Sural Nerve Action Potential Research Articles

Compound Nerve Action Potential of Common Peroneal Nerve and Sural Nerve Action Potential in Common Peroneal Neuropathy

To enhance the accuracy for determining the precise localization, the findings of the compound nerve action potentials (CNAPs) of the common peroneal nerve (CPN) were investigated in patients with common peroneal mononeuropathy (CPM) in the knee, and the sural sensory nerve action potentials (SNAPs) were also analyzed. Twenty-five patients with CPM in the knee were retrospectively reviewed. The findings of the CNAPs of the CPN recorded at the fibular neck and the sural SNAPs were analyzed. The lesion was localized at the fibular head (abnormal CNAPs) and at or distal to the fibular head (normal CNAPs). Seven patients were diagnosed as having a lesion at or distal to the fibular neck, and 18 cases were diagnosed as having a fibular head lesion. The sural SNAPs were normal in all the cases of lesion at or distal to the fibular neck. Among 18 cases of fibular head lesion, the sural SNAPs were normal in 7 patients: two cases of conduction block and 5 cases of mild axon loss. Eleven patients showed abnormal sural SNAPs. Of those, 9 cases were severe axon loss lesions and 2 patients were diagnosed as having severe axon loss with conduction block. The recording of the CNAPs may enhance precise localization of CPM in the knee. Moreover, the sural SNAPs could be affected by severe axonal lesion at the fibular head.

Diagnostic criteria for demyelinating polyneuropathy associated with monoclonal gammopathy

In order to define diagnostic criteria for the demyelinating polyneuropathy associated with monoclonal gammopathy of undetermined significance (MGUS), we compared 30 patients with idiopathic chronic inflammatory demyelinating polyneuropathy (CIDP) without a monoclonal gammopathy, with 29 patients with polyneuropathy associated with MGUS. All 59 patients fulfilled research criteria for CIDP. In the patients with MGUS, sensory symptoms and signs predominated, there was usually no cranial nerve involvement, and the neuropathy was symmetrical with a slowly progressive course. On electrophysiological examination, an abnormal median nerve sensory action potential in combination with a normal sural nerve action potential (AMNS) was not found. In idiopathic CIDP patients, a preceding infection was frequent, motor features predominated, there was often cranial nerve involvement, the neuropathy could be asymmetrical, and AMNS was frequently found. Diagnostic criteria for demyelinating polyneuropathy associated with MGUS are presented. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 73–79, 2000

Quantitative sensory and autonomic testing in male diabetic patients with erectile dysfunction.

To correlate abnormalities of nerve fibres in the lower limbs with erectile dysfunction in male diabetic patients, using a range of quantitative sensory and autonomic function tests. The study included 68 male diabetic patients with symptomatic erectile dysfunction and 11 matched diabetics without erectile dysfunction; none had clinical evidence of peripheral vascular disease or psychological disorder. Patients were evaluated with a symptom questionnaire based on the Michigan Neuropathy Screening Instrument questionnaire and examined clinically. Sural and peroneal nerve-conduction studies, and quantitative sensory and autonomic tests (vibration, thermal, light-touch thresholds, sensory and autonomic cutaneous axon-reflexes) were used to detect nerve abnormalities in the lower limbs, which were correlated with erectile dysfunction. Symptoms of neuropathy were more common in the group with male erectile dysfunction (MED), but statistically significant only for neuropathic pain (53% MED, 18% nonMED, P<0.05, chi-square test) and gastroparesis (44% MED, 0% nonMED, P<0.05). Tests of unmyelinated afferents (warming perception and capsaicin-induced sensory axon-reflex vasodilatation) were most often abnormal, sometimes with no other abnormalities on tests or neurological examination. However, abnormality of warm perception was not significantly different between groups (81% MED, 70% nonMED), suggesting that it is a poorer discriminant than abnormal sensory axon-reflex vasodilatation (89% MED, 22% nonMED, P<0.001). The only other significant test difference was decreased sural nerve action potential (70% MED, 22% non-MED, P<0.01). There appeared to be preferential involvement of unmyelinated sensory fibres that mediate axon-reflex vasodilatation in the limbs of diabetic patients with erectile dysfunction. This test appears to be a helpful indicator of neurological involvement in erectile dysfunction, and may be used to monitor the effect of new treatments.

Subclinical neuropathy in type I diabetic children

Objectives: Small and large, somatic and autonomic nerve fibre functions were neurophysiologically evaluated in 33 asymptomatic neurologically free type 1 diabetic children and 69 age-matched healthy controls. Methods: The evaluation of large and small somatic nerve fibre function was performed by conventional nerve conduction studies, thermal specific and thermal pain sensitivity tests, as well as autonomic nerve fibre functions by sympathetic skin response and R–R interval variation assessment. Results: A significant difference was established between the healthy and the diabetic group. Neurophysiologically determined subclinical neuropathy was found in 87% of type 1 diabetic children. The majority of abnormal recordings were found on the lower limbs. The dysfunction of the somatic motor large nerve fibre type in the lower limbs was altered in 57% of patients, somatic sensory large in 39%, somatic sensory small in 45%, and sympathetic in 45%. The leading abnormal measure was a delayed sympathetic skin response on the foot (42% of diabetic children) followed by a reduced amplitude of sural nerve action potential (36%). The whole spectrum of recordings showed scattered involvement of nerve functions. There was no selective susceptibility of nerve fibre types exposed to a noxious factor. Conclusion: A complex neurophysiological assessment, including standard nerve conduction studies as well as psychophysical examination and autonomic nerve function tests, evaluating the function of small and large nerve fibres, is recommended for evaluating the subclinical neuropathy in asymptomatic type I diabetic children.

Ataxic neuropathy in the elderly--clinicopathological study of six cases

The combination of ataxia with peripheral neuropathy (ataxic neuropathy) is rare. Six elderly patients with peripheral neuropathy who developed ataxia were studied. Of the peripheral neuropathies, ataxic neuropathy was significantly more frequent in patients aged more than 65 years compared with younger patients. Ataxic neuropathy was associated with carcinoma (2 cases), Sjögren's syndrome (1 case), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP, 1 case) and chronic idiopathic ataxic neuropathy (2 cases). The two cases of carcinomatous neuropathy initially showed ataxia, which preceded detection of the carcinomatous lesions in the lung by approximately 1 year. The study cases had many clinical features in common. In the nerve conduction study, sural nerve action potential could not be measured in five of the cases; sural nerve biopsy revealed a decreased density of myelinated fibers in all cases. In particular, the large myelinated fibers were markedly decreased. These findings were common, regardless of the underlying disease, except in the case of CIDP in which there was only a slight decrease in the number of large myelinated fibers. Differential diagnosis based on the clinicopathological features was difficult. Therefore, in cases of ataxic neuropathy, systemic evaluation is necessary to rule out the possibility of carcinoma or various systemic diseases, especially in elderly patients.

Clinical and electrodiagnostic features of X‐linked recessive bulbospinal neuronopathy

We describe four men from two kinships affected with X-linked recessive bulbospinal neuronopathy, and one sporadic case. All developed postural tremor, weakness, and fasciculations, with onset from age 25 to 39 years. Weakness began in the pelvic girdle or hands, with dysphagia or dysarthria occurring years later in two. Sensory symptoms were present in only one, who also had diabetes mellitus. In contrast, sural nerve action potentials were small or absent in all. Needle EMG showed widespread chronic partial denervation with reinnervation. The characteristic twitching of the chin produced by pursing of the lips consisted of repetitive or grouped motor unit discharges, rather than fasciculations. Broader awareness of the distinctive features of bulbospinal neuronopathy will probably increase the frequency of its recognition. Diagnosis is important for purposes of providing a prognosis for affected men and genetic counseling for affected families.

Symptomatic polyneuropathy in human immunodeficiency virus antibody seropositive men with and without immune deficiency: a comparative electrophysiological study.

Symptomatic polyneuropathy in human immunodeficiency virus (HIV) infection was studied in ten men with acquired immunodeficiency syndrome (AIDS) and in ten men without the immune deficiency. In both groups of patients electrophysiological signs of polyneuropathy of the axonal type were present in the sural, median and peroneal nerves. The AIDS patients had a greater reduction of the mean (SD) sural nerve action potential, 3.1 (2.7) microV, than in patients without AIDS, 10.2 (6.1) microV (p less than 0.01) and greater slowing of peroneal nerve conduction velocity, 42.6 (1.4) m/s in AIDS patients versus 52.6 (3.3) m/s in patients without AIDS (p less than 0.0001). These findings indicate that in most HIV infected patients the severity but not the type of neuropathy depends on whether an immune deficient state has developed. Seven patients with symptomatic polyneuropathy were treated with azidothymidine (AZT) for an average of 10 months and compared with a group of five untreated patients with similar symptoms. No effect of AZT treatment on sural or median nerve amplitude or conduction velocity or on the vibratory or temperature thresholds was observed.

Peripheral Neuropathy Associated With Acquired Immunodeficiency Syndrome

We prospectively studied 40 hospitalized patients who had well-established diagnoses of acquired immunodeficiency syndrome. Patients with confounding risk factors for neuropathy were excluded; none of the study patients had known vitamin deficiency, alcoholism, or any metabolic, drug, or toxic factor. Clinical and electrophysiologic evidence of a distal symmetric polyneuropathy was found in 35% (13/37) of the patients. Symptoms and signs of neuropathy were usually mild, and painful dysesthesias were uncommon. Amplitude reduction of sural nerve action potentials distinguished all patients with from those without clinical neuropathy. Results of other electrophysiologic studies of sural, peroneal, and median nerves were typically normal. These results provide evidence of distal axonal degeneration. Neuropathy occurred only in patients with systemic illness longer than five months' duration. When compared with patients without neuropathy, these patients had more severe weight loss and a higher incidence of clinical dementia. Follow-up evaluation showed no evidence of clinical progression over a six-month period. The pathogenesis of this common distal axonal polyneuropathy is unknown and warrants further investigation.

Modulation of the somatosensory evoked potentials by the input information originating from the gastrocnemius and sural nerves in the dog.

Input-output characteristics of the somatosensory system were studied in the dog. Somatosensory evoked potentials were recorded from the scalp at stimulations of the sural and gastrocnemius nerves. There was a sigmoid relationship between the stimulus strength and the amplitude of the sural nerve action potential, which was best described by a logistic equation. The early waves (P1, N1) increased especially at low threshold stimulations of the sural nerve; then they remained either unchanged or decreased at high threshold stimulations within the Group II and III ranges. The late waves (P2, N2) especially increased at high threshold Group II stimulations of the sural nerve, and increased further at strong stimuli. Similar changes were observed at stimulations of the gastrocnemius nerves. The attenuation of the early waves was explained by "gating" mechanisms acting from the sensorimotor cortex onto the sensory relay nuclei. The increase of the late waves at especially high threshold Group II and III stimulations was accounted for by the multisynaptic diffuse projection from the reticular formation and/or the nonspecific thalamic nuclei to the somatosensory cortex. In a three weeks old pup, stimulation of the gastrocnemius nerves evoked somatosensory responses with similar morphology observed in adult dogs, but the latencies of the evoked potential components were relatively long, presumably as a result of the uncompleted myelination in the somatosensory afferent system.

Electrophysiologic deficits in peripheral nerve as a discriminator of early hexacarbon neurotoxicity.

To determine the extent of neurotoxicity of parenterally administered hexacarbons, male Sprague-Dawley rats were given either n-hexane or 2,5-hexanedione for 35 consecutive days. Electrophysiologic measurements showed a lengthening of the sciatic and sural nerve action potentials (slower conduction velocities) and increased refractory periods. These effects correlated with a shift in the nerve membrane sensitivity to potassium-induced depolarization. A similar effect can be induced by ouabain, an Na+, K+-ATPase inhibitor. These effects were seen with both n-hexane and 2,5-hexane-dione. Although the treated animals gained weight more slowly than controls, they showed no loss of motor function when tested behaviorally, and there were no signs of histopathology in the peripheral nerves. These results show that hexacarbons produce a neurotoxicity that can be demonstrated by changes in nerve excitability, prior to overt behavioral neurotoxicity. Furthermore, these electrophysiologic changes may be related to a hexacarbon-induced disruption of nerve-membrane ATPase activity.

Effect of continuous vibration on sural nerve action potentials.

The effects of continuous vibration on sural nerve action potentials were investigated in 15 subjects. The results show that continuous vibration applied to the sural nerve innervated skin area produces an amplitude reduction of the sural nerve action potentials on both painless and painful stimulation conditions. This amplitude decrease is attributed to an impulse blockage of the large diameter afferent nerve fibers.

Juvenile-onset metachromatic leukodystrophy: biochemical and electrophysiologic studies.

A 15-year-old girl with juvenile-onset metachromatic leukodystrophy (MLD) had markedly decreased leukocyte arylsulfatase A activity and low levels of leukocyte beta galactosidase and serum acid phosphatase. There was marked slowing of nerve condition velocity, and metachromasia was seen in biopsied sural nerve. Leukocyte arylsulfatase A activity was decreased in all members of the girl's family, and sural nerve action potentials were abnormal in two asymptomatic siblings. Electrophysiologic studies combined with biochemical studies may aid in the identification of presymptomatic metachromatic leukodystrophy homozygotes or asymptomatic heterozygotes.

The neuropathic factor in the aetiology of diabetic foot ulcers

The nature and severity of changes due to peripheral neuropathy has been assessed clinically and electrophysiologically in 39 diabetic patients, 23 of whom had penetrating ulcers on the sole of the foot. Patients suffering from diabetic foot ulcers were found to have sensory loss to pin prick in the feet more frequently than “controls”. The electrophysiological measurements confirmed the severity of the neuropathy with absent sural nerve action potentials in 95% of the ulcer patients and inexcitability of small foot muscles in 40%. Weakness of small foot muscles due to neuropathy is thought to underlie the foot deformity that leads to maldistribution of weight bearing, and subsequent pressure necrosis of analgesic skin.

In vivo human sural nerve action potentials.

ARTICLESIn vivo human sural nerve action potentialsR. Shiozawa, and H. MavorR. Shiozawa, and H. MavorPublished Online:01 May 1969https://doi.org/10.1152/jappl.1969.26.5.623MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByLower Extremity Sensory Nerve Conduction StudiesPhysical Medicine and Rehabilitation Clinics of North America, Vol. 9, No. 4Coexistent entrapment neuropathies in patients with amyotrophic lateral sclerosisArchives of Physical Medicine and Rehabilitation, Vol. 77, No. 11 More from this issue > Volume 26Issue 5May 1969Pages 623-629 Copyright & PermissionsCopyright © 1969 the American Physiological Societyhttps://doi.org/10.1152/jappl.1969.26.5.623PubMed5781616History Published online 1 May 1969 Published in print 1 May 1969 Metrics