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At least 199 records · Page 11Linked to original sources
PubMed1988

Selective vulnerability of unmyelinated fiber Schwann cells in nerves exposed to local anesthetics.

When peripheral nerves of experimental rats are exposed to local anesthetics, distinctive and reproducible pathologic changes occur involving the perineurial sheath and endoneurial contents. Application of intermediate strength concentrations of the local anesthetics, 2-chloroprocaine, lidocaine, etidocaine, and intermediate or high concentrations of procaine to the surface of rat sciatic nerves resulted in the following changes. By 48 hours, the perineurial sheath exposed to the drug was disrupted and became permeable to granulocytes which infiltrated the subjacent endoneurium in conjunction with edema formation in the endoneurial interstitium. Application of 10% procaine to exposed nerve resulted in extensive demyelination. The most striking pathologic change occurring with either intermediate or high doses was accumulation of lipid droplets in Schwann cells, a phenomenon that occurred often in myelin-producing Schwann cells but much less frequently in unmyelinated fiber Schwann Cells. Lipid accumulation appears to be one of several reactive changes that affect Schwann cells of myelinated fibers and is dose-dependent. On the other hand, while reactive changes were infrequently seen in unmyelinated fiber Schwann cells, these cells appeared more susceptible to injury as shown by electron microscopy. Injury to Schwann cells by local anesthetics is temporary because these cells can replicate quickly. Autoradiographic studies of thymidine incorporation 1 week after procaine administration to the sciatic nerve showed intense proliferation of Schwann cells, but no such activity in controls. These findings support the view that their neurotoxic properties may account in some part for the function of local anesthetics, that Schwann cells of small unmyelinated fibers are more vulnerable to these agents than those of myelinated fibers, and that destruction of their supporting cells is followed by vigorous mitotic activity in the endoneurium.

Anesthetics, Local↗
PubMed1995

[Hypoxic cerebral lesions. X-ray computed tomography and MRI aspects. Apropos of 20 cases. Selective vulnerability of the striatopallidum].

Brain lesions following hypoxic-ischaemic injuries are known from autopsy studies, but their appearance in live patients has been only occasionally described, and only sporadic reports have been published on their CT and MRI images. Over a 2-year period (1991-93) we studied the clinical, MRI and CT features in 20 patients shortly after a severe hypoxia. Clinical examination showed motor extrapyramidal signs in 13 cases and coma in 7 cases. MR with inversion recovery (IR) and T2-weighted spin echo (SE) sequences was performed in 17 patients and CT in 15. Bilateral lesions were found in 11 cases, but in 13 of them CT was normal. Radiological lesions were always symmetrical and bilateral, located in the pallidum in 10 cases, the striatum in 4 cases and the thalamus in 2 cases. Additional white matter lesions were present in only 4 MRI examinations. No relationship was found between the mechanism of hypoxia and the severity of clinical signs. The course of the clinical signs was correlated with the presence of radiological lesions. In comatous patients there was a relation between parkinsonism and abnormalities of basal ganglia. None of the patients who had perinatal asphyxia had radiological lesions. The presence of pallidal or striatal confirmed the hypoxic origin of neurological symptoms, especially in patients with parkinsonism. MRI, particularly in IR sequences, makes it possible to detect small lesions in basal ganglia after hypoxic injuries.

Adult↗
PubMed1995

Diazepam, given postischemia, protects selectively vulnerable neurons in the rat hippocampus and striatum.

Following cerebral ischemia, certain populations of neurons degenerate. Excessive accumulation of excitatory amino acids in the synaptic cleft, activation of excitatory amino acid receptors, and influx of calcium into neurons play a key role in the development of ischemia-induced neuronal death. We hypothesized that neuroprotection may be achieved by enhancing inhibitory (i.e., gamma-aminobutyric acid, GABA) neurotransmission to offset excitation. Diazepam, a drug that increases GABA-induced chloride channel opening, was administered (10 mg/kg, i.p.) to rats 1 and 2 hr following 15 min of transient global ischemia, when hippocampal GABA levels, increased during ischemia, returned to basal. Rats were maintained normothermic during ischemia and became hypothermic following the injections of diazepam. Four days later, rats were sacrificed and the brains were examined for neuronal degeneration and the presence of GABAA receptors labeled by 35S-t-butylbicyclophosphorothionate (35S-TBPS). There was substantial neuroprotection of striatal neurons and pyramidal neurons in the CA1 area of the hippocampus. In addition, diazepam prevented the loss of 35S-TBPS binding sites in the striatum and in the dendritic fields of the CA1 hippocampus following ischemia. Since hypothermia, itself, is neuroprotective, we determined if hypothermia was required for the ability of diazepam to produce neuroprotection. Diazepam was microinjected into the CA1 hippocampus 1 and 2 hr following ischemia, and rats remained normothermic. Four days later, diazepam still produced substantial protection of hippocampal neurons. Thus, postischemic hypothermia may have contributed to the neuroprotection by diazepam when it was administered systemically, but the neuroprotective effect of diazepam did not require hypothermia. We conclude that delayed enhancement of GABAergic neurotransmission directly at the site of vulnerability following an ischemic event protects the vulnerable neurons from death.

Animals↗
PubMed1993

Aging of the human photoreceptor mosaic: evidence for selective vulnerability of rods in central retina.

PURPOSE: Because previous studies suggested degeneration and loss of photoreceptors in aged human retina, the spatial density of cones and rods subserving the central 43 degrees of vision as a function of age was determined. METHODS: Cones and rods were counted in 27 whole mounted retinas from donors aged 27 to 90 years with macroscopically normal fundi. Photoreceptor topography was analyzed with new graphic and statistical techniques. RESULTS: Changes in cone density throughout this age span showed no consistent relationship to age or retinal location, and the total number of foveal cones was remarkably stable. In contrast, rod density decreased by 30%, beginning inferior to the fovea in midlife and culminating in an annulus of deepest loss at 0.5 to 3 mm eccentricity by the ninth decade. Space vacated by dying rods was filled in by larger rod inner segments, resulting in a similar rod coverage at all ages. At the temporal equator, cone density declined by 23%, but rods were stable throughout adulthood. CONCLUSIONS: The stability of both rod coverage and rhodopsin content despite decreasing cell number suggests plasticity of the adult rod system and that age-related declines in scotopic sensitivity may be due to postreceptoral factors. There is no evidence for the massive loss of foveal cones required to explain even modest decrements in acuity, consistent with evidence that visual deficits at high photopic levels may be largely due to optical factors. Why the rods of central retina, which share a common support system and light exposure with the neighboring cones, are preferentially vulnerable to aging remains to be determined.

Adolescent↗
PubMed1995

[Selective vulnerability of neuronal injury after experimental heart arrest].

The study was aimed at the analysis of vulnerability of the olfactory bulb neurons in dogs after experimental heart arrest lasting for 15 minutes and recirculation lasting for 1 hour. By means of the Nauta degenerative neurohistologic method the reactions of individual types of nerve cells in the olfactory bulb were investigated. Nauta-positive granules were observed in the cytoplasm of the mitral and tufted cells of the olfactory bulb, which are of dopaminergic character. The granulations were present in the cellular areas which are rich in Nissl substance. The granular and short-axon cells of GABA-ergic character which contain a small amount of Nissl granules lack the Nauta-positive granules. Similarly, the Nauta-positive granules were absent in the axon hillock of mitral cells which under normal conditions do not contain the Nissl substance. These results justify the conclusion that ischemia lasting for 15 minutes and one-hour recirculation primarily affect the excitatory neurons rich in the Nissl substance. (Fig. 4, Ref. 16.).

Animals↗
PubMed1984

Neurotoxicity of certain environmental substances.

Lead, aluminum, mercury, and ketones and related solvents are discussed because they represent common problems in the environment and because they demonstrate selective vulnerability, selectively attacking some portions of the nervous system, sparing others. The absorption, excretion, distribution, and toxicologic effects of these chemicals and the diseases they are associated with are reviewed, as is the accuracy of screening procedures for detection of these chemicals.

Aluminum↗
PubMed1993

Die Pathoklise [Parkinson's disease].

The history of the concept of selective vulnerability of the basal ganglia with particular respect to the substantia nigra is briefly reviewed. During the past century attention has gradually focussed down from gross lesions of the basal ganglia through cell morphometry and presently to the level of the intracellular neurobiology. Despite an abundance of reported morphological and neurochemical changes it remains unresolved whether these findings indicate primary aetiological factors or secondary consequences of nigral cell death. In this debate, while MPTP has proven to be a most amenable model for the study of secondary parkinsonism it has not resolved the dilemma; equally uncertain are the claims derived from the MPTP hypothesis of nigral vulnerability that selective MAO inhibition has a protective effect on the natural history of Parkinson's disease. Some of the evidence, past and present, will be reviewed in so far that it reflects upon the concept of pathoclisis and the selective vulnerability of nigral cells and recent evidence from clinical trials and from the study of human foetal nigral cells in tissue culture will be presented.

Animals↗