Pathophysiology of Schizophrenia - Research Paper Example

Running head: Intellectual Disabilities and its categories Pathophysiology of Schizophrenia By _________________ Abstract Schizophrenia, a group of related disorders that takes no time to turn into disability, however if given proper concern in this stage, it is lesser probability that it would turn into a disability. These disorders are followed by hallucinations and delusions along with the positive and negative symptoms that lead to schizophrenia. The patient builds certain characters which are not based upon reality and are fictitious, often the patient is found to communicate with those characters which he create in his imaginations. These characters tend him towards social as well as moral isolation, frustration and depression. The outcome is severe personality disorder followed by lack of communicational skills. Such patients possess attitude problem like speech disorder, mental disorder and are often tended towards what we call as 'roller coaster of thoughts'. However, the dilemma remains that this lifelong disease is responsible for conducting many suicidal behaviors, mood instabilities and frustration causing serious crime and is still not given that much attention as it supposed to be given. While considered as a disease, it requires serious steps to be taken in pathophysiology. Pathophysiology of Schizophrenia According to DSM-IV, for a person to be diagnosed with Schizophrenia, they must show two or more of the following symptoms: 1. Delusions 2. Hallucinations 3. Disorganized speech 4. Grossly disorganized behavior 5. Negative symptoms, such as flat mood, lack of motivation etc. (Rapee, 2001:20) Siever et al describes Schizotypal disability as a disorder, which shares common phenomenological, genetic, biologic, outcome, and treatment response characteristics with more severely ill chronic schizophrenic patients. (Siever & Davis) However, at the same time, they are freer from the multiple artifacts that potentially confound research in schizophrenia including the effects of long-term and usually ongoing medication treatment, multiple hospitalizations or institutionalization, and prolonged functional impairment secondary to chronic psychosis and social deterioration. (Siever & Davis) Genetic Factors: Studies have shown that that if one person has schizophrenia, the chance for another person also sharing the disorder depends on the degree of genetic relatedness between them. For example if one twin has schizophrenia, the chance that the co-twin will also have schizophrenia is around 18% if they are non identical twins but 48% if they are identical twins as identical twins share 100% of their genes. (Rapee, 2001:22) Neurotransmitters/ Disconnection Syndrome: The biological models of schizophrenia emphasize neurochemical dysregulation or anatomical changes in the brain. The most widely disseminated and thoroughly developed biological theories include the neurotransmitter model. (Beebe, 2003) The cause of Schizophrenia is followed by one of the most widely accepted theory named "Dopamine Theory". This hypothesis states that schizophrenia can be understood in cognitive terms, as a failure of functional integration within the brain. Functional integration refers to the interactions of functionally specialised systems (i.e., populations of neurons, cortical areas and sub-areas) that are required for adaptive sensorimotor integration, perceptual synthesis and cognition. (Friston, 2002) According to this theory, most of the symptoms of schizophrenia are the result of having excessive levels of dopamine, especially in the mesolimbic pathways of the brain. (Carson & Sanislow, 1993) Several sources support this theory. First many of the drugs that are used to treat schizophrenia seem to work primarily by blocking certain dopamine receptors in the brain. Second certain drugs that have been found to increase levels of dopamine in the brain also produce symptoms that are very similar to those found in schizophrenia. An appropriate example is the Amphetamine abuse, which are stimulants that work by increasing brain dopamine levels. People who abuse large doses of amphetamines often present at hospitals with behaviors that look very "schizophrenic like", including agitation, hallucination and paranoid delusions. Finally, both post-mortem dissections and brain scans using positron emission tomography (PET) have shown that people with schizophrenia have more dopamine receptors in their brains and that these receptors are more active than in other people. (Taubes, 1994) More recently several other neurotransmitters have been hypothesized to be involved in schizophrenia in addition to dopamine. Another theory supporting schizophrenia but to a little extent accepted is diathesis stress theory, which includes that schizophrenia turns out to be a complete disorder when this genetic predisposition reacts with some type of life stress. Cognitive Functioning: Schizophrenic patients not only demonstrate qualitative and quantitative impairment in smooth pursuit tracking but also perform less accurately in antisaccade and in motion detection tasks. Smooth pursuit eye movements are mediated by frontal and temporal cortex, as well as brain stem, while motion detection is mediated by inferior temporal cortex. SPD subjects show impairment in smooth pursuit tracking measured qualitatively and by indices such as tracking gain and saccadic intrusions just as do schizophrenic patients. (Siever & Davis) These abnormalities are particularly correlated with the social deficits and interpersonal isolation of these patients. Schizotypal subjects, whether identified in samples of clinical, volunteer, or relatives of schizophrenic patients, also show deficits in d-prime, a measure of accuracy in performance, on the Continuous Performance Task (CPT), an attentional task that depends on frontostriatal circuitry. Interestingly, schizotypal individuals perform relatively normally under low processing demand conditions such as non-degraded stimulus presentation, but perform more poorly than normal controls and other personality disorder comparison groups when stimuli were degraded or a more challenging identical pair CPT paradigm or a dual task CPT was utilized. Other information processing abnormalities shared between SPD and schizophrenic subjects include latent inhibition, negative priming, and interference. (Siever & Davis) Information Processing: The symptoms of schizophrenia can be interpreted as the result of a defect in the mechanism that controls and limits the contents of consciousness. This defect can be understood as excessive self- awareness. Normally most of the complex information processing which is continuously required by even simple acts of perception, language and thought goes on below the level of awareness; whereas in schizophrenic patients some of this processing, or the results of this processing, not in themselves abnormal, become conscious. This excessive awareness can account for the typical symptoms of schizophrenia and explains many of the specific cognitive abnormalities found in schizophrenic patients. (Frith) Schizophrenia is a disorder that selective damage to cellular or molecular systems mediating either structural or synaptic plasticity. However, there are two simple facts that point schizophrenia to synaptic plasticity. The first is that schizophrenic symptoms can be produced by psychomimetic drugs (Allen R.W). This tells us immediately that the locus of abnormality is likely to be synaptic as opposed to cellular. This is because neurotransmitters in this disorder act at synapses, not at the level of neurogenesis during development. Secondly, the fact that schizophrenia is expressed symptomatically in adulthood points to abnormal modulation of experience-dependent synaptic plasticity, as distinct from the induction and maintenance of connections though epigenetic mechanisms or indeed activity-dependent plasticity in utero. This does not preclude neurodevelopment explanations for schizophrenia, but suggests that the mechanistic endpoint, of any putative aetiology, involves processes that are expressed post-developmentally. (Friston) Community Care: Community acceptance of the mentally ill in most places through many of the subsequent years have been sufficiently poor, however still the services and programs are offered by a community support system in order to counsel individuals through psychosocial rehabilitation and vocational services. Services may be offered to patients in hospital, group homes, independent living or wherever the client can be found, whether it is in jail or a shelter for the homeless. Community support comprises everything the old, long-stay institutions used to furnish and a host of additional services besides, which are essential for community tenure. References & Bibliography Allen RW. Young SJ. Phencyclidine-induced psychosis. Am J Psychiatry. 1978;135:1081-1084. Beebe, Lora Humphrey, (2003) Theory-Based Research in Schizophrenia In Perspectives in Psychiatric Care. Volume: 39. Issue: 2 Carson, R.C., & Sanislow, C.A.III (1993) The Schizophrenias. In P.B. Sutker & H.E. Adams, Comprehensive Handbook of Psychopathology: New York Friston J, Karl (2002) Dysfunctional Connectivity in Schizophrenia. In World Psychiatry: Pubmed Central v.1(2); June 2002, accessed from Frith CD, (1979) Consciousness, Information Processing and schizophrenia in The British Journal of Psychiatry 134:225-235 Rapee M., Ronald, (2001) Abnormal and Health Psychology: Psychological Science. Bond & McConkey Siever J, Larry and Davis L., Kenneth (n.d) accessed from Taubes, G. (1994). Will new dopamine receptors offer a key to schizophrenia Science. Warner Richard, (2004) Recovery from Schizophrenia: Psychiatry and Political Economy: Brunner-Routledge: New York. Read More