Schizophrenia is a neurodevelopmental disorder. Drs John L Waddington and Hanafy A Youssef suggest that schizophrenia patients with tardive dyskinesia have an excess of “developmental (primitive/neonatal) reflexes” and that schizophrenia with anomalies in brain development are particularly susceptible to tardive dyskinesia. Their idea is supported by evidence that some preschizophrenics may already show involuntary movements and by the finding that tardive dyskinesia is especially common in “non-genetic schizophrenia.” The authors also note that a history of pregnancy and birth complications is more frequent in schizophrenia without a family history of psychiatric disorder. Drs S J Cooper and D J King argue that the possible aetiological roles of viral infections and birth complications should be considered separately. The authors agree that viral infections during pregnancy may induce fetal abnormalities leading to perinatal complications. Mednick et al have shown that exposure to the influenza epidemic in 1957 increased the risk of later schizophrenia. Dr M T Abou-Saleh suggests that brain damage caused by obstetric complications explains the scan abnormalities and cognitive deficits in type II schizophrenia. The authors agree and suggest that the deficits of affect and cognition seen in this type of chronic schizophrenia are continuations of longstanding deficits present before the onset of psychosis. Dr Abou-Saleh's point about higher rates of perinatal injury in developing countries is not easily resolved. The authors note that severe mental retardation is a syndrome which numbers obstetric injury among its causes, yet it shows a surprisingly stable global incidence. Dr Abou-Saleh also states that it is difficult to reconcile the neurodevelopmental hypothesis with the genetic basis of the disorder but then suggests that early developmental anomalies might involve the very brain structures which mediate the effects of genetic factors. Mednick et al consider that “a part of the genetic vulnerability to schizophrenia consists of a heightened sensitivity of the brain to perinatal insult.” Evidence implicates the hippocampus, and the genetic predisposition to schizophrenia might well comprise the inheritance of a pattern of neuronal migration into the hippocampus which is especially vulnerable to hypoxic-ischaemic damage.Schizophrenia is a neurodevelopmental disorder. Drs John L Waddington and Hanafy A Youssef suggest that schizophrenia patients with tardive dyskinesia have an excess of “developmental (primitive/neonatal) reflexes” and that schizophrenia with anomalies in brain development are particularly susceptible to tardive dyskinesia. Their idea is supported by evidence that some preschizophrenics may already show involuntary movements and by the finding that tardive dyskinesia is especially common in “non-genetic schizophrenia.” The authors also note that a history of pregnancy and birth complications is more frequent in schizophrenia without a family history of psychiatric disorder. Drs S J Cooper and D J King argue that the possible aetiological roles of viral infections and birth complications should be considered separately. The authors agree that viral infections during pregnancy may induce fetal abnormalities leading to perinatal complications. Mednick et al have shown that exposure to the influenza epidemic in 1957 increased the risk of later schizophrenia. Dr M T Abou-Saleh suggests that brain damage caused by obstetric complications explains the scan abnormalities and cognitive deficits in type II schizophrenia. The authors agree and suggest that the deficits of affect and cognition seen in this type of chronic schizophrenia are continuations of longstanding deficits present before the onset of psychosis. Dr Abou-Saleh's point about higher rates of perinatal injury in developing countries is not easily resolved. The authors note that severe mental retardation is a syndrome which numbers obstetric injury among its causes, yet it shows a surprisingly stable global incidence. Dr Abou-Saleh also states that it is difficult to reconcile the neurodevelopmental hypothesis with the genetic basis of the disorder but then suggests that early developmental anomalies might involve the very brain structures which mediate the effects of genetic factors. Mednick et al consider that “a part of the genetic vulnerability to schizophrenia consists of a heightened sensitivity of the brain to perinatal insult.” Evidence implicates the hippocampus, and the genetic predisposition to schizophrenia might well comprise the inheritance of a pattern of neuronal migration into the hippocampus which is especially vulnerable to hypoxic-ischaemic damage.