Biological Explanation of Schizophrenia - Essay Example

Biological Explanation of Schizophrenia Degree Biological Explanation of Schizophrenia Among the most serious and widespread formsof mental illness today is schizophrenia. According to World Health Organization (2012), about seven out of every one thousand adult population are affected by some degree of schizophrenia, primarily between the ages of fifteen to thirty-five years, and approximately 24 million worldwide. Subsequently, based from National Institute of Mental Health (NIMH) statistical record, there are approximately 2.4 million Americans that are affected by this chronic mental illness (The University of Chicago Medical Center, 2012). Thus, schizophrenia is considered to be one of the most disruptive and disabling of mankind’s afflictions. The various kinds of schizophrenia, according to symptoms experienced by the stricken person, are paranoid, disorganized, catatonic, residual and undifferentiated disorder. As symptom changes over time to an afflicted patient, it is possible that he or she suffers more than one kind of schizophrenia in his/her lifetime (Schoenstadt, 2008). NIMH (2009) stated three broad categories of symptoms of schizophrenia as positive, negative and cognitive. Positive symptoms include hallucinations, delusions, thought and movement disorders. Negative symptoms include dull talking in monotonous voice, lack of pleasure in everyday life, lack of ability to begin and sustain planned activities, often neglect their basic personal hygiene, laziness or unwillingness to help themselves. Cognitive symptoms are quite difficult to recognize unless tests are performed because it involve poor ability to understand information and capacity to use it for decision-making, difficulty in focusing attention, and memory problem. Hence, person suffering from any one of the schizophrenias often withdraw from social life and retreat into an inner imaginary world, to the extent of experiencing delusion or hallucination. Their functioning senses grossly change, as their feelings and behaviors also change. People and objects may take on strange appearances for them, food may taste peculiar to them, odors may become repulsive, sounds may become either unbearable loud or scarcely audible. Regarding the root cause of this chronic mental disorder, researchers are still uncertain whether it is a biological disorder or a transitory emotional disorder brought about by environmental cause, as they explain their current understanding based on their study research that no specific gene has yet discovered, nor biochemical has been confirmed responsible, nor particular stressful event that sufficiently stimulate schizophrenia (Sumrall, 2003). But even no specific gene can cause this mental disease by itself, scientists have accepted the fact that the closer one’s blood relationship to a schizophrenic, most likely he or she will become afflicted because it runs in families. But additionally, scientists also believe that environmental factors, such as exposure to certain viruses or malnutrition before birth, or any other yet unknown psychosocial factors and problems during birth, are contributors to development of this illness (NIMH, 2009). Thus, undoubtedly, schizophrenia as an inherited mental disease is a well-established fact. In fact, as genes of parents are being transferred to their children, about 10% of probabilities to children of either a father or a mother is a schizophrenic tend to develop the disease, while approximately 50% to children whose parents are both schizophrenic (ThinkQuest Internet Challenge Team, 2001). It is now well-established that genes play a role in the development of schizophrenia. Genetic research, which involve studies on family, twin and adoption scheme while employing neurological and clinical observations, have been performed to provide basis of genetic transmission of cases of schizophrenia. One employed scheme is through comparing the concordance rates along with the monozygotic twins (MZ), who share 100% of their genetic substance, against dizygotic twins (DZ), who share only 50% of their genetic material. The results revealed an approximate concordance rate of 53% for MZ pairs while 15% for DZ pairs, hence, three times more likely MZ twins has genetically components of schizophrenia as compared to DZ twins. Moreover, children born to non-schizophrenic parents but were adopted and raised by schizophrenic parent did not show up probable rates of schizophrenia (Faraone, Taylor & Tsuang, 2002). Nevertheless, since no specific gene is found to be responsible to develop schizophrenia, and environmental factors seem to influence fetus before and at birth, Glausiusz, (2001) asserts that Biologists must have rightly assumed that mutant genes pass the probability of developing schizophrenia from parent to offspring. Mutant genes are possibly produced in cases of head injuries, maternal malnutrition and rubella during pregnancy. However, in a more vivid research conducted by virologist Robert Yolken of John Hopkins School of Medicine, after examining the spinal fluid of 35 afflicted, he found the retrovirus that was actively generating RNA, the outline for proteins, while non-schizophrenic individuals have no signs of retrovirus. He believed that this is a product of another infection such as a herpes virus infection. Researchers from the Genetics Institute Inc. in Massachusetts declared “that a gene carried by Yolken’s retrovirus may play an integral role in building the human placenta,” and “the protein for which the gene codes, called syncytin, both prompts placenta cells to knit together to nourish a fetus and enables the virus to fuse with the cells it infects” (para.9). Therefore, it is hypothetically assumed that schizophrenia may possibly initiated during fetal development with faulty neuronal wiring. Psychiatrist Dolores Malaspina of New York State Psychiatric Institute commented that “it could be that it’s a neurodevelopmental disease, in which a flawed gene derails the normal development of brain neurons” (para.9). Robert Freedman, an editor of American Journal of Psychiatry attested that certain studies probe the neuroanatomical substrates of schizophrenia (as cited in Schizophrenia Research Forum, 2007). Furthermore, Foster (2003) also affirmed that schizophrenia might have been developed during pregnancy as a product of maternal infections, but not as a result of active viral infection, but rather an impact resulting from brain damage in the fetus. He also refutes the dopamine hypothesis, “the belief that excess dopamine accentuates and decreased dopamine reduces the positive or hot symptoms of schizophrenia” (p. vii). The dopamine hypothesis was a popular theory during the 1970’s according to Walsh (2008). This hypothesis was based on observations that schizophrenia like symptoms inhibited after overdosing normal participants of amphetamine, enhancer of dopamine activity. After given to schizophrenic patients, their symptoms exaggerated. However, an alternative theory implies that it is the over-activity of some type of dopamine receptor rather than too much dopamine that initiates schizophrenia. Also, studies show that brains of schizophrenic have no more dopamine. On the other hand, some other hypothesis linking schizophrenia to some abnormalities in the dorsolateral prefrontal cortex are also introduced, since anatomical and molecular abnormalities of excitatory neurons are shown in the said cortex. In harmony with the recent findings, the striatal dopamine activity of a schizophrenic patient was abnormally elevated, thus the researchers concluded that these two abnormalities are inversely correlated. So, stimulating prefrontal cortex area affects dismissing of striatal neurons and dopamine release (Asher, 2002). Aside from the frontal cortex, the hippocampus, the brain area that involved various aspects of learning and memory, is also affected as reduction in its volume is being revealed in cases of schizophrenia. Therefore, it also inhibits behavioral and cognitive deficits. Further study provides further proof that hippocampal volume reductions and cognitive difficulties both inhibits in patients suffering schizophrenia (Beenken, 2007). Environmental factors not only affect the development of schizophrenia in the genetic formation of the fetus, but also to the possible victims at the stage of the development of this mental disorder. Somehow, environmental aspects may also influence not only the vulnerability but also the worsening of the case once it is developed. The diathesis-stress model of schizophrenia corroborated the environmental factors that possibly interact with preexistence of this mental disorder. Jones and Fernyhough (2006) cites Walker and Diforio ‘s version of the neural diathesis-stress model that expressed the dependents of neuroendocrine pathways that through stress exposure may result in releasing of cortisol as facilitated by the hypothalamic-pituitary-adrenal axis that may also influence transmission of dopamine. It defines that as cortisol level increases due to stress-related exposures, the abnormality of dopamine neurotransmission will worsen that may result to development of schizophrenia. Walker and Diforo also noted the findings that drugs may raise cortisol levels that may worsen the symptoms. Patients suffering schizophrenia are not dangerous at all. In fact they are more dangerous to themselves than to others because some tend to commit suicide most especially if they are extremely exposed to stress-related circumstances.   References Aher, J., (2002). Schizophrenia linked to defect in prefrontal cortex. UniSci, DailyUniversity Science News. Retrieved April 19, 2012 from http://www.unisci.com/stories/20021/0129021.htm Beenken, B., (2007). Neuropsychological and neuroanatomical deficits in patients with polydipsia and hyponatremia in schizophrenia. UMI Proquest Dissertaions & Thesis. Retrieved April 19, 2012 from http://gradworks.umi.com/32/43/3243872.html Faraone, S. V., Taylor, L., and Tsuang M. T., (2002). The molecular genetics of schizophrenia: an emerging consensus. Expert reviews on molecular medicine. Cambridge University Press. Retrieved April 18, 2012 from http://journals.cambridge.org/download.php?file=%2FERM%2FERM4_14%2FS146239 9402004751a.pdf&code=eae984112914ff93a22b52fd9ff5084a Foster, H., (2003). What really causes schizophrenia. Retrieved April 19, 2012 from http://www.hdfoster.com/sites/hdfoster.com/files/users/user6/Foster_Schizophrenia.pdf Glausiusz, J., (2001). The Biology of . . .Schizophrenia. Discover Magazine. Retrieved April 19, 2012 from http://discovermagazine.com/2001/oct/featbiology Jones, S., and Fernyhough, C., (2006). A new look at the neural diatheses – stress model of schizophrenia: The primacy of social-evaluative and uncontrollable situations. Schizophrenia Bulletins. Oxford Journals. Retrieved April 19, 2012 from http://schizophreniabulletin.oxfordjournals.org/content/33/5/1171.full National Institute of Mental Health, (2009). What are the symptoms of schizophrenia. Retrieved April 18, 2012 from http://www.nimh.nih.gov/health/publications/schizophrenia/what- are-the-symptoms-of-schizophrenia.shtml National Institute of Mental Health, (2009). What causes schizophrenia? Retrieved April 18, 2012 from http://www.nimh.nih.gov/health/publications/schizophrenia/what-causes- schizophrenia.shtml Schizophrenia Research Forum, (2007). News Brief: Neuroanatomy of functional deficits in Schizophrenia. Retrieved April 19, 2012 from http://www.schizophreniaforum.org/new/detail.asp?id=1325 Schoenstadt, A., (2008). Types of schizophrenia. eMed TV. Retrieved April 18, 2012 from http://schizophrenia.emedtv.com/schizophrenia/types-of-schizophrenia.html Sumrall, S., (2003). Schizophrenia. Advanced Behavioral Consultants. Retrieved April 18, 2012 from http://www.healthsurvey.com/schizophrenia.htm The University of Chicago Medical Center, (2012). Schizophrenia. Retrieved April 18. 2012 from http://www.uchospitals.edu/online-library/content=P00762 ThinkQuest Internet Challenge Team, (2001). An eclectic view on schizophrenia. Retrieved April 18, 2012 from http://library.thinkquest.org/C0122164/bio_main.html Walsh, K., (2008). Biological explanations of schizophrenia – the dopamine hypothesis. Retrieved April 19, 2012 from http://alevelpsychology.co.uk/a2-psychology-aqa-a/unit- 4/psychopathology/schizophrenia/biological-explanations-of-schizophrenia-the- dopamine-hypothesis.html World Health Organization, (2012). Schizophrenia. Retrieved April 18, 2012, from http://www.who.int/mental_health/management/schizophrenia/en/ Read More