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Biomedical subjects

F Gray

Publications and source records attributed to F Gray.

At least 199 records · Page 11Linked to original sources
PubMed1986

Infarcts of both inferior parietal lobules with impairment of visually guided eye movements, peripheral visual inattention and optic ataxia.

Clinicopathological correlations are reported in a case with bilateral isolated infarcts in the posterior part of the parietal lobes, due to nonbacterial thrombotic endocarditis accompanying pancreatic adenocarcinoma. The initial left-sided infarct induced right visual neglect, impairment of right-beating optokinetic nystagmus (OKN), optic ataxia, Gerstmann's syndrome and apraxia. After the right-sided infarct, which occurred six weeks later, bilateral visuo-oculomotor disturbances were observed, including peripheral visual inattention, disorder of visually guided saccades, severe impairment of foveal smooth pursuit and OKN slow phase. The lesion on the left involved the upper part of the angular gyrus and a part of the adjacent superior parietal lobule (SPL). That on the right involved the supramarginal gyrus and extended posteriorly into the superoanterior extremity of the angular gyrus, into both margins of the adjacent intraparietal sulcus and into a small part of the SPL. As the oculomotor deficits and the peripheral visual inattention were bilateral after the second infarct, they probably resulted from the lesion of homologous areas in both cerebral hemispheres. The zone damaged in common included a small part of the SPL, the superoanterior extremity of the angular gyrus, and the adjacent intraparietal sulcus and a small portion of the subcortical white matter. This restricted cerebral zone could therefore, in man, be implicated both in the control of all visually guided eye movements and in visual attention. It is further suggested that two corticofugal pathways are implicated in visually guided saccades, the first arising from the frontal eye fields and projecting directly onto the premotor structures in the brainstem, the second arising from the posterior parietal cortex (probably mainly the intraparietal sulcus adjacent to the angular gyrus) and including a relay in the superior colliculus before reaching the premotor structures. Lastly, the findings support the hypothesis that optic ataxia results from interruption of direct and/or crossed occipitofrontal pathways coursing in the deep white matter of the parietal lobe.

Ataxia↗
PubMed1986

Focal perivascular alterations of white matter in herpes simplex encephalitis--a histological and immunocytochemical study.

Several cases of human herpes simplex encephalitis treated with Vidarabin have been investigated with the histological and immunocytochemical techniques. Cases with a subacute evolution revealed areas of focal perivascular myelin destruction in the white matter. The distribution of herpes simplex antigen did not show any preferential localization of the virus in perivascular oligoglial cells. In contrast, a spatial and temporal relationship has been found between the appearance of immunoglobulin-bearing cells around the vessels and that of areas of focal perivascular myelin damage. Therefore, it is postulated that the areas of focal destruction of myelin are not related to the cytotoxic effect of the virus but are rather dependent on the immune response of the host.

Adult↗
PubMed1986

Orthostatic hypotension from a cerebellar gangliocytoma (Lhermitte-Duclos disease). Case report.

A 49-year-old woman presented with orthostatic hypotension. Vertebral angiography and ventriculography revealed a tumor of the left cerebellar hemisphere. Ventriculoperitoneal shunting was followed by complete disappearance of the orthostatic hypotension. The tumor was subsequently removed and microscopic study showed Lhermitte-Duclos disease. Orthostatic hypotension has been rarely reported in association with tumors of the posterior fossa except for those tumors destroying the medullary centers and interrupting the baroreceptor reflex arc. This case is of interest because the tumor was restricted to the cerebellum. The authors have found no previous case in which orthostatic hypotension was a presenting symptom of Lhermitte-Duclos disease.

Cerebellar Neoplasms↗
PubMed1986

[Myoclonic cerebellar dyssynergia (Ramsay-Hunt syndrome) and cerebellar telangiectasia].

A 8 year-old girl presented with generalized epileptic seizures followed by the progressive onset of myoclonic jerks, sometimes associated with willed movements, and a static and kinetic cerebellar syndrome without conspicuous intellectual impairment. Death occurred 10 years after the onset of the disorders. There was no family history. Neuropathological studies showed lesions confined to the cerebellum. Diffuse and bilateral telangiectases were present in the cerebellar white matter. They were associated with patchy cortical alterations of the distal parts of some folia involving mainly the granule-cells ans sparing the Purkinje cells. No Lafora bodies and no abnormal lipofuscin storage were observed. The dentate nuclei, superior cerebellar peduncles and red nuclei were normal as were the inferior olives and inferior cerebellar peduncles. The spino-cerebellar tracts were unaffected. This case confirms the hypothesis that dyssynergia cerebellaris myoclonica corresponds only to a clinical entity. It may be encountered in various degenerative or metabolic disorders involving the cerebellum and/or its pathways. To our knowledge the association of a Ramsay Hunt syndrome with a vascular malformation has not been previously reported.

Adolescent↗
PubMed1986

[Hemiballismus and metastasis to the Luys' body. An anatomo-clinical case].

A 55 year-old man complained of headaches, dizziness and vomiting. Neurological examination only showed a cerebellar syndrome. CT scan revealed two hyperdense round areas in the right frontal lobe and cerebellar vermis consistent with metastases and a lung carcinoma was diagnosed. Two months later he presented with typical right hemichorea. A second CT scan showed another hypodense lesion with slight contrast enhancement in the left subthalamic region. He died 6 months after clinical onset. Post mortem examination showed an adenocarcinoma of the right lung with liver metastases. Neuropathological examination revealed four intraparenchymatous metastases one of which involved the left subthalamic nucleus. Hemichorea secondary to metastatic neoplasm of the corpus Luysii is uncommon; only 6 cases have been reported previously; five of them had a post mortem examination of the brain. In three cases a CT scan was available and had demonstrated the site and nature of the lesion.

Adenocarcinoma↗
PubMed1986

[Non-dominant hemisphere syndrome as a result of a right thalamic infarct: an anatomoclinical case].

A 71 year old man had a massive left sensory deficit and hemiplegia, with left heminanopia, visual neglect and constructional apraxia. Moreover he experienced an extra-left arm and illusions of movements. 3 weeks later he suffered "thalamic" pain on left side; he died suddenly 6 weeks after the stroke. Post-mortem examination revealed: a) a right inner temporal and occipital infarction; b) a right thalamic infarction in the thalamogeniculate and paramedian territories; c) an infarction in the adjacent right internal capsule. Considering this case and pertinent literature on clinicopathological studies of right thalamic infarction, the authors suggest that a simultaneous ischaemia of thalamogeniculate and paramedian territories should be necessary to induce somatognosic and visuospatial disturbances.

Aged↗
PubMed1985

Leukoencephalopathy in diffuse hemorrhagic cerebral amyloid angiopathy.

We have studied 12 patients with diffuse hemorrhagic cerebral amyloid angiopathy clinically and at postmortem examination. The brains in 8 patients had diffuse bilateral loss of myelin in the hemispheric white matter sparing the U fibers, corpus callosum, and internal capsules. The periventricular areas were predominantly affected. Microscopic examination of the white matter showed an association with subacute or chronic edematous lesions: spongiosis, swollen oligodendroglia, widening of the perivascular spaces with edema fluid or siderophages, hyalinization of the blood vessel walls, incomplete myelin loss, and astrocytic gliosis. Three of 8 autopsied patients had undergone computed tomographic examination, which showed bilateral hypodensity of the hemispheric white matter. The brains of 4 patients with illnesses of shorter duration showed only discrete but similar lesions in the centrum semiovale. These white matter changes are similar to those observed in Binswanger's subcortical encephalopathy. We suggest that a common mechanism of hypoperfusion of the distal white matter causes the leukoencephalopathy.

Aged↗
PubMed1985

Dopaminergic and cholinergic lesions in progressive supranuclear palsy.

In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.

Aged↗
PubMed1985

Failure to detect scrapie virus in sheep at slaughter in a highly endemic region of France.

A study was carried out in a sheep slaughterhouse located in a region of France where scrapie has been endemic for several decades. Neuropathological examination of 63 randomly selected lambs and adult sheep revealed no scrapie-related abnormalities, and inoculation of mice with brain, tonsil, lateropharyngeal ganglia, and intestine from the same animals did not transmit scrapie. The failure to detect any evidence of scrapie infection in commercially-bred sheep, the absence of an increased mortality rate for human CJD in the surrounding consumer region, and the absence of a single case of CJD among slaughterhouse personnel, do not support the hypothesis that exposure to potentially scrapie-contaminated products is responsible for CJD in humans.

Abattoirs↗
PubMed1985

Altered capillary permeability in neurogenic pulmonary oedema.

Two cases of fatal neurogenic pulmonary oedema are depicted. The hemodynamic study failed to document any hypertensive crisis or pulmonary hypertension. By contrast, the low values of pulmonary capillary wedge pressures and the high protein concentration in tracheal fluid suggest a pulmonary capillary wall lesion.

Adult↗
PubMed1985

Luyso-pallido-nigral atrophy and amyotrophic lateral sclerosis.

The clinical and pathologic findings in a 34-year-old woman with basal ganglia degeneration and amyotrophic lateral sclerosis are reported. The duration of symptoms was 2 years. A maternal uncle had a parkinsonian syndrome with onset at 45 years of age. Neuropathologic examination revealed extensive neuronal loss and gliosis in the corpus Luysii. Nerve cell loss and gliosis also involved both parts of the globus pallidus, and the substantia nigra. The corticospinal tracts were demyelinated in the spinal cord, and neuronal loss was observed in the anterior horns. Only one similar case of pallido-luyso-nigral atrophy associated with amyotrophic lateral sclerosis has, to our knowledge, been reported previously. Such an association may represent more than a coincidental occurrence.

Adult↗
PubMed1985

[Baló's concentric sclerosis: lesions restricted to the pons].

A clinico-pathological case of Baló's concentric sclerosis is reported. Besides the rarity of the disease, this case was interesting because of the late onset of the illness (50 years) the normality of the CSF and the localization of the lesions which were restricted to the pons.

Autopsy↗
PubMed1985

[Arteriopathic leukoencephalopathy (17 anatomo-clinical cases)].

Seventeen clinico-pathological cases of leukoencephalopathy due to vascular diseases are reported. All of them had diffuse, often spotty demyelination sparing the U fibers, the corpus callosum, the internal capsule and the optic radiations. Microscopic examination of the white matter showed the association of the following lesions: oedema, swollen oligodendroglia, spongiosis, incomplete loss of myelin, astrocytic gliosis with Rosenthal's fibers, widening of the perivascular spaces with oedema fluid or hemosiderin laden macrophages, thickening and hyalinization of the blood vessels walls. Among those cases, 8 were consistent with Binswanger's subcortical encephalopathy (5 males, 3 females, mean age at death: 64 years, mean illness duration: 6, 7 years); all of them were hypertensive and had lacunae in the basal ganglia, hemispheric white matter and pons. Another case could be considered as a cortico-subcortical chronic hypertensive encephalopathy (77 y.o., female, illness duration: 4 years); she was hypertensive and had small cortical infarcts and perivascular bleedings, lobar and cerebellar hematomas, but no amyloid deposits in the blood vessels walls. Eight patients (5 males, 3 females mean age at death: 72 years, mean illness duration: 5, 4 years, 6 normotensive, 2 hypertensive) had diffuse meningocortical amyloid angiopathy with multiple small cortical infarcts, small cortical perivascular bleedings, slit haemorrhages and one or more lobar hematomas. Four of them had numerous senile plaques and neurofibrillary tangles. To our knowledge such a leukoencephalopathy in cerebral amyloid angiopathy has not been yet pointed out. It was present in 8 out of 12 cases of diffuse haemorrhagic form of cerebral amyloid angiopathy observed in the Charles Foix Laboratory of la Salpêtrière, during the last 10 years. A common mechanism with hypoperfusion of the distal white matter and alteration of the blood brain-barrier is suggested for this leukoencephalopathy.

Aged↗