in tibial/peroneal nerves demonstrated high sensitivity (90%) and specificity (99%), with an area under the curve of 0.95, to distinguish neuronal intranuclear inclusion disease patients from healthy controls. The criterion\'s diagnostic performance was validated on an independent cohort of 56 literature reported neuronal intranuclear inclusion disease cases (area under the curve = 0.93, sensitivity = 87.5%, specificity = 99.0%), and in distinguishing neuronal intranuclear inclusion disease from genetically unresolved leukoencephalopathy cases (sensitivity = 90.0%, specificity = 80.0%). In conclusion, mildly to moderately decreased motor nerve conduction velocity in multiple nerves is a significant electrophysiological hallmark assisting the diagnosis of neuronal intranuclear inclusion disease, regardless of CNS- or PNS-predominant manifestations.

OBJECTIVE: Not all patients with chronic inflammatory demyelinating polyneuropathy (CIDP) have evidence of demyelination on nerve conduction studies (NCS). Patients with \"supportive\" evidence of CIDP on cerebrospinal fluid (CSF), magnetic resonance imaging (MRI), ultrasound (US), or nerve biopsy but not on NCS, often receive immunomodulating therapy. We evaluated the treatment response of patients with clinical and supportive features of CIDP lacking NCS evidence of demyelination.
METHODS: Retrospective chart review was conducted on 232 patients who met CIDP clinical criteria and were treated with disease-modifying therapy. Patients included did not have NCS criteria of demyelination, but did have supportive CSF, MRI, or US findings consistent with CIDP. A positive treatment response was defined as at least a one-point improvement in the modified Rankin scale (mRS), or a four-point increase in the Medical Research Council sum score (MRCSS).
RESULTS: Twenty patients met criteria: 17 of the 18 (94%) patients with CSF protein >45 mg/dL, 6 of the 14 (43%) with MRI lumbosacral root or plexus enhancement, and 4 of the 6 (67%) with enlarged proximal nerves on US. Eighteen patients received intravenous immunoglobulin, 10 corticosteroids, one plasma exchange, and six other immunomodulatory therapies. Twelve patients had a positive treatment response on the MRCSS or mRS. The presence of MRI lumbosacral root or plexus enhancement was associated with a positive treatment response.
CONCLUSIONS: A trial of immunomodulating treatment should be considered for patients with clinical features of CIDP in the absence of NCS evidence of demyelination, particularly when there is MRI lumbosacral root or plexus enhancement.

Introduction Nonalcoholic fatty liver disease (NAFLD) presents as a multisystem disorder, heightening the risk of developing type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVDs). Occupation emerges as a significant factor influencing the occurrence of NAFLD. Research indicates that individuals engaged in shift work face an elevated risk of NAFLD, alongside obesity and T2DM, attributed to disruptions in their circadian rhythm, which precipitate hepatic steatosis and inflammation. Remarkably, peripheral neuropathy has been observed in conjunction with advanced liver disorders and NAFLD in the general population. However, the correlation between NAFLD and peripheral neuropathy remains unestablished in shift workers. Objective To identify NAFLD in seemingly healthy rotating shift workers and assess any potential impact of NAFLD on nerve function in this demographic. Methods This cross-sectional study involved 73 apparently healthy nonalcoholic security guards (aged 35 to 60 years) working in rotating shifts. The study included a comprehensive assessment, beginning with a medical history, an evaluation of physical activity, and anthropometric measurements. Confirmation of NAFLD was achieved through abdominal ultrasonography (USG), followed by the analysis of biochemical parameters. Motor and sensory nerve conduction studies (NCS) were conducted on participants with normal vitamin B12 levels using the Aleron electromyograph (EMG) machine (Recorders and Medicare Systems Private Ltd, Budanpur, India). The evaluation encompassed the Median and Common Peroneal motor nerves, as well as Median and Sural sensory nerves. Recorded parameters for motor nerves included distal motor latency (DML), compound muscle action potential (CMAP) amplitude, conduction velocity (CV), and F-wave minimum latency (F-wave), while sensory nerve parameters comprised sensory onset latency (SOL), sensory nerve action potential (SNAP) amplitude, and CV. Results Among 73 healthy security guards working in rotating shifts, 76.1% were diagnosed with NAFLD through abdominal ultrasound. Following participant withdrawals and exclusions due to vitamin B12 deficiency, a comparison of NCS parameters between NAFLD (n=24) and Non-NAFLD (n=12) groups revealed no significant disparities in motor or sensory parameters, except for a slightly diminished CMAP amplitude in the peroneal nerve of NAFLD subjects (8.21±2.83mV vs ±10.22±2.30 mV, p< 0.040). However, these differences fell within normal ranges, indicating no notable impact on peripheral nerve conduction in the presence of NAFLD. Conclusion The results indicate a high prevalence of NAFLD among individuals working rotating shifts. Moreover, the investigation suggests that despite the presence of NAFLD, there is no discernible influence on motor and sensory peripheral nerve conduction, particularly in common peroneal, median, and sural nerves.

Creatine kinase (CK) has been associated with neuropathy, but the mechanisms are uncertain. We hypothesized that peripheral nerve function is impaired in subjects with persistent CK elevation (hyperCKemia) compared to age- and sex matched controls in a general population. The participants were recruited from the population based Tromsø study in Norway. Neuropathy impairment score (NIS), nerve conduction studies (NCS) and electromyography (EMG) in subjects with persistent hyperCKemia (n = 113; 51 men, 62 women) and controls (n = 128; 61 men, 67 women) were performed. The hyperCKemia group had higher NIS score than the controls (p = 0.050). NCS of the tibial nerve showed decreased compound motor action potential amplitude (p < 0.001), decreased motor conduction velocity (p < 0.001) and increased F-wave latency (p = 0.044). Also, reduced sensory amplitudes of the median, ulnar, and sural nerves were found. EMG showed significantly increased average motor unit potential amplitude in all examined muscles. CK correlated positively with glycated hemoglobin and non-fasting glucose in the hyperCKemia group, although not when controlled for covariates. The length dependent polyneuropathy demonstrated in the hyperCKemia group is unexplained, but CK leakage and involvement of glucose metabolism are speculated on.