Abstract
The cause of schizophrenia, a serious mental illness characterized by hallucinations, delusions and a marked deterioration in social functioning, is an enigma that continues to perplex the scientific community. While we know that approximately 80% of the risk of developing schizophrenia is conferred by genes (1), no research group has yet located a gene(s) contributing to the cause of schizophrenia. Moreover, while a significant environmental contribution is indicated by the fact that one-half of monozygotic twins pairs are discordant for schizophrenia, the nature of this environmental contribution is still controversial. The past theory that an abnormal family upbringing was the causative environmental factor has not stood up to scientific scrutiny. In recent years, the search for causative environmental factors has focused on the possibility that some type of prenatal insult predisposes the fetus to develop schizophrenia in early adult life. The initial suspicion of an intrauterine insult was based on indirect evidence. First, dermatoglyphic patterns in patients with schizophrenia were noted to be abnormal. The dermal ridges are laid down between the third and fifth month of gestation, in effect leaving a fossilized record of neurodevelopmental perturbation. Second, minor physical anomalies, typically involving the mouth, ears and eyes, occur with increased frequency in schizophrenia. Much like dermatoglyphic abnormalities, minor physical anomalies represent a disruption of the final phase of the developmental shaping of the face, which takes place in the second trimester. Of course, both abnormal dermatoglyphic patterns and minor physical anomalies may reflect the effects of abnormal genetic regulation of development rather than an extrinsic insult.