Sural nerve myelinated fibre density and size in diabetics.

Js, Chopra; Hurwitz, L. J.

doi:10.1136/jnnp.32.2.149

Cited by 26 publications

(13 citation statements)

References 12 publications

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“…Our findings agree with the laminae. Similar observations were reported by inished density of myelinated fibres of all Bischoff (1965Bischoff ( , 1973, who found, in addition, an s, reported by Chopra and Hurwitz (1969) in increase in the thickness of the individual basal it of nine patients with sensory-motor neuro-laminae, which we did not measure in our patients. hy.…”

Section: Other Ne Uropath Iessupporting

confidence: 92%

“…They considered it an open question whether the axonal loss was secondary to segmental demyelination or occurred independently. Since demyelination but not axonal loss was found in diabetics without neuropathy, Chopra et al (1969) believed segmental demyelination to be the primary abnormality. This confirmed the view of Bischoff (1968) that a metabolic Schwann cell lesion is the primary defect in diabetic neuropathy.…”

Section: Discussionmentioning

confidence: 99%

“…The slowing in conduction which characterises most sensory and motor nerves in diabetic neuropathy (Lamontagne and Buchthal, 1970) has been considered to be due to segmental demyelination (Gilliatt, 1966;Thomas and Lascelles, 1966;Chopra et al, 1969). The use of electron microscopy and teased fibre preparations have led to conflicting results and explanations: is demyelination or axonal loss the primary and main lesion, or does each develop independently of the other?…”

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confidence: 99%

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Nerve biopsy and conduction studies in diabetic neuropathy.

Behse¹,

Buchthal²,

Carlsen³

1977

Journal of Neurology, Neurosurgery & Psychiatry

352

151

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SUMMARY Morphological findings in sural nerves were related to nerve conduction in 12 patients with diabetic neuropathy, five with mainly sensory involvement, four with severe, symme,trical sensory-motor polyneuropathy, and three with multiple mononeuropathy. All had loss of large and small myelinated and of unmyelinated fibres, even early in the disease; segmental remyelination was the most prominent myelin alteration in teased fibres, segmental demyelination was found in only a few fibres. Axonal degeneration and Schwann cell damage seem to proceed independently of each other. The relation between recorded conduction velocity and that expected from the diameter of the largest fibres indicated that slowing of 20 to 30% was due to causes other than fibre loss; a grossly diminished conduction velocity was caused mainly by fibre loss. Electrophysiological findings in the sural nerve were largely representative of findings in other nerves, though abnormalities were less marked in the median nerve. In half the endoneurial vessels from diabetic neuropathy the perivascular space was thickened or contained more layers of basal laminae than normal. The same abnormalities were found in one-quarter of the endoneurial vessels from other acquired neuropathies.

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Section: Other Ne Uropath Iessupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Nerve biopsy and conduction studies in diabetic neuropathy.

Behse¹,

Buchthal²,

Carlsen³

1977

Journal of Neurology, Neurosurgery & Psychiatry

352

151

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“…In a study of Chopra and Hurwitz (1969) of the cross-sectioned sural nerve in 16 diabetics some displacement of frequency-size histograms towards smaller values can be seen [10]. The authors suggest that this result may be due to loss of large fibres or remyelination following segmental demyelination.…”

Section: Discussionmentioning

confidence: 94%

Axonal dwindling in early experimental diabetes. I. A study of cross sectioned nerves

Jakobsen

1976

Diabetologia

172

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Summary. A diminution of the cross sectional area of myelinated fibres in the common peroneal nerve was observed in rats four weeks after the induction of diabetes with streptozotocin. Small fibres were affected more than larger ones and the axon reduction was twice that of the myelin sheath. The fibre diminution and the decreased axon/myelin ratio may explain the slowing of nerve conduction in experimental diabetes.Key words: Streptozotocin diabetes, axons, myelin sheath, nerve degeneration, neural conduction.Peripheral nerves are involved early in juvenile diabetes. Thus Gregersen (1967) demonstrated decreased motor nerve conduction velocity within the first year after the clinical onset of the disease [1]. At this time there were no clinical symptoms of neuropathy. The structural alteration underlying this functional abnormality is still unknown.Also in experimental diabetes, whether induced by streptozotocin, aUoxan or pancreatectomy, slowing of nerve conduction occurs from the very beginning. The morphological lesion has not been identified here either.A few histological studies have reported Schwann cell abnormalities several months after the induction of diabetes [2,3]. However, a recent extensive morphometric study failed to define any pathological alterations at all in diabetic animals [4].In this report of early experimental diabetes quantitative morphological changes, mainly affecting the axon, are demonstrated. The pathological lesion observed in the present study may well explain the functional abnormalitiy of nerve conduction in diabetic animals. Materials and MethodsMale Wistar rats raised on a standard rat chow diet with water ad libitum were used for the experiments. Animals 18 to 20 weeks old weighing between 330 and 380 g were selected at random for the different groups of the experiment. Diabetes was induced in ten rats by intravenous injection of 40 to 45 mg streptozotocin per kg body weight. The animals were maintained for four weeks without insulin treatment.Ten other rats were selected as a control group (control group 1). Both groups of animals were killed four weeks later.For the purpose of imitating the weight loss of the diabetic rats another group of five normal animals was deprived of food for four days and subsequently fed on a restricted daily diet of nearly 50% of the standard diet for 24 days (control group 2). With this diet it was intended to induce a weight loss somewhat greater than that observed to occur in the group of diabetic rats, to compensate for the increase in gastrointestinal filling known to occur in diabetic rats.Body weight was determined weekly in all animals. Blood glucose and 24 h urine output were measured at ten day intervals in the diabetic rats, and at the end of the experiment in the rats of the control groups. Blood samples were taken in the morning as duplicates from non-fasting animals. Blood glucose was determined by a glucose oxidase method [5] and urine glucose by a p-toluidine method. Tissue PreparationPeripheral nerves were initially fixed by vas...

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“…D PN is an axonal neuropathy that involves nerve fiber loss, and probable concurrent degeneration and regeneration within the same peripheral nerve fascicle (1)(2)(3)(4)(5)(6). Among the least understood aspects of DPN is the development of positive sensory symptoms in the extremities, which do not respond to painful stimuli.…”

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confidence: 99%