Neurobiology Of Schizophrenia - Admission/Application Essay Example

 How Well Psychobiology Explanations Account For Schizophrenia As a mental disorder affecting human perception and differentiation of what is real and what is not, Schizophrenia affects a sizeable ratio of the adult population. It accounts for an estimated 1.1 percent of America’s adult populations (18+ years) at any given year. It is characterized by both the failure to recognize reality from illusion (imbalanced perception) and abnormal social behaviors as displayed by affected individuals. In this regard, common symptoms are inclusive of: confused/ unclear thinking, false beliefs, general inactivity, auditory hallucinations and a reduction in emotional expression and social engagement (NIH, 2015). Towards better understanding of the critical influence of this ailment, the paper will include the utility of pertinent psychobiology explanations. Accordingly, both biological and psychological explanations provide a firm basis on which the ailment can be addressed; in terms of symptoms, influences and effects, as well as treatment. Schizophrenia as a chronic ailment is both severe and disabling to the human brain. This is in terms of functionality and balance. As the NIH (2015) portrays, it has and still affects thousands of individuals throughout history. The affected individuals are shunned by the rest of society. Such social reactions were in the past influenced by the unsteady, uncontrollable and often violent nature of the ailment in terms of manifestation within patients (NIH, 2015). Because such individuals often hear voices, which others do not hear, having a belief that other people can control or read their minds or in extreme cases envisaging other people plotting to cause harm to them, patients suffering from schizophrenia are often terrified. This is what leads to a general withdrawal behavior, as well as the often-experienced extreme agitation in patients. Such individuals often do not make sense when they engage in conversations. On the other hand, they may even sit for long periods without talking or moving, thereby necessitating concern from family relations and the society at large (NAMI, 2014). Accordingly, as Mueser and Jeste (2008) portray, both family relations and the society are affected by the ailment, influenced by the fact that a majority of individuals suffering from the ailment are dependent on them. Those suffering from the ailment often are unable to take care of themselves let alone effectively hold a job/ profession, thereby relying more on others for constant help. This is mainly what informs the need for treatment procedures vital in relieving a majority of the symptoms and effects experienced. While the affected individuals often have to cope with such symptoms for life, many are able to lead meaningful and rewarding lives within society, especially when aided through pertinent treatment measures (Mueser & Jeste, 2008). Through continuous R&D, researchers continue to develop more effective medications, thereby further understanding the causal factors of the ailment. As Berrios, Luque and Villagran (2003) aver, in terms of categorization of known causal factors, experts are of the opinion that the ailment is fundamentally based upon genetic and environmental contributions, as well as diverse brain structure and chemistry. Thus, this influences the reason behind use of psychobiology explanations in terms of accounting for schizophrenia. On the one hand, genetic factors are influential in terms of family history studies, which show the tendency of the ailment to often run within family lineages. On the other hand, biochemical factors are informative when accounting for the ailment, based majorly on the dopamine hypothesis. Further pivotal in such a discussion are the pertinent influences of both social and psychological factors. All these encompass the descriptive methodology, through which the ailment can be best accounted for (Berrios, Luque & Villagran, 2003). According to the American Psychiatric Association (APA) (2014), a key aspect of the ailment’s biological explanation is of the suggestion that schizophrenia is transmitted from parents to their children. This is in terms of genetic transfer, where the parent(s)’ genetic makeup is implanted to future generations through genes. It is proven through research that there is a higher chance of an individual suffering from the ailment through direct heritability. However, varying estimates of heritability prevail, influenced by the difficulty encountered in the separation of the causal effects of either the environment or genetics (APA, 2014). In terms of genetics, as provided by Bradley et al. (2012) the greatest risk is presented in the event of plausible diagnosis of a first-degree relative who is categorized as having the risk rate of 6.5%. Concerning monozygotic twins, the presence of either or both parents suffering from the ailment greatly increases the chances of affect to 40% of such children. Thus, in the event of a parent being affected, the chances of the offspring contracting the ailment rise to about 13%. Comparatively, in the event of both parents being affected, the risk of contracting the ailment further escalates to nearly 50% chance rates. This is enough evidence proving that first-degree relatives i.e. siblings, parents and offspring, share 50% of their genetic makeup (Bradley et al., 2012). While there exist a variety of differences and similarities between biological and psychological explanations, the Diathesis-stress model as a theory, delves at both contributions. Accordingly, a blend of critical genetic predispositions towards environmental stresses and diseased conditions does result in the occurrence of abnormal behaviors. It hence suggests that mental disorders are but the result of interaction between nurture and nature, thereby merging psychological and biological approaches in the explanation of schizophrenia (NAMI, 2014). This is in terms of unknown expression and transmission as presented by as well as small effect (Grohol, 2014).Amongst the proposed genetic candidates include: histone protein loci, NOTCH4 and specific copy number variations amongst others. In addition, zinc finger protein 804A is among a few genome-wide associations that have also been linked to the ailment’s occurrence. This is especially informed by the fact that there appears to be a distinguishable overlap in the genetics of both bipolar disorder and schizophrenia (Grohol, 2014). Also influential is that evidence is emerging of the involvement of both rare risk and common variation in the genetic architecture of the ailment. As Siegal et al. (2006) portend, in relation and influential are environmental factors in the occurrence of the illness. This is based upon pre-natal stressors, drug use and/ or the surrounding ‘living environment.’ individual developmental factors i.e. infection and hypoxia, malnutrition and stress etc, especially in the mother during her pregnancy influences fetal development. This may thus result in the slight increase of risk of the ailment later on in life. This is better encapsulated under biochemical analysis, vital in the greater understanding and subsequent treatment of the ailment (Siegal et al. (2006). Researchers are of the opinion that a number of factors play vital roles in the development of the ailment. According to Kumra et al. (2001), researchers envisage the presence of imbalances within the interrelated and complex chemical reactions of the brain. This is in relation to the neurotransmitters glutamate and dopamine amongst others. As substances, which allow communication between, brain cells, neurotransmitters are vital in the proper mental balance of an individual. Through studies of brain tissue, scientists have been able to find small changes concerning the characteristics and/ or distribution of brain cells. These have been linked to a likelihood of occurrence before birth, therefore solidifying the link between the ailment and pre-natal developmental factors. Informative is that problems experienced during pre-natal brain development (Kumra et al., 2001). Accordingly, the core biochemical explanation for ailment’s occurrence is the dopamine hypothesis, with the idea being based upon the role-play of the chemical messengers (neurotransmitters). Neurologically as Kurtz (2005) alludes, the ailment is associated with a number of subtle differences found within the brain structures and chemistry. Influential is that brain structure differences are found in an estimated 40-50% of diagnosed cases with brain chemistry differences occurring more during acute psychotic states. Through studies utilizing PET and fMRI amongst other brain imaging technologies and neuropsychological tests, differences have been shown to occur most commonly in the temporal lobes, frontal lobes and the hippocampus of the brain (Kurtz, 2005). Furthermore, has been the reported presence of brain volume reductions in the temporal lobes and frontal cortex, smaller than those experienced in individuals suffering from Alzheimer’s disease. Such differences have subsequently been linked to prevailing neuro-cognitive deficits that are often associated with the ailment. Pertinent to this has been the suggestion of the ailment being perceived as a collection of specific neuro-developmental disorders. Through the dopamine hypothesis, particular attention is paid to the functional role-play of neurotransmitter chemical dopamine, found within the brain’s meso-limbic pathway (Grohol, 2014). This focus is influenced mainly through the accidental finding of a reduction in psychotic symptoms experienced when the dopamine function is blocked. As Konradi and Heckers (2003) present, this is evident when phenothiazine drugs are introduced into the human system. Further supporting this is that amphetamines conversely increase the prevailing and/ potential psychotic symptoms through the triggering of dopamine release. Accordingly, the hypothesis proposed that the excessive activation of D2 receptors was a critical causal factor of the ailment’s positive symptoms. Further support was gained by way of both SPET and PET imaging studies conducted. The neurotransmitter glutamate further provides an idea on how the schizophrenia develops, based upon the reduced role-play of the NMDA glutamate receptor in individuals suffering from the ailment. Reduced glutamate functional role-play is therefore linked to poor performance in tasks requiring both hippocampal and frontal lobe functionality (Konradi & Heckers, 2003: Jones & Pilowsky, 2002). Kurtz (2005) provides that diagnosis of the ailment is based upon the utility of self-reported experiences of an individual, as well as reported behavioral abnormalities. This is usually followed up by a thorough clinical assessment of an individual by pertinent mental health professionals. Unfortunately, a hindering factor is that the ailment’s associated symptoms occur along a given continuum in any population, thereby necessitating that they reach a specific severity before pertinent diagnosis is made. Because the critical causal factors of the ailment are still unknown, the prevailing treatments mainly focus on the elimination of the existing symptoms (Kurtz, 2005). Thus, critical to the treatment of the ailment are varying psychosocial treatments and antipsychotic medications. Neuroleptic/ antipsychotic drugs ‘dampen’ dopamine effects through blocking of dopamine receptors, thereby aiding in the relief of delusions and hallucinations experienced by suffering individuals. Further influential to optimal treatment procedures is the need for continuous input of illness management skills. This is informed by the fact that those suffering from the ailment can actively take a role in the management of their own forms of illnesses. This is through informed decision making concerning their care as well as the prevention of relapses (NIH, 2015: NAMI, 2014). In addition, the presence of coping skills being inputted is critical in dealing with persistent symptoms. It is known that in individuals suffering from the illness, substance abuse is the most widespread concurring disorder. Thus, the need for input of integrated treatment programs focusing on the illness and drug treatment. This therefore necessitates rehabilitation measures that engage in vocational and social training that is helpful to those suffering from the illness. Further critical are cognitive behavioral therapy, family education and self-help groups, all which focus on the individual’s active participation in various social roles (Bo et al., 2011). The psychodynamic approach as portrayed by Freud puts blame squarely on parents for the illness’ development in children. Thus, both psychological and biological explanations portray many similarities, with both approaches being viewed as deterministic, due to their provision of complete reasons. However, their failure is experienced when they do not consider the aspect of ‘free will’ found in all human beings. Nonetheless, these approaches take into considerable account, the pivotal role-play of the family, exploring family and communal influences with the aim of determining the origin of the disorder. This is in addition to how the illness further builds a foundation basis over the years, upon which the illness is triggered from adolescence and the early twenties (Berrios, Luque & Villagran, 2003). In conclusion, Schizophrenia as a serious mental disorder affects an estimated 2.4 million adults in America, affecting both genders with equal frequency. However, it is experienced more in men during their early twenties or late teenage years vis-à-vis in women who are more affected during their late twenties and/ or early thirties. While finding the root causes of the ailment often has proved difficult because of specificity/ uniqueness in each individual, the aforementioned psychobiology explanations are vital in their account of the ailment. The influences experienced include interference with an affected individual’s overall management of emotions, ability to clearly think, their relationships to others, and pertinent decision-making processes. Through research, various linkages have been proven to the ailment’s occurrence, from a diverse number of causes including environmental and genetic factors, as well as brain structure and chemistry. Treatment procedures therefore vary in nature, based upon the mentioned causal factors. References APA (American Psychiatric Association). (2014). Diagnostic and statistical manual of mental disorders (5th Ed.). Arlington: American Psychiatric Publishing. Berrios, GE, Luque, R & Villagran, J. (2003). Schizophrenia: a conceptual history. International Journal of Psychology and Psychological Therapy, 3 (2): 111–140. Bo, S et al. (2011, July). Risk factors for violence among patients with schizophrenia. Clin Psychol Rev, 31 (5): 711–26. Bradley, WG et al. (2012). Bradley’s neurology in clinical practice 1 (6th Ed.). Philadelphia PA: Elsevier/ Saunders. Grohol, JM. (2014, July 9). Schizophrenia and psychosis: schizophrenia information & treatment (introduction). PsychCentral – Conditions, retrieved from: http://psychcentral.com/disorders/schizophrenia/ Jones, HM & Pilowsky, LS. (2002). Dopamine and antipsychotic drug action revisited. British Journal of Psychiatry, 181: 271–275. Konradi, C & Heckers, S. (2003). Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharmacology and Therapeutics, 97 (2): 153–79. Kumra, S et al. (2001). Childhood-onset schizophrenia: research update. Canadian Journal of Psychiatry, 46 (10): 923–30. Kurtz, MM. (2005). Neuro-cognitive impairment across the lifespan in schizophrenia: an update. Schizophrenia Research, 74 (1): 15–26. Mueser, KT & Jeste DV. (2008). Clinical handbook of schizophrenia. New York: Guilford Press. NAMI (National Alliance on Mental Illness). (2014). what is Schizophrenia? National Alliance on Mental Health: Mental Illnesses – Schizophrenia, retrieved from: http://www.nami.org/Template.cfm?Section=schizophrenia9 NIH (National Institute of Mental Health). (2015). What is Schizophrenia? National Institute of Mental Health, Health and Education: Mental Health Information, retrieved from: http://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml Siegal, GJ et al. (2006). Basic Neurochemistry: Molecular, Cellular and Medical Aspects (7th Ed.). Burlington, MA: Elsevier Academic Press. 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