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Biomedical subjects

P Sham

Publications and source records attributed to P Sham.

98 records · Page 6Linked to original sources
PubMed1992

Genes, viruses and neurodevelopmental schizophrenia.

Recent neuroimaging and neuropathological studies suggest a developmental origin for schizophrenia. Some cases may, therefore, be caused by a genetic defect in the specification of brain development. Early environmental hazards such as obstetric complications, and maternal exposure during pregnancy to influenza epidemics, have also been found to increase the risk of later schizophrenia. The relationship between the prevalence of influenza and birth date has been found more consistently for female than male schizophrenics. Female schizophrenia is also associated with a higher risk of schizophrenia in first degree relatives. This raises the question of whether part of the genetic predisposition to schizophrenia may comprise an abnormal reaction to maternal influenza.

Brain Damage, Chronic↗
PubMed1992

Seasonality of admissions in the psychoses: effect of diagnosis, sex, and age at onset.

A summer peak was found in first admissions to hospitals in England and Wales between 1976 and 1986 for both affective psychoses and schizophrenia, but not for neurotic conditions or personality disorders. There was no significant relationship between age at first admission and season of admission. The summer peak was most prominent for mania, where it was present in both sexes; for schizophrenia, it was present only in females. These findings suggest that schizophrenia in females, and mania in both sexes, have some aetiological or precipitating factor in common.

Adult↗
PubMed1991

Schizophrenia after prenatal exposure to 1957 A2 influenza epidemic.

The birth dates of schizophrenic inpatients in eight health regions in England and Wales were reviewed for any effect of the 1957 A2 influenza epidemic. 5 months after the peak infection prevalence, the number of births of individuals who later developed schizophrenia was 88% higher than the average number of such births in the corresponding periods of the 2 previous and the next 2 years. This finding is in accordance with a study from Helsinki and with clinical and neuropathological evidence of aberrant fetal brain development in the pathogenesis of schizophrenia.

Adult↗
PubMed1991

Tyrosine hydroxylase polymorphisms and bipolar affective disorder.

A reported genetic association between bipolar affective disorder and DNA polymorphisms at the tyrosine hydroxylase gene is not confirmed by the present study. The combined allele frequencies in the patients, from studies published to date, are significantly different from the frequencies in the controls for the TY7/BglII polymorphism.

Alleles↗
PubMed1991

Can future suicidal behaviour in depressed patients be predicted?

The determinants of suicidal behaviour over 18 years were examined in a series of 89 depressed in-patients, using index data on clinical features, personality, and history of past loss. Seven variables were selected from univariate analyses and their relationship with (1) the presence or absence, (2) frequency, (3) intent, and (4) medical threat of suicidal behaviour was then explored by generalised linear modelling. Severe dysphoria, past alcoholism and chronic physical illness were most predictive of suicidal attempting; however, different variables predicted the frequency, degree of intent and severity of medical threat of subsequent suicidal attempts. Thus, our results suggest that different aspects of long-term suicidal behaviour have different determinants.

Adolescent↗
PubMed1991

Does recurrent depression lead to a change in neuroticism?

The hypothesis that recurrent or chronic depressive illness produces a long-term change in neuroticism was examined in a sample (N = 34) from a consecutive series of 89 depressed patients admitted to the Maudsley Hospital in 1965/6. The Eysenck Personality Inventory (EPI) was administered at the time of the index illness both when the patients were depressed and on recovery, and then again at follow-up 18 years later. The change in the neuroticism (N) score over the 18-year-period was compared in good and poor outcome groups defined variously by a global rating of outcome, frequency of episodes, extent of subsequent hospitalization and the presence or absence of subsequent chronicity. The mean N score for the sample as a whole did not change significantly over the 18 years, and no differential change in the N score was observed between any of the good and poor outcome groups. Thus, the hypothesis was not supported.

Adolescent↗
PubMedDate not supplied

[Influence of serotonergic transmission on response to olanzapine].

INTRODUCTION: This study aimed to investigate associations between the response to olanzapine and genetic variations (polymorphisms) in serotonergic transmission related genes in a sample of prospectively studied schizophrenic patients treated with this drug. METHODOLOGY: A total of 51 non-related patients with a DSM-IV diagnosis of schizophrenia were treated with olanzapine (mean dose: 12 mg/day; range: 5-25 mg) and followed-up for at least three months. Response to olanzapine was measured by the difference between baseline and post-treatment scores on the PANSS and GAS scales. The following polymorphisms were studied: serotonin receptor 5-HT2A (102-T/C, His452Tyr), serotonin receptor 5-HT2C (Cys23Ser, -330-GGT/-244-CT), and serotonin transporter (VNTR, 5-HTTLPR). RESULTS: Global clinical improvement, measured with both the GAS and PANSS total scores, was observed. When patients were divided into responders and non-responders, the distribution of genotypic and allelic frequencies was similar to the one observed in previous studies with clozapine. When regression analyses were undertaken, polymorphism 330-GT/-244-CT of the 5-HT2C serotonin receptor and 5-HTTLPR of the serotonin transporter showed a tendency towards the association to olanzapine response. CONCLUSIONS: The present study provides preliminary evidence of the important role of variations in serotonin transmission related genes in determining clinical response to olanzapine. Considering previous studies, it can also be concluded that olanzapine and clozapine may have similar affinities to serotonin receptors.

Adolescent↗