PubMed Health⌕ Search

Biomedical subjects

T J Crow

Publications and source records attributed to T J Crow.

At least 19 recordsLinked to original sources
PubMed1992

Schizophrenia, genetic retrenchment, and epidemiologic renaissance. The Sixth Biennial Winter Workshop on Schizophrenia, Badgastein, Austria, January 26-February 1, 1992.

A distinctive feature of these workshops, in addition to those noted in the introductory overview, is the selection of a relatively isolated location for a 1-week period. This, together with a rich and varied program and an ethos of informality, encourages participants to discuss not only the work presented but also their unpublished work and their intuitions based on preliminary data and analyses. Such an interchange is of inestimable value to the schizophrenia research community. In scientific terms, a panel of concluding discussants (Drs Kendell, Torrey, and Waddington) were in some measure of agreement that genetics, particularly molecular genetics, appears to be experiencing a period of retrenchment, while epidemiology is experiencing something of a renaissance. Maternal influenza was a prominent theme, although the data were far from consistent. It was argued by Dr Wessely that risk for schizophrenia putatively attributable to maternal influenza might be 5% to 10% of all cases, indicating a modest effect. Eclectically, Dr Kendell believed the effect to be "real" but slight and fragile, it being sought against large aggregates that almost inevitably result in differing findings from differing countries or from different data bases within a given country. Gender differences were also among the more prominent themes, not just in an epidemiologic context but also in a variety of other studies. This points anew to disturbances in schizophrenia of factors that regulate, or are intimately associated with, sexual dimorphism in brain development. Abnormalities in cerebral asymmetry continue to pervade a variety of research findings and point further to neurodevelopmental anomalies.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1992

A dementing illness associated with a novel insertion in the prion protein gene.

Following our previous report of an 144-bp insertion in the open reading frame of the prion protein (PrP) gene, we have now identified a larger, 216-bp, insertion in the gene. The insertion which is in frame encodes 9 extra octapeptide repeat sequences in addition to the 5 repeats normally present and represents the largest insertion so far detected in the PrP gene.

Alleles↗
PubMed1992

The Northwick Park 'Functional' Psychosis Study: diagnosis and outcome.

Three hundred and twenty-six consecutively admitted patients with functional psychotic illnesses to which no diagnostic classification had been applied were followed up after 2.5 years. They were examined in social, clinical and psychological terms and the CATEGO programme and DSM-III criteria were applied to data concerning the index episode to derive diagnostic classifications. The deterioration in occupational functioning and the hospital careers of patients with diagnostic classifications of schizophrenia were worse than those in the other groups and positive and negative features were also more severe in patients with a classification of schizophrenia. By contrast, no differences in psychological test performance were found between the groups based upon diagnostic classification. Impaired psychological test performance was found and it was strongly related to concurrent mental state abnormalities, particularly negative symptoms. It is concluded that the diagnostic classifications used were of limited value in predicting outcome in functional psychosis.

Adult↗
PubMed1992

Inherited prion disease with 144 base pair gene insertion. 2. Clinical and pathological features.

A large family with autosomal dominant segregation of presenile dementia, and other neurological and behavioural features is described. At various times, family members have carried diagnoses of Alzheimer's disease, Huntington's disease, Parkinson's disease, myoclonic epilepsy, atypical dementia, Pick's disease, Creutzfeldt-Jakob disease and Gerstmann-Sträussler syndrome. Molecular genetic studies have enabled classification of this disease at the molecular level as one of the group of inherited prion diseases. Here we describe the phenotype of inherited prion disease (PrP 144 bp insertion).

Adult↗
PubMed1992

Who benefits from electroconvulsive therapy? Combined results of the Leicester and Northwick Park trials.

This paper describes the results obtained by combining data from the Northwick Park and Leicester randomised controlled trials of ECT. Patients who suffered from depression in which retardation and delusions were features and who received real ECT had a significantly improved outcome at the end of four weeks of treatment (as measured by improvement in the HRSD) in comparison with those who received simulated ECT. However, this treatment effect was not detectable at six-month follow-up. Patients who were neither retarded nor deluded did not benefit significantly from real as opposed to simulated ECT.

Antidepressive Agents↗
PubMed1992

Prenatal exposure to influenza does not cause schizophrenia.

Claims have been made that maternal infection with influenza during pregnancy is a cause of schizophrenia in the child. These assertions are based upon some apparently significant associations between the timing of influenza epidemics in the general population and birth rates of people who later suffered from schizophrenia. Such associations have not been present in studies of the 1919 and 1957 epidemics, with sample sizes larger than those on which the claims were made. More decisively, in an investigation of the subsequent psychiatric admissions of people born a few months after the 1957 epidemic, it was found that the children of 945 mothers who actually suffered from influenza during the second trimester of pregnancy were at no greater risk of developing schizophrenia than children of mothers who were not infected. In contrast to the predictions of the influenza hypothesis of 26.5 extra cases by broad diagnostic criteria and 15.8 cases by narrow criteria, the numbers observed in children of mothers exposed to influenza in the second trimester were 3 and 1 cases respectively, close to the expected rate. It is concluded that prenatal influenza and schizophrenia are unrelated.

Adolescent↗
PubMed1991

Complications of pregnancy and delivery in relation to psychosis in adult life: data from the British perinatal mortality survey sample.

OBJECTIVE: To evaluate whether events occurring at or around the time of birth contribute to the onset of psychotic illness in adult life. DESIGN-Pregnancy and birth complications as possible causes of adult mental illness were studied in the population sample of the British perinatal mortality survey. Subsequent psychiatric admissions were independently identified through the Mental Health Enquiry and records of regional and special health authorities. Logistic regression was used to compare data on perinatal deaths with those on survivors to determine factors independently associated with perinatal death, and this equation was then used to calculate the risk of perinatal death for each survivor. SUBJECTS: 16,980 people born in a single week in 1958 (the British perinatal mortality survey sample), including 252 patients admitted to psychiatric care; case notes of 235 patients were supplied. MAIN OUTCOME MEASURES AND RESULTS: Patients with a schizophrenic illness (whether defined by "broad" (n = 57) or "narrow" (n = 35) diagnostic criteria) did not have a greater mean risk of perinatal death than the population in general, but there was some evidence of increased liability (relative risk 2.43; 95% confidence interval 1.17 to 5.05) for those with affective psychosis (n = 32). Specific high risk variables for affective psychosis were decreased gestation time (273.9 v 281.2 days; mean difference 7.3 days, 95% confidence interval 3.1 to 11.5; p less than 0.002) and prescription of vitamin K to the child in the first week of life (19% of patients v 5% of controls, p = 0.016). CONCLUSIONS: The findings give no support to theories that factors predicting perinatal mortality contribute significantly to causation of schizophrenic illness. Further investigation of decreased gestation length in relation to affective disorder is required.

Adult↗
PubMed1991

G proteins (Gi, Go) in the medial temporal lobe in schizophrenia: preliminary report of a neurochemical correlate of structural change.

We have measured the amount of Gi (the inhibitory G-protein) or Go (a similar G-protein of unknown function) in 5 areas of the medial temporal lobe of control and schizophrenic brains utilizing pertussis toxin-catalyzed ADP ribosylation. The material used has previously been shown to have asymmetrical structural abnormalities of the ventricular system. The amount of Gi or Go was reduced on the left side in the hippocampus, amygdala and parahippocampal gyrus, the difference reaching significance in the hippocampus. This data is the first report of a neurochemical correlate of the structural change in the brains of patients with schizophrenia. Decreased Gi or Go in hippocampus may relate to other reported neurochemical deficits or other transmembrane signalling abnormalities. Further investigations of these indices of secondary messenger function in relation to structural changes are indicated.

Adenosine Diphosphate Ribose↗
PubMed1991

Insertions in the prion protein gene in atypical dementias.

A number of mutations have been demonstrated in the open reading frame (ORF) of the prion protein (PrP) gene in patients with familial Creutzfeldt-Jakob disease or Gerstmann-Sträussler syndrome. On the basis of detecting an insertion in the ORF of the PrP gene in a patient originally suspected to be suffering from familial Alzheimer-type dementia, we screened 101 individuals with atypical dementias for the known PrP gene mutations. Insertions were found in five individuals, whereas none of the other reported mutations in the PrP gene was detected in the present study. One of the five insertions was larger than that described previously, suggesting that the individuals with these mutations are unlikely to be all lineally related and that insertions in the PrP gene may not be uncommon in prion diseases.

Alzheimer Disease↗