Gliosis, a process of neural scarring, is considered to be the characteristic feature of neuronal degeneration (Holtman C). Research across last few decades has shown conflicting results with respect to gliosis being present or absent in schizophrenic brains.
A couple of decades ago, Stevens and colleagues reported gliosis in approximately 70% of their schizophrenic brain cases (Stevens, 1982). Around the same time, some other research by Roessmann showed that gliosis injury to the brain resulting in schizophrenia can occur as early as the 20th week of intrauterine life (Roessman, 1986). In a separate research, Roberts GW concluded that injury to the brain, specifically in the 3rd trimester of pregnancy, can result in development of gliosis, which can lead to schizophrenia in further life (Roberts, 1991). Some other research has shown completely different results. According to Bertolino, magnetic resonance spectroscopies of schizophrenic brains showed no evidence of increased gliosis, neither in chronic schizophrenia nor at the time of onset of the disease (Bertolino, 1996). This means that damage to the brain is not due to a neurodegenerative process. According to Friede, there is no gliotic response till about the end of 6 months of intrauterine period (Friede, 1989). Thus, inspite of decades of research on the etiology and pathogenesis of schizophrenia, it is not yet certain if presence or absence of gliosis can lead to development of schizophrenia.
Some of the extensive research on the timing of development of vulnerability to schizophrenia has shown certain factors during the prenatal age to have an adverse impact on the developing fetal brain. Factors like obstetrical complications, preeclampsia, and toxaemia were strongly linked to development of schizophrenia at a later stage in life (Buka 1993, Walker 2004). Prenatal exposure to rubella and maternal infections are also responsible for development of the condition later in life (Walker, 2004). Some research has suggested that the risk for development of schizophrenia increases when the affected child is born shortly after an epidemic of influenza (Barr, 1990). Most importantly, the second trimester is an important period for brain development of the developing fetus and injury during this period can lead to different kinds of developmental anomalies.
References:
- Holtam C. The Neurodevelopmental Hypothesis of Schizophrenia. Neurodevelopmental Hypothesis, [Online] Available at: http://www.priory.com/psych/neurodev.htm
- Stevens, JR. (1982) Neuropathology of schizophrenia. Arch Gen Psychiatry, 39, 1131–9.
- Roessmann U. (1986) Pathological reaction of astrocytes in perinatal brain injury: an immunohistochemical study. Acta Neurolpathology, 70, 302-307.
- Roberts G.W. (1991) Schizophrenia: a neuropathological perspective British Journal of Psychiatry, 158, 8-17.
- Bertolino A. (1996) Regionally specific pattern of neurochemical pathology in schizophrenia as assessed by multi-slice proton magnetic resonance spectroscopic imaging. Am J Psych, 153 (12), 1554-1563.
- Friede RL (1989). Developmental neuropathology. Berlin: Springer Verlag.
- Buka SL, Tsuang MT, Lipsitt LP. (1993). Pregnancy/delivery complications and psychiatric diagnosis: a prospective study. Arch Gen Psychiatr, 50, 151–56.
- Walker E, Kestler L, Bollini A, Hochman K. (2004) SCHIZOPHRENIA: Etiology and Course. Ann Rev Psychol, 55: 401-30.
- Barr CE, Mednick SA, Munk-Jorgensen P. (1990) Exposure to influenza epidemics during gestation and adult schizophrenia: a 40- year study. Arch. Gen. Psychiatry, 47, 869–74.
