Diminished cerebral inhibition in neonates associated with risk factors for schizophrenia: parental psychosis, maternal depression, and nicotine use.

Diminished inhibitory gating of cerebral auditory evoked responses is transmitted in families with psychoses as an endophenotype related to the genetic risk for these illnesses. To assess whether the endophenotype is already expressed in infants of parents with psychotic illness and to assess effects of other known risk factors for schizophrenia, ie, maternal cigarette smoking and depression, inhibitory gating of cerebral auditory evoked responses was evaluated by comparing the P1 evoked responses to the first and second of paired auditory stimuli. Cerebral evoked responses were recorded during active sleep from 22 infants with a parent diagnosed with a psychotic illness and 129 infants with parents with no such history. Of these infants, 25 were prenatally exposed to nicotine (16 from the comparison group and 9 from the group with parental psychosis). Mothers of 35 infants had diagnoses of major depressive disorder. Parental psychosis (P = .032) and exposure to maternal smoking (P = .012) both resulted in diminished inhibitory gating in infant offspring. Compared to infants of mothers who did not smoke and who had neither parental psychosis nor maternal depression, diminished inhibitory gating was observed in infants with parental psychosis (P = .027) and in infants with maternal depression (P = .049). Diminished inhibitory gating of auditory evoked response in infants who have risk factors for schizophrenia mirrors reports of its familial transmission in adults. The results further indicate that the phenotypic expression of familial genetic and environmental risks for psychosis is already manifest very early in development.