Sural Sensory Nerve Research Articles

Modulation of Interleukin-8 Production by Vitamin D Supplementation in Indonesian Patients with Diabetic Polyneuropathy: A Randomized Clinical Trial.

ObjectivesWe sought to assess the modulation of interleukin-8 (IL-8) production by vitamin D supplementation in Indonesian patients with diabetic polyneuropathy (DPN).MethodsWe conducted a cohort prospective, randomized, placebo-controlled, double-blind trial. This study was approved by the Local Ethical Committee and conducted from July 2018 to February 2019. We recruited 50 subjects with type 2 diabetes mellitus attending Haji Adam Malik General Hospital Medan, and divided them into two groups. The groups were treated for 10 weeks, either with placebo or vitamin D (D3) supplementation of 50 000 IU/week. They were evaluated by routine nerve conduction study (NCS) in the upper and lower limbs, and their serum vitamin 25-hydroxyvitamin D (25(OH)D) and IL-8 levels before and 10 weeks after placebo or vitamin D supplementation were measured. The role of IL-8 and vitamin D supplementation on the NCS was analyzed using linear regression.ResultsThere was a significant difference between the mean vitamin 25(OH)D (p = 0.001) and IL-8 levels (p = 0.002) before and after vitamin D supplementation. There was no significant correlation between changes in vitamin 25(OH)D and IL-8 levels (p = 0.743). There was significant role of IL-8 on amplitude of the sensory sural nerve (p = 0.047; B = -0.009) and the nerve conduction velocity (NCV) of the motor tibial nerve (p = 0.007; B = -0.027). There was a significant role of vitamin D supplementation on NCSs.ConclusionsHigher IL-8 levels were correlated with poorer amplitude of the sensory sural nerve and the NCV of motor tibial nerves. Lower vitamin 25(OH)D levels were correlated with poorer distal latencies, amplitudes, and NCVs. There was no significant correlation between vitamin 25(OH)D and IL-8 levels. Thus, no sufficient evidence that vitamin D supplementation modulates IL–8 in Indonesian patients with DPN. Vitamin D3 improved NCSs in diabetic patients.

Gluten neuropathy: electrophysiological progression and HLA associations.

Gluten neuropathy (GN) is the term used to describe peripheral neuropathy that occurs in patients with gluten sensitivity (GS) or coeliac disease (CD) in the absence of other risk factors. We aimed to describe the neurophysiological progression rate of GN across time and look into the potential role of genetic susceptibility in its development. This is a cohort study of 45 patients with GN with a mean follow-up period of 8 ± 5years. The assessments included clinical and neurophysiological data and HLA-DQ genotyping. The mean age at diagnosis was 60 ± 12years. The majority of patients had a length-dependent neuropathy (75.6%), whereas the rest were diagnosed with sensory ganglionopathy (SG). DQA1*02-positive patients were more likely to suffer with SG compared to the DQA1*02 negative patients (60% versus 13.8%, p = 0.009). There was also a trend for statistical significance regarding the DQB1*06 allele and the DQA1*01/DQB1*06 haplotype were found more frequently in patients with GN than in healthy controls (p = 0.026 and p = 0.047, respectively). A linear effect of time on the neurophysiological findings was found in radial sensory nerve action potential (1.9% mean annual decrement, p = 0.036), sural sensory nerve action potential (3.3% mean annual decrement, p = 0.013) and tibial nerve motor compound action potential (6.5% mean annual decrement, p < 0.001) amplitudes, independently from age or gender. GN is a late manifestation of GS and CD. The majority of patients have the length-dependent neuropathy with a linear deterioration over time. HLA genotyping of GS and CD patients who suffer from neuropathic symptoms is recommended as it can help identifying patients at risk for developing SG.

Calf Pain-Brazilian Jujitsu Fighter

HISTORY: 29 yo male Brazilian jujitsu fighter with a history of Henoch-Schonlein purpura and eczema presents to clinic for 6 months of right anterolateral calf pain without a clear injury. He reports constant, dull, aching pain, worse with dorsiflexion and resisted plantar flexion. He notes associated pitting edema, dry leathery skin, hypopigmentation, and hyperesthesia that began 3-4 months ago. He has stopped jujitsu due to symptoms. Tib-fib xrays and venous duplex were negative. He tried acetaminophen, ibuprofen, physical therapy, topical clobetasol, and oral prednisone with short-term improvement. PHYSICAL EXAMINATION: Skin of the anterolateral calf is indurated with hair loss, a leathery appearance, and areas of depigmentation. The distal lateral calf is warm and erythematous, with swelling posterior to the lateral malleolus. Tinel’s sign is negative at the fibular head. Pulses are normal bilaterally with ankle plantar and dorsiflexion. Ankle ROM is full. Light touch sensation is intact in L2-S2 dermatomes and strength is 5/5 in lower extremities. DIFFERENTIAL DIAGNOSIS: Complex regional pain syndrome, Cellulitis, Scleroderma, Eosinophilic fasciitis, Chronic exertional compartment syndrome, Vascular insufficiency TEST AND RESULTS: Lab work: inflammatory markers and rheumatologic labs negative except for elevated CK (356) of unknown significance. EMG/NCS: low amplitude right vs left sural sensory nerve suggesting sural neuropathy although within normal limits; no fibular neuropathy or radiculopathy. MRI right leg: nonspecific skin thickening of anterolateral shin with fascial edema and mild fibularis longus myositis. Skin biopsy: linear morphea versus eosinophilic fasciitis FINAL WORKING DIAGNOSIS: Segmental Linear Morphea (localized scleroderma) TREATMENT AND OUTCOMES: Dermatology referral led to biopsy; subsequently, treatment with PO methotrexate (MTX), high dose IV methylprednisolone for three cycles, and topical clobetasol ointment BID. UVA1 phototherapy was also started due to extensive disease and ankle and knee joint involvement. Subjective improvement in ROM, skin stiffness, and strength per patient after 2 cycles of methylprednisolone. Switched to SQ MTX for better absorption and lower cost. Patient continues to improve as he remains on the above treatment protocol.

Systemic lupus erythematosus may have an early effect on peripheral nerve function in patients without clinical or electrophysiological neuropathy: comparison with age- and gender-matched controls.

Asymptomatic electrophysiological peripheral neuropathy is described in systemic lupus erythematosus (SLE) patients. To determine if SLE could have an even earlier effect on peripheral nerve function even before the development of electrophysiological abnormalities, we compared nerve conduction studies (NCS)of SLE patients without electrophysiological or clinical peripheral neuropathy with healthy controls. Consecutive SLE patients without clinical neuropathy (or other known causes of neuropathy) underwent sensory and motor NCS of all four limbs. Results of 61 patients without electrophysiological criteria of neuropathy were compared with age- and gender-matched controls. Although still within the laboratory's range of normal values, significant differences were found in several NCS parameters between patients and controls. SLE patients had lower amplitudes for ulnar, fibular, and tibial compound muscle action potentials (CMAP) and sural sensory nerve action potentials (SNAP); slower conduction velocities for median, ulnar, and fibular motor nerves, and median, ulnar and sural sensory nerves. SLE patients also had longer minimum F-wave latencies for median, ulnar, fibular, and tibial nerves. H reflexes were more often absent in patients. Correlations were found between the number of disease relapses and motor conduction velocities of the fibular and tibial nerves. SLE may have early effect on peripheral nerve function in patients even before they develop electrophysiological or clinical neuropathy.

Relationship between the Diabetic Polyneuropathy Index and the Neurological Findings of Diabetic Polyneuropathy.

Objective To achieve an accurate quantification in diabetic polyneuropathy (DPN), we developed a new electrophysiological index that we called the DPN index. The relationship between the DPN index and the neurological findings in diabetic patients was assessed. Methods The DPN index was calculated by the mean value of percentages of four parameters (tibial compound muscle action potential amplitude / F wave minimum latency, sural sensory nerve action potential amplitude / sensory nerve conduction velocity) against the mean normal values. Twenty healthy subjects were recruited as a control group. Patients A total of 348 diabetic patients who were hospitalized in our hospital during the period from December 2016 to August 2019 were retrospectively studied. The correlations between the DPN index and five neurological findings (subjective sensory symptoms, diminished or absent Achilles tendon reflex, impaired tactile and vibration sense, low coefficient of variation of R-R interval) were evaluated. Results The DPN index in healthy subjects was 129.3±32.7%. The DPN index in diabetic patients with one or more neurological findings was significantly lower than that in diabetic patients without any neurological findings (p<0.01: 89.3±27.8% vs. 118.4±21.2%). For each of the five neurological findings, the DPN index in the group with an abnormality was significantly lower than that in the group without any abnormality (each p<0.01). Spearman's correlation coefficients indicated that a greater number of neurological findings resulted in a lower DPN index (r=-0.711, p<0.01). Conclusion Our study suggested that the DPN index is useful for evaluating the severity of DPN.

The Slipping Slipper Sign: A Poor Man's Test for Severe Diabetic Peripheral Neuropathy.

Neuropathic feet are at very high risk for infection and amputation. The slipping slipper sign (SSS) is elicited by a simple questionnaire test reported to detect the presence of severe diabetic peripheral neuropathy. This test can be administered by non-medical staff. In this study, subjects with and without the SSS were evaluated by nerve conduction studies (NCS) and ultrasound measurements of the right sural nerve diameters as well as with traditional scoring systems for peripheral and autonomic neuropathy. To demonstrate that the Slipping Slipper Sign can be used as an index of severe diabetic peripheral neuropathyMethod:This was a prospective cross sectional study in which 74 patients with diabetes (38 positive and 36 negative for SSS) underwent ultrasonography and NCS of the right sural nerve by an examiner blinded to SSS status. Findings were evaluated against demography, clinical history, anthropometry as well as traditional clinical and autonomic neuropathic scores. Patients without the SSS [median (IQR) = 10.0 years (4.0-20.3)] had a significantly shorter duration of diabetes compared with those with the SSS [median (IQR) = 15.0 years (8.5-25.0)], p = 0.028. The frequencies of retinopathy (36.8% vs 2.8%, p < 0.05) and cerebrovascular accidents (18.4% vs 13.9 %, p < 0.05) were higher among those with SSS compared with those without. Differences in nerve conduction characteristics were markedly significant. The amplitude of the sural sensory nerve action potential (SNAP) was ([median (IQR)] 0 microvolts vs 4.0 microvolts (0.0-10.8) p < 0.002) between those with and without SSS, respectively whilst none of patients with SSS had a recordable SNAP vs 78% without a SSS. Similarly, maximal thickness of the right sural nerve at the ankle 3.0 mm (2.3-3.4) vs 3.5 mm (3.0-3.9), and leg 3.4 mm (2.7-3.8) vs 3.9 mm (3.3-4.2) was reduced, p < 0.01 in patients with the SSS compared with those with a negative SSS. The SSS identifies feet with objective neurophysiological and imaging characteristics of severe neuropathy.

Subclinical peripheral neuropathy in patients with chronic obstructive pulmonary disease without hypoxemia

AIM: The aim of the study was to determine the prevalence of subclinical peripheral neuropathy (PNP) in stable chronic obstructive pulmonary disease (COPD) patients without severe hypoxemia. MATERIALS AND METHODS: Fifty-six (52 men and 4 women) patients with COPD without severe hypoxemia, 25 healthy smokers, and 24 healthy nonsmokers were included in the study. The latency, amplitude, and velocity measurements of right and left median motor nerve, tibial motor nerve, peroneal motor nerve, median sensory nerve, sural sensory nerve, right ulnar motor nerve, and right ulnar sensory nerve were performed. RESULTS: A high proportion of PNP was detected in the COPD group compared to the smoker and nonsmoker control groups (41.1%, 36.0%, and 33.3%, respectively). However, the difference between the groups was not statistically significant (P = 0.784). However, some of the electrophysiological measurements were statistically significantly worse in the COPD group (P 0.05). CONCLUSION: The present study demonstrates that the PNP may be an extrapulmonary manifestation of COPD. The physician should be aware of the possibility of PNP in COPD patients without severe hypoxemia.

Sural Radial Amplitude Ratio: A Study in Healthy Indian Subjects.

Context:The amplitude ratio of sural radial sensory nerve action potential is used as a sensitive measure for the diagnosis of an early distal axonal peripheral neuropathy. There is no age-stratified reference data available.Aim:To establish age-stratified sural radial amplitude ratio (SRAR) reference data in healthy Indian subjects.Study Setting and Design:The study was conducted in the electrodiagnostic laboratory of a tertiary city hospital and is an analytical, prospective, and field trial study.Materials and Methods:A prospective study was conducted on 146 healthy volunteers between 18 and 86 years, stratified into 6 groups, a = 18–30 years, b = 31–40 years, c = 41–50 years, d = 51–60 years, e = 61–70 years, and f = >70 years.Sural:Radial amplitude ratio was calculated.Statistical Methods:Stata 12.1 statistical program was used. Lower limit of SRAR was obtained (mean-2SD of transformed data). ANOVA defined the intergroup variability, and linear regression and Pearson's correlation assessed the statistical significance.Results:The lower limit of normal SRAR, for each age group is as follows: a: 0.30, b: 0.23, c: 0.20, d: 0.17, e: 0.17, and f: 0.08. SRAR of groups a, b, c was significantly different from groups e and f. Similarly, SRAR was significantly different between groups d and f but not between groups d and e or a, b, c, d.Conclusion:This study provides age-stratified reference data for SRAR. There is evidence to suggest that SRAR varies with age; hence, a single value of SRAR should not be used when diagnosing a peripheral neuropathy based on this criterion.

Diet quality and chronic axonal polyneuropathy: a population‐based study

ObjectiveTo investigate the association between diet quality and chronic axonal polyneuropathy.MethodsBetween June 2013 and January 2017, among 1650 participants of the Rotterdam Study (median age 69.1 years, 54.2% women), diet quality was quantified based on food frequency questionnaires as a sum score of adherence (yes/no) to 14 components of the Dutch dietary guidelines. Presence of polyneuropathy was determined based on a questionnaire, neurological examination of the legs, and nerve conduction studies. We used logistic regression to associate diet quality with the presence of chronic axonal polyneuropathy and linear regression to associate with sural sensory nerve action potential (SNAP) amplitude in participants without polyneuropathy. Results were adjusted for age, sex, time between measurements, body mass index, blood pressure, diabetes mellitus, smoking, kidney function, and education.ResultsOverall diet quality was not associated with chronic axonal polyneuropathy (odds ratio [OR] = 0.99, 95% confidence interval [CI] 0.88; 1.12, P = 0.842), nor with sural SNAP amplitude in participants without polyneuropathy (difference = 0.01, 95% CI −0.14; 0.15, P = 0.993). Although not surviving multiple testing, a nominally significant association was found between salt intake ≤6 g/day and presence of chronic axonal polyneuropathy (OR = 0.55, 95% CI 0.35; 0.86, P = 0.008).InterpretationWe did not find an association between diet quality and chronic axonal polyneuropathy.

Sural nerve sensory response in diabetic distal symmetrical polyneuropathy.

The sural sensory nerve action potential (SNAP) amplitude is a measure of the number of axons. We tested the hypothesis that sural SNAP amplitude can be used as a marker in screening, severity evaluation, and follow-up of diabetic distal symmetrical polyneuropathy (DSPN). Patients with type 2 diabetes underwent nerve conduction studies and were followed for 6 years. Composite amplitude scores (CASs) were determined to evaluate DSPN severity. Sural SNAP amplitudes were negatively correlated with CAS (r = -.790, P < .0001), and changes in sural SNAP amplitudes were negatively correlated with those of CAS after controlling for follow-up duration (r = -.531, P = .028). When a patient's baseline sural SNAP amplitude is above zero, it can be used as one measure of DSPN in screening, severity evaluation, and follow-up. However, if the patient's sural SNAP value is zero, CAS can be used as a follow-up measure.

Polyneuropathy and the sural/radial sensory nerve action potential ratio in primary Sjögren’s syndrome

ABSTRACTObjectives: Polyneuropathy is the most common neurological complication in primary Sjögren’s syndrome (pSS). A ratio of sural nerve and superficial radial nerve sensorial action potential amplitudes (SRARs) of <0.4 is an indicator for early axonal neuropathy. We evaluated the polyneuropathies and SRARs in pSS patients.Method: Fifty-two female patients who were diagnosed with pSS according to the European-American Consensus Criteria and 45 healthy controls were enrolled. Nerve conduction studies were performed to diagnose polyneuropathy. Sensory axonal polyneuropathy was diagnosed in three patients, so SRARs were compared in 49 patients and 50 healthy controls.Results: Fifty-two patients with pSS underwent nerve conduction tests. The sural sensory nerve action potential (SNAP) was <6 µV in threepatients and they were diagnosed with sensory axonal neuropathy. SRARs were evaluated in 49 female patients, with a mean age of 51.98 ± 10.79 years and 50 healthy controls with a mean age of 50.52 ± 12.55 years. The mean disease duration was 7.59 ± 6.17 years. The SRAR values were different between the patient and control groups. SRAR was <0.4 in 20.4% of the patient group and <0.4 in 6% of the control group. The SRAR value was not statistically different within the patient group based on anti-Ro and anti-La.Discussion: The potential for neurological involvement in patients with pSS who have no signs or injury should be evaluated because nervous system involvement in pSS is a negative prognostic factor. SRAR in patients with pSS can be used as a marker for the early detection of axonal neuropathy.

Early Detection of Diabetic Polyneuropathy Using Paired Stimulation Studies of the Sensory Nerves

This study seeks to use the relative refractory period, a sensitive parameter for detecting early change in peripheral polyneuropathies, as a tool for early detection of diabetic polyneuropathy. The relative refractory period of the median and sural sensory nerves was measured in 57 diabetic patients (male 31, female 26) and 23 healthy controls (male 16, female 7). The shortest interstimulus interval, where the latency of the response to the second stimulus recovers to normal, was defined as the relative refractory period. The relative refractory period of the median and sural nerves were significantly longer in diabetic patients (3.6 msec, P < 0.001, and 3.8 msec, P < 0.001, respectively) than in the control group (3.0 msec in both nerves). Relative refractory period values of both nerves were also significantly prolonged compared with the control group, even in diabetic patients without diabetic polyneuropathy based on conventional conduction studies (3.3 msec, P = 0.002, for median nerve; 3.5 msec, P < 0.001, for sural nerve) or without any clinical symptoms and signs (3.3 msec, P = 0.007, for median nerve; 3.5 msec, P = 0.001, for sural nerve). The relative refractory period was prolonged in diabetic patients even before other electrophysiologic abnormalities or clinical findings appeared. These results suggest that the relative refractory period can be a possible early indicator of diabetic polyneuropathy.

P75-F Evaluation of deterioration in sensory nerve conduction studies in Amyotrophic Lateral Sclerosis

Background Many neurophysiological and pathological studies showed sensory abnormalities in ALS patients as a part of multisystem disease. In this study, we assessed progression of sensory changes in ALS patients, using nerve conduction studies (sNCS) in two consecutive visits. Material and methods sNCSs were evaluated based on amplitudes and velocities of bilateral dorsal sural (DS), medial plantar, superficial peroneal (SP), sural and left radial sensory nerves. In addition a global Total Sensory Score (TSens) was determined using the amplitudes of these nerves. Results Although, for both visits, TSens was smaller in patients (p = 0.04 and P = 0.01, for consecutive visits) then controls, there was no significant change between two visits of the patients (P = 0.19). ALS patients had significantly smaller amplitudes and slower velocities for bilateral DS, and left radial nerves for both visits. TSens was reduced in 7 (63.3%) but increased in 4 (36.6%) ALS patients. Conclusions Although, ALS patients showed considerable changes in NCS, sensory denervation is probably slowly progressive. The patients with improved sNCS were attributed to possible changes in sensory nerve excitability following corrective measures, e.g. administration of parenteral gastrostomy or high caloric diet.

The nerve conduction study is the key tool for the assessment of a peripheral neuropathy after carbon monoxide intoxication in a young adolescent mimicking a central presentation

Background Peripheral neuropathy after carbon monoxide (CO) intoxication is rarely reported. A peripheral nerve dysfunction mimicking a central presentation has never been reported. Objectives To determine the place of nerve conduction studies (NCS) in the assessment of peripheral neuropathy following CO intoxication. Methods We reported the case of a young patient aged 21 years who was addressed to the electrophysiological department Sahloul to perform NCS one year after a severe CO intoxication. He developed during his hospitalization, a left hemiparesis (lower and upper limbs). The NCS was not performed at this time. The diagnosis was rhabdomyolysis complicated by an acute renal failure due to CO poisoning in a patient with central nervous system complication. Actually the physical examination revealed the left hemiparesis with conserved or even exaggerated reflexes. These clinical features were compatible with a central dysfunction. However, when performing NCS on the left side, sural, superficial peroneal, ulnar, and median sensory nerve action potentials were unobtainable, as well as peroneal and tibial compound muscle action potentials. Such findings evoke a diffuse peripheral neuropathy with axonal dysfunction. This association was not reported after CO intoxication. Results Although demyelinating neuropathy is the mostly common reported form of neuropathy after CO intoxication, axonopathy can also be occurred but needs more times to recover. Rhabdomyolysis and CO itself are the major factors leading to peripheral neuropathy. Conclusion A peripheral neuropathy mimicking a central presentation can occur after CO intoxication. Clinicians should be aware of the major implication of the peripheral nervous system in this context.

Non-invasive assessment of chemotherapy-induced peripheral neuropathy using neuromuscular ultrasound in breast cancer patients.

e23152 Background: Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting toxicity for breast cancer patients that leads to early treatment discontinuation and worse outcomes. Neuromuscular ultrasound (NMUS) is a non-invasive assessment of peripheral nerves that has not been studied in taxane CIPN. Methods: This cross-sectional study enrolled breast cancer patients with subjective complaints of CIPN symptoms during or after taxane chemotherapy and compared nerve cross-sectional area (CSA) by NMUS with historical values in 120 healthy adults. Findings were correlated with self-reported symptom scale (EORTC-QLQ CIPN20, range 0-72, higher more severe); nerve conduction studies; and skin biopsies for intraepidermal nerve fiber density (IENF). Results: We evaluated 20 participants (mean 55.4 ± 10.5 yrs) with NMUS at 74 nerve sites after median 3.7 months (IQR 1.0-6.1) since last taxane (paclitaxel 10, docetaxel 8, nab-paclitaxel 2). Participants reported moderate-to-severe CIPN symptoms which were predominantly sensory (19.1 ±4.9, max 32) as opposed to motor (15.6 ±5.8, max 32) or autonomic (3.3 ±1.6, max 8). Sural sensory nerve CSA was 1.2 mm2 smaller than in historical controls (4.1 vs. 5.3 mm2, 2-sample t-test p = 0.005) and decreased with more days from last taxane (Spearman’s r -0.46, p = 0.04). Tibial motor nerve was not significantly different from controls (p = 0.35). Median nerve CSA was enlarged at the distal wrist crease entrapment site (12.5 vs 10.1, p = 0.03). Older age was associated with smaller sural CSA (r = -0.72, p &lt; 0.001). When controlling for age and days from last taxane, for each 1mm2 decrease in sural CSA, distal IENF reduced by 2.1 nerve/mm2 (p = 0.04, R2 = 0.30). Conclusions: NMUS showed expected sensory predominant distal axonopathy in taxane CIPN. Evaluation of nerve CSA by non-invasive NMUS may serve as an objective point-of-care assessment to risk-stratify women with taxane CIPN prior to the development of debilitating symptoms. Clinical trial information: NCT03139435. [Table: see text]

Close relationship between cardiovagal function and sural sensory nerve action potential in type 2 diabetes

ObjectiveBoth diabetic distal symmetrical polyneuropathy (DSPN) and cardiac autonomic neuropathy (CAN) indicate the length-dependent pattern of disease. Decreased parasympathetic activity has been found in the early phase of CAN and sural sensory nerve action potential (SNAP) imply axonal loss in DSPN. MethodAll patients with type 2 diabetes underwent cardiovascular autonomic function and nerve conduction studies (NCS). We constructed modified composite autonomic scoring scale (CASS) and composite score of NCS to measure the severity of CAN and DSPN, respectively. ResultsPatients with a longer duration of diabetes had a lower heart rate response to deep breathing (HR_DB), Valsalva ratio (VR), and baroreflex sensitivity (BRS), higher CASS, a higher percentage of CAN, lower sural SNAP, higher composite score of NCS, and a higher percentage of DSPN. Multiple linear regression analysis showed that only sural SNAPs were independently associated with mean HR_DB. ConclusionSural SNAP was closely correlated with parameters of cardiovagal functions in patients with different durations of diabetes. The percentage and severity of CAN and DSPN increase with longer duration of diabetes. SignificanceThe independent association of sural sensory nerve action potential amplitude and heart rate response to deep breathing with type 2 diabetes is important because combined testing increases diagnostic sensitivity and specificity.

Effects of Aerobic Exercise on Electrophysiological Features of Diabetic Peripheral Neuropathy

Objective: To investigate electrophysiological effects of exercise on peripheral neuropathy in patients with type 2 diabetes mellitus. Methods: Thirty-five patients (21 women) with diabetic peripheral neuropathy were included with mean (SD) age of 56.9 (6.2) years. We performed electrophysiological studies, and after 8 weeks of exercise, reevaluated the participants. Results: Sural sensory nerve (P &lt; .001) and tibial compound muscle (P = .001) action potential increased, while F-wave (P = .024) and nerve conduction velocity (P = .001) decreased significantly. Conduction velocity for deep peroneal nerve showed a significant increase (P = .001). Conclusion: Aerobic exercise improves electrophysiological features and should be considered in the therapy of diabetic peripheral neuropathy.

Latent autoimmune diabetes of adulthood (LADA) is associated with small fibre neuropathy.

To assess if latent autoimmune diabetes of adulthood (LADA) is associated with small fibre neuropathy. Participants with LADA (n=31), Type 2 diabetes (n=31) and healthy control participants without diabetes (n=31) underwent a detailed assessment of neurologic deficits, quantitative sensory testing, electrophysiology, skin biopsy and corneal confocal microscopy. The groups were matched for age (healthy control without diabetes: 53.5±9.1 vs. Type 2 diabetes: 58.0±6.5 vs. LADA: 53.2±11.6 years), duration of diabetes (Type 2 diabetes: 10.0±8.3 vs. LADA: 11.0±9.1 years) and blood pressure. However, BMI (P=0.01) and triglycerides (P=0.0008) were lower and HbA1c (P=0.0005), total cholesterol (P=0.01) and HDL (P=0.002) were higher in participants with LADA compared with Type 2 diabetes. Peroneal motor nerve conduction velocity (P=0.04) and sural sensory nerve conduction velocity (P=0.008) were lower in participants with latent autoimmune diabetes in adults compared with Type 2 diabetes. Intra-epidermal nerve fibre density (P=0.008), corneal nerve fibre density (P=0.003) and corneal nerve branch density (P=0.006) were significantly lower in participants with LADA compared with Type 2 diabetes. There were no significant differences in the other neuropathy parameters. Despite comparable age and duration of diabetes, participants with LADA demonstrate more severe neuropathy and particularly small fibre neuropathy, compared with participants with Type 2 diabetes.

Total Body Adiposity, Triglycerides, and Leg Fat are Independent Risk Factors for Diabetic Peripheral Neuropathy in Chinese Patients with type 2 Diabetes Mellitus

To evaluate the risk factors associated with diabetic peripheral neuropathy (DPN) in Chinese patients with type 2 diabetes mellitus (T2DM). Between January 2014 and December 2017, 107 participants who had obesity with T2DM and 349 participants who had normal weight with T2DM, matched for age, sex, and duration of diabetes, were recruited. The clinical and biochemical parameters were measured in each patient. DPN was diagnosed based on neuropathy symptom score and neuropathy deficit score. Motor and sensory nerve conduction velocities were measured by electromyography. Body fat mass was estimated by dual-energy X-ray absorptiometry, while hepatic steatosis was evaluated by ultrasonography. The group with obesity had a significant higher prevalence of DPN (66.62%) than that (46.99%) of the group with normal weight. Compared to the patients with normal weight, the sural sensory nerve in the right lower limbs of the patients with obesity was more susceptible to damage. Hypertriglyceridemia in the patients with obesity was a significant independent risk factor for DPN (odds ratio [OR], 3.90 [95% confidence interval (CI), 1.01 to 15.02]; P = .04), while the duration of diabetes (OR, 1.33 [95% CI, 1.07 to 1.65]; P<.01) and leg subcutaneous fat mass (OR, 0.72 [95% CI, 0.57 to 0.90]; P<.01) in the patients with normal weight were independent risk factors for DPN. The presence of obesity alone in patients with T2DM could predict high DPN risk (OR, 3.09 [95% CI, 1.11 to 8.65]; P = .04). Reducing total body adiposity and triglyceride levels, as well as avoiding leg subcutaneous fat atrophy, could be new prevention strategies for DPN in Chinese patients with T2DM. ALB = albumin; ALT = alanine transaminase; AST = aspartate transaminase; AUC = area under the curve; AUCc-p/AUCglu = AUC of C-peptide/AUC of glucose; BMI = body mass index; BP = blood pressure; CI = confidence interval; Cr = creatinine; DBP = diastolic blood pressure; DPN = diabetic peripheral neuropathy; FC-P = fasting C-peptide; FPG = fasting plasma glucose; FFA = free fatty acid; γ-GGT = γ-glutamyl transferase; HbA1c = glycated hemoglobin A1c; HDL-C = high-density-lipoprotein cholesterol; ISI = insulin sensitivity index; ISSI-2 = insulin secretion-sensitivity index-2; LDL-C = low-density-lipoprotein cholesterol; MNCS = motor nerve conduction velocity; OGTT = oral glucose tolerance test; PG = plasma glucose; SAT = subcutaneous adipose tissue; SBP = systolic blood pressure; SNCS = sensory nerve conduction velocity; T2DM = type 2 diabetes mellitus; TC = total cholesterol; TG = triglyceride; UA = uric acid; VAT = visceral adipose tissue; WC = waist circumference.

The Correlation of the Grading of Chemotherapy-Induced Peripheral Neurotoxicity (CIPN) Using the Total Neuropathy Score-Reduced and Various Electrophysiological Parameters in Breast Cancer Patients

Background The accurate grading of chemotherapy-induced peripheral neuropathy (CIPN) represents an unsolved issue. This study evaluated usefulness of the reduced version of Total Neuropathy Score TNS (TNSr) and the correlation of this scale with various electrophysiological parameters. Methods Neuropathic symptoms and quality of life were assessed using the neuropathy symptom scale and the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group Neurotoxicity (FACT/GOG-NTX) scale. A detailed neurologic examination, nerve conduction study (NCS), and the current perception threshold (CPT) were also performed.The TNSr score was calculated by a single examiner. We divided the patients with small fiber neuropathy and large fiber neuropathy and compared each variable between groups. Also, we analyzed correlations of the TNSr score with various parameters (NCS data, CPT score, and neuropathy symptom scales). Results Of 30 recruited patients, 16 (53%) had large fiber neuropathy, and the other 14 (47%) had small fiber neuropathy. Patients with large fiber neuropathy had a lower sural sensory nerve action potential (SNAP) (p=0.000), lower peroneal compound muscle action potential (CMAP) (p=0.002), higher National Cancer Institute-Common Terminology Criteria for Adverse Events (NCI-CTCAE, NTC) sensory grade (p=0.029) and higher TNSr score (p=0.000). There were no differences in any domain of the FACT/G, neuropathy symptom scale, or FACT/GOG-NTX between the two groups. The TNSr score was most significantly correlated with the sural SNAP (p=0.000), NTC-sensory grade (p=0.000), neuropathy symptom scale (p=0.001), FACT/GOG-NTX score (p=0.009), and pin score (p=0.002). Conclusions The TNSr score is correlated with sensory peripheral neurotoxicity and also present the symptom severity in CIPN. Key Words: Breast neoplasms, Polyneuropathies, Neurologic manifestations