PubMed Health⌕ Search

Biomedical subjects

H Nukada

Publications and source records attributed to H Nukada.

14 recordsLinked to original sources
PubMed1992

Mild ischemia causes severe pathological changes in experimental diabetic nerve.

Nerve ischemia is considered one of etiological factors in the development of structural changes in peripheral nerves associated with diabetes mellitus. To assess the effect of mild ischemia on diabetic nerve, a subthreshold dose of polystyrene microspheres was injected intraarterially to occlude microvessels of the sciatic nerve and its branches in 20-week streptozotocin-induced diabetic and control rats. Diabetic sciatic and tibial nerves showed severe pathological change of myelinated fibers, whereas nondiabetic nerves were normal or had minor structural abnormalities. Morphometrical evaluation confirmed a greater frequency of abnormal myelinated fibers in diabetic nerves especially in central fascicular regions. The results indicate that diabetic nerve has an increased morphological susceptibility to nerve ischemia. Endoneurial hypoxia, which may result from hemorheological and vascular abnormalities, is likely to cause a lowered threshold to ischemic tolerance in diabetic nerve. This increased vulnerability to ischemia may render diabetic nerve unduly susceptible to hyperglycemia-induced systemic tissue abnormalities.

Animals↗
PubMed1992

Perineurial window: demyelination in nonherniated endoneurium with reduced nerve blood flow.

The perineurial window, created by surgical incision of the perineurial sheath allowing its contents to herniate into the epineurial space, provides an experimental model of primary demyelination, the cause of which is unclear. Because the injury is localized and involves distortion of tissue at the lesion site, ischemia is suspected as a cause of demyelination. To study the mechanism of demyelination in the perineurial window model, we measured nerve blood flow (NBF) with a laser Doppler flowmeter before and after perineurial rupture in rat sciatic nerve and assessed the spatial distribution of demyelinated fibers, particularly in the nonherniated portion of the endoneurium. Nerve blood flow at the site of the perineurial window was reduced significantly with an average level of NBF approximately 50% of presurgical values 10 minutes, 60 minutes and 6 hours after surgery. By light microscopic examination, most nerve fibers that herniated through the perineurial window underwent demyelination by 7 days. In addition, focal lesions of subperineurial demyelination were found in the nonherniated endoneurium in the adjacent subperineurial region and proximally and distally to the perineurial window. Endoneurial vessels adjacent to the perineurial incision appeared to be compressed. We suggest that ischemia contributes to the process of demyelination in the perineurial window model.

Animals↗
PubMed1990

Hereditary cerebellar degeneration with downbeat nystagmus. A case and it's treatment.

We present a female patient of 48 years with downbeat nystagmus (DBN), moderate impairment of coordination testing and a family history of cerebellar ataxia. We report that a single 2 mg dose of clonazepam (following Currie & Matsuo) resulted in a virtual disappearance of nystagmus and of the patient's symptom of oscillopsia. This result is interpreted in terms of current models of DBN.

Cerebellar Ataxia↗
PubMed1990

[Ischemic neuropathy].

Ischemia plays an important role in the development of neuropathies associated with various disorders, such as peripheral vascular occlusive diseases, necrotizing vasculitides, diabetes mellitus and nerve compression or trauma. Although a multiple mononeuropathy or an asymmetrical polyneuropathy is the usual clinical presentation of ischemic neuropathy, some patients present with a neuropathy that is mainly distal and symmetrical. Pathologically, nerve ischemia results in focal or multifocal central fascicular or sector fiber degeneration. These ischemic lesions tend to begin at mid-upper arm or midthigh level, which is the watershed zone of poor perfusion, and become more diffuse distally. Nerve ischemia at the level of distal small fascicles often induces sub-perineurial crescent lesion rather than central fascicular fiber degeneration. Physiologically, reduced nerve blood flow with endoneurial hypoxia has been demonstrated in experimental diabetic and galactose neuropathies. Endoneurial ischemia/hypoxia in galactose neuropathy appears to be due to increased intercapillary distances and constriction of trans-perineurial vessels resulting from endoneurial edema. Although acute ischemic neuropathy has been well investigated, little is known about functional or structural responses of peripheral nerve to chronic ischemia.

Diabetic Neuropathies↗
PubMed1989

Chronic paroxysmal hemicrania.

Chronic paroxysmal hemicrania consists of unilateral paroxysmal headaches, commonly in women, and relieved by indomethacin. Two patients with the condition are reported, one of whom had essential thrombocythaemia and the headaches remitted when the platelet count returned to normal. Platelet function may be worth exploring in these headaches.

Adult↗
PubMed1989

Is ischemia implicated in chronic multifocal demyelinating neuropathy?

We describe a patient with chronic multifocal demyelinating neuropathy associated with persistent conduction block. Multifascicular lesions in sural nerve included a complete loss of myelinated fibers, demyelination, remyelination, onion bulb formation, and axonal attenuation. On the basis of these morphometric results we hypothesize that nerve ischemia may be involved in the pathogenesis of chronic multifocal demyelinating neuropathy.

Brain Ischemia↗
PubMed1988

Post-traumatic endoneurial neovascularization and nerve regeneration: a morphometric study.

Neovascularization would be expected to play an important role in regeneration after nerve injury, but its mechanism is poorly understood. Quantitative investigations of endoneurial capillaries and myelinated fibers 5 and 15 mm distal to different types of nerve injury have therefore been performed. This study demonstrated that numbers of endoneurial capillaries were significantly increased at the 5 mm level 2, 4, 6 and 8 weeks after crush, transection and ischemic lesions, but not following permanent axotomy. Late neovascularization associated with delayed nerve regeneration was found following nerve ischemia. These results suggest that neovascularization following nerve injury is dependent on two variables, the degree of nerve regeneration and the severity of ischemia. Axonal outgrowth appears to be an important determinant of post-traumatic new capillary formation, while nerve ischemia causes both delayed neovascularization and nerve regeneration.

Animals↗
PubMed1988

Neuropathy in multiple symmetric lipomatosis. Madelung's disease.

With increasing age, peripheral neuropathy becomes more common in multiple symmetric lipomatosis (MSL) and the principal cause of severe disability. High alcohol consumption is frequently associated and the peripheral neuropathy of MSL is often attributed to alcoholism. In this study, sural nerve biopsies from MSL patients revealed an absence of acute axonal degeneration, a significant shift to the left of myelinated fibre diameter distributions, reduced indices of axonal and nerve fibre circularity, and an increase in myelin periodicity. This pathology supports the view that the neuropathy of MSL is not alcohol-induced but that a chronic distal axonopathy is an integral part of the MSL syndrome. Biochemical observations suggest a defect in catecholamine-stimulated lipolysis in MSL at a membrane level, possibly in the amount or function of Gs membrane protein or in the catalytic unit of adenylate cyclase. Evidence is presented that the frequent association of MSL with alcoholism is on the basis of an additional ethanol-induced membrane lesion involving beta-adrenergic receptors.

Adult↗
PubMed1986

Neovascularization after ischemic nerve injury.

Because angioneogenesis is associated with wound repair, neovascularization may play an important role in regeneration after nerve injury. This hypothesis was tested in the present study in which the number and distribution of endoneurial capillaries were determined 6 weeks after ischemic nerve injury. The density of capillaries was increased in the central fascicular regions of the distal sciatic and proximal tibial nerves at sites of ischemic injury. This was accompanied by a decrease in intercapillary distance. Neovascularization may be a response to ischemia or a consequence of nerve degeneration or regeneration, the mechanisms of which are poorly understood.

Animals↗