MINOR PHYSICAL ANOMALIES IN FAMILIAL AND SPORADIC SCHIZOPHRENIA - THEMAUDSLEY FAMILY STUDY

Citation
Td. Griffiths et al., MINOR PHYSICAL ANOMALIES IN FAMILIAL AND SPORADIC SCHIZOPHRENIA - THEMAUDSLEY FAMILY STUDY, Journal of Neurology, Neurosurgery and Psychiatry, 64(1), 1998, pp. 56-60
Citations number
20
Categorie Soggetti
Psychiatry,"Clinical Neurology",Surgery
ISSN journal
00223050
Volume
64
Issue
1
Year of publication
1998
Pages
56 - 60
Database
ISI
SICI code
0022-3050(1998)64:1<56:MPAIFA>2.0.ZU;2-B
Abstract
Objectives-(1) To test the hypothesis that minor physical anomalies ar e increased in patients with schizophrenia and (2) to investigate diff erences in the prevalence of minor physical anomalies in patients with familial and sporadic schizophrenia and their first degree relatives. Methods-A weighted Waldrop assessment was carried out on 214 subjects in five groups: schizophrenic patients from multiply affected familie s; first degree relatives of these familial schizophrenic patients; sp oradic schizophrenic patients; first degree relatives of these sporadi c schizophrenic patients, and normal controls. Broad and narrow criter ia for abnormality were defined based on the distribution of minor phy sical anomalies in the control group. Results-(1) The total schizophre nic group did not have a significant increase in minor physical anomal ies using a narrow criterion of abnormality, but did when a broader cr iterion was used. (2) A significant increase in the proportion of subj ects with an abnormally high number of minor physical abnormalities wa s shown in the group of sporadic schizophrenic patients (uncorrected p <0.01). Separate analyses for males and females showed a significant i ncrease in the male sporadic group (uncorrected p<0.05), and a smaller non-significant increase in the female sporadic group. Neither the fa milial schizophrenic group nor either group of first degree relatives showed any significant increases in the proportion of patients with hi gh abnormality scores. Conclusion-This work supports prenatal developm ental abnormality as a mechanism for sporadic, but not familial, schiz ophrenia.