Psychology PSYA3

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Clinical classifications and explanations of schizophrenia.

Classifications (psychopathology- dominated by biology approach)- it assumes that mental disorders is similar to physical disorders, so it suggests that mental disorders should be treated, diagnosed and classified as physical disorder.

When a disorders is being classified, clinicians used the symptoms and signs to identify the group the disorder is classified into.

Positive symptoms

these are the Symptom, Explanation and Example

* Delusions- False beliefs that the sufferer thought to be true.

* Persecution – having special knowledge or a belief that powers, thought or

actions are being controlled by an external force.

* Hallucinations- Imagined sensory perceptions.

* Auditory – hearing imagined voices (And holding prolonged conversations with

these voices)

* Thought Disorder- Confused thinking that is evident in what they say and how

they say it.

* Incoherent speech – jumping from one subject to another with little or no

logical connection. The grammar may be strange and only makes sense to the

speaker. They may claim that thoughts are being broadcast or stolen from them

or are being controlled or influenced by an alien, demon, or foreign power.

* Bizarre Behaviour- Strange and inappropriate behaviour (Contravening social

norms). Undressing in public or making odd faces, body gestures and postures

for no apparent purpose.

Negative Symptoms

these are the Symptom, Explanation and Example

* Blunted Emotional Responses- No emotional involvement in or response to

things in their immediate environment

* Unchanging facial expression, gestures, or tone of voice regardless of

whether the environment would require a happy or sad response, or an

inappropriate response e.g. laughing at a funeral.

* Loss of drive- Has little interest or motivation to work or enjoy leisure

activities

* Inability to wash and feed to take decisions and being entirely passive,

which leads to social withdrawal from the individual causing a lack of friends

or the difficulty making and keeping friends acquaintances or more intimate

relationships. Also relates in a reluctant and negative way towards social

interaction.

* Poverty of Thought- Considerable reduction in cognitive activity: Thinking

limited to immediate concerns. As well as, a limited amount of speech and may

answer questions with ‘yes’ ‘no’ or ‘I don’t know’.

Genetic Explanations for Schizophrenia:

Sample sizes and modestly positive results do not add up to certainty, however, a summary of

evidence to this end includes:

Twin studies showing

higher than expected probability that if one twin presents symptoms the other is likely to do so;

The closer the genetic relative

to the sufferer, the higher the probability that they might develop

schizophrenia.

Adopted children whose

natural family contained a member

who had developed schizophrenia were more at risk; a child adopted by a family where a

member later develops schizophrenia is no more likely to develop the illness

itself.

Where biological

changes do occur they could be the result of the schizophrenia rather than the

cause, or linked in ways in which has yet to be discover.

The longitudinal Copenhagen

High Risk Study (1962 - early 90’s) examined children who’s mothers were

diagnosed as having schizophrenic symptoms and found them much more likely to

develop the illness compared to those who did not. There was less than 1 in 10,000 chance

(p that these findings could have occurred by chance.

However, this study

cannot differentiate between the effects of genes and the effects of the

environment.

Adoption studies

provide some of the strongest evidence in support of the argument that genetics

play a key role in the development of schizophrenia.

Below shows the evidence indicating strong genetic links between genetics and

schizophrenia. However, it must be remembered that sample sizes are small and that circumstances of each study were

not directly comparable (lacks of population validity- difficult to generalise).

Also, there are issues to do with the fact that NOT ALL SOCIAL GROUPS ARE

EQUALLY LIKELY TO BE DIAGNOISED WITH SCHIZOPHERIA.

Evaluation:

· Research evidence is

pretty persuasive for

genetic linked risk factors;

· Degree of risk for relatives is

never 100% - even with Mz Twins its less than 50%, therefore genetics cant be a complete explanation.

· Search for the

relevant gene: Without knowing the exact

gene it’s impossible to isolate the underlying mechanisms that lead from genetic risk to

symptoms of the disorder. The search for the gene continues.

Biochemical explanations of schizophrenia

Dopamine is a brain chemical that increases the sensitivity of the brain

cells that promote the individual’s awareness of danger or aroused and when

under stress. If, however, the individual’s level of brain activity

is already highly aroused, then the effects of additional dopamine activity may

trigger the onset of a psychotic state, such as schizophrenia.

Neurons that have dopamine as their transmitter

substance (Dopaminergic neurons) are overactive in individuals who exhibit

schizophrenic symptoms.

The dopamine hypothesis suggests that ‘excessive

activity’ in the dopamine neurons leading to increased dopamine production and

limited absorption of existing dopamine is associated with schizophrenia.

An interesting parallel exists with Parkinson’s Disease, where a dopamine

increasing drug (L Dopa) seems to have the opposite effect.

Further support for the dopamine hypothesis comes from the post-mortems (dead patients- corpse) of patients

with schizophrenia. These

have revealed specific increase of dopamine in the left amygdale (Falkai et al.

1988) and increased dopamine receptor density in the caudate nucleus putamen

(Owen et al. 1978)

Wong et al. (1986)

shows in live patients using pet scans that the dopamine receptor density in the caudate nuclei is indeed

greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.

Evaluation of Dopamine Hypothesis:

Positive evaluation

+ Current available evidence

supports some form of the dopamine hypothesis.

+ Effects of different drugs on different sub types (Type I and II)

Negative evaluation

- Drugs alleviate

positive symptoms but are not so effective with negative symptoms.

- Cause or effect can’t be established

Neutral evaluation

-/+ Amphetamines

worsen positive symptoms (associated with acute schizophrenia) and lessen

negative symptoms (Associated with chronic) while phenothiazine's

(Anti-psychotics) alleviate positive symptoms but aren’t as effective in

lessening negative symptoms.

Role of dopamine in other disorders:

Dopamine also implicated in

mania and other disorders which have quite different symptoms. Main evidence in dopamine

schizophrenia is the effectiveness of phenothiazine in alleviating symptoms.

Neuroanatomical explanations

Two such scanning

technologies are Positron Emission

Tomography (PET) and Magnetic Resonance Imaging (MRI).

PET scans are used in the diagnosis of problems in bodily organs,

particularly the brain.

MRI is a complex diagnostic technique whereby a patient is surrounded by

a cylinder that contains a strong magnet.

These technologies have

shown abnormal brain structures in many patients exhibiting schizophrenic

symptoms,the differences in the density of receptor cells for

dopamine in schizophrenia patients who were being treated with anti-psychotic

drugs and those who were not.

Evidence for neuro-anatomical

explanations:

Brown et al (1986) found decreased brain weight and enlarged

ventricles, which are the cavities in the brain that hold cerebrospinal fluid.

Flaum et al. (1995) also found enlarged ventricles along with

smaller thalamic hippocampal and superior temporal volumes.

Buchsbaum (1990)

found abnormalities in the frontal hippocampus and the amygdale. As more MRI

studies are being undertaken, more abnormalities are being identified.

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