ABSTRACT
Prenatal viral infection is emerging as a potentially important risk factor for schizophrenia. As early as the 1960s, a small number of investigators postulated that infection during the prenatal period may playa role in schizophrenia and other neuropsychiatric disorders.1,2 Yet this hypothesis was not formally tested until about two decades later, fueled in part by greater attention to the neurodevelopmental hypothesis of schizophrenia,3 and an increasing number of studies demonstrating an excess of schizophrenia births during the winter and spring.4,5
The neurodevelopmental hypothesis of schizophrenia
The neurodevelopmental hypothesis of schizophrenia postulates that a disruption in the programmed process of brain development increases vulnerability to schizophrenia later in life, possibly as a result of interaction with later brain developmental processes in adolescence or adulthood.6 Evidence supporting this model in schizophrenia includes: childhood neurocognitive, behavioral, and neuromotor disturbances long before onset of the illness/-9 increases in minor physical anomalies;10,11 and gross brain abnormalities in first episode patients,12 including an increased risk of cavum septum pellucidum, a marker of disrupted development because this brain structure normally fuses in utero. 13 The discordance rate of schizophrenia in monozygotic twins is approximately 50%, arguing for the importance of environmental factors in its etiology.
