Peripheral Nerve Conduction in Diabetic Neuropathy

Gilliatt, R. W.; Willison, R. G.

doi:10.1136/jnnp.25.1.11

Cited by 153 publications

(54 citation statements)

References 11 publications

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“…That slowing in motor conduction in our patients scattered less than in other series of patients (Mayer, 1963;Eeg-Olofsson and Petersen, 1966) (Calverley and Mulder, 1960). In addition there was evidence of involvement of distal nerves and muscles with slowing of conduction in the lateral popliteal and the median nerves in agreement with findings in diabetic amyotrophy by Gilliatt and Willison (1962) and Chopra and Hurwitz (1968). The third patient was the only one with electromyograpoic abnormalities in the medial vastus muscles suggestive of myopathy such as has been described in biopsies as atrophic muscle fibres scattered randomly among normal fibres (Bischoff, 1959;Garland, 1961;Locke, Lawrence, and Legg, 1963;Coers, 1966).…”

Section: Motor Conduction and Evoked Muscle Actionsupporting

confidence: 90%

“…These studies concerned patients with or without diabetic neuropathy (Lawrence and Locke, 1961;Mulder et al, 1961;Skillman et al, 1961;Fagerberg et al, 1963;Mayer, 1963;Gamstorp, 1964;EegOlofsson and Petersen, 1966) and mixed groups (Gregersen, 1964(Gregersen, , 1967. In the individual patient, slowing in motor conduction was often borderline in the non-affected nerves of patients with isolated peripheral nerve lesions (Gilliatt and Willison, 1962). Our findings of abnormalities in sensory action potentials in the median nerve of many patients without corresponding clinical signs made it possible to establish the presence of latent involvement in the individual patient.…”

Section: Motor Conduction and Evoked Muscle Actionmentioning

confidence: 81%

“…Previous studies of electrophysiological changes in diabetic neuropathy have dealt with fibrillation potentials, polyphasic potentials, or conduction velocity in motor and, in a few instances, mixed and distal sensory nerves (Downie and Newell, 1961;Lawrence and Locke, 1961;Mulder, Lambert, Bastron, and Sprague, 1961;Skillman, Johnson, Hamur, and Driskill, 1961;Gilliatt and Willison, 1962;Wiesendanger and Bischoff, 1962;Fagerberg, Petersen, Steg, and Wilhelmsen, 1963;Mayer, 1963). Electrophysiological parameters in the same patient have not been compared and there are few studies of sensory conduction and none of conduction along the whole nerve.…”

mentioning

confidence: 99%

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Electrophysiological studies in diabetic neuropathy

Lamontagne

Buchthal

1970

Journal of Neurology, Neurosurgery & Psychiatry

175

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SUMMARY In 30 patients with diabetic neuropathy sensory potentials in the median nerve, motor conduction in the lateral popliteal and median nerves, and electromyographic findings in distal and proximal muscles were compared with the severity of symptoms and signs. All patients had abnormalities in at least one of the electrophysiological parameters. The sensory potentials were the most sensitive indicator of subclinical involvement; abnormalities were found in 24 patients, 12 of whom had no sensory symptoms or signs and five of whom had no other clinical or electrophysiological evidence of neuropathy in the upper extremities. This indicates that sensory nerve fibres may be affected before motor. The next most sensitive parameter was the presence offibrillation potentials, found in more than half the distal muscles examined. Slowing in motor conduction in the lateral popliteal nerve was the only electrophysiological change correlated to the severity of the neuropathy, and no other electrophysiological parameter was correlated to the duration or the severity of the neuropathy or the diabetes. An onset of neuropathy before or simultaneously with the manifestations of the diabetes, as well as the frequent occurrence of asymptomatic changes in sensory conduction, support the evidence at hand that the neuropathy develops concomitantly with and as an integral part of the metabolic disturbance rather than as a consequence of the vascular complications of diabetes. Of three patients with clinical signs or symptoms of a diabetic amyotrophy, two had asymptomatic electrophysiological abnormalities in distal nerves and muscles, consistent with widespread involvement of the peripheral nerves. The third patient had electromyographic changes in the medial vastus muscles suggestive of a myopathy. Motor and sensory conduction in distal and proximal nerves were normal.Previous studies of electrophysiological changes in diabetic neuropathy have dealt with fibrillation potentials, polyphasic potentials, or conduction velocity in motor and, in a few instances, mixed and distal sensory nerves

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Section: Motor Conduction and Evoked Muscle Actionsupporting

confidence: 90%

Section: Motor Conduction and Evoked Muscle Actionmentioning

confidence: 81%

mentioning

confidence: 99%

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Electrophysiological studies in diabetic neuropathy

Lamontagne

Buchthal

1970

Journal of Neurology, Neurosurgery & Psychiatry

175

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“…The nerve dysfunction as a consequence of diabetes is debilitating and can lead to lifethreatening autonomic neuropathy, cardiac diseases, and CNS atrophy (3,4). Dying back of distal peripheral nerve fibers because of glucose toxicity and the ensuing spinal sensitization are thought to be the underlying causes of pain (5)(6)(7)(8)(9). Although hyperglycemia is the initiating cause for diabetic neuropathy, aggressive glycemic control is effective in impeding the progression of neuronal loss and pain, but not in reversing neuropathy (10).…”

mentioning

confidence: 99%

Acute augmentation of epoxygenated fatty acid levels rapidly reduces pain-related behavior in a rat model of type I diabetes

Inceoglu

Wagner

Yang

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The nerve damage occurring as a consequence of glucose toxicity in diabetes leads to neuropathic pain, among other problems. This pain dramatically reduces the quality of life in afflicted patients. The progressive damage to the peripheral nervous system is irreversible although strict control of hyperglycemia may prevent further damage. Current treatments include tricyclic antidepressants, anticonvulsants, and opioids, depending on the severity of the pain state. However, available therapeutics have drawbacks, arguing for the need to better understand the pathophysiology of neuropathic pain and develop novel treatments. Here we demonstrate that stabilization of a class of bioactive lipids, epoxygenated fatty acids (EpFAs), greatly reduces allodynia in rats caused by streptozocin-induced type I diabetes. Inhibitors of the soluble epoxide hydrolase (sEHI) elevated and stabilized the levels of plasma and spinal EpFAs, respectively, and generated dose-dependent antiallodynic effects more potently and efficaciously than gabapentin. In acute experiments, positive modulation of EpFAs did not display differences in insulin sensitivity, glucose tolerance, or insulin secretion, indicating the efficacy of sEHIs are not related to the glycemic status. Quantitative metabolomic analysis of a panel of 26 bioactive lipids demonstrated that sEHI-mediated antiallodynic effects coincided with a selective elevation of the levels of EpFAs in the plasma, and a decrease in degradation products coincided with the dihydroxy fatty acids in the spinal cord. Overall, these results argue that further efforts in understanding the spectrum of effects of EpFAs will yield novel opportunities in treating neuropathic pain.analgesic drug | soluble epoxide hydrolase inhibitor | cytochrome P450 | glucose homeostasis | motor depressant

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“…Peripheral neuropathy is probably one of the most common complications associated with diabetes (Kaur et al, 1982;Ellenberg, 1983), and yet has an elusive pathogenetic mechanism. Mulder et al (1961), Gilliatt and Williamson (1962), , and were among the first to appreciate the abnormalities of the PNS in human diabetics. Several possible mechanisms have been put forth to explain how certain metabolic factors culminate in diabetic complications (Greene et al, 1975(Greene et al, , 1987aClements, 1979;Li et al, 1985;Winegrad, 1987).…”

mentioning

confidence: 99%

Effect of Sorbinil and Ascorbic Acid on myo‐Inositol Transport in Cultured Rat Schwann Cells Exposed to Elevated Extracellular Glucose

Karihaloo¹,

Joshi

Js³

1997

Journal of Neurochemistry

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Abstract:The effect of long-term (2 weeks) exposure to 0-50 mM glucose and 0-1 mM sorbitol on myo-inositol metabolism was studied in cultured rat Schwann cells. Experiments were carried out to determine the effect of sorbinil and ascorbic acid on myo-inositol uptake in rat Schwann cells cultured in the presence of increased extracellular glucose or sorbitol. myo-lnositol uptake and its incorporation into phospholipids decreased significantly when cells were grown itt 30 mM glucose for a period of 2 weeks. This inhibitory effect was partly blocked by sorbinil, an aldose reductase inhibitor, in a dose-dependent fashion. Significant prevention was achieved with 0.5 and 1 mM sorbinil. Ascorbic acid also prevented the reduction in myo-inositol uptake due to excess extracellular glucose, at 3 and 30 bIM concentrations, but not at 300 tiM. Neither sorbinil nor ascorbic acid could prevent the alterations in myo-inositol transport in cells exposed to high sorbitol levels for the same period of time. These data suggest that glucose-induced alteration of myo-inositol transport in Schwann cells is mediated, at least in part, via sorbitol accumulation. This myo-inositol transport impairment is prevented by sorbinil and also by ascorbic acid. Ascorbic acid may hold a fresh promise for the treatment/prevention of diabetic neuropathy/ complications, at least as an adjunct therapy along with known aldose reductase inhibitors.

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Peripheral Nerve Conduction in Diabetic Neuropathy

Cited by 153 publications

References 11 publications

Electrophysiological studies in diabetic neuropathy

Electrophysiological studies in diabetic neuropathy

Acute augmentation of epoxygenated fatty acid levels rapidly reduces pain-related behavior in a rat model of type I diabetes

Effect of Sorbinil and Ascorbic Acid on myo‐Inositol Transport in Cultured Rat Schwann Cells Exposed to Elevated Extracellular Glucose

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