Peroneal Motor Research Articles

The relationship of reduced peripheral nerve function and diabetes with physical performance in older white and black adults: the Health, Aging, and Body Composition (Health ABC) study.

OBJECTIVE—Poor peripheral nerve function is prevalent in diabetes and older populations, and it has great potential to contribute to poor physical performance.RESEARCH DESIGN AND METHODS—Cross-sectional analyses were done for the Health, Aging, and Body Composition (Health ABC) Study participants (n = 2,364; 48% men; 38% black; aged 73–82 years). Sensory and motor peripheral nerve function in legs/feet was assessed by 10- and 1.4-g monofilament perception, vibration detection, and peroneal motor nerve conduction amplitude and velocity. The Health ABC lower-extremity performance battery was a supplemented version of the Established Populations for the Epidemiologic Studies of the Elderly battery (chair stands, standing balance, and 6-m walk), adding increased stand duration, single foot stand, and narrow walk.RESULTS—Diabetic participants had fewer chair stands (0.34 vs. 0.36 stands/s), shorter standing balance time (0.69 vs. 0.75 ratio), slower usual walking speed (1.11 vs. 1.14 m/s), slower narrow walking speed (0.80 vs. 0.90 m/s), and lower performance battery score (6.43 vs. 6.93) (all P < 0.05). Peripheral nerve function was associated with each physical performance measure independently. After addition of peripheral nerve function in fully adjusted models, diabetes remained significantly related to a lower performance battery score and slower narrow walking speed but not to chair stands, standing balance, or usual walking speed.CONCLUSIONS—Poor peripheral nerve function accounts for a portion of worse physical performance in diabetes and may be directly associated with physical performance in older diabetic and nondiabetic adults. The impact of peripheral nerve function on incident disability should be evaluated in older adults.

Routine electrodiagnosis and a multiparameter technique in lumbosacral radiculopathies

This study compares Routine nerve conductions studies (NCS)/needle electromyography (nEMG) with a multiparameter recording method (NC-stat; NeuroMetrix Inc., Waltham, MA, USA) in patients with lumbosacral radiculopathies (LSR). Charts from 34 consecutive patients with a clinical history and/or examination consistent with an LSR were retrospectively reviewed. All underwent both Routine NCS/nEMG studies and NC-stat EDX. NC-stat testing included peroneal and posterior tibial nerve distal motor latencies and amplitudes and F-wave analysis. Twenty-eight patients had magnetic resonance imaging of the lumbosacral spine, and two had post-myelogram computerized tomography scan. In the 24 patients with abnormal routine NCS/nEMG, NC-stat EDX was abnormal in 22. Raw agreement values between specific abnormal Routine and NC-stat EDX parameters ranged from 065 to 0.76. NC-stat amplitude and F-wave data provide reasonable electrodiagnostic 'rule in, rule out' information for LSR. Routine and NC-stat EDX had comparable positive and negative likelihood ratios with radiographic findings based on blinded neuroradiological evaluation. This included good 'stand alone' values for NC-stat F-wave and compound muscle action potential (CMAP) amplitude abnormalities in patients with spinal stenosis. This report supports the value of multiparameter clinical neurophysiological evaluations in patients with LSR including CMAPs and F-waves.

Relevance of Muscle Weight as a Functional Parameter for the Regeneration of the Peroneal Nerve in Rabbits

To evaluate the relevance of muscle weight as a functional parameter of motor regeneration, the nerve-dependent muscle weights were measured and compared with the toe-spreading reflex and the muscle action potential in different designs of nerve conditioning of the peroneal nerve in New Zealand White rabbits. From 100 peroneal nerves in 50 rabbits, 60 nerves received a conditioning crush lesion and 4 weeks later a test lesion--a transection with suturing at different sites. An additional 10 peroneal nerves were solely transected and sutured, 10 peroneal nerves were sham-operated, and 20 peroneal nerves remained unoperated for control. Eleven weeks after the final lesion, when the toe-spreading reflex had returned, the peroneal muscle weight showed a non-significant relation with the toe-spreading reflex (area 0.650, P = 0.149), whereas the relation of the amplitude (area 0.964, P < 0.001) and the conduction velocity (area 0.721, P = 0.033, left side) with the toe-spreading reflex were significant. Despite the lower sensitivity and specificity of the muscle weight, the possibility to measure the weight of all three peroneal nerve-dependent muscles separately represents a more detailed method of evaluation than both the toe-spreading reflex testing and the muscle action potential recording and justifies its use as a functional parameter in the early phase of peroneal motor regeneration in the rabbit.

Nerve conduction velocities in the lower extremity in patients with Raynaud's phenomenon and clinical applications

The purpose of the study is to study the nerve conductivity of the tibial motor, peroneal motor, peroneal sensory, and sural nerves in patients with primary and secondary Raynaud's phenomenon (RP). Twenty each: primary RP, secondary RP, and normal controls. Electromyography using distal latency (DL) and nerve conduction velocity (NCV) as dependent variables. Peroneal nerve DLs were slower and NCVs were weaker for the secondary RP group compared to the primary RP group and controls. Tibial motor nerve DLs from slowest to fastest were: primary RP, secondary RP, and controls. NCV strength order was: secondary RP weakest, primary RP, and controls. Patients with secondary RP generally had the slowest DLs and the weakest NCVs, with differences most pronounced in the motor nerves. With the exception of the tibial motor nerve, patients with primary RP had similar NCVs to the control group. Neural mobilization techniques can be applied to assist with patient symptoms.

Clinical and genetic study of SPG6 mutation in a Chinese family with hereditary spastic paraplegia

Mutations in the NIPA1 gene cause autosomal dominant hereditary spastic paraplegia (ADHSP). To date, little is known about the relationship between genotype–phenotype correlation. In order to examine the gene mutation associated with the genotype–phenotype of Chinese kindred with ADHSP, linkage analysis and mutation detection were performed. For affected family members, clinical analysis, electrophysiological examination and MRI of the brain and spinal cord were also performed. Every effected patient had a c316 (G106R) mutation in the NIPA1 gene. Neurophysiological examination revealed decreased amplitude of compound muscle action potentials (CMAP) from the tibial and peroneal motor nerves in most patients. Sensory nerve action potential (SNAP) from the tibialis nerve was not elicited in most patients. Central motor conduction time (CMCT) to the abductor pollicis brevis muscle (APB), first metatarsal interosseus muscle (FMI) and anterior tibial muscle (AT) were either absent or clearly prolonged in all patients. Spinal cord MRI showed different levels of atrophy in every affected individual. These lesions present an increased spot or patch signal on transverse axis T2WI and an intense signal of continual longitudinal strip on the anteroposterior axis. Our study supports that mutations in the NIPA1 gene cause ADHSP and further demonstrates genotype–phenotype correlations in SPG6.

Zone of Traction Injury of the Common Peroneal Nerve

The history of functional motor recovery after reconstruction of traction injury to the common peroneal nerve is poor, regardless of technique and regardless of the experience of the surgeon doing the reconstruction. The hypothesis tested is that the failure of functional motor recovery after common peroneal nerve traction injury is because the zone of injury extends beyond the visible region of peroneal nerve in continuity injury and into the muscle entry zone of the motor nerve terminations. The opportunity arose to examine pathologically this suspected distal zone of injury in one patient. Histology from this patient was compared with that from a similar zone in a leg amputated for vascular indications. With a peroneal traction injury severe enough to cause disruption of the nerve, histology using Masson trichrome stain for collagen, neurofilament and S-100 stain for nerve fibers and Schwann cells demonstrated collagen deposition between the peroneal nerve and the muscle. This fibrosis was not seen in the in the same location from the amputation specimen. These findings were corroborated by electron microscopy of the myoneural junction in both specimens. It is concluded that stretch/traction injury zone extends into the myoneural junction, preventing otherwise successful neural regeneration through nerve grafts to reinnervate muscle. This suggests that with a distal zone of injury extending into the myoneural junction region, peroneal motor function may be better achieved by direct neurotization than with nerve grafting.

Correlation of vibratory quantitative sensory testing and nerve conduction studies in patients with diabetes

Monitoring the course of diabetic peripheral neuropathy (DPN) remains a challenge. Besides clinical examination, nerve conduction studies (NCS) and quantitative sensory testing (QST) are the most commonly used methods for evaluating peripheral nerve function in clinical trials and population studies. In this study the correlation between vibratory QST and NCS was determined. Patients (N = 227) with diabetes mellitus participated in this multicenter, single-visit, cross-sectional study. QST of vibration measured with the CASE IV system was compared with a composite score of peroneal motor and tibial motor NCS and with individual attributes of peroneal, tibial, and sural nerves. The correlation between QST and composite score of NCS was 0.234 (Pearson correlation coefficient, P = 0.001). The correlations between QST and individual attributes of NCS ranged from 0.189 to 0.480 (Pearson correlation coefficients, P < 0.001). The low to moderate correlation between QST and NCS suggests that these tests cannot replace each other but are complementary.

Subclinical Neuropathy Among Diabetes Control and Complications Trial Participants Without Diagnosable Neuropathy at Trial Completion

We sought to evaluate the prevalence of subclinical neuropathy in intensive and conventional treatment groups at completion of the Diabetes Control and Complications Trial (DCCT). We assessed neuropathy using nerve conduction results obtained at DCCT completion after stratifying the DCCT cohort to exclude subjects with progressively less severe degrees of diagnosable neuropathy. We began with those who had confirmed clinical neuropathy (the primary DCCT end point) and eventually excluded all subjects with any clinical or electrodiagnostic evidence of neuropathy. After excluding subjects with confirmed clinical neuropathy at DCCT completion, 8 of 10 nerve conduction measures (including all lower-extremity measures) were significantly improved in the intensive treatment group (O'Brien rank-sum test across all nerve conduction measures, P < 0.0001). Conduction velocity group differences were substantial, and the peroneal conduction velocity averaged 3.1 m/s faster in the intensive compared with the conventional treatment group (45.1 vs. 42.0 m/s, P < 0.0001). Numerous significant differences in median and peroneal motor conduction velocities favoring the intensive treatment group persisted, regardless of the exclusion criteria applied. Intensive and conventional treatment group subjects without diagnosable neuropathy at DCCT completion had significant differences in electrophysiologic measurements favoring the intensive treatment group. Differences in subsequent incident neuropathy between the original treatment groups may reflect, in part, their levels of subclinical neuropathy at DCCT completion, rather than persistent metabolic effects.

A 16-year-old girl with progressive weakness of the left leg

The patient first noted problems in 1996, almost 3 years prior to evaluation. She had fallen and injured her right knee on a brick. The onset of her left lower extremity problems was uncertain, but she noticed gradual weakness of her left foot subsequent to the injury. In January 1999, the weakness of the left foot was noted to be definite. Her left foot would slap with walking, and her mother would encourage her to “pick up her foot” when she walked. Her grandmother noted that she would often scuff her left foot. The patient experienced no pain with the weakness, and she herself was only aware of it while trying to run. The patient felt she had been unable to run properly for the last 2 to 3 years. Approximately 4 months later, electromyography (EMG) was done at Mayo Clinic at the request of the referring physician (table 1). This showed absent left peroneal motor and sensory responses and absent left sural sensory response. The left tibial motor conduction was normal. Needle examination revealed fibrillation potentials in the tibialis anterior with markedly reduced recruitment in the left peroneal innervated muscles. She was fitted with an orthosis at the local institution to prevent foot drop. View this table: Table 1 Electromyography 1999 In June 1999 at age 12, she was assessed clinically at the Mayo Clinic. She was on no medications. She had no significant past medical history but was overweight. She was born weighing 8 lbs 8 oz at normal gestation without any complications. Development was otherwise normal. She had no known exposure to any toxins and had no history of exposure to alcohol, cigarette smoking, or illicit drug use. There was no known family history of neurologic disease. The patient’s maternal grandmother had “hammer toes.” Her sister had surgically corrected femoral …

Parasacral Sciatic Nerve Block: Does the Elicited Motor Response Predict the Success Rate?

In this prospective, randomized, double-blind study, we compared the tibial and the peroneal evoked motor response with regard to efficacy of sciatic nerve block using the parasacral approach. Twenty-six ASA I-III patients scheduled for elective lower limb surgery were randomized to receive a parasacral sciatic block, using a nerve stimulator technique seeking either a tibial (n = 14) or peroneal (n = 12) motor response. After the evoked motor response was obtained, a solution of 10 mL 2% lidocaine with epinephrine and 10 mL 0.75% ropivacaine (actual final concentration of epinephrine, 1/160,000) was slowly injected through the needle. Sensory and motor blocks were assessed every 5 min for 30 min by an anesthesiologist blinded to the elicited motor response. If the block was not complete 30 min after injection of the local anesthetics, it was considered as failed, and general anesthesia was supplemented. Time to perform the block and level of minimal and maximal stimulation were not different between groups. The success rate of complete block was significantly higher in the tibial compared to the peroneal group (11 of 14 vs 2 of 12; P = 0.002). Eliciting a tibial motor response predicts a higher success rate than eliciting a peroneal motor response with parasacral sciatic nerve block.

A Thoracic Disc Herniation Presenting as an Abdominal Hernia

Thoracic disc herniations (TDHs) occur infrequently, accounting for fewer than 1% of all spinal disc prolapses.1 Although most TDHs present initially with radicular pain, others may demonstrate only myelopathic signs and/or, even less often, ipsilateral abdominal muscle weakness.2,3 A 75-yr-old male who had been successfully treated with intermittent split-table pelvic traction for a T12–L1 disc herniation returned a year later with new, abrupt-onset, severe left-flank and abdominal pain. The physical examination revealed a large abdominal-wall hernia (Fig. 1) involving both the left upper- and lower-abdominal quadrants. The straight-leg raising test was unrestricted. Sensory and motor testing and the deep tendon reflexeswere all normal.FIGURE 1: Large abdominal-wall hernia (arrow) with thoracic disc herniation.However, there was a notable reduction in the motor units of the muscular abdominal wall. No long tract signs were observed, and the bowels and bladder were controlled. Electroneuromyography demonstrated 4+ fibrillationand positive waves in the left paraspinal muscle at the T10–T12 levels, without similar findings in the adjacent abdominal muscle. However, there was a notable reduction in motor units in the abdominal musculature. The peroneal motor nerve conductions were normal. Magnetic resonance imaging revealed a large, left T12–L1 disc herniation (Fig. 2). With persistent pain and associated difficulty in walking, the patient was referred to a spinal surgeon and was restarted on split-table intermittent pelvic traction after thermal therapy.FIGURE 2: Thoracic disc herniation (arrow) at T12–L1.With continuing conservative treatment, the patient’s pain slowly remitted. TDHs account for 0.24–0.75% of all disc herniations, with an overall incidence of 1/1,000,000 patients per year.1 This relative paucity of TDHs has been attributed to the stabilizing influence of the rib cage. When thoracic radicular pain is accompanied by myelopathic signs (i.e., hyperreflexia and Babinski reflexes), they mimic the presence of a spinal cord tumor. Although suggestive, an abdominal hernia in the presence of radicular thoracic pain is not pathognomonic evidence of a TDH. Other sources of thoracic root compromise include, among others, diabetes mellitus and/or viral exanthems (i.e., poliomyelitis), as well as herpes zoster.

Challenges in Design of Multicenter Trials

Assessing clinimetric performance of diabetic sensorimotor polyneuropathy (DSPN) end points in single and multicenter trials. Assessed were placebo-treated patients with DSPN in the Viatris and Eli Lilly trials and an epidemiologic cohort. Test reproducibility in clinical trial cohorts (r(I) approximately 0.7-0.85) approached that in the epidemiologic cohort (r(I) approximately 0.85-0.95). Associations between pairs of end points explained <10% of the variability of data (sometimes 15-35%), being higher in the epidemiologic cohort and the Viatris trial than in the Lilly trial. Most end points did not show monotonic worsening over 4 years. However, sural nerve amplitude and peroneal motor conduction velocity did. A nerve conduction score (Sigma 5 NC nds [5 attributes of nerve conduction expressed as normal deviates]) did not show monotonic worsening in established DSPN. In the epidemiologic cohort followed for 9.5 years, monotonic worsening of small magnitude occurred for sural amplitude, vibration detection threshold, and especially for composite quantitative sensation. The main reason why it is difficult to demonstrate monotonic worsening of neuropathic end points appears to be a very slow worsening of DSPN, a placebo effect for symptoms and signs, and measurement noise. Demonstrating disease progression in controlled trials of DSPN is more likely when 1) patients with developing rather than established DSPN are selected, 2) type 1 diabetic patients are preferentially recruited, 3) patients are selected who cannot or will not achieve ideal glycemic control, 4) end points chosen are known to show monotonic worsening, and 5) a restricted number of centers and expert examiners (trained, certified, using standard approaches, and reference values and interactive surveillance of tests) are used.

Topiramate and physiologic measures of nerve function in polyneuropathy

To evaluate topiramate treatment on nerve function using electrophysiologic methods and a non-inferiority clinical trial design. A double-blind, multicenter, placebo-controlled trial was conducted in patients with painful diabetic polyneuropathy (n = 67). Change in peroneal motor nerve conduction velocity (NCV) was the primary outcome. NCVs of sural sensory and ulnar nerves, and amplitude and latency changes were measured secondarily. Peripheral nerve function was also evaluated in a patient subgroup reporting treatment-emergent paresthesias. Least squares mean decrease in NCV was greater for placebo (-0.2 m/s) than for topiramate treatment (-0.1 m/s) (95% CI: -1.30, 1.42). Secondary measures showed no decrease in nerve function for topiramate-treated patients. Neurophysiologic measures were similar in patients with and without paresthesias. The most common adverse events with topiramate were paresthesias, anorexia, weight decrease, and taste perversion. This nerve conduction study found no evidence that topiramate is associated with deterioration of nerve function.

Simplified Electrodiagnostic Criteria of Diabetic Polyneuropathy in Field Study (KCIS No. 14)

This study sought to determine the sensitivity of sural sensory action amplitude (SAP) and peroneal motor conduction velocity (MCV) for differentiating the status of other nerve conduction velocities and identifying important correlates of diabetic polyneuropathy. Subjects (n = 708) with type 2 diabetes from one community completed a preliminary questionnaire. Among the 298 subjects with positive questionnaire results, 272 completed nerve conduction tests. The means of 6 nerve conduction velocities of subjects with both SAP and MCV abnormalities were compared to those of normal controls. The mean conduction velocities of all motor and sensory nerves were slower (p < 0.05) in subjects with polyneuropathy than without polyneuropathy. Important known correlates of diabetic polyneuropathy can also be identified by this electrophysiological definition. The sural SAP and peroneal MCV together serve as a good diagnostic for diabetic polyneuropathy and can be used as a simplified criterion in field studies.

Effect of conduit repair on aberrant motor axon growth within the nerve graft in rats

After peripheral nerve injury, minimizing axonal misdirection has been a matter of importance to obtain good functional outcomes. In general, it becomes more challenging as the nerve defect length is longer. As previous works suggested that a conduit repair leaving a short gap could induce some target-specific reinnervation, we expected that a distally placed conduit combined with nerve graft would enhance the specificity of reinnervation, especially in dealing with a long gap. To test this, a 14-mm-long gap was created in the rat sciatic nerves and repaired with either 1) whole nerve graft (WG), 2) interfascicular nerve grafts (FG), or 3) whole nerve graft combined with distally placed silicone tube leaving a 5-mm gap (TUBG). At the end of follow up, the extent of target specific reinnervation (measurement of the compound muscle action potentials evoked by stimulation of the sciatic nerve and its tibial and common peroneal fascicles) and the accuracy of motoneuronal projection (sequential retrograde labeling of the common peroneal motor pool) were assessed. Both assessments revealed that groups FG and TUBG had a similar selectivity, which was significantly higher than in group WG. Consistent with these results, the functional recovery as assessed by walking track analysis showed no significant difference between groups FG and TUBG, whereas those were significantly superior to group WG. In contrast, histomorphometric assessment of the regenerating axons and wet muscle weight showed no significant difference among the three groups. In conclusion, conduit repair would have some effects on reducing motor axonal misdirection, and it might be more effective when used in the management of a large defect in combination with nerve graft.

Neurophysiological Changes in Neurologically Asymptomatic Hypothyroid Patients: A Prospective Cohort Study

This is a prospective cohort study on neurologically asymptomatic patients with primary hypothyroidism. It was conducted to evaluate the frequency and pattern of neurophysiological changes in this group of patients. Twenty-three subjects were included over a period of 2(1/2) years. Neurophysiological evaluation included nerve conduction studies (NCS) of median, ulnar, and peroneal motor nerves as well as median palmar and ulnar and sural sensory responses. Electromyography of deltoid, first dorsal interosseous, vastus lateralis, and tibialis anterior muscles was performed with concentric needle electrodes in which duration, amplitude, and stability of motor unit action potentials, recruitment, and interference pattern were evaluated. NCS showed that 52% of the patients had some abnormality, predominantly of the motor demyelinating pattern, as evidenced by prolonged F-wave and distal latencies with normal amplitudes in most affected nerves. Thirty percent of patients had median mononeuropathy consistent with carpal tunnel syndrome. Nondisfigurative myopathic changes in the form of myopathic motor unit action potentials without spontaneous activity were seen in 74% of the patients, most commonly in deltoid (70%). Frequencies of involvement of other muscles were 39% in the vastus lateralis muscle, 26% in tibialis anterior muscle, and 9% in the first dorsal interosseous muscle. We conclude that electromyographic/NCS changes commonly exist in treated, neurologically asymptomatic patients with hypothyroidism and are most frequently myopathic. Median neuropathy is the most common nerve abnormality. Other nerves are involved, with a higher tendency for motor nerve demyelination. We speculate that some neuromuscular changes secondary to hypothyroidism persist after treatment and that motor nerve abnormalities are less likely to be symptomatic than sensory nerve changes in these patients.

Criterion validity of the NC-stat automated nerve conduction measurement instrument

The purpose of this study is to assess the criterion validity of peroneal and posterior tibial nerve conduction measurements obtained with the NC-stat system. Sixty patients referred to the Boston VA EMG laboratory were enrolled. Each subject had a full study of the lower extremity performed using traditional EMG equipment prior to obtaining the NC-stat measurements. These included peroneal and posterior tibial distal motor latency (DML), amplitude (AMP) and F-wave latency (FLAT) measurements. Excellent criterion validity was demonstrated for the peroneal and posterior tibial FLATs and the peroneal AMP. Acceptable criterion validity was identified in the peroneal DML and the posterior tibial AMP. The validity of the posterior tibial DML could not be demonstrated. With the exception of the peroneal DML, criterion validity was maintained in a sub-group analysis of the 50% most abnormal parameter values. The comparability of NCS performed with the NC-stat and in traditional settings has been demonstrated for motor studies of the median and ulnar nerves in previous studies. This study shows that the technology used by the NC-stat for studying the peroneal and posterior tibial nerves compares favorably as well with that obtained with traditional EMG equipment used under neurologist supervision.

Reduced Peripheral Nerve Function Is Related to Lower Hip BMD and Calcaneal QUS in Older White and Black Adults: The Health, Aging, and Body Composition Study

Bone tissue is innervated, and peripheral nerve function may impact BMD. Older black and white men and women (N = 2200) in the Health, Aging, and Body Composition Study with worse sensory and motor peripheral nerve function had lower hip BMD and calcaneal BUA independent of lean mass, strength, physical ability, and diabetes. Poor peripheral nerve function may directly affect bone. Bone tissue is innervated, yet little is known about the impact of nerve function on BMD. Poor peripheral nerve function may contribute to lower BMD and higher fracture risk, particularly in those with diabetic neuropathy. The Health, Aging, and Body Composition (Health ABC) Study included annual exams in white and black men and women 70-79 years of age recruited from Pittsburgh and Memphis. Nerve function in legs/feet was assessed by 1.4- and 10-g monofilament detection, vibration threshold, and peroneal motor nerve conduction velocity (NCV) and amplitude (CMAP). Total hip BMD, heel broadband ultrasound attenuation (BUA), and total fat and lean mass were measured 1 year later (QDR 4500A, Sahara QUS; Hologic). Participants (N = 2200) were 48% men and 37% black. Poor nerve function (lower monofilament detection, higher vibration threshold, lower CMAP, lower NCV) was associated with 1.4-5.7% lower BUA and significant for all but NCV, adjusted for demographics, diabetes, body composition, and physical ability. Results were similar for adjusted hip BMD, with 1.0-2.9% lower BMD, significant for monofilament and CMAP testing. When considering the components of BMD, total hip area was 1.8-4.9% higher in those with the worst nerve function, although BMC showed little difference. Lower monofilament detection and CMAP were independently associated with lower heel BUA (p < 0.01), and monofilament detection was associated with lower hip BMD (p < 0.05) in regression additionally adjusted for lifestyle factors, bone-active medications, and diabetes-related complications. Poor peripheral nerve function may directly related to lower BMD, likely through an increase in bone area in older adults, independent of lean mass, strength, physical ability, and diabetes. Whether those with impaired nerve function are at higher risk for fracture independent of falls needs to be studied.

Exercise training can modify the natural history of diabetic peripheral neuropathy

Background Diabetes is the most important cause of peripheral neuropathy (DPN). No definitive treatment for DPN has been established, and very few data on the role of exercise training on DPN have been reported. Aim of the study We sought to examine the effects of long-term exercise training on the development of DPN in both Types 1 and 2 diabetic patients. Participants and methods Seventy-eight diabetic patients without signs and symptoms of peripheral DPN were enrolled, randomized, and subdivided in two groups: 31 diabetic participants [15 f, 16 m; 49±15.5 years old; body mass index (BMI)=27.9±4.7], who performed a prescribed and supervised 4 h/week brisk walking on a treadmill at 50% to 85% of the heart rate reserve (exercise group: EXE), and a control group of 47 diabetic participants (CON; 24 f, 23 m; 52.9±13.4 years old; BMI=30.9±8.4). Vibration perception threshold (VPT), nerve distal latency (DL), nerve conduction velocity (NCV), and nerve action potential amplitude (NAPA) in the lower limbs were measured. Results We found significant differences on Δ (delta) in NCV for both peroneal and sural motor nerve between the EXE and CON groups during the study period ( P<.001, for both). The percentage of diabetic patients that developed motor neuropathy and sensory neuropathy during the 4 years of the study was significantly higher in the CON than the EXE group (17% vs. 0.0%, P<.05, and 29.8% vs. 6.45%, P<.05, respectively). In addition, the percentage of diabetic patients who developed increased VPT (25 V) during the study was significantly higher in the CON than the EXE group (21.3% vs. 12.9%, P<.05). Change on Hallux VPT from baseline to the end of the study was significantly different between the EXE and CON groups ( P<.05); no significant change in Malleolus VPT between the two groups occurred. Conclusions This study suggests, for the first time, that long-term aerobic exercise training can prevent the onset or modify the natural history of DPN.

Peripheral Neuropathy in Genetic Mitochondrial Diseases

Peripheral neuropathy is an underrecognized but common occurrence in genetic mitochondrial disorders. To gain insight into the frequency and clinical presentation of this complication, nerve conduction studies were performed on 43 subjects with congenital lactic acidosis enrolled in a controlled clinical trial of oral dichloroacetate. Median and peroneal motor conduction studies and median and sural sensory conduction studies were performed on each patient. The mean amplitude of the peroneal motor nerve (P < 0.001) and the conduction velocities of the median (P < 0.001) and peroneal (P < 0.001) motor nerves were uniformly lower in our subjects than in healthy literature control subjects. There were no significant differences in sensory nerve conduction studies. A generalized reduction in motor nerve conduction velocity was the dominant electrophysiological abnormality in the patients in this study and was independent of age, sex, or congenital mitochondrial disorder. We postulate that cellular energy failure is the most likely common cause of peripheral neuropathy in patients with genetic mitochondrial diseases, owing to the high demand for adenosine triphosphate via aerobic carbohydrate metabolism by nerve tissue.