Biological Basis of Schizophrenia - Essay Example

Schizophrenia The basis for the treatment of schizophrenia for many years has been psychological. These have been patients that supposedly had a terrible time with their families and developed schizophrenia either because of that or some other traumatic event. Historically, psychological illness is one of the few illnesses that the medication to treat came before the ability to diagnose. Recently however, there is research to show that may very well not be the basis of schizophrenia. In fact, that basis may be biological and with the development and use of MRI, CAT, PET, and BEAM, theory has changed. This paper will discuss the biological basis of schizophrenia and what has led to that belief. Schizophrenia is a complex debilitating psychotic disorder that involves a disconnection between thought and language. It affects, thoughts, feeling, perceptions, and overall behavior. The usual onset is age 17 to 25. 90% of those that are being treated are 15-55. Onset before 10 and after 60 is rare (Porth & Matfin, 2008). Recent research and data present a complex image of a brain dysfunction with alterations in anatomic structures as well as protein synthesis and functional disturbances. Some of the manifestations include incomprehensible speech, delusions, hallucinations, and sometimes catatonic behavior. It is thought that sounds and color are more vivid and louder to these patients (Porth, et.al., 2008). There is paranoia as they believe people are watching them or out to get them. Though the studies following show some research into the neurophysiology of schizophrenic symptoms, it is still virtually unknown what the pathogenesis is. It is known from the imaging techniques being used that there are abnormalities in the construction of the brain but how do those abnormalities relate to the psychological issues. This is still unknown. It will be important to discern at what age this disease begins to manifest itself. One of the studies noted leads the researcher to believe that it may be a manifestation of development in uterus and not occur post partum. Young children are not often scanned so it is not known for sure (Porth, 2008). It is known, however, that adolescents who have a strong family history and who have been scanned do have the larger ventricles shown in a parental scan. Treatment at this time has not changed much though future study may change that. Presently the goal of treatment is still to attempt to induce remission, and improve behavior and cognitive function. Outcomes from the illness are improved and some patients function at a fairly high level. Medication and psychosocial intervention is important as the disease impacts everyone and the whole family must learn how to deal with it (Porth, 2008). Diagnosis of the biological basis for schizophrenia as noted above is made by the MRI, CAT, PET, and BEAM. The CAT scan shows a two dimensional black and white picture of the brain surface and the inner tissue. It makes it much easier to see abnormalities. The CAT of a schizophrenic brain shows many abnormalities. An MRI or magnetic resonance imaging is even more in depth. MRIs of the schizophrenic brain are quite different than those of the non-schizophrenic patient. The consistent abnormalities found with CAT have been a decrease in the size of the brain and enlarged lateral and third ventricles. It is interesting to note that twins of schizophrenics that are not schizophrenic do not have the same structural abnormalities (Choi, 2003). PET scan permits high resolution sliced images of the subcortical sections and colored indications of the brain activity(Taylor, 1987) The PET scan takes quite a bit of prep time as well as run time and is difficult to do with schizophrenic patients because of this. The rCBF monitors the amount of blood that is flowing through the brain. This test shows that most schizophrenic patients have greatly decreased blood flow to the frontal cortex (Taylor, 1987). Edward Taylor in 1987 discussed the fact that there may be something other than a psychological reason for schizophrenia. He believed that physical and chemical changes that were being found in the brain were reason to believe that this was a biological disease. In his article he reports that on any given day, 600,000 people with schizophrenia are under active treatment and there are at least 100,000 new ones in that group (Taylor, 1987). There are many abnormalities that occur causing this disease. It is unknown why they occur. Many of the changes are structural as well as functional. There are actually many theories as to how these abnormalities happen, some of them are viral infections, genetic makeup, and damage from chemical or hormones which can also include the drugs given to treat schizophrenia (Taylor, 1987). At this time research had been focusing on the frontal and temporal lobes of the brain along with the limbic system. These structures are responsible for the receiving, organizing, selecting, and making sense of internal and external perceptions (Taylor, 1987). It is expected that damage to the limbic system in the human being will produce distortions of perception, hallucinations, feeling of depersonalization, paranoia, and catatonic like behavior. These are, after all, the symptoms of schizophrenia. Neuroleptic drugs are the only drugs that have been known to work in the schizophrenic patient. The side effects of these drugs in some cases can be worse than the disease, however. This is the only thing that has decreased their psychotic symptoms. Therefore, if schizophrenia is not a medical illness why does it respond to this group of medications and not social treatment (Taylor, 2001)? It is interesting to note that the symptoms are present before medication is used and though there is a brain chemistry change from these medications, the overall picture of the brain abnormalities do not change. Certainly neuroleptic drugs do not cause the decreased brain size or decrease in circulation to the frontal lobe so the explanation continues to be a different disease and that would be schizophrenia as a biological disease (Taylor, 2001). Magnetic resonance imaging (MRI) has proven to be an important investigative tool to look for the structural changes in the brain that cause schizophrenia. In most of the studies done, the MRI was used. The studies were affected by sample variation because of the sizes of the sample. This made all of the studies look misleading due to inconsistent positive and negative results (Wright, et.al., 2000). There have also been many different parts of the brain studied but not all in every study. Generally what has been seen however is there are higher ventricle to brain ratios, greater volumes of the lateral ventricles, reduced brain size, reduced cross-sectional area of the corpus callosum, reduced volumes of the bilateral temporal lobe, hippocampus changes and amygdala-hippocampal complex changes. It was felt by Wright (2000) that the problem of with previous studies had not been that the data was not good but that the data had not been combined in such a way that it could be tracked and analyzed. There for he and his team choose to do an in-depth meta-analysis. All of this information was included in the meta-analysis. Once information from the previous studies was categorized and placed in a data base, it revealed many significant factors about the biological basis of schizophrenia. The total numbers from so many studies also gave validity to the work. This study showed absolute total ventricular volume was greater in the patients with schizophrenia than in the comparison subjects. There was a 95% confidence level that these were correct. Absolute volumes of ventricular subdivisions were also greater in patients with schizophrenia (Wright, 2000). The left ventricle was slightly enlarged as compared to the right ventricle and some ventricular subdivisions showed increased and were greater than the global difference. Again the confidence level was 95%. The third ventricular volume was about the same as the global difference . Overall, median temporal lobe structures were fairly small but the volume differences compared were not much different. The left temporal gyrus was small as was the parahippocampus (Wright, 2000). The numbers of basal ganglion structures were larger than most and relative volumes of the thalamus were smaller. This part of the study alone is tremendous proof of the biological differences in the brain of the schizophrenic as compared to the non-schizophrenic patient. There has been an enormous research effort to determine structural brain changes in schizophrenia, as shown by this meta-analysis. Many regions of the brain have been measured in over 1,000 patients which was not clear before performing a meta-analysis on the data. The results of the analysis show the presence of deferent brain volumes (Wright, 2000). Cerebral volume was lower in 98% of the cases and total volume was higher in patients with schizophrenia than in comparison subjects. There appeared to be no difference in pathology between men and women. These comparisons were made in men and women that had been submitted to trauma also but the brains of those diagnosed were not different. Further study into the gene therapy side was done by Choi, Zepp, and Higgs et.al. (2003). Their belief was that a disruption in the normal development of the prefrontal cortex happens and this causes later schizophrenia through cognitive dysfunction (Choi, et.al., 2003). The study was set up as a full gene study, studying method generated genome wide expression profiles of people ranging from the age of one month to 49 years. The study used Affymetrix HG-0133 to do this. There were genes that showed aging and those were matched up with any that had schizophrenic genomes in the PFC. Once that was done a functional annotation analysis was done. The conclusion was that genes related to schizophrenia showed disruption as they aged and this may cause later schizophrenia but there were disruptions from the beginning during the critical period of development that predisposed to schizophrenia. They concluded that not only could schizophrenia be a genetic abnormality but might be caused by disruption of genes causing malformation during fetal development (Choi, 2003). In determining that damage during the fetal cycle can cause gene changes and put a baby at risk for schizophrenia, it is noted that further study is in need of being done to determine what things damage those genes. It also further supports the fact that this is a biological and not a psychological disease. Proteins are present in the brain fluids at all times. However, patients with schizophrenia express different proteins than the average person. These proteins are expressed in the hippocampus (Nesvaderani, Matsumoto, Sivagnonasundaram, 2009). In this study proteins were extracted from fresh postmortem cadavers. They were removed from the posterior and anterior hippocampus from 19 schizophrenia and 19 control patients. There were 48 unique proteins found in the patients with schizophrenia. The anterior hippocampus seems to be more involved when there is schizophrenia than when there is the posterior hippocampus. This would correlate with the other studies we have noted with the changes in the anterior hippocampus as well as the increased fluid levels. They found other issues too. For example they discovered that there was abnormal neuronal cytoarchitecture and function as well as neurotransmission and mitochondrial function (Nesvaderani et.al. 2009). All of these issues noted during this study indicate a biological reason for schizophrenia rather than a psychological one. Twin studies have been done often, in the recent past. Anokhin, Vedeniapin, Heath, et.al. (2007) completed a twin study for schizophrenic tendency. In each group of twins tested, there was one twin with schizophrenia and one without. In every case, the twin with the schizophrenia had the malformations in the brain that were listed earlier and the twins without schizophrenia did not. These malformations were shown by MRI. There was also a finding at the same time of a deficit in sensory gating in the twins with schizophrenia. These were measured by the suppression of P50 auditory ERP which has been noted in the biological studies of schizophrenia before (Anokhin, et.al., 2007). This may, according to this study also affect attentive processing which may explain some of the symptoms of schizophrenia. There are few genetic studies however, at this time, that include this phenomenon and there is reason to extend those studies. In conclusion, for many years Schizophrenia was considered a pyschological illness created by trauma within the family circle. Many of these patients were removed from their family homes. Many were placed on medications that only seemed make things worse. The typical psychotic medications used for so many other psychological illnesses did not seem to help and it was not understood why. More recently, it is well understood that there are biological reasons for schizophrenia. There are malformations in the brain that occur only in the affected person, even in twins. There still is evidence that much of this is hereditary but it is still unknown as to why. Some of the studies noted inform that genes carry this disease but normal genes can also be traumatized during growth and development to change them enough to be born with these malformations. It is still not know why. There is a great need to continue study in this disease as there are as many unanswered questions as there are answered. It is exciting, however, to know that a disease that has been so poorly accepted in the past may be coming to a time when it is better understood. Resources Anokhin, A., Vedeniapin, A., Heath, A. 2007. Genetic and environmental influences on sensory gating of mid-latency auditory evoked responses: A twin study. Schizophrenia Research. 89(3). 312-319. Choi, K., Zepp, M., Higgs, B. et.al. 2003. Expression profiles of schizophrenia susceptibility genes during human prefrontal cortical development. Journal of Psychiatry Neuroscience. 34(6). 450-8. Retrieved April 4, 2010 from http://www.search.ebscohost.com/login.aspx?direct=true&AuthType=IP,cpid&custid=58856 Insel, T. 2010. Faulty circuits. Scientific American. 30(2). pg. 4. Porth, C., & Maffin, G. 2008. Pathophysiology. 8th ed. Lippincott: Boston. pg. 1173. Taylor, E. 1987. The biological basis of schizophrenia. Social Work. Retrieved April 3, 2010 from http://www.ebscohost.com Taylor, E. 2001. Schizophrenia: fire in the brain. Points and Viewpoints. Retrieved April 3, 2010 from http://www.ebscohost.com Wright, I., Rabe-Hesketh, S., Woodruff, P., 2000. Meta-Analysis of regional brain volumes in schizophrenia. American Journal of Psychiatry. 157: 16-25. Retrieved April 3, 2010. Read More