The article discusses the potential neurodevelopmental origins of schizophrenia, suggesting that certain individuals with anomalies in brain development may be more susceptible to tardive dyskinesia. It highlights evidence that some pre-schizophrenic individuals exhibit involuntary movements, and that tardive dyskinesia is more common in "non-genetic schizophrenia." The authors also address the role of viral infections and birth complications, noting that these can lead to secondary perinatal complications and increased risk of schizophrenia. They support the idea that early brain damage from obstetric complications can explain cognitive deficits in type II schizophrenia and that these deficits may be a continuation of longstanding issues present before the onset of psychosis. The article also discusses the genetic basis of schizophrenia, suggesting that genetic vulnerability can increase sensitivity to perinatal insults, such as hypoxic-ischaemic damage.The article discusses the potential neurodevelopmental origins of schizophrenia, suggesting that certain individuals with anomalies in brain development may be more susceptible to tardive dyskinesia. It highlights evidence that some pre-schizophrenic individuals exhibit involuntary movements, and that tardive dyskinesia is more common in "non-genetic schizophrenia." The authors also address the role of viral infections and birth complications, noting that these can lead to secondary perinatal complications and increased risk of schizophrenia. They support the idea that early brain damage from obstetric complications can explain cognitive deficits in type II schizophrenia and that these deficits may be a continuation of longstanding issues present before the onset of psychosis. The article also discusses the genetic basis of schizophrenia, suggesting that genetic vulnerability can increase sensitivity to perinatal insults, such as hypoxic-ischaemic damage.