Etiology and Treatment of Schizophrenia - Essay Example

Schizophrenia is a disorder that is distinguished by a major disruption in cognition and emotion, influencingthe primary areas of language, thought, perception, affect, and self-concept. The range of symptoms, while various and extensive, usually includes psychotic manifestations, such as hearing internal voices or experiencing other sensations unrelated to an apparent source (hallucinations) and assigning unconventional importance to normal events or upholding fixed false personal beliefs (delusions). There is no one single symptom that makes diagnosis conclusive; instead, such diagnosis covers a pattern or an aggregate of signs and symptoms, that concurrently occur with occupational or social malfunction (American Psychiatric Association). The following discussion represents the symptoms of the disorder, and of its etiology and treatment. Symptoms are conventionally divided into those which are positive and those which are negative, because of their outcome on diagnosis and treatment (Crow 471–486). Positive symptoms refer to those that manifest as a reflection of an excess or a disruption of normal functioning (Cuesta and Peralta 227–235). Based on DSM-IV, its diagnosis requires at least one month of manifestation of two or more symptoms, unless hallucinations or delusions are particularly queer. In such cases, one symptom alone is adequate for diagnosis. On the other hand, negative symptoms are those that represent a reduction or loss of normal functions (Roy and DeVriendt 407–414.). These frequently transpire in the lives of people with schizophrenia during periods of low (or absent) positive symptoms. Negative symptoms present difficulties in assessment because they are not as obviously abnormal as positive ones. Moreover, they may be caused by a wide array of other factors as well, for example, as an adaptation to a persecutory delusion. Nevertheless, progress in diagnostic assessment tools may be noteworthy. Having presented a brief description of the disorder, its etiology is next discussed, with solid empirical support of the fact that the disorder is borne out of a combination of genetic and environmental factors. According to DSM IV, the following are some positive symptoms related to schizophrenia: Delusions are firmly held erroneous beliefs due to distortions or exaggerations of reasoning and/or misinterpretations of perceptions or experiences. Delusions of being followed or watched are common, as are beliefs that comments, radio or TV programs, etc., are directing special messages directly to him/her. Hallucinations are distortions or exaggerations of perception in any of the senses, although auditory hallucinations (“hearing voices” within, distinct from one’s own thoughts) are the most common, followed by visual hallucinations. Disorganized speech/thinking, also described as “thought disorder” or “loosening of associations,” is a key aspect of schizophrenia. Disorganized thinking is usually assessed primarily based on the person’s speech. Therefore, tangential, loosely associated, or incoherent speech severe enough to substantially impair effective communication is used as an indicator of thought disorder by the DSM-IV. Grossly disorganized behavior includes difficulty in goal-directed behavior (leading to difficulties in activities in daily living), unpredictable agitation or silliness, social disinhibition, or behaviors that are bizarre to onlookers. Their purposelessness distinguishes them from unusual behavior prompted by delusional beliefs. Catatonic behaviors are characterized by a marked decrease in reaction to the immediate surrounding environment, sometimes taking the form of motionless and apparent unawareness, rigid or bizarre postures, or aimless excess motor activity. Other symptoms sometimes present in schizophrenia but not often enough to be definitional alone include affect inappropriate to the situation or stimuli, unusual motor behavior (pacing, rocking), depersonalization, derealization, and somatic preoccupations. On the other hand, negative symptoms include the following: Affective flattening is the reduction in the range and intensity of emotional expression, including facial expression, voice tone, eye contact, and body language. Alogia, or poverty of speech, is the lessening of speech fluency and productivity, thought to reflect slowing or blocked thoughts, and often manifested as laconic, empty replies to questions. Avolition is the reduction, difficulty, or inability to initiate and persist in goal-directed behavior; it is often mistaken for apparent disinterest. Research on the cause of schizophrenia is not conclusive. However, it supports the idea that schizophrenia is mainly caused by an interaction between genetic and environmental factors. This view assumes that there exists a genetic predisposition to the disorder that leads to an environmental disruption in brain development. Such disruption may be caused by triggers from both genetic and environmental sources, that presumably stimulate and alter the brain. In addition, environmental stressors that may come later in development may either aggravate or improve the exhibition of genetic or neurodevelopmental defects. The main thesis is that the beginning of schizophrenia and its course are most probably attributed to an interaction between genetic and environmental triggers. Family, twin, and adoption studies lend credence to the critical role of genetic factors in the development of schizophrenia (Kendler & Diehl 261–285). Immediate biological kin of individuals with schizophrenia have about 10 times greater risk than that of the general population. With these prevalence rates, this suggests a 5 to 10 percent lifetime risk for first-degree relatives (covering children and siblings) and indicates a strong genetic component to schizophrenia (e.g., Kety 423–429). The genetic role is further supported by findings that the identical twin of a person with schizophrenia is at greater risk than a sibling or fraternal twin, and that adoptive relatives do not share the increased risk of biological relatives. Nevertheless, in about 40 percent of identical twins in which one is diagnosed with schizophrenia, the other never meets the diagnostic criteria. The discordance among identical twins obviously suggests that environmental factors also play an equally critical role (DSM-IV). The diathesis-stress framework purports that schizophrenia is attributed to a genetic predisposition combined with environmental and psychosocial triggers. the so-called diathesis-stress model (Zubin and Spring 103–126). Family studies indicate that individuals have varying levels of congenital inherited genetic vulnerability, ranging from very low to very high, to schizophrenia. That is, whether or not the person does develop the disorder is partly determined by this vulnerability. Concurrently, the development of schizophrenia also relies on the amount and types of stresses the person undergoes over time. A parallelism may be drawn to diabetes by virtue of both genetic factors (e.g., family history) and behavioral factors (e.g., diet, exercise, stress) that interact to determine whether or not a given person develops diabetes. How the interaction works in schizophrenia is not completely known; it is a subject of continuous research (Murray et al 225–235). While a genetic factor in schizophrenia is being implicated, scientists have not yet determined which specific genes are responsible (Kendler & Diehl 261–285). The present consensus is that it is attributed to a multiplicity of genes are responsible (Kendler et al., 1996). Several brain abnormalities have been established in schizophrenia. For instance, patients frequently have unusually large cranial ventricles, cavities in the brain that transport cerebrospinal fluid, more especially the third ventricle (Weinberger 660–669), and reduced cerebral size (Schwarzkopf et al 49–60) in contrast with control groups. Numerous studies point to the idea that this may be more common among males (Nopoulos et al. 1648–1654) whose families do not have a history of schizophrenia (Schwarzkopf et al. 49-60). There is also some proof that at least some people with schizophrenia have unconventional cortical laterality, with dysfunction localizing to the left hemisphere (Braun et al. 489–509 ). To demonstrate laterality, some have suggested a prenatal injury or insult at the time of left hemisphere development, which normally lags behind that of the right hemisphere (Bracha 551–553). The anatomical abnormalities found in various parts of the brain tend to be associated with schizophrenia’s positive symptoms (Barta et al., 1990) and negative symptoms (Buchanan et al. 59–65). Positive symptoms are frequently related to temporal lobe dysfunction, as demonstrated by imaging studies that use blood flow and glucose metabolism. This dysfunction likely associated with abnormal phospholipid metabolism (Fukuzako et al. 629–640). Disorganized speech (taken to be a manifestation of disorganized thinking) has been linked with abnormalities in brain regions related to the regulation of speech (McGuire et al. 231–235.). Negative and cognitive symptoms, specifically those associated with volition and planning, are conventionally correlated with prefrontal lobe dysfunction (Capleton 123–128). This is probably associated to unusual neuronal density and may be more predominant among patients whose families have a history of schizophrenia than those whose do not (Sautter et al. 1–7.). However, mapping patients’ symptoms with brain regions is complicated and varying. Researchers assert that the dysfunctions are manifested in brain circuitry rather than in one or two localized areas of the brain (Andreasen et al. 1648–1654). Dopamine at excess levels has been implicated in schizophrenia studies, although it is inconclusive whether the excess is its main cause of schizophrenia. The other hypothesis is that it may be a result of a more fundamental dysfunction (Grace 1–24). More recent studies point to the dysregulation of dopamine and other neurotransmitter systems (Grace 1-24). Some of these studies link schizophrenia to specific fluctuations in dopamine receptors, while other researches emphasize the serotonin system (Inayama et al. 103–105). However, it must be reinforced that in many cases it is probable that disturbances in neurotransmitter systems may result from complications of schizophrenia, or its treatment, rather than from its causes. The factors studied in schizophrenia encompass a broad array of biological, environmental, psychological and social variables. There is reliable empirical proof that prenatal stressors are related to increased risk of the child developing schizophrenia in adulthood, although the mechanisms for these associations are yet to be fully investigated. Some initial research indicates risk factors include maternal prenatal poverty (Cohen 951–958), poor nutrition (Susser and Lin, 983–988), and depression (Jones et al. 1–25). Other stressors are exposure to influenza outbreaks (Mednick et al. 189–192), war zone exposure (van Os & Selten 324–326), and Rh-factor incompatibility (Hollister 19–24). Their broad variety indicates that other stressors might also be risk factors, under the overall category of maternal stress (Hollister 19–24). As an outcome of such stresses, newborns of low birth weight and short gestation have been associated to increased risk of schizophrenia in adulthood (Jones et al, 1–25), as have delivery complications (Hultman et al. 128–133) and other developmental problems that manifest early on (Brixey et al. 447–456). With children, especially infants, viral central nervous system infections may be linked with increased risk (Rantakallio et al. 837–843). This explains the correlation between schizophrenia and being born or raised in crowded conditions (Torrey and Yolken 321–324) or during the flu-prone winter and spring months (Castrogiovanni et al. 175–181). However, support for these hypotheses is inconclusive (Yolken and Torrey 131–145). In fact, it is probable that prenatal and obstetric complications associated with schizophrenia could represent an already disrupted fetal development, rather than being causes in themselves (Lipska and Weinberger 10-25). In general, across the life span, the chronic stresses of poverty (Cohen, 951–958) and some aspects of minority social status appear to modify the course of schizophrenia. At present, the mechanisms with which these risks contribute to the diathesis-stress interaction for any one individual is unexplained because causes may be distinct (Onstad et al. 203–206). While genetic vulnerability may be hard to manipulate, specific other relevant factors can be addressed with present data. An awareness of these factors that aggravate genetic vulnerability lends information for drafting preventive strategies, such as good prenatal health care and nutrition. Moreover, since life stresses can worsen the course of the illness, availability of effective quality services, social support, and relapse prevention interventions, may have advantageous effects on longer term outcomes (Wiersma et al. 75–85). Concurrently, researchers are struggling to unify findings on both diathesis and stress into models of how schizophrenia develops (Andreasen 1586–1593). Brain biology does exert a significant effect on behavior and experience; in turn, behavior and experience may mold brain biology as well. One potentially useful integrative model is the neurodevelopmental theory of schizophrenia developed by Weinberger and others (Murray and Lewis 681–682). It upholds that schizophrenia stems from “a subtle defect in cerebral development that disrupts late-maturing, highly evolved neocortical functions, and fully manifests itself years later in adult life” (Lipska and Weinberger 10-25). The nature of the defect has not yet been determined and may be a result of a pre- or neonatal insult to the brain. Additional support for the neurodevelopmental theory comes from abnormalities in brain structure that have long been found in people with schizophrenia. Such results have been taken to mean abnormal neuronal migration in early development (Jakob and Beckmann 303–326). Researchers have developed animal models of early neurodevelopmental dysfunctions that present in later behavioral and functional abnormalities (Geyer et al. 361–372) and are influenced by genetic factors (de Kloet et al. 345–356). However promising these theories may be, the causal factors and mechanisms of schizophrenia remain unidentified. Despite this, research has found useful treatments for schizophrenia that are effective in improving symptoms and functional deficits. The following are some chosen treatment recommendations, according to the Schizophrenia Patient Outcomes Research Team: Recommendation 1. Antipsychotic medications, other than clozapine, should be used as the first-line treatment to reduce psychotic symptoms for persons experiencing an acute symptom episode of schizophrenia. Recommendation 2. The dosage of antipsychotic medication for an acute symptom episode should be in the range of 300–1,000 chlorpromazine (CPZ) equivalents per day for a minimum of 6 weeks. Reasons for dosages outside this range should be justified. The minimum effective dose should be used. Recommendation 8. Persons who experience acute symptom relief with an antipsychotic medication should continue to receive this medication for at least 1 year subsequent to symptom stabilization to reduce the risk of relapse or worsening of positive symptoms. Recommendation 9. The maintenance dosage of antipsychotic medication should be in the range of 300–600 CPZ equivalents (oral or depot) per day. Recommendation 12. Depot antipsychotic maintenance therapy should be strongly considered for persons who have difficulty complying with oral medication or who prefer the depot regimen. Recommendation 23. Individual and group therapies employing well-specified combinations of support, education, and behavioral and cognitive skills training approaches designed to address the specific deficits of persons with schizophrenia should be offered over time to improve functioning and enhance other target problems, such as medication noncompliance. Recommendation 24. Patients who have ongoing contact with their families should be offered a family psychosocial intervention that spans at least 9 months and that provides a combination of education about the illness, family support, crisis intervention, and problem-solving skills training. Such interventions should also be offered to nonfamily members. Recommendation 27. Selected persons with schizophrenia should be offered vocational services. Recommendation 29. Systems of care serving persons with schizophrenia who are high users should include ACT and ACM programs (Lehman and Steinwachs 11–20). The treatment of schizophrenia has substantially progressed in the last decade. A battery of treatments may be availed of to alleviate symptoms, to enhance quality of life, and to restore productivity and functioning. Treatment options are frequently related to the clinical phases of schizophrenia, namely the acute phase, stabilizing phase, stable (or maintenance) phase, and recovery phase. When possible, this report links available information to these treatment phases. The most commendable treatment across all phases includes some form of pharmacotherapy with antipsychotic medication, conventionally paired up with various psychosocial interventions. Psychosocial interventions cover supportive psychotherapy, and family psychoeducational interventions, psychosocial and vocational rehabilitation. The treatment of individuals with schizophrenia who are high service users should be coordinated by an interdisciplinary treatment team to guarantee continuity of services (Lehman & Steinwachs 11–20). It may be more beneficial for some to avail of less intensive forms of case management and various self-help and consumer-operated services. It may also be critical to help individuals with schizophrenia in addressing their many interrelated needs, such as for supported housing, transportation, and general medical care. These are among the 30 pivotal treatment recommendations of the Agency for Healthcare Research and Quality (AHRQ)- and NIMH-sponsored Schizophrenia Patient Outcomes Research Team (PORT), which developed its recommendations on the basis of a comprehensive review of the treatment outcomes literature (Lehman and Steinwachs 11-20). Table 2 specifies recommended treatment options. Although the Schizophrenia PORT study recommendations are based in research, it may be worth noting that treatment practices fail to comply with these recommendations. In fact, conformance generally falling below 50 percent (Lehman & Steinwachs 11-20). The troubling gap between knowledge and practice are attributed to the many barriers that exist in the transfer of information about treatment and evidence-based practice to clinicians, family members, and service users. 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