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Nerve Fiber Density (nerve + fiber_density)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Nerve Fiber Density

  • intraepidermal nerve fiber density
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    Selected Abstracts

    Determination of Epidermal Nerve Fiber density.

    ACTA NEUROLOGICA SCANDINAVICA, Issue 6 2003
    Methodological Issues
    First page of article [source]

    Near-nerve needle sensory and medial plantar nerve conduction studies in patients with small-fiber sensory neuropathy

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 9 2008
    K. Uluc
    Background and purpose:, The aim of this prospective study was to show and compare the rate of large-fiber involvement with near-nerve needle sensory (NNNS) nerve conduction study (NCS) and with medial plantar NCS recorded with surface electrodes in a group of patients who had clinically pure small-fiber sensory neuropathy (SFSN) with reduced intra-epidermal nerve fiber density in skin biopsy and with normal routine NCS. Methods and results:, The study included 19 patients with clinically pure SFSN with normal routine NCS results and 17 healthy volunteers. Routine NCS, skin biopsy, medial plantar NCS and NNNS NCS were performed. NNNS NCS data were evaluated both by using univariate analysis methods and by using a multivariate analysis method, principal components analysis (PCA). Eight patients (42%) had abnormal results for medial plantar NCS with surface electrodes. Seven patients (37%) had abnormal results for NNNS NCS with PCA, whilst only four patients with univariate analysis. We found a significant correlation between intra-epidermal nerve fiber densities, medial plantar NCS and PCA results of NNNS NCS. Conclusions:, This study showed that large-nerve fibers are also involved in some patients with pure SFSN and medial plantar NCS can accurately diagnose neuropathy without a need for NNNS NCS in patients with normal routine NCS. [source]

    Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 79

    JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003
    U Del Carro
    Peripheral neuropathy is one of the most common secondary complications of diabetes mellitus, causing severe and prolonged morbidity. However, clinical and experimental studies have reported that careful glucose control may prevent, stabilize, and/or reverse neuropathy and other chronic diabetic complications. Unfortunately, insulin therapy does not prevent the development or progression of chronic lesions in the vessels, kidneys, eyes, or nerves of the diabetic patient. There is great interest in investigating other forms of endocrine replacement therapy, such as transplantation of the pancreas or of the islets of Langerhans (IT). Diabetic polyneuropathy (DP) evolution is characterized by progressive demyelination and axonal loss and is manifested by signs and symptoms on physical examination and abnormalities in nerve conduction studies (NCS). NCS provide reliable, noninvasive, objective measures of peripheral nerve function and constitute the most important technique for the evaluation of the severity of DP in clinical trials. Several research groups have demonstrated that skin biopsy with measurement of intraepidermal nerve fiber density is another method minimally invasive and repeatable that provides direct pathologic evidence of axonal damage in diabetic neuropathy. Fifty-one consecutive IDDM patients with or without end stage renal disease were enrolled at the moment of islet (Is), kidney (KD), kidney-pancreas (KP) or kidney-islet (KI) transplantation. Patients underwent skin biopsy punch, neurologic examination and neurophysiological investigation. Particularly, 20 pts underwent KP tx, 16 KD tx, 10 islet tx and 5 KI. The patients were comparable for duration of diabetes, dialysis (when present), age, lipid profile. In half of the patients a follow-up of 2 years has been reached. After KP tx, and partially with KI, a complete normalization of glycometabolic control has been achieved, with statistically lower HbA1c in comparison with KD group (KP = 6.2; 0.1% vs. KD = 8.4; 0.5%; p < 0.01). In the KI/Is group, a long-term restoration of islet endocrine function has been achieved, with insulin independence. When this has been lost, a persistent secretion of C-peptide was shown for a long period of time. This was correlated with a global improvement quality of life and vascular structure. Preliminary results will be presented. [source]

    Intraepidermal nerve fiber density as a marker of early diabetic neuropathy

    MUSCLE AND NERVE, Issue 5 2007
    T. Umapathi MB
    Abstract The purpose of the study was to reliably identify an early stage of diabetic polyneuropathy (DPN) by measuring injury to epidermal nerve fibers. We compared intraepidermal nerve fiber density (IENFD) at the ankle and thigh of 29 diabetic subjects who had no clinical or electrophysiological evidence of small- or large-fiber neuropathy to that of 84 healthy controls. The mean ankle IENFD of diabetic subjects was 9.1 ± 5.0 mm and that of controls, 13.0 ± 4.8 mm (P < 0.001). The thigh IENFD did not differ significantly. The IENFD ratio (thigh IENFD divided by ankle IENFD) was 2.39 ± 1.30 in diabetic subjects and 1.77 ± 0.58 in controls (P < 0.001), indicating a length-dependent reduction of IENFD in diabetics. Ankle IENFD remained significantly lower and the IENFD ratio higher in diabetic subjects after adjusting for age. Two subjects had parasympathetic dysfunction, two had retinopathy, and two early nephropathy. Age, height, weight, duration of diabetes, and average HbA1c did not influence IENFD among diabetic subjects. We used receiver operating characteristic (ROC) curves to describe and compare the utility of various threshold values of ankle IENFD and IENFD ratio for the diagnosis of early DPN. The sensitivity and specificity of diagnosing DPN using ankle IENFD of less than 10 mm were 72.4% and 76.2%, respectively. Thus, asymptomatic diabetics have a measurable, length-dependent reduction of distal epidermal nerves. Analogous to microalbuminuria in diabetic nephropathy, reliable identification and quantitation of nascent diabetic neuropathy may have potential therapeutic implications. Muscle Nerve, 2007 [source]

    Treatment-induced diabetic neuropathy: A reversible painful autonomic neuropathy

    ANNALS OF NEUROLOGY, Issue 4 2010
    Christopher H. Gibbons MD
    Objective To describe the natural history, clinical, neurophysiological, and histological features, and outcomes of diabetic patients presenting with acute painful neuropathy associated with glycemic control, also referred to as insulin neuritis. Methods Sixteen subjects presenting with acute painful neuropathy had neurological and retinal examinations, laboratory studies, autonomic testing, and pain assessments over 18 months. Eight subjects had skin biopsies for evaluation of intraepidermal nerve fiber density. Results All subjects developed severe pain within 8 weeks of intensive glucose control. There was a high prevalence of autonomic cardiovascular, gastrointestinal, genitourinary, and sudomotor symptoms in all subjects. Orthostatic hypotension and parasympathetic dysfunction were seen in 69% of subjects. Retinopathy worsened in all subjects. Reduced intraepidermal nerve fiber density (IENFD) was seen in all tested subjects. After 18 months of glycemic control, there were substantial improvements in pain, autonomic symptoms, autonomic test results, and IENFD. Greater improvements were seen after 18 months in type 1 versus type 2 diabetic subjects in autonomic symptoms (cardiovascular p < 0.01; gastrointestinal p < 0.01; genitourinary p < 0.01) and autonomic function tests (p < 0.01, sympathetic and parasympathetic function tests). Interpretation Treatment-induced neuropathy is characterized by acute, severe pain, peripheral nerve degeneration, and autonomic dysfunction after intensive glycemic control. The neuropathy occurred in parallel with worsening diabetic retinopathy, suggesting a common underlying pathophysiological mechanism. Clinical features and objective measures of small myelinated and unmyelinated nerve fibers can improve in these diabetic patients despite a prolonged history of poor glucose control, with greater improvement seen in patients with type 1 diabetes. ANN NEUROL 2010;67:534,541 [source]

    Sural nerve biopsy may predict future nerve dysfunction

    ACTA NEUROLOGICA SCANDINAVICA, Issue 1 2009
    S. Thrainsdottir
    Objective,,, Sural nerve pathology in peripheral neuropathy shows correlation with clinical findings and neurophysiological tests. The aim was to investigate progression of nerve dysfunction over time in relation to a baseline nerve biopsy. Methods,,, Baseline myelinated nerve fiber density (MNFD) was assessed in sural nerve biopsies from 10 men with type 2 diabetes, 10 with impaired and 10 with normal glucose tolerance. Nerve conduction and quantitative perception thresholds were estimated at baseline and follow-up (7,10 years later). Results,,, Subjects with low MNFD (,,4700 fibers/mm2) showed decline of peroneal amplitude (P < 0.02) and conduction velocity (P < 0.04), as well as median nerve sensory amplitude (P < 0.05) and motor conduction velocity (P < 0.04) from baseline to follow-up. In linear regression analyses, diabetes influenced decline of nerve conduction. MNFD correlated negatively with body mass index (r = ,0.469; P < 0.02). Conclusion,,, Low MNFD may predict progression of neurophysiological dysfunction and links obesity to myelinated nerve fiber loss. [source]