Unmyelinated Fibres and Schwann Cells of Sural Nerve in Neuropathy

Abstract

Electron micrographs of 45 sural nerves from patients with acquired (22) or heredodegenerative neuropathy (23) were analysed with respect to the number of unmyelinated nerve fibres, 37 nerves with respect to the number of Schwann cell sub-units and of structures connected with Schwann cells. Findings were compared with those in 6 nerves from control subjects and referred to the total number rather than to the number per mm2 to eliminate error due to increase in the transverse endoneurial area, present in more than half the diseased nerves. Ninety-one per cent of the diseased nerves showed one or several abnormalities in unmyelinated fibres of their Schwann cells. The best indicator of fibre loss was an increase in the number of Schwann cell sub-units devoid of axons, found in more than half the nerves. This was the only abnormality related with decrease in number of myelinated fibres. The increase in number of empty Schwann cell sub-units was due both to loss of unmyelinated nerve fibres and to proliferation of Schwann cells. Proliferation was indicated by the higher incidence of Schwann cell nuclei in cross-sections of diseased nerves than in controls. The earliest sign of involvement was an increase in number of profiles and of small isolated Schwann cell projections, observed in 33 of 37 diseased nerves, as the only abnormality in 7 nerves. The number of unmyelinated nerve fibres by itself was of little value to indicate loss of fibres, since regeneration often replaced or more than replaced degenerated fibres. Regeneration was indicated by an increase in number or incidence of small unmyelinated fibres, present in nearly half of 45 diseased nerves; and by an increased in the total number, present in a third of the nerves. An increase in the number of collagen pockets and of fibres undergoing degeneration (loss of organelles) and a decrease in the number of unmyelinated fibres per Schwann cell sub-units was present in only a quarter to a third of diseased nerves and was not related to other criteria of loss of fibres or of regneration.

Combined light- and electron-microscopic study of the rat saphenous nerve

“…Thus, it would seem that autonomic nerves and cutaneous nerves resemble each other with respect to this parameter in a given spe cies. On the other hand, the apparent dilferencesinpercentagedistributionand mean number in two autonomic nerves in two different species [Aguayo et al, 1973[Aguayo et al, , 1976 and in two cutaneous nerves in two different species [present study and Behse et al 1975] seem to suggest that there is a species difference for the autonomic and cutaneous nerves with respect to this parameter.…”

A new combined Bodian-Luxol technique for staining unmyelinated axons in semithin, resin-embedded peripheral nerves: a comparison with electron microscopy

“…Even though UF are involved in most neuropathies [3,5,12,13,18,20], a predominant loss of unmyelinated axons, often associated with selective loss of small-diameter myelinated fibers, has proved a valuable finding with a limited differential diagnosis: leprosy, amyloidosis, small-fiber diabetic neuropathy, and hereditary conditions such as Fabry's disease, Tangier's disease, hereditary sensory and autonomic neuropathies, idiopathic acute pandysautonomia, idiopathic chronic anhydrosis, dimethylaminopropionitrile toxic neuropathy and some forms of alcoholic neuropathy [6,11,15].…”

“…Size-frequency histograms: a minimum of 150 fibers were evaluated, the diameter of each nerve fiber was determined as the mean of the largest diameter and the diameter at right angles to it [3].…”

Neural and vascular regulatory factors of the skin

“…Distal degeneration and axonal sprouting are features of diabetic polyneuropathy, as demonstrated by electron microscopy in sural nerve biopsies [100] and early increases in numbers of cutaneous peptide-containing nerves, as identified by PGP-9.5 and neuropeptide immunostaining, may reflect early stages of neuronal degeneration in diabetes, which arc followed eventually by a diffuse loss of peripheral nerves. These immunohistochemical abnormalities did not correlate closely with neurophysiological autonomic and sudomotor tests, suggesting that different techniques detect different aspects of diabetic neuropathy.…”