Peroneal Motor Nerve Research Articles

Autonomic and electrophysiological studies in patients with signs or symptoms of diabetic neuropathy

Thirty-five patients with symptoms or signs of diabetic neuropathy were tested for autonomic neuropathy by measuring heart rate and blood pressure changes during an orthostatic tilt test, a single deep breath and the Valsalva manoeuvre and these results were related to electrophysiological measurements made on the common peroneal and sural nerves. The sural sensory action potential (SAP) was more strongly correlated with these tests of autonomic function (particularly with the brake index of the orthostatic tilt test ( P < 0.001) and the fall in systolic blood pressure 1 min after tilt ( P < 0.001), than the common peroneal nerve compound motor action potential, its minimum F wave latency or nerve conduction velocities. Patients with a detectable sural SAP had significantly higher brake indices than those with absent sural SAPs. Significant correlations were also obtained with the common peroneal motor nerve conduction velocity (MNCV) and autonomic tests and patients with MNCV 〈and〉 38 m/sec showed significant differences in many autonomic tests. The sural SAP amplitude, being less susceptible to factors that influence nerve conduction velocity, may be useful in identifying patients with an autonomic neuropathy.

Nerf peronier accessoire. Etude electrophysiologique

The extensor digitorum brevis muscle is innervated by the deep peroneal nerve. In some cases it has an additional innervation by the accessory deep peroneal nerve, a branch of the superficial deep peroneal nerve. The motor nerve conduction study with detection on the extensor digitorum brevis allows to detect such an anatomical variation. It has been found in twelve cases out of 67 subjects. In two cases it was bilateral and in two other cases the extensor digitorum brevis muscle was innervated by the accessory deep peroneal nerve alone. That anatomical variation has to be known in order to avoid errors in interpretating the peroneal motor nerve conduction velocity.

Effects of glycemic control and aldose reductase inhibition on nerve conduction velocity

In two studies of patients with diabetes who did not have neurologic symptoms, nerve conduction velocity was increased either by an improvement in glucose control or by the administration of the aldose reductase inhibitor sorbinil. In a 1981 study by Graf et al, glycemic control and motor and sensory nerve conduction velocities were evaluated in 18 patients with non-insulin-dependent diabetes before and after one, three, six, and 12 months of antihyperglycemic therapy. There was an improvement in motor nerve conduction velocity (median motor, p <0.01; peroneal motor, p <0.05; and tibial motor, p <0.05), which was associated with the improvement in fasting plasma glucose levels after three months for some motor nerves (median motor: r = −0.62, p <0.01; peroneal motor: r = −0.50, p <0.05). A direct linear relationship between the change in fasting glucose and glycosylated hemoglobin levels and the change in median motor nerve conduction velocity after 12 months of anti-hyperglycemic therapy was also found. Thus, there was a tendency for those patients who had the greatest improvement in glycemic control to have the greatest improvement in motor nerve conduction velocity. The findings in the first study are consistent with the hypothesis that hyperglycemia contributes to slowed nerve conduction velocity. In a 1983 randomized, double-blind, crossover study by Judzewitsch et al, motor and sensory nerve conduction velocities were evaluated in 39 patients with insulin-dependent or non-insulin-dependent diabetes in whom glycemic control was stable. During nine weeks of treatment with 250 mg per day of sorbinil, nerve conduction velocity was faster in the three tested nerves when compared with the velocities during the placebo period (peroneal motor nerve conduction velocity: +0.70 ± 0.24 m per second, mean ± SEM, p <0.008; median motor nerve conduction velocity: +0.66 ± 0.27 m per second, p <0.005; median sensory nerve conduction velocity: +1.16 ± 0.50 m per second, p <0.035). Although the effect of an improvement in glycemic control and administration of sorbinil in increasing nerve conduction velocity in two groups of neurologically asymptomatic patients with diabetes was small, the findings are consistent with the hypothesis that polyol pathway activity contributes to slowed large-fiber nerve conduction velocity in these patients.

Peroneal motor nerve conduction velocity in diabetic children and adolescents. Relationships to metabolic control, HLA-DR antigens, retinopathy, and EEG.

To investigate incipient diabetic neuropathy, peroneal motor nerve conduction velocity (PMNCV) was measured in 61 diabetic children and adolescents whose type 1 diabetes became clinically apparent before the age of 14 years. PMNCV in diabetic patients (48.3 +/- 5.6 m/s) was significantly lower than in controls (56.5 +/- 5.5 m/s), 23 diabetics (36%) having a value more than 2 SD below the mean for normals. There was a highly significant negative correlation between PMNCV and HbA1 levels concomitant with PMNCV measurement or mean annual HbA1 concentrations preceding PMNCV. The relationship between PMNCV and the clinical score of diabetic control since the onset of the disease was also significant. Age, duration of diabetes and HLR-DR antigens were unrelated to PMNCV. EEG abnormalities and retinopathy, whose pathogenesis is different, were not necessarily associated with subclinical neuropathy. Being easy and sensitive, PMNCV determination provides the paediatric diabetologist and the patient himself with an important motivation to improve diabetic control.

Polychlorinated biphenyl poisoning: Correlation of sensory and motor nerve conduction, neurologic symptoms, and blood levels of polychlorinated biphenyls, quaterphenyls, and dibenzofurans

In 1979 in Taiwan, more than 2000 people were poisoned with rice cooking oil contaminated with polychlorinated biphenyls (PCB). One hundred ten patients were studied within one year of the exposure. The blood PCB levels were 39.3 ± 16.6 ppb. The blood levels of the PCB derivatives, polychlorinated quaterphenyls (PCQ) and polychlorinated dibenzofurans (PCDF), were 8.6 ± 4.8 and 0.076 ± 0.038 ppb, respectively. Both the sensory and motor nerve conduction velocities (NCV) of the patients were significantly lower than the control. Abnormal slowing of sensory NCV was found in 43.6% and abnormal slowing of motor NCV was seen in 21.8%. Patients who had higher PCQ blood levels had significantly slower median nerve sensory NCV than those with lower PCQ levels. Patients with higher PCB blood levels had significantly slower peroneal nerve motor NCV than those with lower PCB levels.

Presence of carpal tunnel syndrome in diabetics: effect of age, sex, diabetes duration and polyneuropathy.

Common thought is that diabetic neuropathy is a predisposing factor to entrapment syndromes. Carpal tunnel syndrome (CTS) is the most frequent entrapment neuropathy; females and old people are most frequently affected (Comi et al., 1978). Prevalence of CTS in diabetics and associated risk factors were studied in 401 patients (208 males and 193 females) with insulin-dependent and non-insulin-dependent diabetes using electrophysiological techniques. Median nerve sensory and motor conduction velocity, ulnar and peroneal nerve motor conduction velocity and sural nerve sensory conduction velocity were investigated in all patients. Diagnostic criteria for CTS were the presence of delayed median nerve sensory conduction velocity in the palm-wrist tract and of increased distal motor latency. Polyneuropathy was defined by slowing-down of conduction velocity in two or more nerves. Forty-five patients (11.2%), 36 females and 9 males, showed CTS. One-hundred-sixty-eight patients (41.8%), 74 females and 94 males, were suffering from peripheral neuropathy. The strongest risk factors for CTS, in order of importance, were: female sex, older age and presence of neuropathy. Polyneuropathy but not CTS was related to duration of diabetes.

Influence of continuous subcutaneous insulin infusion (CSII) treatment on diabetic somatic and autonomic neuropathy.

Near-normal plasma daily glucose profile was induced by Continuous Subcutaneous Insulin Infusion (CSII) treatment in order to evaluate its influence on diabetic somatic and autonomic neuropathy. Twelve insulin-dependent diabetic subjects with somatic neuropathy were studied before and after a short term CSII treatment of 10 days. Four out of these subjects, all affected by autonomic neuropathy, were followed for 1 yr with controls every four months. Metabolic equilibrium was monitored by mean daily plasma glucose (MPDG) profile and by Glycosylated Hemoglobin (GHb) evaluation. Somatic neuropathy was studied assessing conduction velocity at peroneal motor (PMCV) nerve, ulnar motor (UMCV), ulnar sensory (USCV) and sural sensory (SSCV) nerves. Autonomic neuropathy was assessed by means of a battery of five cardiovascular autonomic tests: Valsalva Manoeuvre (VR), Deep Breathing (DB), Lying-to-Standing (LS), Sustained HandGrip (SHG) and Postural Hypotension (PH). Short-term CSII treatment induced a near normalization of metabolic parameters, a significant improvement in VR (p less than 0.05) and DB (p less than 0.01) values, but no changes in NCV. The prolongation of CSII treatment in 4 subjects induced a significant (p less than 0.05) improvement in VR, DB and LS values and in PMCV and UMCV after 4 months. This improvement did not increase with the longer CSII treatment (1 yr).(ABSTRACT TRUNCATED AT 250 WORDS)

Non-linear effects of age on nerve conduction in adults

The effects of age on conduction and amplitude in median and ulnar (motor and sensory), superficial radial, sural and common peroneal (motor) nerves of adults were prospectively investigated. Four routinely recorded parameters, including conduction velocity, amplitude and duration, were considered for each sensory nerve and measurements of conduction velocity, terminal motor latency and amplitude were made for each motor nerve. The resulting 25 sets of data were analysed using both linear and quadratic regression. The three sets of terminal motor latency data showed no age dependence while in six other instances there was a linear relationship with age (three of these being motor amplitude). The remaining 16 sets of data were statistically best represented by quadratic analysis. The shapes of the paraboli were remarkably similar, reaching a maximum (conduction velocity and amplitude) or minimum (duration) value in the fourth decade and thereafter declining or rising respectively at an accelerating rate. With only one exception, quadratic curves of the same parameter were shown to be parallel. Tables of normal data which make accurate adjustments for the aging effect can be constructed from this analysis for use in routine clinical investigation.

Anticonvulsant therapy and its possible consequences on peripheral nervous system: a neurographic study.

We studied 80 epileptic patients receiving antiepileptic drugs in mono- or polytherapy. For every patient, peroneal and median nerve motor conduction velocities and median nerve sensory conduction velocity were calculated. The average conduction velocity values were remarkably slower than those of a group of 55 normal subjects. We found at least one abnormal conduction velocity value in patients treated with carbamazepine (CBZ), phenobarbital, and phenytoin. There was no specific prevalence of one of these drugs. We found a noticeable relationship between conduction velocity slowing and daily dosage for CBZ only. There was no relationship between conduction velocity slowing and drug blood levels or duration of treatment.

Effects of prior activity on the conduction in single motor units in man.

The slowing of the conduction of an impulse travelling in the relative refractory period of a prior impulse was studied in single short toe extensor motor units in man. Paired electrical stimuli were delivered to the peroneal nerve and single motor unit recordings were achieved by special electromyographic techniques. The delay of the second impulse, propagated during the relative refractory period of the prior impulse, limited the unit discharge, frequency. The shortest motor unit response interval ranged from 3 to 5 ms and was inversely related to the axonal conduction velocity. The delay of the second impulse in the proximal nerve segment was most pronounced close to the stimulus point but continued during propagation for several milliseconds. Further delay occurred distally. The slowing of the conduction of the second impulse after delivering paired electrical nerve stimuli offers a new parameter in single motor unit studies and also makes it possible to measure the axonal refractory period after electrical nerve excitation without using blocking nerve impulses.

Glycemic control and nerve conduction abnormalities in non-insulin-dependent diabetic subjects.

The influence of therapy of hyperglycemia on the progression of diabetic neuropathy is unclear. We studied variables of glycemia and motor and sensory nerve conduction velocity in a group of 18 non-insulin-dependent diabetic subjects before and after institution of diabetes therapy. Diabetes therapy significantly reduced variables of glycemia after 1, 3, 6, and 12 months. Conduction velocity of the median motor nerve was improved from baseline at each time tested during treatment. In addition, peroneal and tibial motor nerve conduction velocities improved in patients whose levels of hyperglycemia were lowered. Moreover, extent of improvement of conduction velocity of some motor nerves was related to the degree of reduction of hyperglycemia. Sensory nerve conduction velocity was not altered by diabetes therapy. These findings support the hypothesis of a metabolic component to diabetic neuropathy and suggest that optimal glycemic control may be beneficial to patients with this disorder.

Diabetic neuropathy and plasma glucose control

Diabetic neuropathy is defined, and theories of its pathogenesis are reviewed. Recent studies designed to investigate the influence of plasma glucose on nerve function in noninsulin-dependent diabetic patients are summarized. Motor nerve conduction velocities in the median and peroneal nerves were measured using a double-stimulus technique, and sensory conduction velocity was measured by conventional methods before and after therapy with oral agents or insulin. The degree of hyperglycemia was assessed by measurement of fasting plasma glucose and glycosylated hemoglobin concentrations. The degree of slowing in motor nerve conduction velocity in untreated patients was found to correlate with the fasting plasma glucose and glycosylated hemoglobin concentrations, but sensory nerve function, although abnormal, did not show such correlation. Reduction of hyperglycemia was associated with improvement in motor nerve conduction velocity in the peroneal and median motor nerves of these patients, but sensory nerve conduction velocity showed no such improvement. Improvement in median motor nerve conduction velocity was directly related to the degree of reduction in fasting plasma glucose concentration. These findings suggest that metabolic factors related to hyperglycemia are important in the impaired motor nerve function seen in noninsulin-dependent patients with maturity-onset diabetes.

Dietary myo-inositol intake and peripheral nerve function in diabetic neuropathy

The effect of variations in dietary myo-inositol intake upon plasma myo-inositol concentrations, urinary myo-inositol excretion, motor nerve conduction velocities in the median and peroneal nerves, and sensory nerve conduction velocities in the median and sural nerves was studied in six nondiabetic subjects and in twenty patients with symptomatic distal symmetrical diabetic polyneuropathy. Diets were developed which provided either a low, a normal, or a high intake of myo-inositol. In control subjects, the low- myo-inositol diet was found to decrease, while the high- myo-inositol diet increased both the preprandial plasma myo-inositol concentrations and the daily urinary excretion of myo-inositol. These diets had little effect upon measured nerve function in the control subjects, although the high- myo-inositol diet appeared to slightly reduce the median sensory nerve conduction velocity in this group. In the neuropathic diabetics, the low- and high- myo-inositol diets were found to have similar effects upon the plasma myo-inositol concentrations and urinary myo-inositol excretion, but did not affect the plasma glucose concentrations. When analyzed by groups, no statistically significant changes were observed in any of the measured nerve conduction velocities in the diabetic patients. However, when the change in nerve conduction velocity was analyzed, it was found that the ingestion of the high- myo-inositol diet resulted in a statistically significant increase in the median sensory (+1.92 m/sec, p < 0.001) and the sural sensory nerve conduction velocity (+6.67 m/sec, p < 0.001). In contrast, ingestion of the low- myo-inositol diet produced a statistically significant decrease in the median motor (−2.35 m/sec, p < 0.001) and the peroneal motor nerve conduction velocity (−1.18 m/sec, p < 0.001). Thus, ingestion of a diet enriched in myo-inositol may have a salutory effect upon peripheral nerve function in the patient with symptomatic diabetic neuropathy and appears to be without significant side effects in this patient group.

Peripheral Motor Nerve Conduction Velocities in Children Undergoing Chronic Hemodialysis

Peroneal motor nerve conduction velocities (MNCVs) were performed on 58 children aged 20 months to 12 years undergoing chronic hemodialysis. No patient had any clinical manifestations of uremic polyneuropathy. The mean MNCV in 21 children at the onset of dialysis was 42.0 m/sec; significantly slower than the control group of 51.4 +/- 5.3 m/sec (p less than 0.001). 16 studied performed between the 1st and 6th month had a mean MNCV of 43.2 +/- 5.7 m/sec, also slower than the normal controls (p less than 0.001). We conclude that peroneal MNCVs are reduced in most children at the initiation of chronic hemodialysis and do not change significantly during the next 6--12 months and that the routine practice of obtaining such studied is of no value in the clinical management of children undergoing chronic hemodialysis.

Peripheral nerve function in long‐term therapy with diphenylhydantoin

Forty-five patients treated with diphenylhydantoin (DPH) for more than 10 years were examined for clinical and electrophysiologic evidence of a peripheral neuropathy. Plasma anticonvulsant drug levels were determined concurrently. The mean peroneal nerve (motor) and sural nerve (sensory) conduction velocities in the lower extremities showed a small but significant reduction compared with the velocities in a cointrol group and in normal subjects. Twenty-six percent of the patients showed neurogenic changes on needle elec-tromyography. Other electrodiagnostic abnormalities occurred more frequently and were inore marked in patients having either plasma DPH levels of more than 20 mcg per milliliter, an overall intake of DPH of more than 3 kg, or clinical evidence of a peripheral neuropathy. All patients had normal serum B12 and folate levels.

Spinal conditioning

A classical conditioning paradigm was performed on acute paralyzed cats which had undergone spinal section at T-12. Electrical stimulation to the superficial peroneal nerve served as the CS and to the ankle skin as the UCS. Responses from the deep peroneal motor nerve indicated in two separate studies that CS-UCS pairing produced response amplitude increases not seen in unpaired or CS-only controls. A third study indicated that long-lasting sensitization due to the UCS could not account for the results.

Reappraisal of alcoholic myopathy. Clinical and biopsy study on chronic alcoholics without muscle weakness or wasting.

To determine if alcoholic neuropathy which causes denervation of the distal muscles of chronic alcoholics also produces a subclinical myopathy of their proximal muscles, we studied 11 chronic alcoholics who had no muscular weakness or wasting. Six patients demonstrated distal hyporeflexic (ankle jerks) sensory neuropathy on clinical examination. Four patients, one of whom was asymptomatic, had slow peroneal motor nerve conduction velocities. Patterns of neuropathy were present in the electromyograms of the proximal muscles of two patients. Muscle biopsy studies with enzyme histochemistry indicated denervation atrophy and myopathic changes in the contralateral quadriceps muscles of eight patients. As denervation atrophy was present, we concluded that these myopathic changes represented the effects of denervation of these muscles. We conclude, therefore, that the proximal subclinical alcoholic myopathy, previously described as primary by ourselves and others, is the result of denervation due to the well-known alcoholic neuropathy.