Schizophrenia: Introduction and Overview
Running head: THE IMPACT OF SCHIZOPHRENIA
Schizophrenia: Introduction and Overview
Student ID: 2540 (AP205)
Southern Cross International College
(Path Education Singapore)
Schizophrenia: Introduction and Overview
Diseases of the brain and mind have occupied humanity from ancient times. Syndromes recognizable as forms of psychosis appear in the writings of Plato and Hippocrates. Psychosis is a syndrome such as a constellation of symptoms that reflects the distortion of the person's thoughts and perceptions such that there is a loss of boundaries between what is real and what is unreal, between himself or herself and the external world. And Schizophrenia, itself is a form of psychosis, characterized by a multiplicity of symptoms affecting the most fundamental human attributes: cognition, emotion and perception - a mind that is torn asunder. The early age of onset, varying degree of intellectual and psychosocial impairment, possibility of long-term disability and above all associated stigma, often brings to its victims and their family's emotional and financial distress, which makes schizophrenia one of the most severe and devastating mental illness (Thaker and Carpenter, 2001).
Symptoms of schizophrenia are generally divided into three categories: positive, negative and disorganized symptoms (Andreasen, 1995 pg. 477 - 81). Positive symptoms refer to the presence of mental features that should not be normally present. These include delusions which are false beliefs without any basis in reality and which are not in keeping with the person's educational, cultural and religious background. Other symptoms are hallucinations which are perceptions of stimuli that have no external reality, like auditory, visual, tactile, olfactory and gustatory hallucinations. And Andreasen, 1995 further identified the following symptoms of Negative and disorganized symptoms that normally present:
Negative symptoms refer to a lack or reduction of emotional responses and psychological functioning that should normally be present. These are manifested as affective flattening (difficulty in expressing emotions), alogia (limited or poverty of speech with consequent inability to initiate or maintain a conversation), avolition (extreme apathy with lack of initiation, drive or energy which result in academic, vocational and social deterioration), anhedonia (lack of interest or pleasure in life), asociality (social withdrawal and few social contacts) and attentional impairment.
Disorganized symptoms refer to disturbances in thinking and speech, and bizarre behavior. The disturbance in thinking (thought disorder) is inferred from the person's speech, which usually reflects the loosening of the link between one thought to another. The person may shift from one topic to another completely unrelated topic without realizing it makes no logical sense. New words may be made up that have no meaning to others. Behavior may also be abnormal and manifested as strange mannerisms, doing seemingly senseless things or assuming bizarre postures.
However, Andreasen, (1995) stressed that although positive, negative and disorganized features suggestive of schizophrenia may be present, none of these clinical features are pathognomic. Physical disorders and psychosis often overlap and it is essential for patients to have a comprehensive physical assessment to exclude psychosis arising from medical and/or organic causes.
The course of illness can be divided into four major epochs: premorbid adjustment, onset of illness, middle course, and late course (Sadock B.J. and Sadock, V.A., 2001 p. 1106). Premorbid adjustment refers to symptoms that appear prior to the onset of positive symptoms, which may be manifested as poor social and scholastic adjustment or diminished social drive; decreased emotional responsivity; withdrawn, introverted, suspicious, or impulsive behavior; idiosyncratic responses to ordinary events or circumstances; short attention span; and delayed developmental milestones or poor motor and sensorimotor coordination. Childhood asociality - a trait that has been referred to in the past as a poor prognostic indicator, is probably more appropriately conceptualized as the early morbid manifestation of deficit symptomatology. Disturbances in social behavior have been picked up as early as infancy by workers who have noticed a lack of responsiveness and emotional expression in infants who later developed schizophrenia. It is also evident, however, that deficit symptoms may have their onset following psychosis and become part of the progression of the illness during the initial years of psychosis. Subtle forms of positive formal thought disorder may also be manifest before overt hallucinations and delusions occur. Studies have evaluated the development of the offspring of mothers with schizophrenia have observed cognitive difficulties during the pre-teen and teenage years in these high-risk children (p. 1106). And in terms of family relations, there is some evidence that parents of schizophrenics are emotionally disturbed more often than the patterns of normal children and that more of the mothers have schizoid personality traits. Moreover, it is claimed that the parents of schizophrenics seem to be in conflict with one another more often than the parents of other psychiatric patients, and that the mothers are more concerned about and protective towards their children (Johnstone and Lawrie, 1998 p. 404).
The etiology process or processes by which a causal agent creates the pathophysiology of schizophrenia is not yet known. However, while the reliability of the schizophrenia diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), there is evidence to suggest that genetic vulnerability and environmental stressors can act in combination to cause schizophrenia (Harrison & Owen, 2003). The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to ...
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The etiology process or processes by which a causal agent creates the pathophysiology of schizophrenia is not yet known. However, while the reliability of the schizophrenia diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), there is evidence to suggest that genetic vulnerability and environmental stressors can act in combination to cause schizophrenia (Harrison & Owen, 2003). The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to be a disorder of complex inheritance (analogous to diabetes or high blood pressure). Thus, it is likely that several genes interact to generate risk for schizophrenia (Owen, et al. 2005). This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution as some researchers estimate schizophrenia to be highly heritable. However, genetic evidence for the role of the environment comes from the observation that one identical twin does not universally develop schizophrenia if the other one does. A review of the genetic evidence by Torrey, et al. (1994) suggested a 28% chance of one identical twin developing schizophrenia if the other already has it.
There is also considerable evidence indicating that stressful life events can cause or trigger schizophrenia (Day, et al. 1987); Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life (Schenkel, et al. 2005) as well as negative attitudes towards individuals with (or with a risk of developing) schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, and intrusive or controlling attitudes (termed 'high expressed emotion' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures (Bebbington & Kuipers, 1994) (see also Dixon, Lehman & Levine, 1995 and Leff, et al. 1982).
Symptoms of schizophrenia usually emerge in the late teens to mid-20s for men and the late 20s to 30s for women (Sadock B.J. and Sadock, V.A., 2003), when the brain is undergoing important maturational changes. Some investigators believe that the disease process of schizophrenia begins prenatally, lies dormant until puberty, and then causes a period of neural degeneration that causes the symptoms to appear, suggesting that the symptoms may either appear suddenly or evolve gradually, and men tend to have more severe symptoms and a more difficult time with the effects of schizophrenia than women. The second epoch, onset of illness, typically refers to the onset of positive symptoms such as hallucinations, delusions, and positive formal thought disorder. The onset of positive symptoms is insidious in about half of the patients, with the earliest signs of involvement occurring many years before the appearance of the more blatant manifestations of psychosis. In other cases, onset is relatively sudden or acute, with the onset of positive symptoms marking a sharp deviation in development. Patients with the insidious type of onset are very likely to have poor intermediate course and a poor long-term outcome. In contrast, patients with normal development and ordinary personality attributes who experience a relatively sudden appearance of hallucinations, delusions, and disorganized thought vary widely in their intermediate and long-term outcomes (Sadock B.J. and Sadock V.J., 2001 p. 1107) - A youth, whose previous behavior has been unremarkable, slowly becomes more withdrawn and introverted and slowly drifted away from his friends. He also loses his drive and determination and later failed to complete his degree and his apprenticeship that had previously seemed well within his grasp. His parents may be worried by his failures, his apparent lack of interest in achievement and his progressive estrangement from them but they do not suspect that he is ill until one day, months later; it suddenly becomes apparent that he is entertaining delusional ideas and hearing voices, suggesting an acute onset. He becomes convinced that he is being watched or followed that someone is trying to impose their will on his. And the subject's interpretation of these phenomena, which lie beyond the bounds of normal experience, shall depend on his cultural background, such as may attribute to authority agencies, or that his colleagues are conspiring against him (Johnstone and Lawrie, 1998 p. 394). Although the rate of schizophrenia is relatively similar in women and men, there are gender differences in age onset. In males, the peak age of onset ranges from 17 to 27, whereas females tend to have a wider and flatter window of vulnerability, with age of onset generally between ages 17 and 37 (Sadock B.J. and Sadock V.J., 2001 p. 1107).
The patient's affect during the acute illness is as variable as his thought content but is nearly always disturbed in some way. Perplexity is a common and characteristic feature of acute schizophrenic illnesses. The subject suspects that something strange is going on around him but is not sure what, and ideas may come and go in rapid succession as he seeks to integrate his changing perceptions and affective state with his premorbid experience (delusional mood). At other times, the subject may be depressed, elated or angry, and it is sometimes difficult to tell whether the content of the delusions and hallucinatory voices is derived from the prevailing mood or vice versa (Johnstone and Lawrie, 1998 p. 394).
The middle eopch of illness may be subdivided into two subepochs. The first 5 - 10 years of illness are characterized by multiple exacerbations of positive symptoms, during which a patient may return to an asymptomatic baseline between episodes, or remain actively psychotic without achieving full recovery. This subepoch is followed by a plateau phase, in which patients experience a stabilization of their symptoms and a decrease in the number of exacerbations. Recent studies have made it evident that the underlying deterioration associated with schizophrenia principally occurs during the onset of illness and the first half of the middle phase, rather than over the remaining course of illness. However, complications caused by the illness lead to ever increasing impediments to normal existence, so that secondary effects may be progressive even though the primary pathology has plateau. For example, patients who live in under stimulating environments will lose social skills and work capabilities even if their symptoms improve. Thus, effective treatment late in the course of a chronic disease will diminish morbidity, but it will not restore lost experience and opportunity, and a history of disabling schizophrenia is a serious social and occupational burden regardless of the degree of recovery (Sadock B.J. and Sadock V.J., 2001 p. 1107).
In the late epoch, there is a tendency for the intensity of positive symptoms to diminish, and many patients with long-term impairments regain some degree of social and occupational competence, suggesting that the more rapidly patients are treated; the more benign is the course of illness. This observation has led to an increased interest in establishing a methodology for early detection and the development of intensive therapeutic interventions, which combine pharmacological and psychosocial treatments (p. 1107).
Although no present treatment approach can prevent or cure schizophrenia, some approaches have had remarkable remedial effects on course such as cognitive behavioral therapy (CBT) which is beneficial in reducing the symptoms (especially the positive symptoms) of schizophrenia (Garety et al., 2000); Psycho education and family intervention which can help reduce relapse rates (Dixon, Lehman, & Levine, 1995); and Social skills training which could improves social adjustment and coping skills, thereby reducing relapse rates (Benton and Schroeder, 1990).
CBT is a form of psychotherapy that helps the patient to search for an explanation for his or her psychotic experiences and reduce the distress of the illness. The techniques have been adapted and integrated with motivational interviewing principles for patients with poor medication compliance or substance abuse comorbidity. Two recent studies led by Sensky et al (2000) randomized 90 patients, who had at most partially responded to chlorpromazine, to an equal amount of manualized CBT or 'empathic, non-directive' befriending. Blind raters assessed positive and negative symptom severity at baseline, treatment termination and after 9 months follow-up. The results showed that both treatments appeared effective on both measures at the end of treatment, but the group treated with CBT showed further improvements at follow-up whereas the befriended group lost some of their earlier gains, suggesting that CBT may be effective for treatment resistance and negative symptoms (Johnstone and Lawrie, 1998 p. 413).
Discharging patients from hospital when adequate community facilities are not available may also place a heavy burden on relatives, a burden which service providers may do little to relieve. Thus a preventive strategy is to try to alter the attitudes and behavior of the relatives, and various forms of family therapy where the patient and the family members are educated about the illness and its management, prognosis, as well as the various medications, the anticipated side effects and costs, about how to incorporate support from one another to avoid high expressed emotion environment, problem-solving, and crisis intervention support (Dixon, Lehman, & Levine, 1995). In one study led by Leff et al, (1982), 24 schizophrenics who were living in a 'high expressed emotion' environment, were randomly allocated either to routine outpatient care or to receive a special package of social interventions consisting of factual talks to their relatives about schizophrenia, fortnightly group meetings for the relatives designed to help them share experience, and regular family therapy sessions in the patient's home designed to lower expressed emotion and face to face contact. Results shows that after 9 months, the relapse rate was 50% in the controls but only 9% in the treatment group, and the only patients in the treatment group relapse were two in whom no reduction in expressed emotion (EE) or face to face contact was achieved - suggesting that high expressed emotion can provoke relapse and that reduced face to face contact is protective. Thus it does not reveal which elements of the treatment package were most important, but rather, there is no single good evidence that any one therapeutic model is better than another (Johnstone and Lawrie, 1998 p. 412), and thus a structured and educational approach may use to improve social and interpersonal skills (Benton and Schroeder, 1990). Behavioral learning techniques such as coaching, modeling and positive reinforcement are used to train the patient to handle social situations, hence adding these elements into these treatments may enhance their efficacy thereby reducing relapse rates.
In pharmacological treatments, many studies have focused upon the role of antipsychotic drugs in reducing schizophrenic relapse reduction. Davis (1976) reviewed 24 controlled studies and concluded that the evidence for the efficacy of maintenance antipsychotic treatment was overwhelming. The drugs do not, however, abolish the tendency to relapse. In a 2-year follow-up study of oral antipsychotics versus placebo, the rate of schizophrenic relapse in placebo-treated patients was 80%, whereas that of patients on active antipsychotics was 84% (Hogarty et al, 1974). And Gilbert et al (1995) systematically reviewed studies comparing medication maintenance and withdrawal, found an overall 37% reduction in relapses over an average of about 8 months in the continuation groups. And compliance is one major problem when patients with schizophrenia are often unreliable at taking tablets once their acute symptoms have subsided and they left hospital. Reason being is that they may not accept that they have been ill, and even if they do, may not accept that there is any risk of the illness recurring and the drugs often cause akathisia and other unpleasant side-effects (Johnstone and Lawrie, 1998 p. 409) where it can take up to 2 weeks for psychotic symptoms to begin to respond to medication and prospective studies show that it can take several weeks to achieve response to treatment and many months for remission. For these reasons, depot preparations capable of producing adequate serum levels when administered at intervals of 2 weeks or more have been developed to elaborate follow-up arrangements to ensure that patients do not miss their regular injection every 2, 3 or 4 weeks. They are probably a significant advance, but it is important to note that no trial comparing long-term relapse rates on daily tablets and fortnightly injections has demonstrated any clear advantage for the latter. However, long acting depot medications are not usually used for acute episodes because they may take 3 to 6 months to reach a stable steady state and are eliminated very slowly (Marder et al, 1989). And if the patient has improved with a particular medication regimen, he or she should be monitored, whenever possible, while taking the same medication and dose for the next 6 months, because reducing or stopping medication, even after a prolonged period of maintenance and well-being, is a risk for relapse (Johnstone and Lawrie, 1998 p. 409). Here, the patient should continue with the lowest effective dose of antipsychotic medication, such as dose reductions may be considered for stable patients without positive symptoms, and continue to reduce the medication dose gradually as long as the patient remains stable (Schooler, 1991). And finally, once the patients have reach the stage of a single episode of positive symptoms and asymptomatic on maintenance therapy for a period of one year, may be then considered for a trial period without medication (Dixon and Lehman, 1995).
Having reviewed the impact of Schizophrenia, we may say that schizophrenia is an important mental health disorder where the chronicity of the condition and the associated social stigma, adds on to the burden of illness for patients, their families and societies at large. And the field is closer to understanding risk factors at the level of causal mechanism, and new treatments are being developed at an increasing rate. However, more studies are needed to explore and examine further on the effectiveness of drug treatments and psychosocial therapy so that it will lead to further improvement on clinical outcomes.
References
Andreasen, N. C. (1995). Schizophrenia: Positive and Negative Symptoms and Syndromes. Basel; New York : Karger p. 477 - 81.
Bebbington, P., & Kuipers, L. (1994). The Predictive Utility of Expressed Emotion in Schizophrenia: An Aggregate Analysis. Journal of Psychological Medicine, Vol. 24 (3), p. 707-18.
Benton, M.K., & Schroeder, H.E. (1990). Social Skills Training with Schizophrenics: A Meta-Analytic Evaluation. Journal of Consult Clinical Psychology, Vol. 58. p. 741 - 747.
Davis, J.M. (1976). Sighted in Eve, C. Johnstone, Stephen, M. Lawrie. (1998). Companion to Psychiatry Studies: Schizophrenia and Related Disorders. Edinburg; NY: Churchill Livingstone, 6th ed. p. 409.
Day, R., Nielsen, J.A., Korten, A., Ernberg, G., Dube, K.C., Gebhart, J., Jablensky, A., Leon, C., Marsella, A., & Olatawura, M. (1987). Stressful Life Events Preceding the Acute Onset of Schizophrenia: A Cross-National Study from the World Health Organization. Journal of Culture, Medicine & Psychiatry, Vol. 11 (2), p. 123-205.
Dixon, L.B., Lehman, A.F., & Levine, J. (1995). Sighted in Conventional Antipsychotic Medications for Schizophrenia. Journal of Schizophrenia, Vol. 21. p. 567 - 577.
Eve, C. Johnstone, Stephen, M. Lawrie. (1998). Companion to Psychiatry Studies: Schizophrenia and Related Disorders. Edinburg; NY: Churchill Livingstone, 6th ed. p. 394, 404, 409, 412 & 413.
Garety, P.A., Fowler, D., & Kuipers, E. (2000). Cognitive-Behavioral Therapy for Medication-Resistant Symptoms. Journal of Schizophrenia, Vol. 26, p. 73 - 86.
Gilbert, P.L., Harris, M.J., McAdams, L.A., & Jeste, D.V. (1995). Neuroleptic Withdrawal in Schizophrenic Patients: A Review of the Literature. Sighted in Eve, C. Johnstone, Stephen, M. Lawrie. (1998). Companion to Psychiatry Studies: Schizophrenia and Related Disorders. Edinburg; NY: Churchill Livingstone, 6th ed. p. 409.
Harrison, P. J., & Owen, M. J. (2003). Genes for schizophrenia? Recent Findings & Their Pathophysiological Implications. The Lancet, Vol. 361, (9355), p. 417 - 419.
Hogarty, G.E., Goldberg, S.C., Schooler, N.R., & Ulrich, R.F. (1974). Drug & Sociotherapy in the Aftermath of Schizophrenic Patients, II: Two Year Relapse. Sighted in Eve, C. Johnstone, Stephen, M. Lawrie. (1998). Companion to Psychiatry Studies: Schizophrenia and Related Disorders. Edinburg; NY: Churchill Livingstone, 6th ed. p. 409.
Leff, J., Kuipers, L., & Berkowitz, R. (1982). Sighted in Eve, C. Johnstone, Stephen, M. Lawrie. (1998). Companion to Psychiatry Studies: Schizophrenia and Related Disorders. Edinburg; NY: Churchill Livingstone, 6th ed. p. 412.
Marder, S.R., Hubbard, J.W, Van Putten, T., & Midha, K.K. (1989). The Pharmacokinetics of Long-Acting Injectable Neuroleptic Drugs: Clinical Implications. Journal of Psychopharmacology, Vol. 98. p. 433 - 439.
Owen, M. J., Craddock N., & O' Donovan, M. C. (2005). Schizophrenia: Genes at Last? Trends in Genetics, Vol. 21 (9), p. 518 - 525.
Sadock, B. J., & Sadock, V.A. (2001). Textbook of Comprehensive Psychiatry: Schizophrenia Philadelphia: Lippincott Williams & Wilkins. pg. 1106 - 1107.
Sadock, B. J., & Sadock V. A. (2003). Behavioral Sciences/Clinical Psychiatry: Schizophrenia. Philadelphia, Pa : Lippincott Williams & Wilkins, 9th ed. p. 471 - 504.
Schenkel, L.S., Spaulding, W.D., Dilillo, D., & Silverstein, S.M. (2005) Histories of Childhood Maltreatment in Schizophrenia: Relationships with Premorbid Functioning, Symptomatology, and Cognitive Deficits. Schizophrenia Research, Vol. 76 (2 - 3), p. 273 - 286.
Schooler, N.R., (1991). Maintenance Medication for Schizophrenia: Strategies for Dose Reduction. Journal of Schizophrenia, Vol. 17. p. 311 - 324.
Sensky, T., Turkington, D., & Kingdon, D. (2000). A Randomized Controlled Trial of Cognitive-Behavioral Therapy for Persistent Symptoms in Schizophrenia Resistant to Medication. Sighted in Eve, C. Johnstone, Stephen, M. Lawrie. (1998). Companion to Psychiatry Studies: Schizophrenia and Related Disorders. Edinburg; NY: Churchill Livingstone, 6th ed. p. 413.
Thaker, G. K., & Carpenter, W. T. (2001). Advances in Schizophrenia. Journal of Nature Medicine, Vol. 7 (6), p. 667 - 671.
Torrey, E. F., Bowler, A. E., Taylor, E. H. & Gottesman, I.I (1994). Schizophrenia & Manic Depressive Disorder. NY: Basic Book.
The Impact of Schizophrenia