Schizophrenia is a complex illness; wide in its nature, debatable in its causes and generic in its symptoms.
In terms of nature, Psychologists attempt to explain its symptomatology, distributions among the population (male or female, rich or poor), and age of onset. In terms of causes, factors fall into either environmental (expressed emotions in families) or biological explanations (genetic heritability). Lastly, in terms of treatments, there are debates as to whether psychological treatments methods are more effective than the traditional pharmacological ones (drugs).
This paper will look at some of these arguments in each category, assess their strengths and weakness, and conclude, firstly, that there are no single underlying explanations accounting for the nature and treatments of the disorder. And lastly, that there is a strong link suggesting Schizophrenia as being a genetic disorder.
There are two groups of symptoms which are generally identified when diagnosing Schizophrenia. Positive and Negative. Positive symptoms entail the presence of something unusual or not observed in people with a normal psychotic predisposition; such as hallucinations, either visual or auditory (Sartorius et al 1974). Other symptoms include delusions, disorganised thought processes and, in some cases, catatonic behaviour (the holding of a strange statute position for hours).
Negative symptoms on the other hand correspond to the absence of something normal; a common observation associated with this is flat affect. Flat affect is a reduction of, or absence of, a suitable facial expression. For example, smiling. Other types of negative symptoms range from the absence of social skills, to life skills in general, making relationships and jobs difficult to sustain.
For an official psychiatric diagnoses, DSM-IV-TR criteria state that at least two or more positive, or negative symptoms, followed by six months of disturbance are sufficient. However, it is important to note that symptoms vary amongst individuals, making diagnoses often difficult.
Psychologists have come to a general consensus that the onset of Schizophrenia appear to be approximately during adolescence; however, research has found symptoms in infants as young as three years of age (Russell et al 1989), which may imply a genetic significance in its etiology. But findings in this area of research are difficult to interpret for the reason being that Schizophrenia in early childhood is very rare (Burd and Kerbeshian, 1987) as findings cannot be accurately validated.
Further studies have found Schizophrenia to affect approximately 1% of the general population, or 1 in 125 (although this is not the case in all countries). Other studies have found that male populations are more prone to Schizophrenia than female populations (Hambrecht et al 1993), leading to research in predominately male environments, with others focusing on the biological aspects of gender.
Psychologists and Psychiatrists have therefore endeavoured to find its primary cause. There are no definite answers, but, broadly speaking, they can be generalized into either environmental or biological factors.
Environmental factors focus on the individuals’ world as a possible cause of Schizophrenia. Such explanations have lead researchers to study parental attachment, emotions and communication styles amongst family members. Gordon Parker studied the responses of patients’ mother and father in a simple questionnaire, and found that people with Schizophrenia tended to have high relapse rates amongst parents with parental styles as either neglectful or affectionless.
Another area Psychologists have been concerned with is the amount of expressed emotion (EE) and communication in families whose relatives have Schizophrenia. Broadly speaking, high expressed emotion and poor inter-familial communication have been related to higher relapse rates (Brown et al 1972). In support of this, Norton et al (1982) designed a longitudinal study assessing EE in 52 patients, by studying voice tone, and negative content in communication they found that high EE was very accurate in predicting relapse. Furthermore, Doane et al (1982) discovered that parents with a pathologic style of communication and high levels of communication deviance, produced schizotypal behaviour in their offspring.
There are however, some difficulties with these studies. Firstly, both samples contained people with Schizophrenia already. Therefore these studies don’t explicitly explain cause, but rather the effect of living under stressful environments. Secondly, there is evidence to suggest that high EE does not necessarily contribute to Schizophrenia (Parker et al 1988), implying individual differences in terms of reactions to stress.
In addition to these environmental factors, there appears to be stronger evidence from a biological perspective. These factors attempt to define Schizophrenia as having an underlying biological cause. For example, observations have been made during the menopause that an imbalance of certain chemicals can influence the symptoms of Schizophrenia (Mitchell 1974). Other studies have focused on the brain and have noticed differences in ventricle size; with people with Schizophrenia tending to have larger ventricles (Nopolus, Flaum & Andreason, 1997), while other studies have noted excessive amounts of dopamine levels. However, explanations in the etiology of these factors remain controversial. It is possible that a diathesis-stress model explains them, but on the other hand, there is the possible that there are innate biological predispositions. This leads on to a very heavily researched area in the eitiology of Schizophrenia, genetic inheritance.
The most effective way in testing for genetic pre-dispositions has been by comparing non-identical twins and identical twins. In a large study, Cannon et al (1998) used the Finish National Population Register and compared 9562 liked-sexed twins and found an 83% concordance rate in Schizophrenia amongst identical twins (Monozygotic) but only a 17% for non-identical twins (Dyzogotic). In his book, Schizophrenia Genesis, Gottesman (1991) compared four twin studies across
Europe between 1963 to 1987 and found an average of 48%
concordance rates amongst monozygotic twins, in comparison to 17% for dyzygotic
twin pairs. Both studies add weight to
the argument that Schizophrenia is influenced by genetic factors. However, Psychologists point out that because
concordance rates are not 100%, other explanations are responsible, for example
environmental factors. Alternatively,
others may point out that Cannon’s participants were more prevalent to
Schizophrenia, as he, rightly, pointed out that prevalence rates in Finland are
1.3% as opposed to 1% in the UK.
Despite this, Kety (1988) argued that we have more reason to believe that genetic factors are better explanations for the etiology of Schizophrenia than environmental ones. His justification is based on his national study in
where people with Schizophrenia were adopted away from their relatives. He claimed that if these people went on to
the develop Schizophrenia then this would strongly imply a genetic cause. His findings proved significant as 5 cases of
Schizophrenia were found compared to 0 in the control group (p=0.3). More significant however was the finding that
11% of latent Schizophrenia were found in comparison to 0.9% of controls
In light of these explanations, there are a variety of treatments available. Again, we can group these into two main categories; pharmacological and psychological.
Pharmacological treatments that are commonly used are drugs. The most widely accepted are Antipsychotic drugs such as Clozapine. These types of drugs can help alleviate the negative symptoms of the disorder with mixed results. Drugs appear to be very particular. Studies have shown that different Antipsychotic drugs have different effects. For example Claus et al (1992) found Risperidone statistically significant in the overall psychopathology in comparison to other drugs, whereas, Peuskens (1995) did not find any statistical significance. On the other hand, Olanzapine was found to be effective in reducing positive symptoms only, but failed to reduce the negative symptoms.
Drugs, however, are not the only solution. A more evasive approach has been developed by utilization of a short electric current passed through the patient’s brain. This process is known as ECT, and is used as a last resort. Despite the evasiveness of the treatment, Brandon et al (1985) argues against its use as lack of significant evidence has been found in reducing the symptoms of Schizophrenia, leaving this method risky as well as dangerous.
Other types of treatment available are Psychological treatments. These attempt to treat the behaviour of someone suffering from Schizophrenia. One approach developed is known as Social Skills Training. This form of treatment provides the individual therapy, with the aim of improving life skills and reduces relapses. More than 40 studies have found improvements in these areas, but a further study found with the combination of educating those close by to the person with Schizophrenia found a zero relapse rate in their first year of treatment (Corrigan 1991).
Herz (2000) on the other hand believes that Psychological treatments are more effective than Pharmacological ones with the finding that 22% of patients receiving Psychological treatments were re-hospitalized in comparison to 34% patients receiving Pharmacological ones.
The agreements and disagreements in Schizophrenia imply its complex nature, Firstly, there is no single symptom that Psychiatrist can rely on in diagnoses; rather, there are a range of symptoms complicated by the fact that they vary within patients. Secondly, there is no specific drug that can alleviates the symptoms of Schizophrenia, some work well for some people but for others not. This has lead to a number of treatments available on the market. Thirdly, in terms of etiology, environmental explanations do not explain the causes of Schizophrenia, but only its effect on relapse rates. But there is however, a general consensus now that Schizophrenia is a predominately genetic disorder; this is evident in twin and adoption studies. Although singling out the gene or group of genes responsible remains difficult, relatively recent research has found links between certain chromosomes associated with Schizotypal behaviour (Bassett et al 1988). Once this gene has been located, more effective treatments can be engineered in the hope of developing a cure, and making Schizophrenia a thing of the past.
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