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J A Corsellis

Publications and source records attributed to J A Corsellis.

At least 19 recordsLinked to original sources
PubMed1986

Postmortem evidence of structural brain changes in schizophrenia. Differences in brain weight, temporal horn area, and parahippocampal gyrus compared with affective disorder.

The brains of 232 patients with a case-note diagnosis of schizophrenia or affective disorder who died in one mental hospital over a period of 22 years were weighed, and were assessed in a coronal section at the level of the interventricular foramina. From this sample were eliminated the brains of patients whose illnesses did not meet the Washington University criteria for a diagnosis of definite schizophrenia or primary affective disorder and those brains that showed significant histopathologic evidence of Alzheimer's-type change or cerebrovascular disease. This left a sample of 41 patients with schizophrenia and 29 patients with affective disorder. With age, sex, and year of birth controlled for, the brains of the patients with schizophrenia were 6% lighter, had lateral ventricles that were larger in the anterior (by 19%), and particularly in the temporal, (by 97%) horn cross section, and had significantly thinner parahippocampal cortices (by 11%). The findings provide postmortem confirmation of reports of ventricular enlargement in radiological studies and suggest that such enlargement is associated with tissue loss in the temporal lobe. The changes in schizophrenia were of a lesser degree than those seen in a sample of brains of patients with Alzheimer's-type dementia and Huntington's chorea.

Aged↗
PubMed1984

Serotonin receptor changes in dementia of the Alzheimer type.

Serotonin receptors were assessed in post-mortem brains of control and Alzheimer-type dementia (ATD) patients using ligand binding techniques. Differential losses of serotonin S1 and S2 receptors were present in neocortex, hippocampus, and amygdala of ATD patients, whereas no significant changes were observed in basal forebrain and basal ganglia. Losses of S1 receptors were significantly age-related in the ATD group, suggesting they occurred at a later stage of the disease process. Losses of S2 receptors were considerably greater (with a reduction to 35% of control in temporal cortex) and were not age-related in ATD. Significant correlations were observed within the ATD group between S2 receptor binding and somatostatin immunoreactivity in temporal and frontal cortices. Thus the loss of S2 receptors in ATD may be a relatively early change in the disease process, and may precede the changes in ascending serotonergic neurones.

Aged↗
PubMed1983

Neuropeptides in Alzheimer type dementia.

Five neuropeptides (cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), somatostatin (SRIF), neurotensin (NT) and substance P (SP)) were measured in 14 brain areas (4 cortical areas, hippocampus, amygdala, 3 striatal areas, 2 thalamic areas and 3 subcortical areas-- septum, substantia innominata and hypothalamus) in 12 brains with neuropathologically confirmed Alzheimer type change and in 13 control brains. Choline acetyltransferase (CAT) activity was assessed in 6 of these areas. Levels of SRIF, but not those of the other peptides, were reduced in several cortical areas in Alzheimer-type dementia (ATD). The distribution and magnitude of the reduction in SRIF were less than that of CAT activity and the temporal cortex was the only region in which there was a significant relationship between CAT and SRIF deficits. Peptide levels were unchanged in hippocampus, amygdala, thalamus, hypothalamus and striatum (except for an increase in SP in the putamen). SRIF levels were increased in substantia innominata in ATD. NT and SRIF were significantly, and VIP and SP non-significantly, reduced in the septum in ATD. Thus, apart from these alterations in the septum, SRIF was the only neuropeptide for which major changes were identified and these did not follow either the pattern of neuropathological change (e.g. in amygdala and hippocampus) or of CAT deficits (e.g. in substantia innominata).

Aged↗
PubMed1978

The late effects of necrotizing encephalitis of the temporal lobes and limbic areas: a clinico-pathological study of 10 cases.

The clinical and neuropathological features are reported of 10 patients who had suffered, usually for several years, from the after effects of an acute or sub-acute necrotizing encephalitis of the limbic grey matter and of the adjacent temporal lobes. Emphasis is laid on the memory disturbance and on the behavioural and emotional aberrations that tended to occur and that are in some ways reminiscent of the Klüver-Bucy syndrome.

Adult↗
PubMed1977

Evidence for a secular increase in human brain weight during the past century.

7397 post-mortem records have been studied. These comphrhend all 20- to 50-year old men and women who had been autopsied in The London Hospital since 1907. Fresh brain weight, body weight and height were abstracted and analysed statistically according to sex and to year of birth, any person with a cerebral or skeletal abnormality having been excluded. Fresh brain weight in men increased gradually by an average of 0-66 g per year from a mean of 1372 g for those born in 1860 to 1424 g in 1940-a total of 52 g. The weight of the female brain increased by 0-28 g per year from 1242 g to 1265 g over the same period. No appreciable rise in fresh brain weight occurred in women until 1900, after which date the increase was of the same order in the two sexes. Evidence of secular increases in body height and in body weight is also given.

Adult↗
PubMed1975

Recovery of adenovirus type 7 from human brain cell cultures.

A strain of adenovirus type 7 was recovered from cultured brain cells, taken at necropsy from a patient aged 71 years with chronic schizophrenia. This recovery may indicate the reactivation of a latent infection with one of the few adenoviruses that has regularly-if rarely-been associated with clinical encephalitis.

Adenoviridae↗
PubMed1971

Focal dysplasia of the cerebral cortex in epilepsy.

An unusual microscopic abnormality has been identified in the lobectomy specimens removed surgically from the brains of 10 epileptic patients. The abnormality could seldom be identified by palpation or with the naked eye. Histologically, it consisted of congregations of large, bizarre neurones which were littered through all but the first cortical layer. In most, but not in all cases, grotesque cells, probably of glial origin, were also present in the depths of the affected cortex and in the subjacent white matter. This kind of abnormality appears to be a malformation. The picture is reminiscent of tuberous sclerosis but too many distinguishing features, both in the clinical and in the pathological aspects, make this diagnosis untenable. The cases are therefore looked on provisionally (since all but one are still alive) as comprising a distinct form of cortical dysplasia in which localized, exotic populations of nerve cells underlie the electrical and clinical manifestations of certain focal forms of epilepsy.

Adolescent↗