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Biomedical subjects

C M Shaw

Publications and source records attributed to C M Shaw.

At least 73 records · Page 4Linked to original sources
PubMed1980

True traumatic aneurysm of the vertebral artery: case report.

A patient is reported in whom a true aneurysm of the vertebral artery developed following head trauma. The histology of the aneurysm and parent vessel is presented, and its implications regarding the mechanism of formation of posttraumatic true aneurysms are discussed.

Brain Injuries↗
PubMed1979

Has myelin basic protein received a fair trial in the treatment of multiple sclerosis?

Autosensitization to some central nervous system antigen still remains one of the best hypotheses for the continuing pathogenesis of multiple sclerosis (MS). Enough is now known about the cause, pathogenesis, and treatment of experimental allergic encephalomyelitis (EAE) to test this hypothesis. Reports of therapeutic failure of the encephalitogen myelin basic protein (BP) in the treatment of MS have their counterparts in similar therapeutic failures in EAE. Only highly inbred strain 13 guinea pigs respond consistently to BP therapy, and this only when BP is administered in relatively high doses. Noninbred guinea pigs respond much less well to simple BP therapy, and monkeys hardly at all. In both strains of monkeys so far studied, a nonspecific adjunctive factor--an antibiotic in Macaca mulatta and a steroid in Macaca fascicularis--is also required. Accordingly, human trials of the therapeutic efficacy of BP in MS should include its administration in large concentrations together with an adjunctive agent.

Adjuvants, Immunologic↗
PubMed1979

Myelin basic protein treatment of experimental allergic encephalomyelitis in monkeys.

Treatment of experimental allergic encephalomyelitis (EAE) in two strains of monkeys with large amounts of myelin basic basic protein (BP) fails unless an adjunct is also used. In both strains the adjunct by itself is more effective than BP by itself, but in the one strain which could be investigated sufficiently, the combination can be made almost totally effective in reversing EAE. The adjunct varies with the strain of monkey, an antibiotic in Macaca mulatta and a steroid in Macaca fascicularis. Similar adjunctive treatments should be considered in the management of multiple sclerosis, for EAE remains one of the best studied models.

Amino Acids↗
PubMed1979

The pathology of occipital encephalocoele and a discussion of the pathogenesis.

The midline structures of 5 infant brains with occipital encephalocoeles were studied. Though all cases showed a uniform finding of a midline defect of the occipital bone with a herniated mass, the extent of the bony defect, the amount and nature of the herniated tissues and the degree of distortion of the intracranial structures varied markedly. Two of the cases showed multiple associated systemic malformations and another case had an inverse cerebellum. In spite of such a marked variability in presentation, the common findings of herniation and displacement of the mesencephalon and roof of the diencephalon allowed us to postulate that the primary defect of occipital encephalocoeles is an abnormality of the tissues overlying the mesencephalon of the developing brain. Initial herniation of the mesencephalon and subsequent movement of the rest of the brain as a result of growth determines the tissues present in the hernia sac at birth. Other theories of genesis of occipital encephalocoeles are discussed.

Encephalocele↗
PubMed1978

Progressive myoclonus and epilepsy with dentatorubral degeneration: a clinicopathological study of the Ramsay Hunt syndrome.

Ramsay Hunt's progressive myoclonus and epilepsy associated with dentatorubral degeneration is a rare disorder. We report a 19 year old woman with this clinical syndrome who also has a more mildly affected brother. Neuropathological in addition to dentatorubal involvement. The evidence suggests that this is a distinctive hereditary disorder producing neuromal degeneration at several levels in the central nervous system.

Adult↗
PubMed1978

Fast-neutron irradiation of glioblastoma multiforme. Neuropathological analysis.

Various modes of therapy, alone or in combination, have had little effect in improving the survival of patients with glioblastoma multiforme. Recently, in a pilot study, 34 patients with glioblastoma were treated by fast-neutron-beam irradiation of the whole brain. Following treatment, the patients became steroid-dependent and pursued a gradual downhill course with increasing obtundation. Although there was no improvement in the length or quality of survival of these patients, neuropathological studies in the 13 patients who came to autopsy showed the following: 1) extensive coagulative necrosis of much of the tumor mass; 2) dense infiltration by collagenous connective tissue; 3) minimal phagocytic reaction; 4) marked reduction in the amount of viable tumor; 5) abnormal astrocytic proliferation, which may represent either astrocytoma or a radiation-induced bizarre gliosis, and 6) areas of gliosis and white matter degeneration in the brain stem, remote form the tumor site. These observations suggest that continued efforts to further refine this mode of therapy for glioblastoma are warranted.

Adult↗
PubMed1977

Phenytoin-related cerebellar degeneration without seizures.

Cerebellar changes have been reported in relationship to epilepsy alone as well as to phenytoin therapy for the control of seizures. The cliniconeuropathological correlation between these changes and epilepsy or the anticonvulsant is usually complicated by the presence of both variables. Experimental evidence suggests that phenytoin alone may be sufficient to cause cerebellar changes following intoxication. We report a case of cerebellar degeneration in a patient treated with isoniazid and prophylactically treated wtih phenytoin who never had a seizure.

Cerebellum↗
PubMed1976

Herpesvirus hominis encephalitis and retinitis.

A previously healthy 44-year-old man died three weeks after the simultaneous onset of encephalitis and retinitis. Fundus changes were bilateral and included papillitis, rapidly progressive central retinal vein obstruction, and massive exudative retinal detachment. A 16-fold rise in herpesvirus hominis antibodies occured between the 10th and 20th days of illness. At autopsy, the brain showed changes characteristic of herpetic encephalitis, and cultures of the brain yielded Herpesvirus hominis type I. Intranuclear inclusion bodies typical of those produced by Herpesvirus were found by light microscopy in brain, optic nerves, retina, and choroid. Herpesvirus particles were found by electron microscopy in brain, optic nerve, and retina.

Adult↗
PubMed1976

Fast neutron beam radiotherapy of glioblastoma multiforme.

Twenty-one patients with glioblastoma multiforme were treated with fast neutron beam irradiation of the whole brain. Therapy was well tolerated up to calculated doses of 1.850 radn+y in 12-18 increments over 6 weeks. The survival rate 6 month after initiation of treatment was 62%, not significantly different from conventional photon therapy; average posttreatment survival appears to be shortened compared to photon therapy. No improvement or prolonged maintenance of existing neurologic function was observed. Autopsy findings in seven patients showed replacement of tumor by coagulative necrosis persisting at least 16 months posttreatment, paucity of tumor cells with infrequent mitosis, and suppression of macrophage response. These findings differ from those in conventionally irradiated patients. No treatment-related changes were documented by conventional gross and histologic studies of the irradiated brains distant from the tumors. Thus the deaths of patients in this study appear to be related to unexplained causes other than progressive growth of tumor.

Brain Neoplasms↗
PubMed1975

Do neurological signs occur in experimental allergic encephalomyelitis in the absence of inflammatory lesions of the central nervous system?.

Guinea pigs with paralysis or other severe neurological signs of experimental allergic encephalomyelitis (EAE) always exhibited typical histological inflammatory lesions. A few animals inoculated with either the encephalitogenic emulsion or only the control adjuvant emulsion had mild weakness or slowness but no histologic lesion. In some instances, these signs were explained by coincidental non-neural disease or trauma. Therefore, such mild clinical signs cannot be considered pathognominic of EAE. Reports from the literature suggesting that animals have developed clinical signs without histological lesions in EAE are considered invalid because of the nonspecificity of clinical signs, the occurrence of intercurrent diseases, the inadequacy or incorrect timing of histologic evaluations, and the lack of controls for specificity of the signs. There is no basis for the supposition that autoimmunity can cause major neurological signs in the absence of inflammatory lesions in the nervous system.

Animals↗
PubMed1975

Variability of neuropathologic lesions in experimental methylmercurial encephalopathy in primates.

Acute and chronic intoxications of rhesus monkeys with methylmercury produced lesions in the central nervous system (CNS) with different distributions. Neuronal degeneration and astroglial proliferation predominated in the dentate nucleus, lateral geniculate nucleus, thalamus and pontine nuclei in 2 monkeys that received 2 mg/kg/day for 17 and 18 days, whereas pseudolaminar necrosis and astroglial proliferation were observed in the cerebral crotex, maximally in the calcarine and insular regions, in 4 monkeys that received 0.5 to 0.8 mg/kg/day for 3 to 8.5 months. Mercury concentrations in the CNS were much higher in the acutely intoxicated animals than in the chronically intoxicated animals, but the correlation between concentrations of mercury and the histologic destruction was not precise.

Animals↗