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Biomedical subjects

H Nukada

Publications and source records attributed to H Nukada.

At least 55 records · Page 3Linked to original sources
PubMed1985

Spatial distribution of capillaries in rat nerves: correlation to ischemic damage.

Computerized imaging was used to assess the spatial distribution of capillaries (number, density, and intercapillary distance) in normal rat sciatic nerve and its branches, to be able to make inferences about their distribution to central fascicular degeneration typical of ischemic nerve injury. Capillary density was significantly less in the central regions of fascicles than in outer contour areas in sciatic and proximal tibial nerves, the difference being greater in large fascicles. The mean of the minimum intercapillary distance was significantly greater in the central fascicular region of fascicles of the sciatic but not of the tibial and peroneal nerves. These anatomic characteristics may be a factor in ischemic-induced central fascicular degeneration. A decrease in the number of capillaries in a region might lead to impaired oxygen diffusion when blood flow to the region is compromised.

Animals↗
PubMed1984

Decreased axon caliber and neurofilaments in hereditary motor and sensory neuropathy, type I.

The axons of large- and intermediate-diameter myelinated fibers of sural nerves of patients with hereditary motor and sensory neuropathy, type I (HMSN-I), were previously found to be attenuated relative to their myelin spiral length. We inferred that axonal atrophy might account for secondary segmental demyelination and remyelination. To assess whether the observed axonal atrophy could be explained by a decrease in neurofilaments, we have evaluated the number of neurofilaments, microtubules, and other axon organelles in sural nerves of patients with HMSN-I. Whereas the density per square micrometer of neurofilaments or microtubules in diseased nerves was not significantly different from that in control specimens, the number of neurofilaments per axon as related to myelin spiral length was significantly less for intermediate and large myelinated fibers in HMSN-I nerves. The regression lines for the number of microtubules per axon on myelin spiral lengths were also less steep in HMSN-I, but the difference did not reach statistical significance. These results indicate that the number of neurofilaments is proportional to axon diameter but significantly below that expected considering myelin spiral length. Decreased neurofilament synthesis, assembly, or transport may underlie the axonal atrophy in HMSN-I.

Adolescent↗
PubMed1984

Peripheral nerve morphometry in stroke patients.

Sural nerve biopsy specimens from affected and non-affected limbs of stroke patients were examined morphometrically. Two principle abnormalities of peripheral nerve were found in hemiparetic and hemiplegic limbs. First, the frequency of abnormal teased nerve fibers was significantly increased with abnormal internodes frequently "clustered" and showing a 50% or more reduction in myelin thickness. Second, the mean diameter of myelinated nerve fibers was reduced. These results suggest a primary atrophy of peripheral nerve fibers in the affected limbs of stroke patients with secondary demyelination. Possible aetiological factors include disuse, transynaptic degeneration, ischemia, pressure effect, and decreased axoplasmic flow. It would seem that the structural integrity of peripheral nerve is frequently compromised following a cerebral lesion.

Adult↗
PubMed1984

Microsphere embolization of nerve capillaries and fiber degeneration.

Polystyrene microspheres, the size chosen to plug capillaries and precapillaries, were injected into the arterial supply of rat sciatic nerves. They produced widespread segmental occlusion of capillaries in lower limb nerves. The clinical and pathologic effect was dose-related. One million microspheres produced selective capillary occlusion but no nerve fiber degeneration; approximately 6 million microspheres also produced selective capillary occlusion and associated foot and leg weakness, sensory loss, and fiber degeneration, beginning in a central core of the distal sciatic nerve; 30 million microspheres caused both capillary and arterial occlusion and a greater neuropathologic deficit. From these observations it is inferred that 1) occlusion of isolated precapillaries and capillaries does not produce ischemic fiber degeneration; 2) occlusion of many microvessels results in central fascicular fiber degeneration, indicating that these cores are watershed regions of poor perfusion; and 3) stereotyped pathologic alterations of nerve fibers and Schwann cells are related to dose, anatomic site, and time elapsed since injection.

Animals↗
PubMed1984

Spatial pattern of nerve fiber abnormality indicative of pathologic mechanism.

Estimates of the number, density, and size distribution of myelinated fibers at selected levels of roots, spinal tracts, and sampled levels of peripheral nerves may be used in the detection and characterization of alterations of motor, sensory, and autonomic neurons and their axons with development, aging and disease. Use of imaging techniques, now available, increases the reliability, versatility, and speed of such analysis. In this study, the authors evaluated the spatial pattern of fibers in sampled frames and contour areas of transverse sections of nerve fascicles, utilizing, the coefficient of variation and index of dispersion (ID), the latter extensively employed by plant ecologists. The ID was used for recognization of increased, normal, or decreased variability of density within fascicles, between fascicles, and between nerves in health and in various experimental neuropathies. In addition, various morphometric measurements were made in transverse sections at defined levels along the hind limb nerves of rats in acute and chronic ischemia, after rhizotomy and in galactose neuropathy. These stereomorphometric studies, emphasizing the number, size, shape, and spatial pattern of fibers, revealed differences among experimental neuropathies and may be found to be helpful in the characterization and prediction of pathologic mechanisms in neuropathies of unknown cause. Specifically, these approaches could be used for study of whether fiber loss in human diabetic neuropathy is multifocal and determination of the levels of such losses.

Acute Disease↗
PubMed1983

Comparison between fascicular and whole sural nerve biopsy.

Sural nerve regeneration and sensation were evaluated in 16 subjects five or more years after fascicular or whole nerve biopsy. Conduction studies demonstrated successful nerve regeneration in all subjects who had whole nerve biopsy. Postbiopsy interrogation revealed no long-term pain or paresthesias but a high incidence of tactile-induced dysesthesias. No significant difference was seen when areas of sural sensory loss were compared in fascicular and whole nerve biopsy groups. We conclude that whole nerve biopsy should be recommended in preference to fascicular biopsy since it is simpler, has greater diagnostic potential, and allows for a more complete morphological evaluation.

Action Potentials↗
PubMed1983

Thin axons relative to myelin spiral length in hereditary motor and sensory neuropathy, type I.

The relationship of axonal to myelin area in semithin transverse sections of myelinated fibers obtained from sural nerves at the ankle level was morphometrically assessed using computer imaging. Ten patients with hereditary motor and sensory neuropathy, type I and 41 control subjects were examined. In large- and intermediate-diameter myelinated fibers of diseased nerves, axons were significantly attenuated relative to the amount of myelin. Using electron micrographs, a similar finding was obtained when axon area was regressed on myelin spiral length. The altered relationship was found to be greater with more severe fiber loss. These data, plus other evidence, indicate that in this disorder there is a progressive atrophy of axons, usually most severe in distal aspects of lumbosacral neurons and associated with secondary segmental demyelination and remyelination and hypertrophic neuropathy, preceding distal axonal loss. Because the process may begin in utero or in infancy, not only atrophy but also maldevelopment of axons may be involved.

Adolescent↗
PubMed1983

Peripheral neuropathy in Tangier disease.

Peripheral nerve morphometry was assessed in four patients with Tangier disease. Three patients with a relapsing and remitting multiple mononeuropathy had prominent peripheral nerve demyelination and remyelination with affected internodes clustered along particular nerve fibres. Putative lipid vacuoles were almost exclusively confined in this multifocal neuropathy syndrome to Remak cells. By contrast a fourth patient with a slowly progressive syringomyelia-like neuropathy had advanced peripheral nerve degeneration and a more global distribution of lipid vacuoles within peripheral nerve. A review of Tangier disease in the literature indicated the possibility of additional peripheral nerve syndromes. The clinical heterogeneity raises the possibility of different metabolic errors in Tangier disease or a common metabolic error subject to genetic influences. The results of this study indicate that normal serum cholesterol levels do not exclude a diagnosis of Tangier disease. It is therefore advisable to determine both high density lipoproteins and serum cholesterol levels in patients with undiagnosed multifocal neuropathy or syringomyelia-like syndromes.

Adult↗
PubMed1982

The clinical spectrum and morphology of type II hereditary sensory neuropathy.

Consistent morphological features were found in sural nerve biopsies of four sporadic cases of sensory neuropathy. The morphological finding of marked fascicular atrophy, a profound loss of myelinated fibres and a relative preservation of unmyelinated fibres are typical of those previously found in the recessive form of hereditary sensory neuropathy (HSN-II). Variable clinical manifestations contrasted with this morphological specificity. Where clinical doubt exists, the value of nerve biopsy in distinguishing HSN types I and II is emphasized. Long-term clinical follow-up and a comparison of repeat nerve biopsy data indicated that HSN-II is a progressive disorder.

Adult↗
PubMed1981

Disulfiram neuropathy. A morphometric study of sural nerve.

This report describes peripheral nerve morphology in 3 patients whose acute polyneuropathy followed disulfiram therapy. In all patients a combination of axonal degeneration with segmental demyelination and remyelination was seen, suggesting a varying degree of toxicity to both cytons and Schwann cells. The observed randomness of abnormal internodes argued against primary axonal atrophy and secondary demyelination. While large myelinated fibres were preferentially lost, ultrastructural studies also suggested degeneration of unmyelinated fibres. Because of high chloral consumption at the onset of peripheral nerve disease in 2 patients, the possibility of disulfiram-chloral interaction was considered. Present evidence suggests that the combined use of chloral or its derivatives with disulfiram is best avoided.

Adult↗
PubMed1981

Experimental cold injury to peripheral nerve.

Focal non-freezing injury to rat sciatic nerve resulted in nerve conduction block and cessation of axoplasmic transport. Rats showed early functional recovery but subsequently developed a slowly progressive sciatic nerve paralysis. Horseradish peroxidase studies revealed prominent nerve oedema with early enhanced pinocytosis and later, passive leakage through damaged endoneurial capillaries. Detailed microscopy indicated a striking selective vulnerability to cold based on nerve fibre diameter. Unmyelinated fibres were spared while large myelinated nerve fibres showed severe axonal degeneration. Paranodal and segmental demyelination were infrequent findings and may have resulted from early axonal swelling. Possible pathogenic mechanisms to explain the degeneration of myelinated fibres in hypothermic injury are discussed. It is concluded that the gradient of clinical severity seen in limb hypothermic injuries has a pathological correlate in peripheral nerve.

Animals↗
PubMed1980

Clinical and morphological features of gold neuropathy.

Three cases of gold-related neuropathy are reported. Clinical features include an acute, symmetrically progressive polyneuropathy, focal or generalized myokymia and a tendency for initial neurological deterioration followed by improvement, after cessation of chrysotherapy. The degree of clinical recovery related to maximal disability. Morphological findings on sural nerve biopsies revealed both axonal degeneration and segmental remyelination. Similar peripheral nerve histology was seen in a parallel animal study in which the severity of the neuropathy was dose-related.

Adult↗