No abstract

This study provides normative values for HRU, and it suggests that further research with age- and gender-specific distributions must be a key priority in the development of HRU for use as a diagnostic test for peripheral nerve diseases.

OBJECTIVEThe prevailing hypothesis that early subclinical small-fiber injury precedes largefiber damage in diabetic sensorimotor polyneuropathy (DSP) is based on lower intraepithelial nerve fiber density in type 2 prediabetic patients despite normal nerve conduction studies (NCSs). We aimed to confirm the same hypothesis in type 1 diabetic patients by examining whether: 1) subjects without DSP include a spectrum with both normal and abnormal small-fiber measures and 2) subjects with DSP have concurrent evidence of abnormal small-fiber measures. RESEARCH DESIGN AND METHODSA healthy control population (n = 53) was used to generate threshold values for four small-fiber tests: cooling detection thresholds (CDTs), laser Doppler imaging of heat-evoked flare (LDI flare ), heart rate variability (HRV), and corneal confocal microscopy. Based on NCS results, type 1 diabetic patients (n = 131) were dichotomized according to the presence or absence of DSP. RESULTSThreshold values derived from healthy control subjects were 26.58C, 1.4 cm 2 , 13%, and 12.9 mm/mm 2 for CDT, LDI flare , HRV, and corneal nerve fiber length, respectively. Among type 1 diabetic patients, 57 of 131 had evidence of DSP, and 74 of 133 did not. Using abnormality of any small-fiber test to define small-fiber dysfunction, 55 of 57 (96.5%) DSP patients and 39 of 74 (52.7%) control subjects without DSP had concurrent small-fiber damage. The severity of small-fiber abnormalities worsened with an increasing number of NCS abnormalities (ANOVA, P < 0.01). CONCLUSIONSOur findings in type 1 diabetes support the prevailing hypothesis that small-fiber dysfunction occurs early in DSP. However, further research is required to determine which combination of small-fiber tests is most suitable as a surrogate marker in clinical trials.Diabetic sensorimotor polyneuropathy (DSP) is a common complication of diabetes, affecting 28-55% of patients (1). A prospective Finnish study found evidence of probable or definite neuropathy in 8.3% of diabetic patients at the time of diagnosis, 16.7% after 5 years, and 41.9% after 10 years (2). Diabetes-related peripheral neuropathy results in serious morbidity, including chronic neuropathic pain, leg

In our patient population, the EFNS and Neuropathy Association criteria stand out due to high sensitivity and specificity.

No abstract

Peripheral nerves are enlarged diffusely in diabetic patients, including sites not susceptible to bony compression. The number of enlarged CSA values can help predict the presence of DSP. Muscle Nerve, 2016 Muscle Nerve 55: 171-178, 2017.

No abstract

OBJECTIVEMild demyelination may contribute more to the pathophysiology of nerve fiber injury in diabetic sensorimotor polyneuropathy (DSP) than previously thought. We investigated the clinical and electrodiagnostic classifications of nerve injury in diabetic patients to detect evidence of conduction slowing in DSP.RESEARCH DESIGN AND METHODSType 1 diabetic subjects (n = 62) and type 2 diabetic subjects (n = 111) with a broad spectrum of DSP underwent clinical examination and nerve conduction studies (NCS). Patients were classified as having axonal (group A), conduction slowing (group D), or combined (group C) DSP based on electrodiagnostic criteria. Patients with chronic immune-mediated neuropathies were not included. The groups were compared using ANOVA, contingency tables, and Kruskal-Wallis analyses.RESULTSOf the 173 type 1 and type 2 diabetic subjects with a mean age of 59.1 ± 13.6 years and hemoglobin A1c (HbA1c) of 8.0 ± 1.8% (64 ± 19.7 mmol/mol), 46% were in group A, 32% were in group D, and 22% were in group C. The severity of DSP increased across groups A, D, and C, respectively, based on clinical and NCS parameters. The mean HbA1c for group D subjects (8.9 ± 2.3% [74 ± 25.1 mmol/mol]) was higher than for group A and group C subjects (7.7 ± 1.4% [61 ± 15.3 mmol/mol] and 7.5 ± 1.3% [58 ± 14.2 mmol/mol]; P = 0.003), and this difference was observed in those with type 1 diabetes.CONCLUSIONSThe presence of conduction slowing in patients with suboptimally controlled type 1 diabetes indicates the possibility that this stage of DSP may be amenable to intervention via improved glycemic control.