Clinical Flashcards

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1
Q

Outline what is meant by mental illness using the 4 D’s

Give examples of the 4 D’s in terms of dysfunction etc.

A

Deviance –is the behaviour rare? Deviate from the norm eg Shouting randomly is not normal

Dysfunction – does behaviour interfere with everyday life? May not be instantly obvious eg unable to work in a workplace

Distress – does the behaviour cause upset. This is treated in isolation as people may appear to cope or be able to function in some areas. Subjective opinion eg behaviour is followed by crying or complaining

Danger – danger to self and others, seen on a scale, and classed as risky eg seeing hallucinations can be dangerous as they may lead you to being distracted and run into a road

Duration- many behaviours may address the above but be short term. Eg Only occurs for a day

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2
Q

Evaluate and explain the limitations and strengths of the 4’Ds as a form of
diagnosis

A
  1. Gives clinicians power, to remove rights under Mental Health Act, serious issues with labelling and life changes. Ethics
  2. Subjectivitybyclinicianininterpretingclient/patients experience for example, DEVIANCE – can be very subjective as it ignores culture and time. What may be the norm in one culture may not in another. Definitions of deviance change over time. Reliability
  3. Reliability–the4Dsarenotstandardisedinreallife, clinicians may focus on some or every factor
  4. Basedoninterviews,structured/unstructured,issueswith
    self report, e.g. honesty, socially desirable answers, shame etc. Validity
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3
Q

Describe the DSM5 as a diagnostic tool

A

Has 3 sections:

  1. Introductions and instructions on how to use it.
  2. Classification of main mental health disorders and their symptoms. Like the ICD it groups mental disorders into families e.g. Mood disorders (unipolar depression, bipolar ect).
  3. Other assessment measures such as cultural formulation interviews to help diagnose those from other cultures.
    - The multi axis system describes the 5 axis needed to diagnose someone e.g. 5 is the ability to cope with normal life.
    - Patients needs to show 5 symptoms or more to be diagnosed with a mental disorder.
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4
Q

Evaluate the DSM 5, in terms of reliability. Focus on at least two forms of reliability

A

1) Goldstein (1988)** – found that the DSM III was reliable as she tested two experts, using a single blind technique, to diagnose a patients and found high levels of inter rater reliability.
2) Brown et al (2001)*- 362 American patients were interviewed by 2 different experts using the anxiety disorders interview schedule for DSM IV. Brown et al found high levels of inter rater reliability
- Burnham et al found that American Mexicans were more likely to be diagnosed with auditory hallucination as opposed to non-Mexican Americans. This how’s that the DSM is not reliable as it cannot account for cultural differences.

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5
Q

Evaluate the DSM5 in terms of validity, focus on at least two forms of validity

A

+ Hoffmann – Found that the diagnosis of alcohol abuse had no differences using the DSM or computer interview. The symptoms from the interview matched the DSM so it has concurrent validity.
- Kirk and Kutchins – argued that there had been insufficient training and supervision of interviews. The studies took place in a specialised research setting so its lacks ecological validity and cannot be generalised to real life setting.

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6
Q

Outline what is meant by schizophrenia

A

It is a long term disorder involving a breakdown in the relationships between thought, emotion and behaviour. It can lead to faults in perception and inappropriate actions and feelings. It is often referred to as a type of psychosis, which means the person may withdraw from reality and from relationships.

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7
Q

Describe the symptoms of schizophrenia, including positive and negative

A

Positive Symptoms (Type 1) – symptoms that change behaviour or thought, effectively adds to normal behaviour, e.g. Hallucinations, delusions.

Negative Symptoms (Type 2) – symptoms that cause a withdrawal or lack of function, effectively takes away from normal behaviour, e.g. Social withdrawal, mutism, avolition.

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8
Q

Describe the features of schizophrenia

A

25% of sufferers only experience one episode.

  • 25% of sufferers will have symptoms continuously without any breaks.
  • 50% of sufferers experience periods of symptoms and periods of recovery.
  • With treatment 60 % of patients manage a relatively normal life.
  • 1% of the population are diagnosed with schizophrenia.
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9
Q

Evaluate the diagnosis of schizophrenia, in terms of validity and reliability giving examples

A

According to the DSM V
1. Hallucinations (us. auditory or somatic) 2. Delusions (oft. linked to hallucinations) 3. Disorganised speech
4. Disorganised or catatonic behaviour
5. Negative symptoms
PLUS
Social & occupational dysfunction Duration of at least one month

Which is reliable as this is for all individuals but lacks reliability as can be subjective
However lacks validity as on occasions people with schizophrenia don’t count as having as doesn’t fit criteria for example may only have a duration of 1 week

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10
Q

Describe the neurochemical explanation of schizophrenia

A

The dopamine hypothesis’ which is a biochemical theory which suggests that schizophrenia is caused by excessive activity at synapses that use dopamine as their primary neurotransmitter. Dopamine is a neurotransmitter that helps control the brain’s reward and pleasure centres as well as being associated with regulating movement and emotional responses. Research suggests that the presence of an excess number of dopamine D2 receptors at the synapse is the main contributing factor to the mental disorder. According to this hypothesis, the increased number of D2 receptors means that there is a faster rate of D2 receptor dopamine complexes formed per unit of time. This therefore causes abnormal functioning of dopamine dependent brain systems by increasing or decreasing brain activity, resulting in schizophrenic positive and/ or negative symptoms. It is possible that an increase in dopamine activity in the mesolimbic pathway contributes to positive symptoms including auditory hallucinations and delusions associated with psychosis. Likewise, it is also possible that dysfunction with dopamine functioning in the mesocortical pathway contributes to the negative symptoms like social withdrawal and alogia. Using evidence from post mortem studies, It is suggested that sensitivity to dopamine can arise from brain lesioning or prefrontal cortex damage. This may lead to lack of dopamine inhibition in the striatum which is an area associated with multiple aspects of cognition including; decision making motivation, reinforcement and reward perception.

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11
Q

Evaluate the neurochemical explanation of schizophrenia using PACEE

A

P. The dopamine hypothesis has lead to the development of antipsychotics such as haloperidol which work by blocking the D2 receptors that bind with dopamine. This has allowed many to carry on with their lives as productive members of society.

Individual Differences may not work for all

A. Cognitive explanations states that the cause of schizophrenia is due to dysfunctions cognitive processes leading to the development of schizophrenia.

However this can’t be empirically tested like with biological by measuring dopamine levels

C. Is a creditable theory as it has been empirically testedand the theory is supported by measurable concepts such as drug trials making the theory more credible.

The brains of schizophrenics are only ever studied after a diagnosis has been made, we cannot look at the brain before diagnosis
This means that we do not know if the dopamine is the cause of sz or whether developing the illness changes the brain chemistry.

E. - Seeman – found high numbers of D2 receptors in the brain post-mortem. These have a higher chance of bonding with dopamine, leading to higher dopamine activity.

Gottseman and Shield – 48% concordance rate in MZ twins whereas strangers only 1%

EV. - Seeman – there is a problem with direction of causality as it is not clear if higher number of D2 receptors cause schizophrenia or if schizophrenia caused a higher number of D2 receptors.
  • Gottesman and Shield did not find a concordance rate of 100% showing that there are other causes of Schizophrenia such as the effects of environment.
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12
Q

Describe one other biological explanation of schizophrenia for example
genetic explanation or diathesis-stress explanation.

A

Argues there is a gene for the disorder which is inherited and therefore is innate.

  • Individuals have a predisposition for developing schizophrenia but can be triggered by environmental factors.
  • The risk of developing schizophrenia in a lifetime is 1% however this increases to 2-6% if you have a second degree relative with schizophrenia. This shows there is a genetic factor to schizophrenia.
  • The genetic basis is largely corroborated by the twin study carried out by Gottesman and Shield. Study conducted on 62 patients found concordance rates of 48% for MZ twins and 17% for DZ twins. This suggests that there is a genetic factor to schizophrenia.
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13
Q

Evaluate the genetic explanation of schizophrenia using PACEE

A

P

Can predict if a baby may have sz by looking at family history and can help from a young age
A

C

Single gene has not been identified or isolated as a cause of schizophrenia suggesting that there are other factors contributing to schizophrenia.

Twin studies are difficult to use as its hard to separatenature and nurture, as families share the same environment and MZ twins are reared (brought up similarly).

E.
Gottseman and Shield – 48% concordance rate in MZ twins whereas strangers only 1%

F. Seeman – found high numbers of D2 receptors in the brain post-mortem. These have a higher chance of bonding with dopamine, leading to higher dopamine activity.

Ev
Gottesman and Shield did not find a concordance rate of 100% showing that there are other causes of Schizophrenia such as the effects of environment.

Seeman – there is a problem with direction of causality as it is not clear if higher number of D2 receptors cause schizophrenia or if schizophrenia caused a higher number of D2 receptors.

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14
Q

Describe the cognitive explanation, of schizophrenia using key terminology

A

Frith’s Model:
- Model distinguishes between conscious and preconsciousprocessing:
➢ Conscious processing: where highest level of cognitive functions takes place, we are aware of this level. Has a limited capacity and carries out one task at a time.
➢ Preconscious processing: takes place without our awareness; its an automatic process and carries out a number of tasks at once.
- Delusional Thinking is a result of the attention filter breaking down allowing unimportant information to get into the conscious level, leading to it being interpreted as something important that needs to be acted upon.
- Auditory Hallucinations are a result of the conscious/preconscious filter breaking down allowing all sounds to enter the conscious level, this results in non-speech sounds being interpreted as speech and experienced as voices.

Hemsley’s Model:

  • Schizophrenics are unable to give meaning to new sensory input as they cannot activate or access their schemas.
  • This leads to an overload of sensory information that they do not know what to attend to or how to attend it.
  • All information they receive is interpreted as a completely new experience to them, external stimuli such as drilling may be interpreted as danger as they have no corresponding schema to the noise.
  • Internal speech and thoughts are recognised as external voices causing auditory hallucinations.
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15
Q

Evaluate the cognitive explanation of schizophrenia using PACEE

A

P. The cognitive explanation of schizophrenia has lead to the development of cognitive behavioural therapy and coping therapy. These treatments have helped schizophrenics to cope with positive symptoms of schizophrenia e.g. Hallucinations.

A. The dopamine hypothesis (biological explanation) would argue that the cause of schizophrenia is due to overactivity of dopamine at the synapses.

C. Is a creditable theory as it has been empirically tested however concepts are theoretical therefore are not falsifiable meaning the theory is not scientific and therefore less credible.

E. Bentall et al found that schizophrenics with hallucinations performed worse compared to normal people and schizophrenics with no hallucinations, as they found cognitive tasks demanding due to limited capacity at the conscious level. They are unable to filter out important information.

EV. The experiment was conducted in a laboratory environment meaning that it has high internal validity however has low ecological validity.

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16
Q

Describe the features of depression

A

Depression affects over 3.5 million people in the UK.

  • Women are 4 times more likely then men to be diagnosed with depression, 9% women and 2-3% men.
  • 10% diagnosed with depression will commit suicide.
  • If left unattended lasts about 6 months.
  • Can occur at any pint, more prevalent in early adulthood.
17
Q

Describe the symptoms of depression

A

5 or more symptoms must be present for 2 weeks for a diagnosis to be made.

  1. Physiological: weight gain/loss, fatigue, hypersomnia (excessive sleep).
  2. Cognitive: suicidal thoughts, negative thinking.
  3. Behavioural: social withdrawal, lack of concentration, loss of pleasure in activities.
  4. Emotional: excessive guilt, extreme sadness, low self esteem.
18
Q

Describe the neurochemical explanation for depression, serotonin.

A

Monoamine Hypothesis:
- Depression is caused by an an imbalance in the neurotransmitters noradrenaline and serotonin.
Noradrenaline: Regulates mood, too little leads to depression.
Serotonin: regulates noradrenaline activity; too little allows abnormal fluctuations in noradrenaline.
- The imbalance is caused by two processes:
1. Reuptake – Occurs when serotonin is reabsorbed back into the neurone. Once reabsorbed, it is recycled and used again. If it keeps being reabsorbed it means no new serotonin is produced which when is low causes abnormal fluctuations with noradrenaline.
2. Monoamine oxidise – This is an enzyme that breaks down serotonin once it has been used and sent its message. This break down means there are low levels of serotonin which when is low causes abnormal fluctuations with noradrenaline.

19
Q

Evaluate the neurochemical explanation of depression using PACEE.

A

P. The monoamine hypothesis lead to the development of effective drug treatments such as the development of SSRIs and MAOIs, they work by either stopping the reuptake of serotonin or stopping the monoamine oxidisefrom breaking down serotonin leading to a decrease in symptoms of depression.

A. The cognitive explanation as posed by Beck would state that the cause of depression largely stems from the fact there is faulty cognition at work.

C. - Is a creditable theory as it has been empirically tested.
- However is a reductionist model as it only takes into account neurotransmitter activity and does no take into account life events nor cognitive factors, therefore the theory is less credible overall.

E. - Versiani et al – found that people taking antidepressants showed more improvement than placebos, this shows that there is an underlying biological reason for depression.
- Teuting – found that depressed people had higher levels of compound produced from breakdown of serotonin, by monoamine oxide, in urine sample compared to non-depressed people. This shows that low levels of serotonin causes depression.

EV. - Kirsh et al however found that the success of antidepressants was due to the placebo effect this means there are conflicting results with Versiani.
- Teuting’s study follows a controlled procedure that was standardised meaning it’s a reliable study as can be replicated to find similar results.

20
Q

Describe Beck’s cognitive explanation for depression the cognitive triad and

A

According to Beck, depression is caused by negative thinking about:

  1. The Self
  2. The future
  3. Experiences
    e. g. I’m a bad person (1), Things will not improve (2), My life is terrible (3).

Faulty Thinking Strategies:
With the Triad, Beck developed ‘faulty thinking strategies’ which are listed bellow:
- Selective thinking: Focusing on only negative details e.g. ‘I dint get 100% on a test’.
- Arbitrary inference: Drawing negative conclusions from insufficient evidence e.g. ‘I failed once so I always will’
- Overgeneralisation: Drawing conclusions based on a single factor e.g. ‘I failed my exam so I will fail in life’.
- Catastrophising: Exaggerating a minor incident to make it a disaster eg. ‘My teacher hates me because I didn’t do the HW’ and then avoiding the teacher.
- Personalising: Taking blame for everything e.g. ‘Im to blame for my parents divorce’.
- Black & White thinking: seeing everything as a successor failure e.g. ‘I either pass or fail’.

21
Q

Evaluate the cognitive explanation for depression using PACEE

A

P. Led to the development of cognitive behavioural therapy (CBT) which targets the patients faulty cognition and aims to change it by challenging it.

A. The monoamine hypothesis would argue that depression is the result of imbalances in neurotransmitters leading to symptoms of depression.

C. Is a creditable theory as it has been empirically tested, however concepts are theoretical and therefore are harder to operationalise and test making the concept less credible. The theory also lacks credibility as does not explain the root cause of depression.

E. - Beck – compared the dysfunctional attitude scales (DAS), scores from depressed and non-depressed people. He found that depressed people scored higher indicating they thought more negatively about themselves (negative schemas).
- D’Alessandro – found students negative views about their futures were strongly associated with increased depressive symptoms. This supports the triad as it suggests negative thinking leads to depressive symptoms.

EV. - ‘Normal’ individuals experience cognitive processing first before emotional processing. Demasico found through neuro-imaging techniques, that emotional processing occurs before cognitive processing.

  • Beck used a standardised procedure so it can be easily replicated to find the same or similar results.
  • D’Alessandro used only students and as a result its not representative of wider depressed people at different ages and as a result cant be generalised to them.
22
Q

Describe one biological treatment of schizophrenia (drug treatment e.g.

A

TYPICAL – how do they work?
• Reduce level of dopamine in the brain associated with the symptoms.
• By blocking the dopamine receptors in the areas of the brain affected.
• This prevents the dopamine binding to the receptors in the synapse and depolarizes the neurons, calming them down.

ATYPICAL
• They work in the same way, however there is evidence that they do not bind to receptors so tightly, and they only do this temporarily (which is reducing tardive dyskeneisa) and that they also block serotonin receptors.
• This may be linked to the less side effects for the atypical medication.

23
Q

Evaluate drug treatment for schizophrenia using TEARS.

A

T.Antipsychotics take 2-3 weeks to start showing improvements, in the first weeks symptoms of schizophrenia actually increase before improving (down regulation). Treatment is continuous and lasts a lifetime.

E.Meltzer et al – conducted an experiment on 481 patients, and separated with some receiving haloperidol, antipsychotic which blocked D2 receptors, and some receiving placebos. He found that those taking haloperidol displayed reduced symptoms of schizophrenia showing that drug treatments lead to reductions in symptoms.
A.The treatment has considerable side effects that are persistent throughout the life’s of those taking the drugs this leads to drug treatment being undesirable as a method of treatment. Symptoms also increase beforedecreasing meaning schizophrenics would again see treatment as undesirable.

R. Hollon found a 76% relapse rate in patients with schizophrenia who took antipsychotics. Factors that may have contributed to this is severe side effects.

S.Antipsychotics have severe side effects, common side effects include insomnia, blurred vision, fatigue, nausea and weight gain/loss. Some specific antipsychotics have potentially harmful side effects such as creating suicidal thoughts or in the case of risperidone increasing the risk of strokes.

24
Q

Describe a cognitive treatment for schizophrenia, for example CSE, Coping

A
  1. Assessment, including current problems and ways of coping with symptoms e.g. Some schizophrenics may self medicate or partake in self harm.
  2. Selecting coping methods for the symptoms.
  3. Intervention (when coping strategies are put in place)
  4. Review to see how well these coping methods are working for dealing with the symptoms.

The CSE – semi structured interview:
This happens at the start of the CSE and during the ‘review’.
1. Form and content – nature, frequency, duration.
2. Emotional response – how it makes you feel.
3. Prior warnings or triggers before symptoms appear.
(Emotion, behaviour, physical reaction, thoughts and beliefs)

25
Q

Evaluate the cognitive treatment for schizophrenia using TEARS

A

T.CSE takes a considerable longer time than drug therapy, it typically lasts for 12-20 sessions over a 6 month course.

E.- Tarrier found a 50% improvement in people who received CSE compared to other treatments. A follow up in 6 months showed continued improvement this shows CSE provides long term solution/benefits.
- Chadwick & Lowe found that 10 out of 12 patients in their study displayed significant reductions in delusions.

A.CSE is intense and can be uncomfortable as some strategies encourage engagement and acknowledgment of auditory hallucinations which many would not want to do. Treatment is difficult and challenging contributing to the 47% attrition rates.

R. There are low relapse rates as patients are taught coping strategies which are practiced at home so they learn life long skills.

S.There are no physical side effects however engaging with hallucinations can place psychological strain such as stress and heigh anxiety levels.

26
Q

Describe the biological treatment for depression SSRI’s and MAOI’s.

A

Selective Serotonin Reuptake Inhibitors (SSRI):

  • Examples: Citalopram, Paxil, Prozac.
  • How it works: Prevents the reuptake of serotonin in the pre-synaptic neurone. This means that SSRIs increase neurone activity which means that noradrenaline is regulated preventing any fluctuations. 14 days before symptoms are eased.
  • Side effects: Dry mouth, tremors, nausea, fatigue, low sex drive, weight gain.
  • Withdrawal symptoms: Fatigue, muscle spasms and pains.

Monoamine Oxidise Inhibitors (MAOI):

  • Examples: Nardil, Parnate, Marplan.
  • How it work: MAOIs inhibit the activity of the monoamine oxidise preventing it from breaking down serotonin, this means there will be heightened levels of serotonin in the pre-synaptic neurone, thereby regulating noradrenaline.
  • Side effects: Dizziness, insomnia, weight gain, headaches. Eating foods like chocolate can increase blood pressure to dangerous levels.
  • Withdrawal symptoms: Fatigue, muscle spasms and pains.
27
Q

Evaluate the biological treatment for depression using TEARS

A

T.Takes up to 2 weeks to alleviate symptoms where in this time there is a depleting of mood as natural serotonin production increases this poses a risk as it can lead to suicide.

E.- Kane et al – found that 80-90% of people improved with drug treatment in some way.
- Royal Collage of Psychiatrists – 50-65% of patients treated with antidepressants showed improvement compared to 25-30% patients taking placebos.

A.Drug treatment allows a person to continue with their lives and once again become productive members of society without much inhabitation, this means its widely acceptable treatment, and seen more time effective than therapy.

R. Hogarty found that 40% of patients relapse within 6 months of taking antidepressants, this means that people build up a tolerance to the drug and therefore have to increase the dosage which can lead to addiction.

S.Physical side effects of SSRIs such as prozac include dizziness and decreased sex drive, side effects of MAOIs such as nardil include chest pain and vomiting.

28
Q

Describe Rosenhan ‘Sane in an insane place’ 1974 Experiment-classic study.

A

8 pseudopatients (fake patients), 3 women and 5 men, none of them had any history of any mental health problems.

  • 12 hospitals ranging from good, bad, new and old institutions across 5 states in America.
  • Pseudopatients phoned admissions office looking to make appointments about ‘hearing voices’.
  • At admission meeting they reported hearing the words ‘empty’, ‘thud’ and ‘hollow’. They were given fake names and jobs but everything else they disclosed was true to their lives e.g. Life events and family relationships.
  • All were admitted with schizophrenia except one who was admitted with manic depression with psychosis.
  • Once admitted, they behaved normally and showed nosymptoms and tried convincing staff they were not inane. All observations made were recorded.

Results:
- Average stay in the hospital was 19 days with the shortest being 7 days and the longest 52 day.
- When contact was initiated towards the nurses 71% of the time they were ignored.
- Staff made normal behaviour conform to the symptoms of schizophrenia e.g. Note taking was referred to as ‘writing behaviour’.
- Out of 185 reasonable questions asked towards the staff, none were answered.
Follow up:
- Hospital asked Rosenhan to send fake patients in the next 3 months, however he did not send any pseudopatients.
- After the 3 months the hospital claimed to have identified 41 fake patients.

29
Q

Evaluate Rosenhan using GRAVE.

A

G.Research used a small sample of only 8 participants this is not representative of the wider population and cannot be generalised. However they used 12 hospitals across 5 states which varying quality. It can be seen therefore this is a representative of hospitals across America and therefore treatment in these institutes are representative and can be generalised.

R.Research is reliable as the experiment was standardised, for example each of the 8 participants described the same symptoms in the admissions interview. As a result the experiment can be easily replicated to find the same or similar results.

A.Displayed at the time that psychiatric diagnosis was not reliable. This lead to the change of the DSM II to improve diagnosis especially schizophrenia, and also lead to changes in practice in psychiatric institutions e.g. Have more time to spend with patients.

V.- Ecologically valid as the experiment was carried out in psychiatric institutes as a result the findings can be generalised to that setting.
- Less internally valid as extraneous variables were not controlled as a result of inducting in a naturalistic environment.

E.- Consent from hospital staff was not obtained as well as the fact that they were deceived.
- Staff identities in the institutions however were not published and were kept confidential.

30
Q

Describe contemporary study for schizophrenia Carlsson (1999).

A

Aim:

  • Review studies into the relationship between levels of neurotransmitters, especially dopamine and glutamate, on symptoms of schizophrenia.
  • The main assumptions of the causes of schizophrenia were hyperdopaminergia (high levels of dopamine) and hypoglutamatergia (low levels of glutamate).
  • To develop a better treatment with fewer side effects.

Procedure:
Carlsson conducted meta-analysis on 33 studies.
1. Study reviewed research investigating neurochemical levels in patients diagnosed with schizophrenia. Brain scans provided by Abi-Dargham et al found high levels of dopamine is linked to psychosis.
2. Study looked into research about recreational drugs known to induce psychosis. Studies found link of amphetamines (increases dopamine) and PCP (‘angel dust’) with schizophrenia.
3. Evidence of effectiveness of drugs and the effects they had on the brain to support the hypothesis that other neurotransmitters are associated with schizophrenia.

Results:

  • Evidence found to support low levels of glutamate and development of psychotic symptoms. Reduced levels of glutamate was found to be linked with increased dopamine release.
  • PCP which when used inhibited NDMA receptors (glutamate receptors) reducing the action of glutamate in areas of the brain resulting in psychosis.
  • Glutamate failure in the cerebral cortex lead to the development of negative symptoms, and glutamatefailures in the basal ganglia resulted in positive symptoms.
  • Clozapine a antipsychotic reduces levels of dopamine and serotonin in the brain and is a highly effective treatment. Serotonins link with glutamate therefore suggest that glutamate is also responsible for the development of psychosis.
31
Q

Evaluate the contemporary study by Carlsson (1999) GRAVE.

A

G.- Research used a large range and number of studies, Carlsson actually reviewed 33 different studies. Therefore the studies are representative meaning the findings can be generalised.
- Some studies however used animal studies therefore it is difficult to generalise findings to humans.

R.Research used secondary data that is largely accessible to anyone. As a result it means anyone can conduct a review on the same studies to find the same or similar results.

A.Found that glutamate has a strong connection in the development of psychosis, as a result it can lead to development of different drugs as a form of treatment which can possibly have fewer side effects.

V.Great deal of secondary data was used from a verity of different studies and there is no way of knowing the validity of these original studies therefore it can question the overall validity of Carlsson’s review.

E.Is a review study therefore there were no participants in the study meaning that there was no breach of any ethical guidelines.