Biological explanations and treatments Flashcards

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Q

Keywords: Genetics

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Genetics - Inherited as genes and transmitted from parent to child. Passed down through genetics.
Dopamine hypothesis - The theory than an excess in the neurotransmitter dopamine is implicated in schizophrenia.
Neural correlates - Which parts of the brain are implicated in schizophrenia.
Family studies - Whether an individual has inherited genes from families and the concordance rate of sz.
Twin studies - Looking at monozygotic and dizygotic twins and the concordance rate.
Concordance rate - The likelihood two related people both have schizophrenia.
Adoption studies - When twins are adopted at birth. They consider the concordance rate of sz and eliminate the environmental factors.
Candidate genes - Genes that have been implicated in the development of schizophrenia eg. COMT regulates dopamine.
Polygenic disease - Requires a number of different factors to work. Different combinations of genes can lead to the condition.
Neurotransmitters - A chemical messenger in the brain.

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2
Q

Twin studies:

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Monozygotic (identical) twins - Single egg fertilised by single sperm, then splits in two.
They SHARE 100% of their GENES.
Dizygotic (non-identical) twins - Separate eggs fertilised by separate sperm.
They SHARE 50% of their GENES.

If monozygotic twins are MORE CONCORDANT than dizygotic, then this suggests that THE GREATER SIMILARITY IS DUE TO GENETIC FACTORS, as dizygotic share 50% and monozygotic share 100%.
Joseph (2004) - Calculated that the data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins.
More recently, methodologically sound studies have tended to report A LOWER CONCORDANCE rate for MZ twins THAN EARLIER STUDIES.
Despite this, such studies STILL SUPPORT the GENETIC POSITION, because they show a concordance rate for MZ twins that is MANY TIMES HIGHER than for DZ twins.

Criticism of twin studies:
Twins ALL SHARE THE SAME ENVIRONMENT, so you CANNOT DISTINGUISH what is GENETICS and what isn’t.

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3
Q

Family studies:

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Gottesman and Shields, 1991 - Family studies find individuals who have schizophrenia and determined whether their biological relatives are similarly affected MORE OFTEN than non-biological relatives.
THE CLOSER THE DEGREE OF GENETIC RELATEDNESS, THE GREATER THE RISK OF DEVELOPING SCHIZOPHRENIA.
Example from study: Children with TWO schizophrenic PARENTS had a CONCORDANCE RATE of 46%. Children with ONE schizophrenic PARENT had a RATE of 13%. Children with a sibling having it had a CONCORDANCE rate of 9%. Uncles/Aunts had a 2% concordance rate.
Criticism: Can’t distinguish between environmental influence or genetics.
All share the same environment –> cannot definitely say it’s due to genetics and not the environment.

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4
Q

Adoption Studies

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Tienari et al (2000) - Done in Finland - Criticism: May not use the same classification system.
Studies of genetically related individuals who have been REARED APART are used, because of the difficulties of separating genetic and environmental influences within twin and family studies.
164 adoptees - biological Mothers had been diagnosed with SZ.
Findings:
11 (6.7%) - ALSO received a DIAGNOSIS of schizophrenia.
4 (2%) of the 197 CONTROLS adoptees (born to non schizophrenic Mothers).
Investigators concluded that these findings SHOWED THAT THE GENETIC LIABILITY TO SZ HAD BEEN DECISIVELY CONFIRMED.

Piece of research TO SUPPORT a genetic basis of sz.
Heston (1966) - Compared 47 adopted children whose biological Mother had schizophrenia with a control group of adopted children with NO HISTORY OF sz in biological family.
Findings - NONE OF THE CONTROL GROUP WAS DIAGNOSED, 16% of offspring children of sz Mothers were diagnosed.

Support: Establish environmental factors
Criticism: Are RARE

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5
Q

Polygenic and candidate genes

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TEN different genetic variants have been identified.
Schizophrenia is A POLYGENIC disease, as no candidate gene has been identified.
A region in the CHROMOSOME 22 might confer SUSCEPTIBILITY to schizophrenia.
This SEGMENT of DNA harbours genes for the enzyme that can influence NEUROTRANSMISSION.
COMT!!!
COMT - Crucial for dopamine metabolism -
Any GENETIC VARIANCE THAT ALTERS ACTIVITY OF THIS ENZYME COULD LEAD TO AN IMBALANCE OF THIS NEUROTRANSMISTTER.
A DNA sequence variation (single-nucleotide-polymorphism) on the COMT gene CATABOLIZES (breaks down) dopamine at up to 4 times the rate of the HEALTHY GENES.
This results in POSITIVE SYMPTOMS of schizophrenia, including HALLUCINATIONS.
Having these genes DOES NOT necessarily mean an individual WILL develop schizophrenia.

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6
Q

Research into polygenic genes:

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Ripke et al (2014) - 108 GENETIC VARIATIONS
Thought to be a result of genetic factors AND environmental factors. Genetically vulnerable and the environment can act as a trigger.
Associated with variations in multiple genes.
Ripke scanned for GENE VARIATIONS associated with schizophrenia across the ENTIRE GENOTYPE.
Compared genotypes of almost 37,000 sz patients to a LARGE CONTROL group of 113,000.
Researchers found sz to be associated with variations in 108 genes. SUPPORTS POLYGENIC MODEL!

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7
Q

Research into candidate genes:

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COMT, DRD4 , AKT1 –> All three implicated in the processes of dopamine transmission in the brain.
Benzel et al - 2007 –> They have been associated with excess dopamine in specific D2 RECEPTORS, which leads to acute episodes.
There was strong evidence for the role of genetic interactions in INCREASING SUSCEPTIBILITY to schizophrenia.

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8
Q

A03 - Evaluation

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Supports A01:
P) Supporting evidence for genetic vulnerability to sz from a variety of sources, such as Gottesman’s 1991 study.
E) Tienari et al (2004) - Found that children of sz sufferers are still at HEIGHTENED RISK of developing the disorder, even if they are ADOPTED into families with NO HISTORY of schizophrenia.
E) Furthermore - Sorri et al (2004) conducted a longitudinal study of 21 years on FINNISH adoptees, who had BIOLOGICAL MOTHERS with sz and considered FAMILY REARING STYLES among adoptive families. Findings: adoptees with a high genetic risk were MORE SENSITIVE to NON-HEALTHY rearing patterns, which could INCREASE their chance of DEVELOPING schizophrenia.
L) Therefore, genetic + environmental factors play a role in developing schizophrenia.

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9
Q

A03 - Evaluation

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Supports A01:
P) Supporting research for mental illness running in families.
E) Heston (1966) - If one identical twin suffers with sz, the other has a 90% LIKELIHOOD developing a SIMILAR MENTAL DISORDER, involving NEUROTIC symptoms. INCREASES the validity of the role of genetics.
Furthermore, Cardno et al (2002) found a concordance rate of 26.5% for MZ twins and 0% for DZ twins.
C) Although this provides strong evidence for a genetic component, there are problems with this type of research. MZ twins are quite rare in the population and of those, only 1% would be expected to have schizophrenia, therefore the SAMPLE SIZE IS SMALL. This might explain the large difference in concordance rate found by different researchers.
C) However, it is clear that even when the relative is GENETICALLY IDENTICAL (MZ), the chance of developing schizophrenia is WELL BELOW 100%, suggesting that other factors must contribute eg. the environment.

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10
Q

A03 - Evaluation

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Challenges A01:
P) Challenge - The idea that sz running in families may be more to do with COMMON REARING PATTERNS or OTHER FACTORS which have NOTHING to do with heredity.
E) Example - A NEGATIVE EMOTIONAL CLIMATE in some families - may lead to stress beyond an individual’s coping mechanisms, thus triggering a SZ episode.
C) After all, the probability of developing schizophrenia even if your identical twin has it is less than 50%. However, MZ twins are treated more similarly, encounter more similar environments, do more things together and are treated as “twins” rather than TWO DISTINCT INDIVIDUALS like Dz twins, which could influence them both developing a disorder like sz.
C) Therefore, OTHER FACTORS not to do with genetics may play a more important role in the development of schizophrenia.

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11
Q

The Dopamine Hypothesis

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Dopamine - A neurotransmitter that generally has an excitatory effect and is associated with the sensation of pleasure.
Hypothesis - A statement of prediction.

THE DH centres on the idea that the neurotransmitter dopamine is linked to the onset of the disorder.
Cognition - Hallucinations and delusions
Movement - Catatonic behaviour eg. repetitively playing with your hair

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12
Q

Initial dopamine hypothesis

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Only able to explain positive symptoms eg. hallucinations and delusions.
High levels due to neurons firing too EASILY or too OFTEN or due to ABNORMALLY HIGH LEVELS of D2 receptors, which could be due to the COMT gene producing more.
Non - schizophrenic - Less receptors (D2), normal amount
Schizophrenic - More receptors (D2), excessive amount

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13
Q

The revised dopamine hypothesis

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Davis and Kahn (1991) -
Positive symptoms of sz - caused by an EXCESS of dopamine in the SUBCORTICAL areas of the brain, particularly in the MESOLIMBIC pathway.
Negative + cognitive symptoms of sz - thought to arise from a DEFICIT of dopamine in areas of the PREFRONTAL CORTEX (the MESOCORTICAL pathway).
Evidence:
Neural imaging eg. Patel et al (2010)
Used PET scans to assess dopamine levels in schizophrenic and normal individuals.
Found LOWER levels of dopamine in the DORSOLATERAL PREFRONTAL CORTEX of schizophrenic patients COMPARED to their normal controls.
Animal Studies eg. Wang and Deutch (2008)
Induced dopamine depletion in the prefrontal cortex in rats.
Resulted in cognitive impairment (memory deficits)
The researchers were able to reverse using olanzapine, an atypical antipsychotic drug thought to have BENEFICIAL EFFECTS on negative symptoms in humans.

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14
Q

A03: Evaluation

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Agonist - Increases dopamine
Antagonist - Decreases dopamine
Anti-psychotic drugs –> Dopamine antagonists - block the activity of dopamine in the brain.
Parkinson’s disease - They have low dopamine levels, so they are given L-DOPA to raise their dopamine levels. This can produce symptoms very similar to schizophrenia - Grilly , 2002.
Parkinson’s type symptoms are also side effects of anti-psychotic drugs, which reduce dopamine levels.
Low dopamine levels - parkinson’s symptoms eg. tremors + negative symptoms
High dopamine levels - schizophrenia (positive) symptoms

Post Mortems and PET scans - Post mortems on sz show high levels of dopamine in the brain, especially the limbic system - Iversen, 1979
Too many D2 receptors

Amphetamines eg. Cocaine - Give similar symptoms to those of excessive dopamine eg. hallucinations and delusions.
Pet scans show that schizophrenics are more sensitive to amphetamines.
It is now widely accepted that instead of there being too much dopamine, it seems that schizophrenics have too many or over-active dopamine receptors and therefore are utilising too much.

Leucht et al (2013) - Meta analysis, 212 studies - Analysed the effectiveness of different anti-psychotic drugs compared with a placebo.
Findings: All drugs tested were significantly more effective than placebo in the treatment of positive and negative symptoms, achieved through the normalisation of dopamine.

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15
Q

A03 - Evaluation

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Supports A01:
P) Strength - Supporting evidence for the role of antipsychotics.
E) Animal studies: Wang + Deutch (2008) induced dopamine depletion in the pre-frontal cortex of rats. This led to cognitive impairment eg. memory deficit. This was revered by using olanzapine, an atypical drug, which is thought to have beneficial effects on negative symptoms in humans.
C) Weakness - Extrapolation - Can’t generalise animal studies and their findings to humans, which lowers the validity.
C) Therefore, there is supporting evidence for the idea that low levels of dopamine lead to negative symptoms and antipsychotics can combat this.

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16
Q

A03 - Evaluation

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Supports A01 + Challenges A01:
P) Supporting evidence for the dopamine hypothesis.
E) Patel et al (2010) - Neural imaging - Used PET scans to assess dopamine levels in sz compared to normal individuals. Findings: lower levels of dopamine in the dorsolateral prefrontal cortex in sz patients compared to their normal controls.
C) However, Noll (2009) claims there is strong evidence AGAINST both of the dopamine hypothesises. He argues that anti-psychotic drugs do not alleviate hallucinations and delusions in about 1/3 of patients. Additionally, in some people, hallucinations and delusions are present, despite levels of dopamine being normal. Therefore, blocking the D2 receptors has little/no effect on their symptoms.
C) In conclusion, there is supporting evidence for the DH, however also contradictory, as individual differences are evident.

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Q

A03 - Evaluation

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Supports A01:
P) Post mortems studies - Show that there are high levels of dopamine in the brain, especially in the limbic system. Much of the evidence supporting the dopamine hypothesis comes from the success of drug treatments that attempt to change levels of dopamine activity in the brain.
E) Leucht et al (2013) found that anti-psychotic drugs were significantly more effective than placebo in the treatment of positive and negative symptoms.
C) Furthermore, Curran et al (2004) argues that dopamine agonists (increase the level) MAKE SZ worse and can PRODUCE schizophrenia-like symptoms in NON SUFFERERS.
C) This supports the idea that high levels of dopamine causes schizophrenia symptoms.

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Q

A03 - Evaluation

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Challenges A01/Weakness of RM:
What comes first the chicken or the egg?
Does too much dopamine activity cause schizophrenia
OR
Does schizophrenia cause high dopamine levels?
This is not discussed within research around dopamine and schizophrenia.

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Q

Neural Correlates

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Neural correlates - A relationship between parts of the brain and schizophrenia.
Measurements of the structure or function of the brain that correlate with the symptoms of schizophrenia.

There is a growing body of evidence which suggests that schizophrenia may be caused by ABNORMALITIES to BRAIN STRUCTURE.

20
Q

Brain volume

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Johnstone et al (1976) - Enlarged ventricles appear to be associated with negative symptoms. This is fluid filled cavities due to the loss of subcortical brain cells. The ventricles of a person with sz are about 15% bigger than normal.
This implies that the brain areas around the border of the ventricles have SHRUNK or DECREASED in volume, so the ventricular space has become larger and brain weight has decreased as a result.
The enlarged ventricles may be the result of POOR BRAIN DEVELOPMENT or TISSUE DAMAGE.

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Q

Specific Brain Areas

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Many brain regions and systems operate ABNORMALLY in schizophrenia.
Allen et al (2007) - Found abnormalities for positive symptoms in the SUPERIOR TEMPORAL GYRUS and the ANTERIOR CINGULATE GYRUS. Reduced activity in these two areas of the brain is a neural correlate for AUDITORY hallucinations.

Frontal lobe: Critical to problem solving, insight, other high level functioning. Low fl activation when engaging in mentally challenging tasks. In SZ, this leads to difficulty in planning actions and organising thoughts.

Ventral striatum: AVOLITION is a loss of motivation. Motivation involves the anticipation of a reward and the vs is involved in this. Therefore, avolition is linked to this area.

Limbic System (Amygdala): Involved in emotion - DISTURBANCES are thought to contribute to the AGITATION frequently seen in schizophrenia.

22
Q

Neural correlates of positive symptoms

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Prefrontal cortex - Helps people think logically and organise thoughts.
LOWER activity –> linked to DELUSIONS and DISORGANISED thoughts.
Visual cortex and auditory cortex –> Process information received from the eyes and ears.
The SAME activity in these areas when they HALLUCINATE as sane people have visual and auditory experiences.

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Q

Neural correlates of negative symptoms

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Amygdala - Responsible for basic feelings eg. fear.
SMALLER in schizophrenics, so can lead to loss of emotion which is the FLAT AFFECT.

Basal Ganglia - Located deep inside the brain. Affects movement and thinking skills. LARGER in schizophrenics, which could cause MOTOR DYSFUNCTION.

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Q

A03) Evaluation

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Weakness of RM:
P) Limitation of the neural correlates theory is that it can ONLY EXPLAIN negative symptoms.
E) Johnstone et al (1976) found that schizophrenics had ENLARGED VENTRICLES, while non-sufferers did not, which suggests that sz is related to a loss of brain tissue.
C) However, this is NOT TRUE OF ALL schizophrenic sufferers, as Weyandt (2006) suggested enlarged ventricles are ONLY ASSOCIATED with negative symptoms. Although studies of nc are useful in flagging up brain systems that may not be working properly, this evidence DOES NOT PROVE that the activity in the brain region causes the symptom.
For example, Yoon et al (2013) - Suggested that something was wrong in the ventral striatum - which causes negative symptoms of sz. However, it is possible that the NEGATIVE SYMPTOMS THEMSELVES mean that LESS INFORMATION passes through the striatum, resulting in its REDUCED ACTIVITY.
C) Links back to what came first? Therefore, neural correlates studies DO NOT PROVE that the ACTIVITY causes THE SYMPTOM.

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A03) Evaluation
Challenges A01: P) Challenge - The idea that brain tissue differences are an effect of having the disorder rather than being due to genetic factors. E) Boos et al (2012) - performed MRI scans on 155 schizophrenics and 186 of their non schizophrenic siblings. Findings: Schizophrenics had REDUCED GREY MATTER DENSITY AND CORTICAL THINNING. Therefore, there are a number of neural correlates of sz symptoms (positive + negative). C) However, does the unusual activity in a brain region cause the symptom? There could be other explanations for this correlation. For example, the correlation between levels of activity in the ventral striatum and avolition. It is possible that something is wrong in the striatum, causing the negative symptoms. On the other hand, it could be that the NEGATIVE SYMPTOMS THEMSELVES means that LESS INFORMATION passed through the striatum, resulting in REDUCED ACTIVITY. C) Links back to what comes first?
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A03) Evaluation
Challenges A01: P) The existence of NC in sz tells us little in itself. E) Sz can take place in the ABSENCE of a family history of the disorder. One explanation for this - a mutation in parental DNA eg. sperm cells. Can be caused by radiation, poison or a viral infection. C) Evidence for this comes from a study by Brown et al (2002) which showed a POSITIVE CORRELATION between PATERNAL AGE and RISK OF SCHIZOPHRENIA. Increasing from 0.7% with Fathers UNDER 25, to over 2% in Father OVER 50. C) Therefore, there alternative explanations which are backed up by studies.
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Treatments: Drug therapy - Typical and Atypical antipsychotics (antagonists)
Antipsychotics - Drugs used to treat schizophrenia. Typical antipsychotics - Traditional, old drugs, first line developed to treat schizophrenia. Atypical antipsychotics - Newer drugs Antagonist - Blocks dopamine, lowers the level. Agonist - Increases transmission, heightens the level. D2 receptors - Receptors for dopamine on the post synaptic neuron. Agranulocytosis - A side effect of the drugs, reduces the white blood cells. White blood cells are responsible for fighting infections. Tardive dyskinesia - A side effect of the drugs, causes tremors and pacing. Globally, around $14.5 BILLION is estimated to be spent on antipsychotics each year.
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Typical Antipsychotics -
Used PRIMARILY to COMBAT the POSITIVE SYMPTOMS, such as hallucinations and thought disturbances, which are products of an overactive dopamine system. Developed in the 1950's, known as "conventional" antipsychotics. The basic mechanism is to REDUCE THE LEVEL OF DOPAMINE AND SO REDUCE THE SYMPTOMS. Dopamine ANTAGONISTS - They bind to but do not stimulate dopamine receptors (particularly in the mesolimbic dopamine pathway), thus BLOCKING THEIR ACTION. By reducing stimulation of the dopamine system in the mesolimbic pathway, antipsychotics ELIMINATE the hallucinations and delusions. Hallucinations and delusions --> Usually diminish within a FEW DAYS of beginning medication. However, other symptoms may take SEVERAL WEEKS before a significant improvement is seen. The effectiveness of the dopamine antagonists in reducing these symptoms, led to DH development. Kapur et al (2000) estimate --> between 60% and 75% of D2 receptors must be BLOCKED for these drugs to be effective. However, to do this, a similar number of D2 receptors in OTHER AREAS of the brain need to be BLOCKED, leading to undesirable side effects. To address this problem, atypical antipsychotic drugs have been developed. Criticism: Don't help negative symptoms and are expensive.
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Atypical Antipsychotics-
"Second generation" antipsychotics Three main differences to the first gen: - Lower risk of extrapyramidal side effects eg. inability to sit still, tremors, stiff muscles, involuntary facial movements. - Have a beneficial effect on negative symptoms and cognitive impairment. - Suitable for treatment - resistant patients. Like with typical drugs, these also block D2 receptors. However, they only TEMPORARILY occupy the D2 receptors and then RAPIDLY DISASSOCIATE to allow NORMAL DOPAMINE TRANSMISSION. This rapid dissociation of atypical antipsychotics is thought to be RESPONSIBLE for the less side effects found within these drugs compared to conventional ones. They have very little effect on the dopamine systems that control movement, so tend NOT to cause MOVEMENT PROBLEMS (found with typical). However, atypical antipsychotics have a STRONGER AFFINITY for SEROTONIN receptors and a LOWER AFFINITY for D2 receptors. This explains the different effects of atypical compared to typical.
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A03) Evaluation
Weakness of RM: P) Weakness - Likelihood of side effects, ranging from mild - serious - fatal. E) Typical --> associated with dizziness, agitation, sleepiness, stiff jaw, weight gain and itchy skin. Long term use --> Tardive dyskinesia Most serious side effect of typical --> neuroleptic malignant syndrome --> leads to high temp, delirium, coma ---> can be fatal. C) Contrast --> Atypical ones have fewer side effects, because of their mechanism of action --> but do still have side effects eg. agranulocytosis. C) Suggests that AP's may not be appropriate for all patients and should be PRESCRIBED WITH CAUTION. Side effects can be so distressing for patients that they STOP taking the medication entirely --> impacts the effectiveness of the drugs.
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A03) Evaluation
Supports A01: P) Strength of chlorpromazine - supporting studies for its effectiveness. E) Thornley et al (2003) - Reviewed studies comparing the effects of chlorpromazine and a placebo. Data from 13 trials of 1121 pp's found that CP was associated with better overall functioning and reduced symptom severity. E) Furthermore, Leucht et al (2012) - Meta analysis of 65 studies involving nearly 6000 participants. All had been given antipsychotics. Some were taken off theirs and given a placebo instead. Findings: Within 12 months, 64% of those on the placebo had relapsed. 27% relapsed on the AP drugs. E) Meltzer et al (2012) --> concluded that clozapine is more effective than typical AP's and other atypical AP's and that it is effective in 30-50% of treatment - resistant cases, where typical AP's have failed. L) This provides strong evidence for the effectiveness of antipsychotics, especially chlorpromazine and clozapine.
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A03) Evaluation
Weakness of RM: P) Ethical issues with anti-psychotics E) Laing - Anti Psychiatry movement - Says they restrict the mind and are "chemical straitjackets". He also states that if psychedelics eg. magic mushroom can be banned, why can't anti-psychotics, especially because the side effects are much worse. C) Contrast point - Protects themselves and others from harm. Could be supporting ethics (protection from harm). C) However, they do go against free will, as patients are sectioned and drugs are given on time relapse, which could be a major ethical issue.
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A03) Evaluation
Weakness of RM: P) Weakness - Side effects, death and psycho-social consequences. If these were taken into account, a cost-benefit analysis of its advantages would probably be negative. E) USA - Large out of court settlement --> awarded to a tardive dyskinesia sufferer on the basis of the Human Rights Act --> no one should be subjected to inhuman or degrading treatment/punishment. C) Additionally, it is widely believed that AP's have been used in hospital to make patients calmer and easier to deal with, rather than for the patients benefit. Additionally --> Ethical - patient w/ severe symptoms --> may not be able to give fully informed consent. C) Highly unethical - breaks human rights, mostly negative.
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A03) Evaluation
Challenges A01: P) Challenge --> Their effectiveness may be highly exaggerated. E) Healy (2012) - Argued that some successful trials of their effectiveness have had their data published MULTIPLE times. Exaggerates the evidence for + effects. C) Furthermore --> As AP's have calming effects --> easy to demonstrate that they have some positive effects on patients. NOT THE SAME as saying they REALLY REDUCE the SEVERITY of symptoms. C) Not really a wide range of data to support their effectiveness. Highly exaggerated.
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Typical Antipsychotics
Chlorpromazine - Blocks dopamine receptor sites. Thus decreases dopamine activity. Side effects: muscle tightening in neck and jaw, tardive dyskinesia, depression, NMS - epilepsy. Barlow + Durand (1995) - Effective in reducing schizophrenic symptoms in about 60% of cases. Most impact on +, still suffer from severe - symptoms. Haloperidol - Blocks dopamine receptor sites. Thus decreases dopamine activity. 55% relapse rate - Schooler et al (2005) Side effects: muscle tightening in neck and jaw, tardive dyskinesia, decrease in emotional spontaneity and motivation, weight gain, NMS. Schooler et al (2005) - Randomly allocated 555 patients in first episode of sz. Either treated w/ haloperidol or risperidone. 75% in both groups showed a reduction in symptoms. However, 75% drop out.
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Atypical Antipsychotics
Clozapine - Blocks both dopamine and serotonin receptor sites. Side effects: Similar to typical AP's, but tardive dyskinesia is much reduced. Fewer side effects than typical or first gen anti-psychotics. Rare side effect: agranulocytosis - dangerously low level of white blood cells can be FATAL. Pickar et al (1992) - Compared it with other neuroleptics and a placebo --> found clozapine to be the most effective in reducing symptoms, even in patients who had previously been treatment resistant. 72% compliance rate. Risperidone - Blocks both dopamine and serotonin receptor sites. 45% relapse rate compared to 55% with haloperidol (Schooler et al-2005) Side effects: Fewer than haloperidol; weight gain, severe anxiety, sedation, sexual dysfunction, low blood pressure, stuffy nose. Emsley (2008) - Found that patients who were injected with it early in the course of the disorder had LOW relapse rates and HIGH remission rates. 84% of patients showed at least a 50% reduction in both + and - symptoms. 64% went into remission.