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Schizophrenia Symptoms A Bio psychosocial Perspective

schizophrenia symptoms
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Abstract

The aim of the present study is to examine the causes that play a pivotal part in occurrence or prevalence of schizophrenia symptoms. There are several models presented through different researches that claim schizophrenia to be caused by one or another reason including disturbance of dopamine level, genetically predisposition, petrochemical imbalance, and malnutrition in prenatal period by mother while some relates it to social isolation or unemployment.

The article under custody reveals the etiology of schizophrenia on bio psycho and social predispositions. Schizophrenia is a spectrum disorder and a multimodal approach is necessary to understand its causes and bio-psychosocial approach is quite applicable in this regard to better understand the cause of this illness

 Background

Schizophrenia is a mental disorder that is prevalent in every one person out of every hundredth and it was Eugene Bluer who very firstly described it as schizophrenia means splitting of mind.

Purpose

Purpose of this study is to give a multimodal approach with the biological, psychological and social perspective to understand the basic causes of schizophrenia.

Method

Data was collected from online journals and articles and to keep all the previous researches in mind, a new model of bio-psychosocial perspective was described.

Results

Results claims that schizophrenia is caused by several factors that are of biological psychological and social nature and to better understand its etiology of schizophrenia bio-psychosocial predispositions model is needed to understand and employed.

Key words

Schizophrenia, predisposition, biology, psychology, social

Introduction

Schizophrenia is a prevalent mental disorder distressing probably one half to one percent of the earthly bipeds. It is a disorder that can cause hallucinations, paranoia, bizarre delusions, disorganized thought and speech pattern. Schizophrenia often caused with other mental disorders (Sim et al. 2006). One out of every hundredth person in the world suffers from schizophrenia in his life (American Psychological Association [APA], 2000). Schizophrenia unveils itself in symptoms and signs that include the wide range of mental activity (Andreasen, 2000).

Its symptoms categorized into positive and negatives. Positive involve delusions, heightened speech disorganized thinking and hallucinations while negative consists of poor speech, flat affect, loss of volition, and social withdrawal (Comer, 2005).

Schizophrenia manifests and caused

Schizophrenia manifests and caused in variety of ways (Peralta and Cuesta 2000).  While in history different names tried to claim its causes in different ways as Olney and Faber in 1995 suggested that NDMA receptor hypo functioning is responsible to schizophrenia (Keshavan et al. 2008).  Another model by Crow in 1995 recommend a de-synchronization of hemispheric development due to genes involved in evolution of language is mainly a cause of schizophrenia (Keshavan et al. 2008, p.101).

Another model claims stress as a reason and cause of schizophrenia (Corcoran et al. 2003). While after the era of nineties several model was proposed that claims schizophrenia as a multimedia approach predisposed by biology psychology and environment because the notion that schizophrenia is one single disease proved incorrect (Keshavan et al. 2008).

In the past dozen years, a number of theoretical models of predisposition schizophrenic have been proposed and the article in hand argues the bio psychosocial perspective of schizophrenia.

schizophrenia symptoms

Biological Predispositions

Kendler et al. 1993 stated high risk of schizophrenia first degree relatives of patients as 6.5%, and it rises to more than 40% in monozygotic twins (Picchioni and Murray, 2007), Schizophrenia can also be caused by deletions or duplications of DNA sequences in genes that are considered responsible for the purpose of neuronal signalization in the process of brain development (Walsh et al. 2008).

A research was conducted on schizophrenic twins that reveal schizophrenic twins showed significantly more brain abnormalities than the healthy twins including the reductions in different brain regions and increased size of their ventricles which are caused with schizophrenia in several other researches (Howes et al., 2003).

Hoffman and McGlashan

It is also suggested by Hoffman and McGlashan in 2001 that volume of grey matter in some areas of the brain can be a reason for reduction in the amount of neurons that causes schizophrenia in most of the cases (Hoffman and McGlashan 2001). Some researches claims that abnormal connection between different gene networks is common in every patient of schizophrenia after brain imaging techniques (Broyd et al. 2009).

The function of dopamine in the mesolimbic and mesocortial pathways of the brain is also considered as most obvious causes of schizophrenia (Seeman et al. 2005). According to some recent findings genes coding in dopamine functioning is also prevalent in schizophrenics (Arguello and Gogos 2008). Levels of glutamate a neurotransmitter, is also considered responsible in case of schizophrenia as low level of glutamate in body is linked with schizophrenia (Lahti et al. 2001).

Current few researches unveils that malfunction in receptors for the neurotransmitter glutamate causes an abnormality in the balance of dopamine and serotonin and schizophrenia is linked with such imbalance (Comer, 2005).

 Researches claims that the  implicate N-methyl-D-aspartate (NMDA) receptor hypo functioning in body, opposition of NMDA receptors by N-acetyl aspartyl glutamate (NAAG) and resultant oxidative stress, reduction in gamma-amino butyric acid (GABA) and within neuron inhibition of pyramidal neurons in the cingulated cortex of brain are pathogenic mechanisms of schizophrenia (Lieberman, 1999).

 Researches proved the effects on different drugs in form of schizophrenia. One such study claims drug significantly increases the risk of schizophrenia but it cannot be an only cause (Arsenault, Cannon, Witton, & Murray, 2004). Amphetamines are also linked with schizophrenia especially in triggering positive symptoms (Laruelle et al. 1996). As a research reveals that heavy use of hallucinogens also found in the patients of schizophrenia (Mueser at al. 1990).

schizophrenic behavior

Genes such as neuregulin 1 (NRG1),as well as the genes that are considered as dopamine regulators, like catechol-O-methyltransferase (COMT) gene are associated with production of schizophrenic behavior (Howes et al., 2003). Other associated genes with schizophrenia are dysbindin (DTNBP1), regulator of G-protein signaling 4 (RGS4), disrupted-in-schizophrenia 1 (DISC1) gene G72 (Harrison and Weinberger, 2005). COMT is taken as receptive genes because it is responsible in monoamine metabolism (Harrison and Weinberger, 2005).

Post-mortem proof of reduced thickness of prefrontal cortex without a reduction in the number of cell bodies reveals it causality in schizophrenia (Cannon et al, 2003).

During pregnancy labor pain and other situations problems like lack of oxygen leads to schizophrenia and its chances are 67%, significantly higher than the rate of normal (Comer, 2005).

Wright et al. highlighted that presence of neural infections such as influenza and lower birth weight can be responsible of schizophrenia (McDonald et al., 2000).

Hypoxia is a deficiency of oxygen fetus and can affect the various parts of the brain and can cause hypoxic damage which leads to schizophrenia (Cannon et al., 2003).

Psychological Predisposition

In adulthood different environmental stressors are active such as social isolation, migrant to different areas and urban incipient schizophrenia (Picchioni and Murray, 2007). Many studies reported an increased stress in life in few weeks before the onset or relapse of schizophrenic illness (McDonald et al., 2000).

Van Os et al. stated that th risk for schizophrenia associated with neuroticism and extraversion in human personality and extraversion rated at the age of 16 has relation to adult schizophrenia as revealed through then cohort of 5362 individuals by MMPI results (Van Os and Jones, 2001).

Freud in 1984 said that hysteria, obsession neurosis and hallucinatory confusion are three forms of defense mechanisms that a person used that are the primary characteristics of schizophrenia (Freud, 1894) . Freud further claims that delusional thinking arises as a result of the reaction-formation and projection of threatening unconscious homosexual wishes (Chalus, 1977).

Scheff in1966 stated that  labelling theory claims individuals labelled in the way they start perceiving themselves the same way and schizophrenic mostly do ( Scheff’s 1966).

Social Predisposition

In schizophrenia inherited genes cause structural brain abnormalities which can be related to environmental factors. People with environmental risk factor have a higher risk of schizophrenia while those with a unlike genotype remains at low risk (McDonald and Murray, 2000). There are several risk genes associated while we interact with each other and the environmental factors they cause schizophrenia (Picchioni and Murray, 2007).

Another research shows a concordance about 10% in dizygotic twins and 40% in monozygotic twins, which indicates that schizophrenia, cannot only be due to genetic factors (Andreasen, 2000).

Fetal prenatal malnutrition is also related with schizophrenia. A study by Susser et al. exposed that severe malnutrition during the first trimester increased the risk of schizophrenia in adult life (McDonald et al., 2000).

It is exposed through researches that severe stressors such as death of a spouse, unwanted pregnancy and experience of war, tornado or nuclear explosion can influence neurodevelopment growth at the feto-placental-maternal interface (Khashan et al., 2008).

Schizophrenics is particularly marked among those patients born in urban settings there the population increases the probability of disease transmission in population comparatively rural settings (McDonald et al., 2000).

A research in Denmark reveals that the individuals born in Copenhagen areas have four times the risk of schizophrenia as those born in rural areas which later on generalized to overall population of the world after different researches (McDonald et al., 2000).

The role of social isolation is anticipated and collaborative as a social cause of schizophrenia recent interest several studies linked birth and raising in an urban area increases the risk of schizophrenia (Howes et al., 2003).

Schizophrenia patients with low socio economic status have much more likelihood to have a relapse compared to low family there is also evidence that familial stress can speed up the onset of schizophrenia (Picchioni and Murray, 2007). Tienari et al shown that offspring of mothers with schizophrenia are placed in well-adjusted families related to lower risk of developing schizophrenia (McDonald and Murray, 2000).

Conclusion

Several researches claimed as schizophrenia is caused by biological deficits including prenatal environment, maternal malnutrition, drug abusage, neurotransmitters upheaval especially low level of dopamine while some researches paid more emphasis on social conditions and there are those who reasoned schizophrenia as psychological disturbance but more or less schizophrenia is described by the role of biological, psychological and socially predisposition disorder altogether. A bio-psychosocial model can bitterly explain the root causes of schizophrenia as it is a spectrum disorder and its etiology is described in a model of spectrum of reasons.

References

Arguello.JA. 2008. A signaling pathway in schizophrenia. J llin Invest   118(6): 2018–  

          021.

Arsenault L, Cannon M, Witton J, Murray, RM. 2004. Causal association between   

        cannabis and psychosis: examination of the evidence. Br J Psychiatry 184: 110-7.

Corcoran C, Walker E, Huot R, Mittal V, Tessner K, Kestler L, Malaspina

D. 2003. The Stress Cascade and Schizophrenia: Etiology and Onset. Schizophrenia Bull  

          29(4): 671-92.

Boydell, J., Van Os, J., McKenzie, K., Allardyce, J., Goel, R., McCreadie, R.G., &

         Murray,

R.M. (2001). Incidence of schizophrenia in ethnic minorities in London: ecological

         study into interactions with environment. British Medical Journal, 323, 1336-1338.

Cannon, T.D., van Erp, T.G.M., Bearden, C.R., Loewy, R., Thompson, P., Toga, A.W.,

Huttunen, M.O., Keshavan, M.S., Seidman, L.J., & Tsuang, M.T. (2003). Early and late  

            neurodevelopmental influences in the prodome to schizophrenia: contributions of    

           genes, environment, and their interactions. Schizophrenia Bulletin, 29, 653-669

Comer, R.J. (2005). Fundamentals of abnormal psychology. New York: Worth         

           publishers.

Freud, S. (1894). The Neuro-Psychoses of Defence. SE, Volume III, 41-61. 1755- 5 Weiner,I.B.(1966). Psychodiagonosis in Schizophrenia. N.Y: John, Wiley & Sons

            949.2010.00223.x.

Harris A. 2010. Pharmacological Treatment of Schizophrenia [Lecture on the Internet]            

           2010. Sydney: University of Sydney [cited 2010 Nov 8]. Available            rom:http://sydney.edu.au/medicine/psychiatry/workshops/presentations/pharmacological_treatment_schiz.pdf

Harrison PJ, Owen MJ. 2003. Genes for schizophrenia? Recent findings and their  

              pathophysiological implications. Lancet 361(9355): 417-9.

Hoffman RE, McGlashan TH. 2001. Neural network models of schizophrenia.

              Neuroscientist 7: 441-54.

Howes, O.D., McDonald, C., Cannon, M., Arseneault, L., Boydell, J., & Murray, R.M.   

                (2003).

Pathways to schizophrenia: the impact of environmental factors. International Journal

                 of Neuropsychopharmacology, 7, (Suppl. 1), S7-S13.

Khashan, A.S., Abel, K.M., McNamee, R., Pedersen, M.G., Webb, R.T., Baker, P.N.,  

            Kenny, L.C., & Mortensen, P.B. (2008). Higher risk of offspring schizophrenia   

            following antenatal maternal exposure to severe adverse life events. Archives of  

            General Psychiatry, 65, 146-152.

Lahti AC, Weiler MA, Tamara Michaelidis BA, Parwani A, Tamminga CA.2001. Effects         

            of ketamine in normal and schizophrenic volunteers neuropsychopharmacology               

           25(4): 455–67.

Laruelle M, Abi-Dargham A, van Dyck CH, Gil R, D’Souza CD, Erdos J,McCance E,   

            Rosenblatt W, Fingado C, Zoghbi SS, et al. 1996. Single photon emission  

            computerized tomography imaging of amphetamine-induced dopamine release in  

           drug-free schizophrenic subjects. Proc Nat Acad Sci USA 93(17): 9235-4

Lieberman, J.A. (1999). Is schizophrenia a neurodegenerative disorder? A clinical and

             neurobiological perspective. Biological Psychiatry, 46, 729-739.

McDonald, C., & Murray, R.M. (1999). Early and late environmental risk factors for

             schizophrenia. Brain Research Reviews, 31, 130-137

Mueser KT, Yarnold PR, Levinson DF, et al. 1990. Prevalence of substance abuse in             

             schizophrenia: demographic and clinical correlates. Schizophr Bull 16 (1): 31-56.

Seeman P, Weinshenker D, Quirion R, Srivastava LK, Bhardwaj SK,Grandy DK,   

             Premont RT, Sotnikova TD, Boksa P, El-Ghundi M, et al. 2005. Dopamine  

               supersensitivity correlates with D2High states, implying many paths to    

               psychosis. Proc Nat Acad Sci USA 102(9): 3513–18.

 Sim K, Chua TH, Chan YH, Mahendran R, Chong SA. (2006). Psychiatric comorbidity  

                     in first episode schizophrenia: a 2 year, longitudinal outcome study. J    

                     Psychiatric Res 40(7):656–63.

Peralta V, Cuesta MJ. 2000. Clinical Models of Schizophrenia: A Critical Approach to  

                    Competing Conceptions. Psychopathology 33(5): 252-58.

Picchioni, M.M. & Murray, R.M. (2007). Schizophrenia. British Medical Journal, 335,  

                  91-95.

van Os J. 2004. Does the urban environment cause psychosis?. Br J Psychiatry 184: 287-

                  8.

Walsh T, McClellan JM, McCarthy SE, Addington AM, Pierce SB, Cooper GM, Nord   AS, Kusenda M, Malhotra D, Bhandari A, Stray SM, Rippey CF, Roccanova P,                et al. 2008. Rare structural variants disrupt multiple genes in schizophrenia.

Science 320(5875): 539-43.

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