The etiology of schizophrenia has long been debated and findings have indicated that there are genetic predispositions and family history to consider. Schizophrenia is a debilitating psychiatric disorder that widely impacts about 2-3% of the total adult population (Liu, 2015). Schizophrenia is known to be “without a cure” and patients with schizophrenia may endure lifelong disturbances in their daily living even with consistent use of medication to alleviate the symptoms. There has been expensive research done to assess the prodromal symptoms and etiologies of this disorder in hopes that it will aid in developing preventable measures. However, this blog post will focus in on the research done on the link between prenatal infections and a higher risk of schizophrenia. Recent findings have shown that there are certain gestational infections that increase the risk of schizophrenia in later years (Brown, 2010) due to alteration of brain development. The alternation is believed to cause an increase susceptibility for developing schizophrenia. An increasing number of research shows that there is a significant link between exposure to infections particularly during the first half of the pregnancy term is positively attributed to a higher risk of developing schizophrenia as an adult (Meyer, 2007).
The focus for these research studies was done on patients who were right on the age cutoff for an appropriate adult schizophrenia diagnosis, which is 18 years old. The studies honed in on information for any neurologic complications seen in the patients postnatal, any development delays that were seen, and any other coexisting physiologic or psychiatric disorders. For a majority of these patients, there was a noticeable delay in development in the patients’ younger years. These delays may include cognitive, sitting, standing, walking, speech, and cognitive impairments as well (Liu, 2015). Prenatal exposure to infections have been directly linked in the past to CNS development defects and also to physiological and metabolic diseases (Labouesse, 2015). Research now shows that just as infection in utero may cause an increase in neurologic disorders such as autism, mental retardation and cerebral palsy, it can also be linked to an increase risk for schizophrenia (Labouesse, 2015). It is known that maternal infection can damage critical brain structural development and may cause cognitive functional delays (Brown, 2002). The infection can cause a significant disruption in normal fetal brain development. As children with schizophrenic symptoms have been seen to have a loss of gray matter, increased ventricles, and a decrease in hippocampal size including an overall decrease in brain size, it is safely believed that these neurologic changes were present before the symptoms manifested itself (Brown, 2002). However, research is still being done to determine the exact mechanism in which maternal exposure to infections can cause lasting damage on fetal neurodevelopment.
It is believed that there is a fivefold increase in the risk for schizophrenia based on whether the prenatal infection happened within the first half of the pregnancy (Babulas, 2015). With a longitudinal study done with mothers who had been exposed to herpes simplex virus type 2, there was a positive link to those exposed to the virus in utero developing psychotic symptoms as adults (Buka, 2001). The virus would cross through the placenta and enter the fetal bloodstream, which could then affect neurodevelopment of the fetus. The study followed the postnatal babies and assessed their development and treatment of schizophrenia as gathered from hospital data (Buka, 2001). The study found a positive link between prenatal exposure to herpes simplex type 2 and an increased risk of developing schizophrenia. An older research conducted a longitudinal study on Finnish patients who had been exposed to the influenza epidemic in 1957 (Mednick, 1988). Although there were some holes in the study that have yet to be filled, there was also a positive correlation between the fetus that have been exposed to influenza during the epidemic and a higher number of schizophrenia in the participants of the study. This study also introduced the consideration that those who were born in winter months during which the influenza epidemic was most detrimental were also more likely to develop schizophrenia (Brown, 2002). In this study, however, there was a significant increase of patients with schizophrenia who were specifically exposed during the second-trimester of the pregnancy. This brings to question the importance of the timing of prenatal exposure and what are some preventable measures that can be taken. The more recent research on influenza exposure focuses on diagnostic criteria of influenza rather than focusing on the fetus being in utero during an influenza outbreak (Brown, 2002). Recent research has shown that diagnosed infection while the fetus is in utero has been positively linked to a significant increase (fivefold) in the development of schizophrenia (Brown, 2002).
This topic has many epidemiological implications for ways to consider some preventable measures for prenatal infections. An increase in screening and treatment through antibacterial or antiviral medication would easily solve the problem of infections. Many of these infections go undetected when pregnant women come in for regular checkups and thus would result in lasting neurological effects on the fetus. Due to many infections being treatable or even preventable by antibiotics, it would be a simple cure that may potentially prevent significant neurologic damage and ultimately decrease the risk of developing schizophrenia. It would, first, be crucial that mothers be appropriately diagnosed for any exposure or any infection during their gestational period. Then, treated appropriately so that it will not have lasting effects on fetal neurodevelopment.
Brown, A. S. and Derkits, E. J. (2010). Prenatal infection and schizophrenia: A review of epidemiologic and translational studies American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 167, 261-280.
Brown, A. S. and Susser, E. S. (2002), In utero infection and adult schizophrenia. Mental Retardation Developmental Disabilities. Res. Rev., 8: 51–57. doi: 10.1002/mrdd.10004
Buka, S. L., Tsuang, M. T., Torrey, E. F., Klebanoff, M. A., Bernstein, D., Yolken, R. H. (2001). Maternal infections and subsequent psychosis among offspring. Arch Gen Psychiatry. 58:1032–1037
Labouesse, M. A., Langhans, W., Meyer, U. (2015). Long-term pathological consequences of prenatal infection: Beyond brain disorders. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 309, R1. doi:10.1152/ajpregu.00087.2015
Liu, C. H., Keshavan, M. S., Tronick, E., & Seidman, L. J. (2015). Perinatal risks and childhood premorbid indicators of later psychosis: Next steps for early psychosocial interventions. Schizophrenia Bulletin, 41, 801-816. doi:10.1093/schbul/sbv047
Mednick, S. A., Machon, R. A., Huttunen, M. O., Bonett, D. (1988). Adult schizophrenia following prenatal exposure to an influenza epidemic . Archives of General Psychiatry, 45, 189-192. doi:10.1001/archpsyc.1988.01800260109013
Meyer U., Yee B. K., Feldon J. The neurodevelopmental impact of prenatal infections at different times of preg- nancy: the earlier the worse? (2007). Neuroscientist;13. 241–56.