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Biomedical subjects

F Gray

Publications and source records attributed to F Gray.

At least 289 records · Page 16Linked to original sources

'Expanding cerebral lacunae' in a hypertensive patient with normal pressure hydrocephalus.

A hypertensive patient who had been treated successfully for normal pressure hydrocephalus (NPH), died from a left thalamic haemorrhage. Neuropathological examination showed recent and old thalamic haematomas and numerous parenchymal cavities or 'cerebral lacunae'. Two lacunae bulged into the lateral ventricles, and had all the characteristics of so called 'expanding lacunae'. They were surrounded by a single layer of epithelial-like cells, contained a normal, patent, arteriole, and presented as space occupying lesions. Only two similar cases have been reported previously. The complexity of the neuropathological features of 'cerebral lacunae' is emphasized and the relationships between cerebral hypertensive disease, NPH, and expanding lacunae are discussed.

Aged↗

Pathology of the central nervous system in 40 cases of acquired immune deficiency syndrome (AIDS).

The central nervous system was examined in 40 AIDS patients who died between August 1982 and 1987. The cases included two children born to intravenous drug abusers and 38 male adults. The brains of eight patients who had no clinical or radiological evidence of central nervous system involvement showed non-specific changes which included microglial nodules, perivascular mononuclear cuffs, mineralization of blood vessels and granular ependymitis. In 32 brains from patients with neurological symptoms, toxoplasmosis was the most frequent finding (19 cases) manifested by multifocal, necrotic lesions or a diffuse pseudo-encephalitic process. Other opportunistic infections included cytomegalovirus (eight cases), progressive multifocal leucoencephalopathy (two cases), cryptococcosis (one case), aspergillosis (one case), multiple bacterial microabscesses (one case) and Mycobacterium avium intracellulare (one case). Two patients had cerebral lymphoma. Subacute encephalitis with white matter lesions and multinucleated giant cells characteristic of HIV infection was present in 15 cases. Various combinations of all these infections were encountered in the same brain, sometimes in the same area and, occasionally, in the same cell.

Acquired Immunodeficiency Syndrome↗

Expanding cerebellar lacunes due to dilatation of the perivascular space associated with Binswanger's subcortical arteriosclerotic encephalopathy.

An 80-year-old hypertensive woman developed right hemiplegia and died 24 hours after admission. Neuropathologic examination revealed multiple cerebral infarcts of various ages and diffuse subcortical arteriosclerotic encephalopathy. Clusters of asymptomatic "expanding" lacunes, due to dilatation of the perivascular spaces, were found in both dentate nuclei. These cavities, which presented as space-occupying lesions, were surrounded by a single layer of flattened cells and contained 1 or more sections of normal-looking arterioles. Such a topographic grouping of lacunes in the dentate nucleus has not been described previously. The mechanism of widening of the perivascular compartment remains unclear; its occurrence in a hypertensive patient and its association with typical Binswanger's subcortical arteriosclerotic encephalopathy and severe atherosclerosis with multiple infarcts suggest a common pathophysiologic mechanism possibly including an alteration of the blood-brain barrier.

Aged↗

Neuropathology and neurodegeneration in human immunodeficiency virus infection. Pathogenesis of HIV-induced lesions of the brain, correlations with HIV-associated disorders and modifications according to treatments.

A variety of HIV-induced lesions of the central nervous system (CNS) have been described, including HIV encephalitis, HIV leukoencephalopathy, axonal damage, and diffuse poliodystrophy with neuronal loss of variable severity resulting, at least partly, from an apoptotic process. However, no correlation could be established between these changes and HIV dementia (HIVD). From our study of HIV infected patients, it appeared that neuronal apoptosis is probably not related to a single cause. Microglial and glial activation, directly or indirectly related to HIV infection, plays a major role in neuronal apoptosis possibly through the mediation of oxidative stress. In our patients with full-blown AIDS, this mechanism predominated in the basal ganglia and correlated well with HIVD. Axonal damage, either secondary to microglial activation, or to systemic factors also contributes to neuronal apoptosis. Although massive neuronal loss may be responsible for HIVD in occasional cases, we conclude that neuronal apoptosis is a late event and does not represent the main pathological substrate of HIVD. The dementia more likely reflects a specific neuronal dysfunction resulting from the combined effects of several mechanisms, some of which may be reversible. Introduction of highly active antiretroviral therapy dramatically improved patient survival, however, its impact on the incidence and course of HIVD remains debatable. In our series, the incidence of HIVE has dramatically decreased since the introduction of multitherapies, but a number of cases remain whose cognitive disorders persist, despite HAART. The poor CNS penetration of many antiretroviral agents is a possible explanation, but irreversible "burnt out" HIV-induced CNS changes may also be responsible.

AIDS Dementia Complex↗

[Delayed radionecrosis of the cerebral hemispheres following betatron electron beam irradiation for scalp cancer. Pathological and clinical findings in one case (author's transl)].

Three years following an irradiation by the Betatron's electron beam of an epithelioma in left parieto occipital area of the scalp in a female patient aged 77, early suffering from high blood pressure, a fatal pseudo-tumoral brain necrosis occurs presenting as a rapidly increasing from of Wernicke's aphasia. The necropsy shows intense radionecrosis lesions of the brain and the bone, free of any parenchymatous malignant proliferation note-worthy for the striking density of microvascular changes as previously described in radiation therapy. The case observed some years ago, allows to definite again the limits doses of the extracranial irradiations now estimated at 1760 rets. That is the "Nominal Standard Dose" (NSD) measured by rets and taking into account the number of seances (N) and the duration of irradiation (T) which would be to take the place of "the total dose" (D) (rads). These dosimetric criteria themselves must be adjusted to the age and the vascular features of each patient.

Age Factors↗

Dengue: neuropathological findings in 5 fatal cases from Brazil.

Neuropathological examination of 5 patients with dengue who died of shock in Rio de Janeiro during an outbreak in summer 1987, showed nonspecific lesions (edema, vascular congestion, hemorrhagic foci and perivascular lymphocytic infiltrates). In one case with delayed marked neurological symptoms, several foci of perivenous demyelination were observed. Neurological manifestations are various and not uncommon in dengue, but their anatomical substratum is not known. An immunopathological mechanism has been postulated in some cases but has never been demonstrated morphologically. The perivenous leukoencephalitis observed in one of our cases could represent the morphological substratum of such an immunological mechanism.

Adolescent↗

Post-anoxic delayed encephalopathy with leukoencephalopathy and non-hemorrhagic cerebral amyloid angiopathy.

A 74 year-old woman with an early-stage senile dementia developed severe hypertonia and akinetic mutism two weeks after exposure to methane. A CT scan showed a diffuse area of decreased density extending symmetrically into the white matter of both cerebral hemispheres. Neuropathology revealed a senile dementia, Alzheimer's type, with severe non-hemorrhagic cerebral amyloid angiopathy and a diffuse spotty demyelination of the cerebral hemispheres sparing the U fibers, corpus callosum and internal capsules. The close resemblance between Grinker's myelinopathy, secondary to CO exposure or to other non-CO anoxic causes, and the leukoencephalopathy associated with cerebral amyloid angiopathy is emphasized.

Aged↗

[Sigmoid perforation during the course of cholesterol emboli simulating polyarteritis nodosa (author's transl)].

Cholesterol emboli have only recently been recognized as a pathological entity and their clinical picture is still not clearly defined. A case is reported of a patient presenting signs of a severe systemic affection with distal arteriolitis and also general and biological signs of a severe inflammatory process having the particular characteristic of apparent corticoid sensitivity. The patient died following ischemic necrosis of the sigmoid from perforation and peritonitis, also related to the presence of cholesterol emboli.

Aged↗

[Acute pseudobulbar palsy related to bilateral infarction of a part of the anterior choroidal arteries territory; a case report (author's transl)].

A 73 year old man had a pure, acute pseudobulbar syndrome. The pathological study showed only two infarcts of different ages. They involved uncompletely the territories of both anterior cohroidal arteries. On semi-serial sections, both cortico-bulbar tracts were destroyed whereas the cortico-spinal tracts were spared.

Acute Disease↗

[Strümpell Lorrain's familial spasmodic paraplegia. An anatomical and clinical review and report on a new case (author's transl)].

The authors describe the anatomical and clinical findings in a case of the pure form of Strümpell Lorrain's familial spasmodic paraplegia. This hereditary condition of the dominant autosomic type has very monomorphic pathognomonic features which are found in all patients affected. The slowly progressive isolated spastic hypertonia appears exclusively in the upright position and the extent of the disease can be ascertained by clinical observation during walking. The myelino-axial degeneration which is strictly limited to the spinal cord has an elective localization in the crossed pyramidal tracts, is less evident in the direct tracts and is mainly predominant in the lumbosacral and low dorsal regions of the cord. The extension of the process beyond the limits of the extrapyramidal tracts confirms the generally accepted unity of spinocerebellar degenerations. In this case the spinocerebellar tracts were less involved than the lumbar spinal ganglia, as well as their distant axial continuation to Goll's tracts only at the cervical level and until the bulber nucleus gracilis.

Brain↗

[Eosinophilic myositis and Shulman syndrome (author's transl)].

Three cases with eosinophilic infiltration of fascia and muscle are described. In every case at least one relapse occurred. One patient exhibited clinically the definite features of eosinophilic fasciitis. About two cases a tentative diagnosis of Shulman's syndrome is discussed. In these patients, all known causes of eosinophilic myositis had been excluded.

Diagnosis, Differential↗