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Critically consider and evaluate two different psychological theories of Schizophrenia Biological/Cognitive

Schizophrenia is diagnosed using the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), which stipulates five characteristic symptoms:
1. Delusions
2. Hallucinations
3. Disorganized speech
4. Disorganized or catatonic behaviour
5. Negative symptoms (i.e. abilities or traits that are lost, usually at the onset of schizophrenia)
For a diagnosis of schizophrenia to be made the patient must demonstrate two or more of the DSM-IV listed symptoms, which must have been evident for a significant part of least one month (or less if successfully treated at any earlier stage). The description of schizophrenia has changed little since Kraepelin’s original definition in 1878.

The DSM-IV also defines various subgroups of schizophrenia; Paranoid, Catatonic, Disorganized, Undifferentiated and Residual. The subgroups describe how any of the five key diagnostic criteria outlined above may be more or less prevalent in different individuals. Paranoid schizophrenia produces mainly positive symptoms, whereas the remainder describe various combinations of negative and positive symptoms. Positive symptoms can include:
▪ An impaired ability to think logically (formal thought disorder);
▪ False beliefs that are maintained despite convincing evidence to the contrary (delusions);
▪ False perceptions, often presenting as voices being heard only by the patient (hallucinations)
▪ Loss of insight, characterised by an impaired ability to appreciate that symptoms are a result of illness and are not reality

It is reasonably well accepted that positive symptoms are attributable to a biochemical imbalance. The most widely accepted biochemical theory of schizophrenia is the dopamine hypothesis, which suggests that schizophrenic patients suffer from an over-activation of the neurotransmitter, dopamine. The main premise for this argument is that many neuroleptic drugs, such as sulpiride, pimozide and flupenthixol are effective treatments for schizophrenia. These drugs have been shown to be relatively “clean” dopamine blockers, preventing the uptake of dopamine by neurotransmitters (neuroreceptors are structures within the brain that receive neurotransmitters such as dopamine).

It could be argued that these drugs also block other neurotransmitters, so the effect they have in reducing symptoms could be attributable to their effect on dopamine, or their effect on another transmitter. However, Seeman (1980) reviewed the evidence in relation to the dopamine receptor blocking properties of neuroleptics and concluded that they have an important pharmacological action, as they are able to reverse the effects of dopamine enhancing drugs (i.e. amphetamines) and increase the metabolic turnover of dopamine.

Seeman conducted a further study in 1987, reviewing the evidence of studies on the post-mortem brains of schizophrenic patients. Almost all these studies showed evidence of a large increase in dopamine receptors in the brain. This is not conclusive evidence for the dopamine hypothesis however; it maybe the case that as many of these patients would have been treated with neuroleptic drugs for many years, then the brain may have tried to compensate by creating more receptors.

Hence Lee and Seeman tried to control for this factor and used 11 schizophrenic brains that had never been drug treated; they found no significant difference in the level of dopamine receptors in the untreated as opposed to the treated patient. However, there were significantly increased levels of dopamine receptors than in the general population. This is conclusive evidence that high levels of the neurotransmitter dopamine are linked to schizophrenia.

More evidence for the dopamine hypothesis is provided from studies on amphetamine psychosis. Amphetamines block dopamine receptors, and can produce schizophrenic-like symptoms. The immediate effects of amphetamine use are not similar to schizophrenic symptoms, but studies (Angrist & Gershon, 1970, Griffith et al, 1968) have demonstrated that if amphetamine is taken in larges doses over 1-5 days, then psychotic symptoms will appear, such as delusions, hallucinations and sometimes formal thought disorder. These mirror the symptoms in schizophrenic patients very closely. However, one must also consider that neuroleptic drugs tend to be effective in treating only positive symptoms. This suggests there are other contributatory factors in schizophrenia that are not accounted for by the dopamine hypothesis.

Kraepelin first identified “Dementia praecox” (later renamed “schizophrenia” by Bleuler) in 1878. Kraepelin defined this dementia as a slow decline in cognitive processing, which he categorised into four subtypes; a) simple cognitive functioning, whereby a slow social deterioration was evidenced by withdrawal from society and general passivity; b) paranoia, apparent by fear and ‘persecutory’ delusions; c) hebephrenic, identified by incoherent speech and inappropriate emotion and finally; d) catatonic, whereby the patient displays severely limited movement and expression.

Kraepelin believed a disorder of attention was “frequently conspicuously developed” in schizophrenic patients. He believed that many schizophrenic patients demonstrated decreased vigilance, with difficulty in maintaining attention on any dimension. However Kraepelin emphasised the biological nature of schizophrenia and felt a biological degeneration was the primary impairment in schizophrenia, leading onto cognitive deterioration:

“"...We thus come to the conclusion that, in dementia praecox, partial damage to, or destruction of, cells of the cerebral cortex must probably occur" (Kraepelin, 1899 pg 154)

However, many theorists believe schizophrenic patients have a deficit in their ability to selectively attend to stimuli. Some argue schizophrenic patients are continually over-whelmed by indiscriminate environmental stimuli, whereas others argue attention is focused particularly on threatening material. Bleuler first identified the term schizophrenia in 1908 and emphasised the psychological, as opposed to biological, facets of schizophrenia – however he believed attention span to be normal in schizophrenia, with vigilance increased or decreased depending upon the individual and their presentation of symptoms. Bleuler did not believe there was any particular attentional impairment linked with schizophrenia. Nevertheless Bleuler’s belief in the cognitive basis of schizophrenia led to the birth of many papers considering cognitive dysfunction as the pathogenesis.

McGhie & Chapman first formally identified defective attention as a potential pathogenesis of schizophrenia. They applied the concept of abnormal sensory filtering to schizophrenia, having noted that many patients showed attentional changes early on in their illness. They noticed patients showed heightened awareness of their surroundings; they described the attention of patients as being easily caught. Schizophrenic delusions were then further described by Frith (1979), in the context of selective attention deficit theory. He gave a convincing account of how attention filters are defunct and therefore irrelevant stimuli enter consciousness, resulting in the individual believing the stimuli are of significance. However, the hypothesis was theoretical in nature, not empirically tested.

Many researchers were interested in Firth’s theory and a multitude of attention deficit testing with schizophrenic patients followed. The majority of studies utilised Broadbent’s dichotic listening procedure. However, most studies focused on chronic patients and unsurprising 7/9 of these studies found a deficit in attention. Given that the majority of acute schizophrenic patients will perform poorly on any cognitive test, this is not convincing evidence for this theory.

Later, Bentall (1990) empirically tested his Cognitive Processing Bias Theory, which states there maybe an attentional bias in schizophrenia to stimuli of an alarming and emotive character (there are similar theories attempting to explain depression). The Emotional Stroop test has given weight to Bentall’s theory, by demonstrating that patients experiencing delusions do tend to focus more on threatening, frightening stimuli than control stimuli. Bentall argues that this attentional bias may lead to delusions as threatening stimuli is overly processed.

McKenna (1994) reviewed the methodology of these studies and found that the majority of studies to be empirically unsound, often as they did not use a control group. Of the two studies identified by McKenna that demonstrated defective attention in schizophrenic patients, one of these involved a particularly difficult listening task, whilst the other involved sedation of 50% of the schizophrenic group 30 minutes prior to the administration of the test. McKenna states these studies cannot be relied upon and further research is required.

Even if we accept there is some limited evidence for attentional bias in schizophrenia, it does not account for the full range of symptoms. Although defective selective attention could perhaps explain why a paranoid schizophrenic who suffers from delusions feels continually threatened, such theories do little to explain catatonic or residual schizophrenia, for which delusions are not present, or are a small part of the clinical picture.

A cognitive explanation alone is difficult to accept; many schizophrenics perceive a very distorted reality, for them what they see and hear is very real. Hallucinations and delusions are an unconscious process – they are not recognised by the patient as a problem in themselves, as for the schizophrenic the “reality” is the problem. This does not sit well with the usual cognitive explanations of mental illness whereby cognitive processes and schemas are identified and attempts made to modify. Therapy and Freudian psychoanalysis have proven to be ineffective treatments. Cognitive psychological explanations of schizophrenia tend to focus on positive symptoms e.g. delusions, hallucinations, thought disorder and bizarre behaviour, and look to explain symptomatology. Little attention is given to underlying aetiology. Chapman & Chapman (1973) noted that the majority of schizophrenic patients will perform poorly on any test given – therefore it is erroneous to give to much weight to such theories.

Schizophrenia is also characterised by negative symptoms, described as deficits in normal behaviour, which may exhibit as:
▪ social dysfunction
▪ affective flattening (loss of emotional reaction)
▪ loss of motivation
▪ loss of concentration
▪ inability to articulate
It has been argued that the presence of negative symptoms is a result of emotionally anxiety, or trauma, brought about by the disturbing symptoms the patient experiences; however this seems an unlikely explanation, as it is widely recognised that negative symptoms often appear at the onset of schizophrenia, prior to other positive symptoms.

There are a few alternative explanations of negative symptoms. For example, an extensive review of research by Hirsch & Leff (1975) concluded that a significant number of schizophrenic patients have mothers who show more concern and protectiveness than mothers of “normal” children. This was a feature of parenting both before and during their child’s illness. It would seem reasonable then that the child may become withdrawn, unable to focus or socially ineffective, as shown in negative schizophrenic symptoms. However, we cannot infer causality from these studies; it maybe that mothers were able to detect something worrying about their children long before schizophrenic symptoms became obvious and this would account for their heightened concern. At present there is little research considering the aetiology of negative symptoms in schizophrenia, although it is accepted that an interplay of environmental and genetic factors contribute to positive symptoms.

There is evidence that schizophrenia has a heredity factor. Gottesman (1991) conducted a review of 40 studies and pooled the data to consider heredity of schizophrenia. He found an almost 50% concordance in monozygotic twins (twins who began as a single fertilized ovum), who have an identical genetic make-up. This contrasts sharply with the approximately 1% lifetime risk of schizophrenia in the general population, and 15% risk in dyzygotic twins (where the egg has separated into two embryos). Children born of two schizophrenic parents are at a 46% risk of developing schizophrenia, again a figure far higher than that of the general population. This suggests genetic influence, as environmental factors are expected to be similar for identical and non-identical twins.

Overall, there is convincing evidence for a genetic predisposition to schizophrenia, as evidenced by twin studies. Neither of the biological or cognitive accounts discussed here alone offer a particularly convincing explanation of schizophrenic symptoms – it seems likely there is an interplay between the two elements. It appears there is a heredity element that is then triggered by an environmental factor; there is a greater than 50% chance of a monozygotic twin not developing schizophrenia even if the other twin does, suggesting this is not solely a genetic issue.

To conclude, there is certainly a wealth of research papers and hypotheses regarding the pathogenesis of schizophrenia; the continuing difficultly is finding an explanation that is able to account for the range of symptoms described within the DSM-IV. In his original writings, Bleuler believed schizophrenia was not a single psychoses, but in fact a group of several different ones. It maybe the case that the underlying aetiology is slightly different within each subgroup of schizophrenia and therefore the pathogenesis of each needs to be researched separately.

Bibliography

American Psychiatric Association (2000) Quick Reference to the Diagnostic Criteria from DSM-IV-TR. USA. American Psychiatric Association.

Choure, J. & Muzina, D. (2004). SCHIZOPHRENIA. Cleveland. The Cleveland Clinic Foundation

Feltham, C. & Horton, I. (eds) (2000) Handbook of counselling and psychotherapy. London. SAGE Publications.

McKenna, K. (1997). Schizophrenia and Related Syndromes. East Sussex. Psychology Press Ltd.

Walters, R (date unknown) Schizophrenia: A cyclical and heterogeneous dysfunction of cognitive and sensory processing? (online). Available from: http://www.cellscience.com/shdss2.html (accessed 20.04.05)