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 Denmark
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
(p=.0004).
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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