The Cause of Schizophrenia, an Unsolved Mystery in Psychiatry - Essay Example

?The Cause of Schizophrenia: An Unsolved Mystery in Psychiatry Introduction Schizophrenia and similar disorders have traditionally been ified asmore neurologically-based than other mental disorders like depression, anxiety, and others. As a result, the number of available studies on the neurological basis of schizophrenia exceeds that of other mental illnesses. The findings of these studies practically show that there is a vast number of inconsistent or abnormal discoveries about schizophrenia. High-risk individuals and medically recovered patients have high levels of neurological test anomaly, showing that neurological disorder is not only an indicator of ongoing mental illness (Pincus & Tucker 2003, 106). Hence, it is evident that impaired neurologic functioning in schizophrenia is common and inherent to the illness. This essay discusses the neurological basis of schizophrenia and tries to determine if there is a single underlying cause. Neurological Basis of Schizophrenia All forms of illness or impairment of the central nervous system may generate behavioural symptoms that resemble those of schizophrenia. The differential diagnosis depends greatly on the medical record, the type of onset, the form of existing symptoms, and history of psychosis (Pincus & Tucker 2003, 98). There are other conditions, besides schizophrenia, that can stimulate mental disorders, though drug-stimulated psychoses, emotional problems, and schizophrenia are without a doubt the most widespread sources of this syndrome in young adults (p. 98). Due to its elevated prevalence, there is a great tendency to identify schizophrenia every time a young adult shows symptoms of an acute mental disorder (Mueser & McGurk 2004, 2065). Nevertheless, occurrences that resemble schizophrenia have been identified in relation to other mental illnesses and with other neurological disorders like tumour, cerebral trauma, and so on. Even though psychoses are generally identified in such disorders, they hardly ever imitate schizophrenia’s symptoms perfectly; confusion, memory loss, disorientation, and erratic conditions of consciousness that are common in several neurological disorders are rarely identified in schizophrenia (Nasrallah & Lasser 2006, 59). Basically, the complexity in distinguishing neurological disorders from schizophrenia emerges mostly in the early onset of neurological disorder. Neurological anomalies in schizophrenic people have long been determined but have been mostly disregarded by scholars until the recent decades. Trevor Turner, in a study of the medical histories of patients who had been confined in Ticehurst House Asylum in England from 1850 to 1889 “A particular feature was the extraordinary prevalence of abnormal movements and postures. Terms like grimaces, fidgets, jerkiness and twitching recur constantly” (Torrey 1994, 127). In the past, clinicians believed that neurological disorders were a usual parallel to these symptoms. According to Torrey (1994), throughout these earlier periods, the dominant belief among clinicians was that schizophrenia was stimulated by psychological circumstances during childhood—‘functional’ psychosis-- contrary to mental disorders induced by brain tumours or syphilis—‘organic’ psychosis (p. 127). Neurological disorders, which signify an organic diagnosis, did not match the ‘functional’ theory; hence numerous researchers easily discarded them. Gary Tucker and Jonathan Pincus, in 1974, claimed that “Minor neurologic abnormalities are commonly found in schizophrenia. This is not what one would expect in a ‘functional’ disease and for this reason the presence of such signs is often overlooked or they are considered epiphenomena” (Torrey 1994, 128). Neurologic tests of schizophrenic individuals are different from the examinations of healthy individuals, yet the medical ramifications of this are vague. The common medical role of the neurologic test in people with psychosis is to exclude ‘organic’ or minor psychoses. This role has been buried by the overflow of findings showing that neurologic symptoms are common in the ‘functional’ psychoses; hence their manifestation cannot be considered as proof of further neurologic impairment (Robbins 1992, 434). Moreover, there is an insufficient availability of findings comparing neurologic test results from individuals with major and minor psychoses. Nearly all neurological disorders will either disappear or advance to observable neurological syndrome. The error usually made by novice psychiatrists is to classify as schizophrenic all silent, delusional, confused, or odd behaviour that cannot be simply identified by a common medical disorder. Psychiatrists confronted with hallucinations and delusions, usually fail to notice obvious symptoms of Babinski reflexes, tremor, disorientation, memory deficit or other obvious indications that the condition is neurological (Pryse-Phillips 2009, 32). Besides disordered memory and disorientation, there are several uncomplicated rules for the differentiation of traditional schizophrenia from serious neurological illnesses. In serious neurological illnesses there are normally (Pincus & Tucker 2003, 99): (1) Abrupt changes in mental condition. The individual is confused one day, then totally balanced and sane the next: even though sudden changes can also be observed in a number of people with schizophrenia, they are normally not that abrupt. Even when the mental condition of a schizophrenic individual appears to recover all of a sudden, s/he will still manifest several symptoms of delusional thoughts or odd behaviour; (2) a highly erratic mood, temper, behaviour, and capacity to perform tasks at home and at work: the rapidness of the development of this syndrome confirms a neurological basis; (3) a satisfactory social history before the onset of the illness: the patient did not encounter any difficulties at home and at work and was mostly accommodating and affectionate rather than anxious or distressed , as is quite frequently observed in schizophrenia. Noticeable changes in mental conditions are, generally, more symptomatic of serious neurological disorder than schizophrenia. The changes in the mental condition of people with neurological disorder may go together with changing motor functioning. The patient may show destructive urges and get involved in aggressive acts at a particular instant but later on express regret and attempt to mingle with the people s/he has harmed (Walker et al. 2004, 408). The form of behaviour during this time usually has a motivated value to it, as has been discovered by Kahn (1934) and Goldstein and Scheerer (1941) in patients with brain injuries (as cited in Pincus & Tucker 2003, 99). A patient with a serious neurological problem is normally resistant to psychiatric treatment. Psychopharmacological intervention, instead of regulating behaviour, may bring on a comatose or numbed condition depending on the core illness (p. 99). Numerous patients who display silent and odd behaviour are brought right away to the psychiatric specialist. Even serious neurological symptoms can be missed or diagnosed as part of the ‘functional’ psychosis of the patient (Wildgust & Beary 2010, 42). However, noticeable behavioural anomalies should not prevent psychiatrists from identifying neurological signs. Neurological aberrations suggest “that there is some dysfunction of the areas of the brain that control the cranial nerves coming directly from the brainstem, or of the nerves that emanate from the spinal cord” (Zillmer, Spiers, & Culbertson 2008, 138). Usually, these neurological aberrations have been classified into ‘soft signs’, which “involve more complex behaviours for which it is not yet possible to specify which part of the brain is affected,” (Barlow & Durand 2011, 535) and ‘hard signs’, wherein “it is possible to specify with some precision which part of the brain is affected” (Finger 2001, 56). Some examples of soft neurological signs are ‘constructional apraxia’—inability to perfectly draw two crisscrossing pentagons-- and ‘astereognosis’—inability to recognise the kind of object without taking a look at it (Pryse-Phillips 2009, 245). Some examples of hard neurological signs are the long-term grasp reflex and ‘patellar tendon reflex’ (Brookshire 2003, 64). Robert Buchanan and Douglas Heinrichs (1988), in a simple report about the soft signs identified most often in schizophrenic individuals, state that soft signs indicate dysfunctions in “three higher-order functional areas: the integration of more complex sensory units, the coordination of motor activity, and the sequencing of motor patterns” (as cited in Torrey 1994, 129). In truth, what is recognised as neurological anomaly in schizophrenia is somewhat subjective. Studies on people with this illness has manifested defect in ‘vestibular function, dichotic listening, eye movements, and skin conductance patterns’ (Torrey 1994, 129). Each of these signify neurological defects as well, but they are normally not classified per se. It must be stressed that neither soft nor hard neurological symptoms are only found in schizophrenia and could be identified in almost all neurological illness. Soft signs are diagnosed in individuals with attention deficit disorders and dyslexia, and have been diagnosed as well in bipolar disorder, though with lower prevalence compared to schizophrenia (Boyd 2005, 575). As a result, the data on major soft or hard neurological symptoms cannot be applied to make a diagnosis of a schizophrenic individual but only as proof of an imprecise neurological impairment. Even though there have been findings of hard sign anomalies in schizophrenia, like damaged gag reflex and long-term grasp reflex, soft symptoms have been the primary concern (Pincus & Tucker 2003, 107). The contemporary period of focus on neurological symptoms in schizophrenia started in 1960 with the finding of Margaret Kennard of common neurological defects in schizophrenic teenagers. Afterwards, seven other findings were made public. In 1983, these were summed up by Larry Seidman, who stated (Torrey 1994, 129): The frequency of abnormal neurological examinations using soft signs is consistently between 36 percent and 75 percent for those studies providing frequency data… A second clear-cut finding is that schizophrenics have more frequent neurologic abnormalities than other psychiatric patients (e.g., affective disorder) and normal controls… The data are very consistent from study to study and consequently are rather convincing. Soon after publishing this study, several further studies have been made public demonstrating that neurological soft-sign defects arise more often in schizophrenic people than in healthy people. Another discovery is that there is no sole soft or hard neurological symptom that is diagnosed consistently in people with schizophrenia and that can thus be concluded to be characteristic of the illness. In earlier studies of neurological defects in schizophrenic people, soft-sign defects took place more often than hard-sign defects (Finger 2001, 294). A number of neurological aberrations took place at a significantly greater rate in impaired people, such as right-left disorientation, defective coordination, etc (Torrey 1994, 129-130). Yet, no sole neurological symptom prevailed. The general neurological data show a scattered disease mechanism that does not impact exactly the same area of the brain in each affected individual. On the whole, earlier and current efforts to determine particular structural alterations in the brain that are related to neurological abnormality failed. This could be because of the absence of certainty in the assessments of neurological processes, the absence of accuracy in assessments of brain functioning, or the likelihood that the incorrect processes are being assessed. On the other hand, the absence of connection could be due to the fact that brain dysfunction in schizophrenia is not limited to a small number of processes but instead is more scattered, with few, diffused areas of concern scattered in such a manner as to generate neurological defects, which do not automatically associate with extensive structural alteration (Wildgust & Beary 2010, 44). This could be the more probable reason. A more current explanation for disregarding neurological defects in schizophrenic individuals is that the antipsychotic medications administered to cure the illness can also bring about these defects. It is hence concluded by numerous psychiatrists that all neurological defects diagnosed in schizophrenic individuals must be because of the antipsychotic drugs they are receiving or have received previously (Sachdev & Keshavan 2010, 397). This is mainly factual for involuntary movements, most of which are believed to be rooted in the tardive dyskinesia condition—an impairment caused by repetitive, involuntary movements (Boyd 2005, 115). Indeed, studies have demonstrated that related involuntary movements arise in a small number of schizophrenic patients who have never received any medications. Is There a Single Underlying Cause? In spite of almost a hundred years of research, the underlying cause of schizophrenia is still unknown. This failure to determine the underlying cause of the disorder may be attributed to three likely explanations (Taylor 2006, 13): (1) schizophrenia could be rooted in something not yet discovered up to now; (2) schizophrenia may not develop or occur as a single disorder; and (3) there could be numerous causes of schizophrenia. The failure to determine the cause of schizophrenia may suggest incorrect categorisation of disorders under a single concept. However, valuable ideas about this complicated illness have been produced by population-based research. Two primary findings are widely recognised. First, the medical symptoms schizophrenia is scattered and can be diagnosed consistently in diverse populations. Nevertheless, current findings have a tendency to challenge the idea that a single, universal pathophysiology and general genetic mechanism can possibly give explanation for the entire range of schizophrenia’s symptoms (Weinberger & Harrison 2011, 1936). There is currently proof to show that disparities in prevalence and disease vulnerability can be identified in populations at the local, national, and global stage. According to Weinberger and Harrison (2011), comprehensive investigation of these differences in the prevalence of schizophrenia could offer new evidence on the pathogenesis and aetiology of the illness (p. 1936). The second finding is that no sole environmental risk factor of main impact on the prevalence of schizophrenia has been identified thus far. Additional research drawing on large samples is needed to assess possible precursors, predictors, and risk factors for which the current finding is questionable. Contemporary epidemiological studies are drawing on massive databases to verify assumptions about risk factors (Weinberger & Harrison 2011, 1936). The union of epidemiology and genetics will create mechanisms for the understanding of the gene-environment relationship that are possible answers to the underlying cause of schizophrenia (p. 1936). Even if scientists discover a single underlying cause for schizophrenia, it will not essentially result in a solution to prevent or successfully cure the disease. Even though it may not possess the same strength as the identification of a single underlying cause, the discovery of risk factors and an accurate knowledge of how these risk factors affect the brain’s structure and its functioning may in fact become a more effective strategy. Several risk factors could be controllable. Other risk factors could direct clinicians to past procedures of diagnosis. And by understanding how these risk factors cause alterations in the brain, clinicians may in fact be capable of blocking the psychological or biological channels that bring about impairment and weaknesses related to schizophrenia (Stirling 1997, 436). It is important for clinicians to work persistently to determine schizophrenia’s causes. These studies are likely to generate valuable evidence on how the disease can be averted and result in enhanced care and interventions. Even though it is somewhat impossible thus far to be able to totally determine how the entire host of contributing factors work together to generate schizophrenia in any individual, it appears probable that each of these factors influences an ultimate universal pathway. Identifying the features of this pathway will be difficult. Nevertheless, with advanced brain imaging technologies there has been remarkable development in the recent decade. Much knowledge has been produced about learning, attention, memory, and language mechanism. The neurological basis of schizophrenia has some particularly valuable information coming from studies of patients prior the onset of the disorder. In numerous instances, patients are healthy prior to the development of schizophrenia. Others behave or perform more defectively than usual and show slight behavioural and neurological signs indicative of an early neuro-developmental disorder. The propensity of drugs to bring about positive symptoms like delusions and hallucinations points to dopamine (Hoffman & Mcglashan 2001, 445). Many of the areas in the brain responsible for emotions, perception, and thoughts are governed by dopamine. Conclusions As suggested in some studies, patients with schizophrenia have problems carrying out psychological activities. The nature of such abnormalities offers several ideas about the areas in the brain concerned. Empirical findings are still inconclusive, but they seem to imply that there could be continuous structural alterations in the initial stages of disorder consistent with, but not automatically associated with, neurological abnormality. However, even though still inconclusive, several of these findings have repercussions for psychiatric intervention or treatment, and the initial attempts to develop more useful and effective treatments and new, non-pharmacological interventions. Finally, these studies offer some insights into the weaknesses of existing theories and approaches and how a more accurate knowledge of the single underlying cause of schizophrenia could lead to a better knowledge of human consciousness. References Barlow, D. & Durand, M. (2011) Abnormal Psychology: An Integrative Approach. Mason, OH: Cengage Learning. Boyd, M.A. (2005) Psychiatric Nursing: Contemporary Practice. Philadelphia, PA: Lippincott Williams & Wilkins. Brookshire, R. (2003) Introduction to neurogenic communication disorders. New York: Mosby. Finger, S. (2001) Origins of Neuroscience: A History of Explorations into Brain Function. Oxford: Oxford University Press. Hoffman, R. & Mcglashan, T. (2001) ‘Book Review: Neural Network Models of Schizophrenia’, The Neuroscientist, 7(5), 441-454. Mueser, K.T. & McGurk, S.R. (2004) ‘Schizophrenia’, Lancet, 363, 2063-72. Nasrallah, H. & Lasser, R. 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(2004) ‘Schizophrenia: etiology and course’, Annual Review of Psychology, 55, 401-30. Weinberger, D. & Harrison, P. (2011) Schizophrenia. London: John Wiley & Sons. Wildgust, H. & Beary, M. (2010) ‘Review: Are there modifiable risk factors which will reduce the excess mortality in schizophrenia’, Journal of Psychopharmacology, 24(4), 37-50. Zillmer, E., Spiers, M., & Culbertson, W. (2008) Principles of Neuropsychology. Mason, OH: Cengage Learning. Directly Consulted References Barlow, D. & Durand, M. (2011) Abnormal Psychology: An Integrative Approach. Mason, OH: Cengage Learning. Boyd, M.A. (2005) Psychiatric Nursing: Contemporary Practice. Philadelphia, PA: Lippincott Williams & Wilkins. Brookshire, R. (2003) Introduction to neurogenic communication disorders. New York: Mosby. Finger, S. (2001) Origins of Neuroscience: A History of Explorations into Brain Function. Oxford: Oxford University Press. Hoffman, R. & Mcglashan, T. 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(1997) ‘Progress in research into the neurobiological bases of schizophrenia: A review and commentary’, Nursing Times Research, 2(6), 434-440. Taylor, D. (2006) Schizophrenia in Focus. London: Pharmaceutical Press. Torrey, E.F. (1994) Schizophrenia and manic-depressive disorder: the biological roots of mental illness as revealed by the landmark study of identical twins. New York: Basic Books. Walker, E. et al. (2004) ‘Schizophrenia: etiology and course’, Annual Review of Psychology, 55, 401-30. Weinberger, D. & Harrison, P. (2011) Schizophrenia. London: John Wiley & Sons. Whalley, H. et al. (2005) ‘Neural Correlates of Enhanced Genetic Risk for Schizophrenia’, The Neuroscientist, 11(3), 238-249. Wildgust, H. & Beary, M. (2010) ‘Review: Are there modifiable risk factors which will reduce the excess mortality in schizophrenia’, Journal of Psychopharmacology, 24(4), 37-50. Winterer, G. & Weinberger, D.R. (2004) ‘Genes, dopamine and cortical signalto-noise ration in schizophrenia’, Trends in Neurosciences, 27, 683-690. Zillmer, E., Spiers, M., & Culbertson, W. (2008) Principles of Neuropsychology. Mason, OH: Cengage Learning. Word Count (excluding the reference page): 2,687 Read More