title: Physical manifestations of neurodevelopmental disruption: are minor physical anomalies part of the syndrome of schizophrenia?
abstract: The well-documented excess of minor physical anomalies (MPAs) among individuals with schizophrenia generally supports the neurodevelopmental model, which posits that both genetic and environmental factors contribute to structural and functional brain changes in the intrauterine and perinatal periods that predispose one to developing schizophrenia. This review synthesizes select areas of research findings on MPAs to address the question, Are MPAs part of the syndrome of schizophrenia? Although MPAs are not specific to schizophrenia, their presence in some patients indicates that aberrations in the development of the nervous system contribute to risk for the disorder. The broadly defined, heterogeneous MPA construct may be of limited value in further elucidating the specific pathophysiology of schizophrenia, though particular anomalies, such as those pertaining to nasal volumes, palatal abnormalities, or craniofacial morphology, may be informative. Given the availability of more sophisticated microarray technologies, and in light of recent findings on spontaneous mutations in patients with schizophrenia, it is possible that MPAs will prove to be useful in identifying etiologic subtypes and/or the loci of genetic risk factors. It remains to be determined whether MPAs-which, of course, are fixed markers present throughout childhood and adolescence well before the onset of the prodrome and psychosis-may have utility in terms of risk stratification for future preventive efforts. Taken together, research findings on MPAs indicate that these minor anomalies are indeed part of some schizophrenia syndromes, representing a stable systemic or physical set of manifestations of the underlying neurodevelopmental processes that lead to the illness.
authors.affiliation: Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 49 Jesse Hill Jr Drive, SE, Room No. 333, Atlanta, GA 30303, USA. Michael.Compton@emory.edu
authors.forename: Michael T
authors.initials: MT
authors.lastname: Compton
authors.forename: Elaine F
authors.initials: EF
authors.lastname: Walker
mesh_terms: D015415:Biomarkers; D003072:Cognition Disorders / Q000235:genetics / Q000503:physiopathology; D000013:Congenital Abnormalities / Q000235:genetics / Q000503:physiopathology*; D019465:Craniofacial Abnormalities / Q000235:genetics / Q000503:physiopathology; D044127:Epigenesis, Genetic; D005260:Female; D006801:Humans; D008297:Male; D009154:Mutation / Q000235:genetics; D010641:Phenotype; D012307:Risk Factors; D012559:Schizophrenia / Q000235:genetics / Q000503:physiopathology*; D013577:Syndrome
chemical_list: D015415:Biomarkers