Schizophrenia as Critical Psychiatric Disorder - Essay Example

SCHIZOPHRENIA Schizophrenia Schizophrenia is listed among the most complicated and critical psychiatric disorders, causing an early onset of clinical features. It usually manifests in the age group of 15 and 30, and as it enters into a chronic phase it causes more serious disabling features for the patients. Apart from the serous signs and symptoms, this psychiatric disorder also has an immense impact on the close environment and relatives of the patients, due to its severe nature. The earliest description of schizophrenia is given by a French psychiatrist as a form of dementia and was termed “dementia praecox” (Mueser& Jeste 2008). Prevalence of this psychotic disorder in USA is recorded to fluctuate from 0.3 to 4.7 per 1000 people (Shean 2004). A difference in prevalence is observed in the rural and urban areas as well. According to an estimate, a three-fold greater prevalence was observed in the urban areas of Baltimore in USA rather than in rural areas. According to the WHO-Ten Country Study, the age at which schizophrenia manifests in any country depends directly to the degrees north to the equator (Weinberger, Harrison 2011). Schizophrenia is termed as a heterogeneous disorder as it can neither be explained and defined by any particular clinical feature nor diagnosed by a specific test. After excluding all other psychotic disorder signs, an individual is diagnosed with the schizophrenia if he presents with the symptoms of delusions, hallucination and thought disorder. However there are certain individuals that will present with negative symptoms, for instance lack of energy, communication skills, emotions, and stress and speech disturbances. Such patients respond weakly to the conventional treatments of schizophrenia. Cognitive disturbances are another striking feature of this disorder. The patients have difficulty concentrating at work, speaking, understanding things, memorizing and performing various daily functions. These features have been established as a stable feature in schizophrenia patients in spite of manifesting either positive or negative symptoms (Ross, et al 2006). The studies have brought to light that schizophrenia has a neurodevelopmental component in its etiology. This means that there are certain disturbances in the normal course of development and function of the brain which lead to the first episode of schizophrenia in a person. This occurs in the absence of any degenerative process in the brain. On the other hand, neurodegenerative etiological evidence has also been established where there is degradation of neurons due to various factors leading to the signs and symptoms of schizophrenia (Mueser& Jeste 2008). According to the Diagnostic and Statistical Manual of Mental Disorders (DSM), a handbook used widely in USA for classification of mental disorders, schizophrenia clinical features and diagnosis is described by the DSM fourth revision, DSM-1V. The DSM-1V describes the symptoms of schizophrenia as disorganized behavior and speech, negative symptoms, hallucinations and delusion. DSM-1V provides a set of six guidelines to diagnose a schizophrenic individual which includes poor functioning, manifesting over a time period of six months and excluding any mood disorder. The symptoms should also not be caused by any substance abuse and should also not be a feature of autism (Eaton 2006). DSM-1V describes positive symptoms as hyperactivity of the usual and normal cognitive functions while the negative symptom is a depression of the normal functions. The positive symptoms have a “psychotic dimension” and a “disorganization dimension” (Mueser & Jeste 2008). The subject of the case, Shonda, exhibits a history of 12 years since she was first diagnosed of schizophrenia. Her major symptoms include auditory hallucinations and delusions that she might be under surveillance. However, recently she has showed an increase in the hallucinations and she is experiencing disturbed speech and thought process. She also shows a family history of an undiagnosed psychiatric disorder in her family. The case exhibited psychotic symptoms of hallucination and delirium, and they were suppressed by the usage of anti-psychotic drugs. These symptoms were caused by the excitatory and inhibitory actions of the neurotransmitters. The role of neurotransmitters in the patho-physiology of schizophrenia was understood through the concepts of pharmacological studies. It was observed that if stimulants of dopamine were given to normal people, it induced symptoms of psychosis in them. Similarly, in the schizophrenic patients it exaggerated the signs and symptoms. This was termed as the “dopamine hypothesis” and gave evidence about the involvement of dopamine in causing the schizophrenic symptoms. Glutamate is another neurotransmitter of important role in this disorder (Ross et al 2006). In 1943, Albert Hoffman experimented with LSD which induced psychotic symptoms and it was discovered that this chemical compound enhanced the action of serotonin in the brain. Hence, this led to the discovery that serotonin is another neurotransmitter whose hyperactivity causes schizophrenic symptoms. However, the importance of serotonin in the patho-physiology is yet to be established. Glutamate has an excitatory action on the brain’s activity. Evidence about this neurotransmitter was found when antipsychotic drugs blocked the NMDA receptors and inhibited the action of glutamate. Other neurons found to be involved in schizophrenia are aspartate, glycine and GABA (Mueser & Jeste 2008). Shonda shows a family history of an aunt who had a “nervous breakdown” and was not treated by any doctor. This points out towards a positive family history of similar cases. Studies have shown that schizophrenia has a familial trait and familial factors lead towards occurrence of schizophrenia or even other psychotic disorders. Carrier forms can be present and susceptibility genes can be present in families who may or may not present with the manifestations (Kendler & Diehl 1993). Many genetic risk factors have been established that can result in the causation of schizophrenia. Neuregulin 1 is one gene located on chromosome 8p locus that is associated with schizophrenia. Recent studies have pointed out that the activity of this gene signaling is exacerbated in schizophrenia patients. Dysbindin located on chromosome 6p is another gene, which performs the function of glutamate neurotransmission. Mutations in this gene are related with schizophrenia. There is a reduction in the expression of the Dysbindin gene and this results in the reduced function of glutamate as a consequence. D amino acid oxidase activator (DAOA) is present on the 13 chromosome locus. This gene has the function of activating the D amino acid oxidase which acts as a co-agonist with the NMDA receptors for glutamate. COMT and chromosome 22 deletion is strongly associated with schizophrenia. COMT gene produces a protein that clears the excess dopamine from the synaptic regions of the neurons and mutations lead to increased dopamine levels. Some genetic abnormalities occur due to gene translocations; however they are not a major cause of schizophrenia (Ross et al., 2006). The major brain abnormalities found in the schizophrenic patients are divided according to their anatomic site. These include global region, cortical, sub cortical and white matter of the brain. These abnormalities are described under the neurodevelopmental model of the brain of the schizophrenic person. The global brain findings include reduced brain volume and ventricular enlargement. This increase in the ventricular size measured by ventricular-brain ratio affects the presentation of the disease. Prefrontal region of the brain cortex is involved with the normal cognitive and behavioral functions. An important finding in neuroimaging was an increased neuronal packing which was specifically increased in the dorso-lateral part of the cortex. This area is specifically associated with the diminished cognitive functions in the patients. Reduced volume of the medial temporal lobe is seen and the regions of the brain which are affected by this include amygdala, hippocampus and parahypocampal gyrus. Variations in neuron pack density and reduced superior temporal gyrus volume has been associated with audio hallucinations and thought disturbances. Abnormalities in cerebellum cause a disturbance in higher cognitive functions. A theory of disconnectivity describes that different parts of the brain do not connect and communicate normally with each other that leads to different signs and symptoms. This can be explained by dysfunctional neurotransmission. Abnormal distribution and increased cell density of oligodendrocytes and myelin, a part of the white matter has also been detected in prefrontal cortex of the schizophrenic patients (Mueser & Jeste 2008). According to the case-study, Shonda experiences auditory hallucinations and delusions which point towards the fact that the major brain abnormality might be in the amygdala-hippocampal-paraphypocampal gyrus complex and the superior temporal gyrus as they are strongly associated with these symptoms. Shonda has been given a variation of antipsychotics but currently she is being given a neuroleptic called Haloperidol. The recommended dosage of the drug is 6-12 mg. It is a chemical structure of the butyrophenones which is a type of FGAs (Aronson 2009). Currently 11 different classes of anti-psychotic drugs are used for treatment in USA. The first generation antipsychotics (FGAs) include phenothiazines, butyrophenones and thioxanthenes. The second generation anti-psychotics (SGAs) include clozapine, risperidone, olanzipine, quietiapine, ziprasidone, sertindole and zotepine. These are also called the atypical drugs. Aripiprazole is considered as a “next-generation antipsychotic” and has a partial dopamine agonist mechanism of action (Miyamoto 2005). The use of ECT in USA is quite limited such that only about 1% patients receive this therapy. This therapy is only recommended for those patients who fail to respond to medications and psychotherapy. With only 0.0002% rate of mortality, this treatment is mainly safe and free of any severe harm (Mueser & Jeste 2008) There is no history of any other treatment given to Shonda other than anti-psychotic drugs, which has been proved thorough various researches as an effectual strategy. According to research carried out on five different treatment methods of schizophrenia in 2011 by Philip R. A. Mary and A. Hussain Tuma it was concluded that patients who were treated with medications alone or with psychotherapy exhibited the best therapeutic results. The five types of treatment strategies that were experimented included; drugs alone, drugs with psychotherapy, only psychotherapy, electroshock therapy and control treatment devoid of any above mentioned strategies. The patients with ECT and only psychotherapy showed poor results as compared to those treated with drugs and psychotherapy together (May & Tuma 1965). Out of the three types of drugs available for the treatment for schizophrenia, the second generation anti-psychotics have proved to be better and more beneficial than the first generation drugs (Miyamoto 2005). They have a lesser tendency for the dopamine receptors in the basal ganglia of the brain and hence they cause lesser adverse effects as compared to the FGAs (Aronson 2009). The FGAs have a high tendency for the dopamine receptors in the brain. Neuroimaging results have proved that optimal doses of these drugs block the D2 receptors in certain areas of brain which include the limbal cortical areas and the cortex. The action of SGAs is described by the serotonin-dopamine antagonist theory and the “fast-off D2 theory”. The first theory suggests that these drugs have a higher tendency for the serotonin receptors as compared to D2 receptors. Drugs like clozapine and risperidone have the affinity to occupy 80% or even more serotonin receptors. This explains their high efficacy. The therapeutic importance of SGAs can also be described by their ability to act at other receptors like D1 and D3, muscuranic cholinergic receptors and histamine receptors. Some SGAs also possess the tendency to increase the activity of serotonin which results in an improvement in cognition due to its action on the frontal cortex (Miyamoto 2005). Haloperidol might have been given to the patient because of its high affinity for dopamine and keeping in consideration the symptoms of the patient. Haloperidol, which is the current treatment of the subject, is a typical neuroleptic and is associated with extrapyrimadal symptoms. FGAs are effective in curing the positive symptoms of schizophrenia but some patients show no or little response to this treatment. They are comparatively less effective against the negative symptoms and may cause exacerbations or no effect at all. All FGAs have the potency to cause Parkinson like symptoms, dystonia, akathasia and tardive dyskinesia. They can also lead to hyperprolactemia. The SGAs are superior to the FGAs in their safety levels as they do not cause tardive dyskinesia and extrapyrimidal symptoms like dystonia. However, they are associated with a different set of adverse effects which include increase in weight, diabetes mellitus, cardiovascular problems and prolonged QTc interval. Clozapine is one SGA that has given evidence of least cases of hyper-prolactemia and EPS (Miyamoto 2005). When compared with clozapine, haloperidol shows fewer improvements in occupational and daily work activities. It has also been associated with dry mouth and less improvement in negative symptoms. Through studies it has been showed that quality of life improves more significantly with atypical drugs (Aronson 2009). References Aronson, J. K. (2009). Meylers side effects of psychiatric drugs. Amsterdam: Elsevier. Eaton. W. (2006).“Schizophrenia and Bipolar Disorders: Diagnosis, Descriptive Epidemiology, and Natural History. Johns Hopkins Bloomberg School of Public Health. Web. 1 January 2011. http://ocw.jhsph.edu/courses/PsychiatricEpidemiology/PDFs/Lecture11.pdf Kendler, K. S., & Diehl, S. R. (January 01, 1993). The genetics of schizophrenia: a current, genetic-epidemiologic perspective. Schizophrenia Bulletin, 19, 2, 261-85. Miyamoto, S., Duncan, G. E., Marx, C. E., & Lieberman, J. 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