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Aims/Introduction: Although several studies have shown the association between continuous glucose monitoring (CGM)‐derived glycemic variability (GV) and diabetic peripheral neuropathy, no studies have focused on outpatients or used NC‐stat®/DPNCheck™, a new point‐of‐care device for nerve conduction study (NCS). We investigated the association between CGM‐derived GV and NCS using DPNCheck™ in outpatients with type 2 diabetes, and further analyzed the difference in results between patients with and without well‐controlled HbA1c levels. Materials and Methods: All outpatients with type 2 diabetes using the CGM device (FreeStyle Libre Pro®) between 2017 and 2022 were investigated. Sural nerve conduction was evaluated by sensory nerve action potential (SNAP) amplitude and sensory conduction velocity (SCV) using DPNCheck™. Associations of CGM‐derived GV metrics with SNAP amplitude and SCV were investigated. Results: In total, 304 outpatients with type 2 diabetes were included. In a linear regression model, most CGM‐derived GV metrics except for the mean amplitude of glucose excursion and low blood glucose index were significantly associated with SCV, but not with SNAP amplitude. The significant associations of most CGM‐derived GV metrics with SCV remained after adjustment for possible confounding factors, but not after adjustment for glycated hemoglobin (HbA1c). Most CGM‐derived GV metrics were significantly associated with SCV after adjustment for HbA1c in patients with a HbA1c ≤ 6.9%, but not in those with a HbA1c ≥ 7.0%. Conclusions: In outpatients with type 2 diabetes, multiple CGM‐derived GV metrics were significantly associated with SCV obtained by DPNCheck™. GV may have independent impacts on peripheral nerve function, particularly in patients with well‐controlled HbA1c levels. [ABSTRACT FROM AUTHOR]

ABSTRACT Aims/Introduction Although several studies have shown the association between continuous glucose monitoring (CGM)‐derived glycemic variability (GV) and diabetic peripheral neuropathy, no studies have focused on outpatients or used NC‐stat®/DPNCheck™, a new point‐of‐care device for nerve conduction study (NCS). We investigated the association between CGM‐derived GV and NCS using DPNCheck™ in outpatients with type 2 diabetes, and further analyzed the difference in results between patients with and without well‐controlled HbA1c levels. Materials and Methods All outpatients with type 2 diabetes using the CGM device (FreeStyle Libre Pro®) between 2017 and 2022 were investigated. Sural nerve conduction was evaluated by sensory nerve action potential (SNAP) amplitude and sensory conduction velocity (SCV) using DPNCheck™. Associations of CGM‐derived GV metrics with SNAP amplitude and SCV were investigated. Results In total, 304 outpatients with type 2 diabetes were included. In a linear regression model, most CGM‐derived GV metrics except for the mean amplitude of glucose excursion and low blood glucose index were significantly associated with SCV, but not with SNAP amplitude. The significant associations of most CGM‐derived GV metrics with SCV remained after adjustment for possible confounding factors, but not after adjustment for glycated hemoglobin (HbA1c). Most CGM‐derived GV metrics were significantly associated with SCV after adjustment for HbA1c in patients with a HbA1c ≤ 6.9%, but not in those with a HbA1c ≥ 7.0%. Conclusions In outpatients with type 2 diabetes, multiple CGM‐derived GV metrics were significantly associated with SCV obtained by DPNCheck™. GV may have independent impacts on peripheral nerve function, particularly in patients with well‐controlled HbA1c levels.

Carpal Tunnel Syndrome (CTS) is a median nerve entrapment neuropathy that alters primary somatosensory cortex (S1) organization. While electro-acupuncture (EA), a form of peripheral neuromodulation, has been shown to improve clinical and neurophysiological CTS outcomes, the role of EA-evoked brain response during therapy (within and beyond S1) for improved outcomes is unknown. We investigated S1-associated whole brain fMRI connectivity during both a resting and sustained EA stimulation state in age-matched healthy controls (N = 28) and CTS patients (N = 64), at baseline and after 8 weeks of acupuncture therapy (local, distal, or sham EA). Compared to healthy controls, CTS patients at baseline showed decreased resting state functional connectivity between S1 and thalamic pulvinar nucleus. Increases in S1/pulvinar connectivity strength following verum EA therapy (combined local and distal) were correlated with improvements in median nerve velocity (r = 0.38, p = 0.035). During sustained local EA, compared to healthy controls, CTS patients demonstrated increased functional connectivity between S1 and anterior hippocampus (aHipp). Following 8 weeks of local EA therapy, S1/aHipp connectivity significantly decreased and greater decrease was associated with improvement in patients' functional status (r = 0.64, p = 0.01) and increased median nerve velocity (r = −0.62, p = 0.013). Thus, connectivity between S1 and other brain areas is also disrupted in CTS patients and may be improved following EA therapy. Furthermore, stimulus-evoked fMRI connectivity adds therapy-specific, mechanistic insight to more common resting state connectivity approaches. Specifically, local EA modulates S1 connectivity to sensory and affective processing regions, linked to patient function and median nerve health. [ABSTRACT FROM AUTHOR]

Carpal Tunnel Syndrome (CTS) is a median nerve entrapment neuropathy that alters primary somatosensory cortex (S1) organization. While electro-acupuncture (EA), a form of peripheral neuromodulation, has been shown to improve clinical and neurophysiological CTS outcomes, the role of EA-evoked brain response during therapy (within and beyond S1) for improved outcomes is unknown. We investigated S1-associated whole brain fMRI connectivity during both a resting and sustained EA stimulation state in age-matched healthy controls (N = 28) and CTS patients (N = 64), at baseline and after 8 weeks of acupuncture therapy (local, distal, or sham EA). Compared to healthy controls, CTS patients at baseline showed decreased resting state functional connectivity between S1 and thalamic pulvinar nucleus. Increases in S1/pulvinar connectivity strength following verum EA therapy (combined local and distal) were correlated with improvements in median nerve velocity (r = 0.38, p = 0.035). During sustained local EA, compared to healthy controls, CTS patients demonstrated increased functional connectivity between S1 and anterior hippocampus (aHipp). Following 8 weeks of local EA therapy, S1/aHipp connectivity significantly decreased and greater decrease was associated with improvement in patients' functional status (r = 0.64, p = 0.01) and increased median nerve velocity (r = −0.62, p = 0.013). Thus, connectivity between S1 and other brain areas is also disrupted in CTS patients and may be improved following EA therapy. Furthermore, stimulus-evoked fMRI connectivity adds therapy-specific, mechanistic insight to more common resting state connectivity approaches. Specifically, local EA modulates S1 connectivity to sensory and affective processing regions, linked to patient function and median nerve health.

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. [ABSTRACT FROM AUTHOR]

Background: Poor glycemic control and diabetic neuropathy cause the plantar foot diabetic ulcer. Glycemic control improvement has been done to heal the plantar foot diabetic ulcer. Thus, knowing the glycemic control and peripheral nerve function after plantar foot diabetic ulcer is very important. However, the study to evaluate the glycemic control and peripheral nerve function assessment after healed of plantar foot diabetic ulcer has not been conducted yet in Indonesia. Purpose: The purpose of the study was to evaluate the levels and correlation of glycemic control and peripheral nerve function after healed of plantar foot diabetic ulcer in Semarang, Indonesia. Methods: A cross-sectional study was conducted in patients with healed plantar foot diabetic ulcers selected consecutively at two hospitals in Semarang Indonesia. Data on glycemic control was measured using HbA1c levels. Peripheral nerve functions were measured using the Diabetic Neuropathy Examination (DNE) scores. Data were analyzed using the Pearson correlation test. Results: Fifty patients with recently healed plantar foot diabetic ulcer (≤ 12 months) were included in this study. About 42% of the subject had very poor glycemic control (HbA1c>10%) and 92 % had dysfunction of peripheral nerve. There was a significant correlation of glycemic control and function of peripheral nerve after healed plantar foot diabetic ulcer (r = 0.328, p = 0.006). Conclusion: Most of the patients with healed plantar foot diabetic ulcers had very poor glycemic control and peripheral nerve dysfunction. There was a positive correlation between glycemic control and peripheral nerve functions significantly in patients with healed plantar foot diabetic ulcers. This study recommends that have to make an intensive intervention to improve glycemic control and peripheral nerve function after healed of plantar diabetic foot ulcer. [ABSTRACT FROM AUTHOR]

To report the incidence of clinically detectable nerve injuries when utilizing transcranial electrical motor evoked potentials (MEPs) during shoulder arthroplasty. A retrospective review of patients undergoing shoulder arthroplasty with continuous IONM was performed. The criteria for nerve alerts was an 80% amplitude reduction in MEPs. The primary outcome measure was post-operative clinically detectable nerve deficit. An additional retrospective analysis on a subset of cases using an all-or-none (100% amplitude reduction) criterion applied to the deltoid was performed. Two hundred eighty four arthroplasty cases were included. There were no permanent post-operative nerve injuries and two transient nerve injuries (0.7%). MEP alerts occurred in 102 cases (36.2%). Nineteen (6.7%) cases did not have signals return above alert threshold at closure. These cases were significantly associated with post-operative nerve injury (p = 0.03). There were no false negatives, making sensitivity 100% and specificity was 93.9%. In the subset of cases in which an all-or-none criterion was retrospectively applied to just the deltoid, MEP alerts occurred in just 17.9% of cases; specificity improved to 98.0%. We conclude that utilization of the real-time diagnostic MEP data during shoulder arthroplasty aids surgeons in decision making regarding impending peripheral nerve injuries. [ABSTRACT FROM AUTHOR]

The objective of this study is to systematically review the relationship between lower-extremity peripheral nerve function and mobility in older adults. The National Library of Medicine (PubMed) was searched on March 23, 2015 with no limits on publication dates. One reviewer selected original research studies of older adults (=65 years) that assessed the relationship between lower-extremity peripheral nerve function and mobility-related outcomes. Participants, study design and methods of assessing peripheral nerve impairment were evaluated and results were reported and synthesized. Eight articles were identified, including 6 cross-sectional and 2 longitudinal studies. These articles investigated 6 elderly cohorts (4 from the U.S. and 2 from Italy): 3 community-dwelling (including 1 with only disabled women and 1 without mobility limitations at baseline), 1 with both community-dwelling and institutionalized residents, 1 from a range of residential locations, and 1 of patients with peripheral arterial disease. Mean ages ranged from 71-82 years. Nerve function was assessed by vibration threshold (n=2); sensory measures and clinical signs and symptoms of neuropathy (n=2); motor nerve conduction (n=1); and a combination of both sensory measures and motor nerve conduction (n=3). Each study found that worse peripheral nerve function was related to poor mobility, although relationships varied based on the nerve function measure and mobility domain assessed. Six studies found that the association between nerve function and mobility persisted despite adjustment for diabetes. Evidence suggests that peripheral nerve function impairment at various levels of severity is related to poor mobility independent of diabetes. Relationships varied depending on peripheral nerve measure, which may be particularly important when investigating specific biological mechanisms. Future research needs to identify risk factors for peripheral nerve decline beyond diabetes, especially those common in late-life and modifiable. Interventions to preserve nerve function should be investigated with regard to their effect on postponing or preventing disability in older adults. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Oxidative stress and microvascular damage have been implicated in the pathogenesis of diabetic neuropathy, with manganese superoxide dismutase 2 (SOD2) responsible for superoxide detoxification in mitochondria. We hypothesised that patients with recently diagnosed type 2 diabetes would show an altered cutaneous expression of SOD2 and endothelial cell area. Methods: In this cross-sectional study, we assessed skin biopsies using immunohistochemistry, peripheral nerve function and heart rate variability in 69 participants of the German Diabetes Study with recently diagnosed type 2 diabetes and 51 control individuals. Results: Subepidermal SOD2 area in the distal leg was increased by ~60% in the diabetic group vs the controls (0.24 ± 0.02% vs 0.15 ± 0.02%; p = 0.0005) and was correlated with an increasing duration of diabetes ( r = 0.271; p = 0.024) and with the low frequency/high frequency ratio ( β = 0.381; p = 0.002) as an indicator of sympathovagal balance. The area of the subepidermal endothelial cells (measured by CD31 staining) did not differ between the groups. Conclusions/interpretation: Cutaneous antioxidative defence is enhanced in relation to the duration of diabetes and is linked to a cardiac sympathovagal imbalance towards a sympathetic predominance in individuals with recently diagnosed type 2 diabetes without evidence of endothelial cell damage. Whether cutaneous SOD2 levels can predict the development of diabetic neuropathy remains to be determined in prospective studies. [ABSTRACT FROM AUTHOR]

Background. Poor peripheral nerve function is common in older adults and may be a risk factor for strength decline, although this has not been assessed longitudinally. Methods. We assessed whether sensorimotor peripheral nerve function predicts strength longitudinally in 1,830 participants (age = 76.3 ± 2.8, body mass index = 27.2 ± 4.6kg/m², strength = 96.3 ± 34.7 Nm, 51.0% female, 34.8% black) from the Health ABC study. Isokinetic quadriceps strength was measured semiannually over 6 years. Peroneal motor nerve conduction amplitude and velocity were recorded. Sensory nerve function was assessed with 10-g and 1.4-g mono-filaments and average vibration detection threshold at the toe. Lower-extremity neuropathy symptoms were self-reported. Results. Worse vibration detection threshold predicted 2.4% lower strength in men and worse motor amplitude and two symptoms predicted 2.5% and 8.1% lower strength, respectively, in women. Initial 10-g monofilament insensitivity predicted 14.2% lower strength and faster strength decline in women and 6.6% lower strength in men (allp < .05). Conclusion. Poor nerve function predicted lower strength and faster strength decline. Future work should examine interventions aimed at preventing declines in strength in older adults with impaired nerve function. [ABSTRACT FROM AUTHOR]

Objectives To assess the relationship between sensorimotor nerve function and incident mobility disability over 10 years. Design Prospective cohort study with longitudinal analysis. Setting Two U. S. clinical sites. Participants Population-based sample of community-dwelling older adults with no mobility disability at 2000/01 examination (N = 1,680; mean age ± SD 76.5 ± 2.9, body mass index 27.1 ± 4.6; 50.2% female, 36.6% black, 10.7% with diabetes mellitus). Measurements Motor nerve conduction amplitude (poor <1 mV) and velocity (poor <40 m/s) were measured on the deep peroneal nerve. Sensory nerve function was measured using 10- and 1.4-g monofilaments and vibration detection threshold at the toe. Lower extremity symptoms included numbness or tingling and aching or burning pain. Incident mobility disability assessed semiannually over 8.5 years (interquartile range 4.5-9.6 years) was defined as two consecutive self-reports of a lot of difficulty or inability to walk one-quarter of a mile or climb 10 steps. Results Nerve impairments were detected in 55% of participants, and 30% developed mobility disability. Worse motor amplitude ( HR = 1.29 per SD, 95% CI = 1.16-1.44), vibration detection threshold ( HR = 1.13 per SD, 95% CI = 1.04-1.23), symptoms ( HR = 1.65, 95% CI = 1.26-2.17), two motor impairments ( HR = 2.10, 95% CI = 1.43-3.09), two sensory impairments ( HR = 1.91, 95% CI = 1.37-2.68), and three or more nerve impairments ( HR = 2.33, 95% CI = 1.54-3.53) predicted incident mobility disability after adjustment. Quadriceps strength mediated relationships between certain nerve impairments and mobility disability, although most remained significant. Conclusion Poor sensorimotor nerve function independently predicted mobility disability. Future work should investigate modifiable risk factors and interventions such as strength training for preventing disability and improving function in older adults with poor nerve function. [ABSTRACT FROM AUTHOR]

Abstract: Objective: While neuropathy is common in the elderly, nerve conduction (NC) reproducibility in older adults is not well-established. We sought to evaluate intraobserver reproducibility of peroneal motor NC measures in a diverse sample of older adults. Methods: We measured peroneal motor NC amplitude and velocity in a subset of participants (mean age=82.9±2.7, n =62, 50% female, 51.6% black, 35.5% DM) in the Health, Aging, and Body Composition Study. Using coefficients of variation (CVs), intraclass correlation coefficients (ICCs), and Bland Altman Plots, we compared two sets of measurements taken by the same examiner hours apart on the same day. Results: Low CVs (2.15–4.24%) and moderate to high ICCs (0.75–0.99) were observed. No systematic variation was found across measures. Despite small numbers in some subgroups, we found no differences in reproducibility by diabetes, race or study site. Conclusion: NC measures have moderate to high intraobsever reproducibility in older adults and are not affected by diabetes, race, or gender. Significance: These data provide evidence to support use of these measures in aging research. [Copyright &y& Elsevier]

Background: Low vitamin B12 and high homocysteine (Hcy) levels are common in older adults and may be associated with worse neurological function. The aim of this study is to determine whether changes in B12 or Hcy levels are associated with longitudinal changes in peripheral nerve function and clinical neurological signs and symptoms. Methods: Participants aged 60 years and older at baseline (n = 678; 72.2 ± 6.2 years; 43.5% male) were from the InCHIANTI Study. Low B12 (<260 pmol/L) and high Hcy (≥13 μmol/L) were measured at baseline and 3-year follow-up. Neurological function was assessed by peroneal nerve conduction amplitude (compound motor action potential) and velocity, neurological examination, and peripheral neuropathy symptoms at baseline, 3-year, and 6-year follow-up. Results: At baseline, 43.8% had low B12 levels and 58.6% had high Hcy levels. Over 6 years, 12.4% declined to poor compound motor action potential (<1 mV) and 42.1% declined to poor nerve conduction velocity (<40 m/s). In mixed models analyses, sustained high Hcy was associated with worse compound motor action potential compared with sustained normal Hcy (p = .04), adjusting for demographics, diabetes, and folate level. Participants whose Hcy level became high at follow-up were more likely to become unable to detect monofilament at 6-year follow-up compared with those with sustained normal Hcy (odds ratio: 5.4; 95% CI: 1.5–19.0), adjusting for demographics, diabetes, body mass index, and peripheral arterial disease. There was no association with vitamin B12 level or with symptoms. Conclusions: High Hcy may be associated with worse sensory and motor peripheral nerve function. Because poor nerve function has been associated with lower strength and physical performance, these results have important implications for disability in older adults. [ABSTRACT FROM PUBLISHER]

We determined whether more adverse calf muscle characteristics and poorer peripheral nerve function were associated with impairments in self-perceived physical functioning and walking ability in persons with lower extremity peripheral artery disease (PAD). Participants included 462 persons with PAD; measures included the ankle—brachial index (ABI), medical history, electrophysiologic characteristics of nerves, and computed tomography of calf muscle. Self-perceived physical functioning and walking ability were assessed using the 36-Item Short Form Health Survey (SF-36) and the Walking Impairment Questionnaire (WIQ). Results were adjusted for age, sex, race, ABI, body mass index, comorbidities, and other confounders. Lower calf muscle area was associated with a poorer SF-36 physical function (PF) score (overall p-trend < 0.001, 33.76 PF score for the lowest quartile versus 59.74 for the highest, pairwise p < 0.001) and a poorer WIQ walking distance score (p-trend = 0.001, 29.71 WIQ score for the lowest quartile versus 48.43 for the highest, pairwise p < 0.001). Higher calf muscle percent fat was associated with a poorer SF-36 PF score (p-trend < 0.001, 53.76 PF score for the lowest quartile versus 40.28 for the highest, pairwise p = 0.009). Slower peroneal nerve conduction velocity was associated with a poorer WIQ speed score ( p-trend = 0.023, 30.49 WIQ score for the lowest quartile versus 40.48 for the highest, pairwise p = 0.031). In summary, adverse calf muscle characteristics and poorer peripheral nerve function are associated significantly and independently with impairments in self-perceived physical functioning and walking ability in PAD persons. [ABSTRACT FROM AUTHOR]

Abstract: The purpose of this study was to describe age-related changes in vibrotactile sensitivity in participants of the Baltimore Longitudinal Study of Aging and to identify factors that are associated with impairment in vibrotactile sensitivity independent of age. Participants (n =523, age: 26–95 years) underwent measurements of vibration perception threshold (VPT, 100Hz) under the 2nd metatarsal head, glucose tolerance, serum inflammatory markers, nerve conduction parameters, movement time and cognition. Univariate and multivariate regression analyses were performed to identify factors that predicted VPT independent of age. Structural equation modeling was used to describe relationships between these variables. VPT was progressively higher with older age. Adjusting for age and height, VPT was similar in men and women and the slope of age-related decline was similar in the two genders. Age, height, peroneal nerve conduction velocity and peroneal nerve amplitude were independent predictors of VPT. Structural equation model demonstrated a direct relationship between peripheral nerve function and VPT. Height and circulating inflammatory markers may influence age-related decline in vibrotactile sensitivity through their negative impacts on peripheral nerve function. [Copyright &y& Elsevier]

Abstracts Aims Sorbitol and myo-inositol levels and morphology of sural nerve were compared with nerve function and clinical neuropathy in men with diabetic, impaired (IGT), and normal glucose tolerance. Methods After neurography of sural nerve and determinations of sensory thresholds for vibration, warm and cold on the foot, whole nerve sural nerve biopsy was performed in 10 men with Type 1 diabetes mellitus, 10 with IGT, and 10 with normal glucose tolerance. Polyol levels were assessed by gas–liquid chromatography/mass spectrometry. Results Sural nerve amplitudes were significantly lower and sorbitol levels significantly higher in diabetic patients (median (interquartile range)) (3.7 (3.5) μV and 643 (412) pmol/mg protein, respectively) both compared with IGT (11.3 (10.6) μV; P = 0.04 and 286 (83) pmol/mg protein; P = 0.0032, respectively) and normally glucose tolerant (10.0 (11.6); P = 0.0142 and 296 (250) pmol/mg protein; P = 0.0191, respectively) subjects. There were no differences in nerve morphology between the three groups. Nerve myo-inositol levels correlated, however, positively with cluster density (rs = 0.56; P = 0.0054). In diabetic and IGT subjects, sural nerve amplitudes (2.6 (3.8) vs. 12.1 (10.6) μV; P = 0.0246) and myelinated nerve fibre density (MNFD; 4076 (1091) vs. 5219 (668) nerve fibres/mm2; P = 0.0021) were significantly lower in nine subjects with clinical neuropathy than in 10 without. Conclusions Nerve degeneration (i.e. MNFD) correlated with clinical neuropathy but not with glucose tolerance status whereas nerve myo-inositol levels positively correlated with signs of nerve regeneration (i.e. increased cluster density). [ABSTRACT FROM AUTHOR]

It has been proposed that increased polyol pathway activity resulting from hyperglycaemia induces neuropathy in diabetic patients. Recently, it has been demonstrated that erythrocyte sorbitol content is a reflection of polyol pathway activity in nerve. In the present study the relationship of erythrocyte sorbitol and glycosylated haemoglobin (HbA1) levels to peripheral nerve functions were investigated in 62 diabetic patients. Peroneal and median motor nerve conduction velocities, H-M intervals of the Hoffmann reflex, thermal discrimination thresholds and vibratory perception thresholds, either singly or in combination, were not significantly correlated with erythrocyte sorbitol or HbA1 levels. These findings show that a single measurement of erythrocyte sorbitol or HbA1 content cannot predict impairment of nerve function in diabetic subjects. [ABSTRACT FROM AUTHOR]

The objective of this study is to systematically review the relationship between lower-extremity peripheral nerve function and mobility in older adults. The National Library of Medicine (PubMed) was searched on March 23, 2015 with no limits on publication dates. One reviewer selected original research studies of older adults (≥65 years) that assessed the relationship between lower-extremity peripheral nerve function and mobility-related outcomes. Participants, study design and methods of assessing peripheral nerve impairment were evaluated and results were reported and synthesized. Eight articles were identified, including 6 cross-sectional and 2 longitudinal studies. These articles investigated 6 elderly cohorts (4 from the U.S. and 2 from Italy): 3 community-dwelling (including 1 with only disabled women and 1 without mobility limitations at baseline), 1 with both community-dwelling and institutionalized residents, 1 from a range of residential locations, and 1 of patients with peripheral arterial disease. Mean ages ranged from 71-82 years. Nerve function was assessed by vibration threshold (n=2); sensory measures and clinical signs and symptoms of neuropathy (n=2); motor nerve conduction (n=1); and a combination of both sensory measures and motor nerve conduction (n=3). Each study found that worse peripheral nerve function was related to poor mobility, although relationships varied based on the nerve function measure and mobility domain assessed. Six studies found that the association between nerve function and mobility persisted despite adjustment for diabetes. Evidence suggests that peripheral nerve function impairment at various levels of severity is related to poor mobility independent of diabetes. Relationships varied depending on peripheral nerve measure, which may be particularly important when investigating specific biological mechanisms. Future research needs to identify risk factors for peripheral nerve decline beyond diabetes, especially those common in late-life and modifiable. Interventions to preserve nerve function should be investigated with regard to their effect on postponing or preventing disability in older adults.