schizophrenia Flashcards

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1
Q

define schizophrenia

A

-schizophrenia is a serve mental disorder where contact with reality and insight are impaired. The sufferer may experience delusions or hallucinations

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2
Q

concordance rates of schizophrenia

A

Concordance rate of schizophrenia is higher in men than it is women – onset = late adolescence and early adulthood

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3
Q

5 types of schizphrenia

A

-Undifferentiated –> variation between symptoms and not fitting into a particular type

-Residual –> absence of prominent delusions. A presence of negative symptoms

-Paranoid –> preoccupied with false beliefs (delusions) about being persecuted or punished by someone. Their thinking, speech and emotions remain fairly normal

-Disorganized –> often are confused and incoherent with nonsensical speech. Their outward behaviour may be emotionless/falt etc. Disrupt their ability to perform normal daily activites like preparing meals etc

-Catatonic –> generally immobile physically and unresponsive to the world around them. Their bodies are often very rigid and stiff and unwilling to move. Increased risk of malnutrition etc

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4
Q

factors in the development of schizophrenia

A

-genetics (hereditary) –> passed from parents to children

-Brain chemistry –> imbalance of certain chemicals in the brain e.g dopamine. Dopamine levels affects the way the brain reacts to certain stimuli

-brain abnormality

-environmental factors -> poor social interactions, highly stressful situations or hormonal changes between teen and adult years

-no lab tests to diagnose schizophrenia so x-rays, blood tests etc are used to rule out a physical illness

-early diagnosis of schizphrenia can help avoid or reduce frequent relapses

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5
Q

positive vs negative symptoms

A

-positive symptoms = additions of something (delusions and hallcunations)

-negative symptoms = loss of something (speech poverty and avolition)

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6
Q

delusions

A

Delusions –> beliefs that have no basis in reality e.g belief there are victim of conspiracy.

-Paranoid delusions = someone is attempting to hurt them

-belief they have an imaginary power

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7
Q

hallucinations

A

Hallucinations –> experiencing sensations that arent caused by anything or anybody around the,. Most common is hearing voices. Feels very real to the person experiencing them. No basis is reality/distorted perceptions

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8
Q

speech poverty

A

Speech poverty –> Social withdrawal + difficulty in starting a conversation

-involves reduced frequency and quality of speech

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9
Q

avolition

A

Avolition –> loss of motivation to carry out tasks and lowered activity levels. No interest in socialising or hobbies

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10
Q

treatments

A

CBT + antipsychotics

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11
Q

DSM vs ICD

A

DSM-5 = 2 or more positive or negative symptoms of schizphrenia must be present for a diagnosis (American)

ICD-10 = range of subtypes for schizophrenia e.g paranoid (more international)

  • Despite both requiring persistence of symptoms for at least 1 month, the DSM-V has more specific diagnostic criteria and so requires at least 2 or more of delusions, hallucinations, disorganized speech and catononic behaviour, whereas the ICD-10 takes a broader approach to diagnosis, simply stating that “the clinical picture is dominated by relatively stable, often paranoid delusions, usually accompanied by hallucinations
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12
Q

Rosenhan (1973)

A

-experiment into how accurate psychiatrists are at diagnosing abnormality

-involved the use of pseudopatients who stated they kept hearing the word thud in an attempt to gain admission to psych hospital. These patients told the doctors they felt fine and hospital staff failed to detect a single pseudopatients

-41/193 identified as pseudopatients

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13
Q

evaluating the reliability and validity of schizphrenia

A

-symptom overlap between symptoms

-co-morbidity

-gender bias = men more commonly diagnosed than women

-culture bias

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14
Q

reductionist nature of clinical diagnosis

A

Reductionist nature of clinical diagnosis = despite evidence that schizophrenia and bipolar disorder overlap they continue to be treated as separate illnesses

Critics argue there is no diagnostic boundaries in diagnosis

DSM-5 = eurocentric

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15
Q

strengths = validity and reliability

A

-classification = real life applications in treatment

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16
Q

limitations = validity and reliability

A
  • There is a significant co-morbidity (high frequency of diagnosis of two disorders together) between schizophrenia and other mental health disorders, such as OCD and post-traumatic stress disorder, as suggested by Buckley et al (2009). These researchers found that 29% of their SZ patients suffered from post-traumatic stress disorder, whilst 50% suffered depression. Particularly in the case of depression, this suggests that if schizophrenia is so frequently diagnosed with other psychiatric disorders, then these two disorders may actually be the same, and so a more accurate and valid method of diagnosis would be to combine these two. Therefore, there are issues of validity in the diagnosis of SZ and attempting to differentiate its symptoms from that of other disorders.

-— There may be gender bias in the diagnosis of schizophrenia, as suggested by Longenecker et al (2010), who could not find an explanation for the sudden increase in the number of male SZ diagnoses made after 1980s. Cotton et al (2009) suggests that because there are no differences in genetic susceptibility for men and women in terms of SZ, then gender bias must be to blame. Dispositional traits of most women, such as high interpersonal functioning and being able to work even when suffering, means that such traits may mask the symptoms of schizophrenia or distort their severity so that they are not serious enough to call for a diagnosis. This means that the current system of the diagnosis of SZ does not account for these biases or differences in functioning between men and women, increasing the likelihood of inaccurate diagnoses.

— A second type of bias which may reduce the validity of the diagnosis of SZ is the problem of cultural bias, as suggested by Escobar et al (2012). For example, African Americans are far more likely to be diagnosed with SZ compared to patients belonging to Western cultures, due to their increased openness about admitting to certain SZ symptoms which may appear normal in their respective cultures. For example, the phenomenon of hearing voices may be considered a desirable sign of increased spirituality and connectedness with ancestors, and so may even be encouraged. However, both classification systems would view this as a hallmark characteristic of SZ and, combined with the potential distrust in African Americans that white psychiatrists may have, could increase the likelihood of false diagnoses.

-poor reliablity = Cheniaux et al 2009 = two psychiatrists independently diagnose 100ppl using both DSM and ICD. Inter-rater reliability was poor = 26 for DSM but 44 for ICD compared to 13 DSM and 24 ICD

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17
Q

biological explanations of schizphrenia

A

-genetic basis, dopamine hypothesis, neural correlates

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18
Q

genetic factors

A

-genetic component that predisposes people to the illness

-schizophrenia runs in familes suggesting evidence for a genetic link because family members tend to share the same aspects of their environment as well as their genes

-adoption studies = Heston 1966 = compared 47 adopted children whose biological mother has schizophrenia = higher risk even when raised in non-schizophrenia families

-higher associations of genetic similarity = higher likelihood of developing schizophrenia

-candidate genes = individual genes are believed to be associated with a level of inheritance. Schizophrenia is polygenic and aetiologically heterogenous (different combinations of factors can lead to the condition)

-Stephen Ripole et al (2014) –> genome-wide studies = 108 genetic variations associated with an increased risk of schizophrenia comparing 37,000 diagnosed and 113,000 controls

-genes affecting functioning of neurotransmitters such as doapamine

-10-20% concodrance rates in DZ twins but 40-50% in MZ twins

-Tierni (2004) = 5.8% in functional families and 36.8% in disfunctional families

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19
Q

Gottesman (1991)

A

Gottesman (1991) demonstrated a positive correlation between the increasing genetic similarity of family members and their increased risk of developing schizophrenia. The concordance rates are as follows = Monozygotic twins (48%), dizygotic twins (17%), siblings (9%) and parents (6%). This, particularly due to monozygotic twins sharing 100% of their genes, strongly suggests a genetic basis and the existence of candidate genes for schizophrenia. However, it is important to note that there are no 100% concordance rates, therefore demonstrating that there are environmental influences acting on the development of SZ e.g. the schizophrenogenic mother and dysfunctional thought processing.

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20
Q

strengths = genetic explanation

A

-multiple sources of evidence for genetic predisoposition = Gottesman 1991, adoption studies. Evidence suggests genetic susceptibility is very important

21
Q

Limitations = genetic explanations

A

deteministic

diathesis stress

22
Q

dopamine hypothesis

A

-dopamine is a neurotransmitter, causes neurons to fire in the brain

-original dopamine hypothesis stated that schizophrenia sufferes had an excessive amount of dopamine = too many messages

-amphetamines increase the amount of dopamine = give paranoid behaviour similar to schizophrenia

-antipsychotic drugs block dopamine receptors

-hyperdopaminergia in the subcortex = role of high levels of dopamine in the subcortex e.g brocas area associated with speech poverty

-hypodopaminergia in the cortex = Rakic et al 2004 = role of low levels of dopamine in the pre-frontal cortex is reponsible for negative symptoms of schizophrenia

Goldman Rakic et al (2004) suggested that hypodopaminergia in the prefrontal cortex may be responsible for negative symptoms of SZ, such as speech poverty and avolition. This is because the prefrontal cortex is associated with logical thinking, so abnormally low dopamine levels in this area may impair an individual’s ability to construct grammatical sentences that are focused upon one topic (speech poverty) or the ability to make decisions about how to function in day to day living (avolition).

23
Q

strengths dopamine hypothesis

A

-practical application = antipsychotic drugs (Tausher et al 2014) –> important role of dopamine for schizophrenia. Genes that increase dopamine = Riker et al

24
Q

limitations dopamine hypothesis

A

-mixed evidence for dopamine hypothesis –> increase dopamine = schizophrenic like symptoms but not the disorder (Curran et al 2004)

-correlation doesn’t mean causation

25
Q

neural correlates

A

-patterns of structure or activity in the brain that occur in conjunction with an experience

-negative symptoms = avolition = ventrical striatum = involved in motivation and anticipation of a reward. Judel et al = lower levels o activity = severity of negative symptoms

-Allen et al (2007) concluded that “the mis-identification of self-generated speech in patients with 6 auditory verbal hallucinations is associated with functional abnormalities in the anterior cingulate and left temporal cortex”, as SZ patients’ brain activity was recorded using fMRI during auditory hallucinations, and compared to a control group who identified pre-recorded words as their own or not. Therefore, this suggests that speech poverty (a positive symptom) may be associated with this neural correlate, as shown by the SZ group also making more mistakes compared to the control group

26
Q

strengths neural correlates

A

-There is evidence supporting the biological and genetic basis of schizophrenia. For example, Brown et al (2002) found that the risk of having offspring with SZ increased by over 1.3% if the father was over 50 years old, compared to if the father was under the age of 25. Therefore, this suggests that mutations in the sections of DNA containing the candidate genes, such as those coding for serotonin and dopamine production specifically, means that SZ is likely to have a strong heritability coefficient and biological basis. This supports the use of family studies and neural correlates as ways of studying and explaining incidence rates of SZ.

27
Q

limitations = neural correlates

A

-— The main issue associated with the use of neural correlates as a means of explaining schizophrenia is that such evidence is correlational and so does not take into account the ‘third variable problem’, whereby a third unstudied factor could be affecting both outcomes. Taking the example of the link between lower levels of activation in the superior temporal gyrus and anterior cingulate gyrus, and the experience of auditory hallucinations, one explanation would be the lowered activation levels causing the hallucinations, or the hallucinations themselves causing the lowered activation levels. A third possible explanation would be the third variable problem. Therefore, this demonstrates that correlational research cannot be used to reliably demonstrate a ‘cause and effect’ relationship between two variables.

-— The evidence for the dopamine hypothesis can be best described as ‘mixed’. On the one hand, support comes from Tauscher et al (2014) who found that antipsychotics, which act as dopamine antagonists and so reduce dopamine activity by binding to complementary receptors on the post-synaptic membrane, alleviated the symptoms of SZ, suggesting that dopamine has a key role in its development, in line with the predictions of the dopamine hypothesis. On the other hand, some researchers such as Moghaddam and Javitt (2012) have criticised the dopamine hypothesis and biological explanations of SZ as emphasising the role of dopamine too far. For example, the neurotransmitters glutamate and serotonin may also play a key role, as evidenced by the antipsychotic Clozapine acting upon both of these substances and being more effective than other atypical antipsychotics in reducing SZ symptoms, as suggested by Meltzer (2012).

28
Q

antipsychotic medication

A

-drugs are effective in treating the most disturbing forms of psychotic illness

-helps the person with the disorder function as well as increasing feelings of subjective wellveing

-example = chlorpromainze

-combat hallucinations and thought disturbances which are thought to be the products of overactive dopamine

-Antipsychotic medications are effective treatments for several mental health conditions. This group of medications is divided into two classes: typical and atypical antipsychotic medications. Typical antipsychotics tend to more strongly block dopamine. Atypical antipsychotics have greater effects on serotonin.

29
Q

psychological explanations to schizophrenia

A

-family dysfunction (poor family communication etc), cognitive explanations (mental processes), dysfunctional thought processing (informational processing is abnormal)

-role of internal mental processes and irrational cognitive thinking in the development of schizophrenia

30
Q

Stirling et al

A

Stirling et al (2006) –> studied the performance of people with schizophrenia and non-patient groups on the stroop test (neural psychological test to focus on cognitive stimulus). Epople with SZ are slower than control group in cognitive test. SZ patients had increased interference

31
Q

family dysfunction = schizophreogenic mother

A

-Fredia-Fromm-Reichman (1948) proposed a psychodynamic explanation for schizophrenia based on accounts she heard from her clients about their childhood. The schziophrenogenic mother = cold, rejecting and controlling and tends to create a fairly tense climate

-leads to distrust and paranoid delusions

32
Q

double bind theory

A

-Gregory Bateson et al (1972) –> agreed that family climate is important to the development of schizophrenia but emphasises the role of communication style within a family

-the developing child regularly finds themselves trapped in situations where they fear they are doing the wrong thing

-feel unable to comment on the unfairness of a situation or ask for clarification

-when getting something wrong the child is often punished by loss of love

33
Q

expressed emotions

A

-the level of emotion (particularly negative) expressed to a person with schizophrenia by their carers e.g hostility towards the person including anger and rejection.

-emotional over-involvement

-verbal criticism

34
Q

cognitive explanations

A

-focuses on the role of mental processes –> disruption to normal thought processing

-reduced processing in the ventral striatum is associated with negative symptoms whilst reduced processing of information in the temporal cingulate gyri are associated with hallucinations

-Frith et al (1992) –> 2 types of dysfunctional thought processing could underline some symptoms

-metarepresenation –> cognitive ability to reflect on feelings of thought and behaviour. Allows an insight into intentions and goals. Explains hallucinations as they cannot distinguish between reality

-central control –> cognitive ability to suppress automatic responses while we perform deliberate actions instead. Disorganized speech could result from the inability to repress automatic thoughts

35
Q

strengths of psychological explanations to schizophrenia

A

-support for family dysfunction as a risk factor –> difficulty in family relationships are associated with an increased risk of schizophrenia. Read et al (2005) reviewed 46 studies of child abuse and concluded that 69% o adult women inpatients with a diagnosis of SZ faced abuse. Barry et al = adults with insecure attachment style more likely to have SZ. However results have been inconsistent.

-strong evidence to support dysfunctional thought processing –> and that faulty central control skills may be responsible for some SZ symptoms, as demonstrated by Stirling et al (2006). The researchers found that SZ sufferers made significantly more mistakes and twice as long to complete the task, compared to a healthy neurotypical control group. However, it should be emphasised that dysfunctional thought processing can only offer explanations for the indirect, proximal causes of SZ, and not the distal causes, meaning that such theories can explain the symptoms but not the origin of SZ. This limits the utility of psychological explanations for schizophrenia.

36
Q

limitations of psychological explanations to schizophrenia

A

-critisised theory for parent blaming

-lack temporal validity

-little empirical research

-gender bias = focus on schizophrenogeic mother

-weak evidence for family based explanations –> lack of emprical evidence supporting double bind. Both theories are based on clinical observations

-evidence for biological factors is not adequatly considered e.g diathesis stress model

-cannot conclude cause and effect relationship

37
Q

psychological therapies for schizophrenia

A

CBT, family therapy, token economies

38
Q

family therapy + research

A

-aims to reduce stress within the family that might contribute to a persons risk of relapse

-reduce high levels of expressed emotions

-all family members share their experiences of schizophrenia

-develop practical coping skills that enable everyone to manage having schizophrenia in the family. Family may feel angry or impatient but are encouraged to express these in constructive ways

-lasts 3-12 months

-recognise signs of relapse and respond quickly

Pharoah et al 2010 = identified a range of strategies that aim to improve the functioning of a family. Reducing stress of caring fo a relative with schizophrenia. Reduction of anger and guilt.

39
Q

CBT + research

A

-cognitive explanations view the symptoms of schizophrenia as resulting from dysfunctional thought processes leading to fault interpretation of events. CBT assumes delusions influence a persons behaviour in a maladaptive way

-offering cognitive explanations for the existence of delusions and hallucinations can help reduce anxiety

-challenge irrational beliefs by reality testing to reduce distress

-Coping strategy enhancement = cognitive strategies to cope with their hallucinations

-Pilling et al 2002 = conduct meta-analysis of CBT that included a total of 392 ppts and concluded that CBT was effectve in improving the mental state of patients

40
Q

CSE

A

-specific form of CBT

-identify triggers for schizophrenia e.g people, being on their own etc

-develop strategies such as distraction or relaxation techniques or loud music to drown out voices etc

41
Q

token economies

A

-reward systems used to manage the behaviour of patients with schizophrenia

-for those who have been instiutionalised for a long period of time and who have developed bad habits

-based on the principles of operant conditioning

-staff give patients token when they perform desirable behaviours

-tokens are secondary reinforcers as they only have value when the patient recieves the reward

42
Q

strengths of psychological explanations to schizophrenia

A

-evidence for effectivness e.g Turkington et al (2004), who found that CBT could be used to challenge a patient’s paranoid beliefs about being targeted by the Mafia. More effective behaviours are put into place by questioning the reality of the patient’s beliefs and considering other, more reasonable alternatives. For example, beliefs about the Mafia can be rationalised as simply being based upon a single day where an individual was staring at the patient for an extended period of time, perhaps lost in thought.

-CBT gives patients autonomy in their own treatment = long-term strategies but not always appropriate for everyone

-no side effects = more likely for people to try = more inclusive

43
Q

limitations of psychological explanations to schizophrenia

A

-subjective = only useful for patients who have the motivation

— None of the three psychological therapies above actually treat the patient and ‘cure’ their schizophrenia. Instead, these therapies simply improve their quality of life through making the symptoms more manageable. For example, token economies increase the likelihood that the patients act in accordance with hospital rules and breaks disruptive patterns of behaviour, whilst family therapies reduce stress within a schizophrenic family and so increase the likelihood of the patient complying with their medical advice, whereas CBT improves the patient’s understanding of their symptoms. This suggests that an interactionist approach towards treatment is best adopted: biological therapies can treat the distal causes of SZ, whilst psychological therapies can treat the proximal symptoms!

  • There are serious ethical issues associated with the use of psychological therapies, and specifically concerning token economies. For example, some may argue that the ‘privileges’ that patients receive upon displaying appropriate behaviours are actually rights. Preventing patients from calling home or exercising outside may increase their stress and so aggravate their condition further. In addition, patients with the most severe SZ may find it near impossible to comply with these rules, and so will bear the most negative consequences. Similarly, CBT raises ethical issues because the therapist essentially has control over the patient’s views. This means that by challenging the idea of a Mafia as a controlling government instead, for example, the therapy is infiltrating into the patient’s personal beliefs. These changes can be anything, and not always beneficial.

-alternative psychological therapies

-token economies only help with negative symptoms

44
Q

antipsychotics

A

Antipsychotics = drugs used to reduce the intensity of symptoms particularly positive symptoms

45
Q

typical antipsychotics

A

-first generation

-phenothiazines known as chloropromazine –> taken orally, injection or by syrup

-inhibitiory effect

-dopamine antagonists (Working against the action of dopamine)

-They block the action of D2 dopamine receptors on the post-synaptic neuron by binding to them but not simulating them. This reduces the activation of dopamine

-improvement in positive symptoms such as hallucinations (claming + sedative effect)

-strong association between chloropromazine and the dopamine hypothesis

46
Q

atypical antipsychotics

A

-second generation

-examples = clozapine (reduce negative symptoms) or risperidone (reduce positive)

-introduced to minimise side effects and address both positive and negative symptoms

-dopamine antagonist

-lower affinity = bind temporality to D2 receptors then rapidly dissociate for normal dopamine transmission

-allows endogenous dopamine to work

-reduces positive and negative symptoms

-also a serotonin antagonist = blocks 5-HT(2a) receptor = lead to reduction in negative symptoms like avolition

-The key advantage of Clozapine is the improvements in cognitive functioning and mood which patients experience when taking it. This is particularly useful considering that SZ has a 50% comorbidity rate with depression - however, these benefits may be offset by the serious side effect of agranulocyotis, which is a severe and dangerous leukopenia which has caused several deaths in the past.

47
Q

strengths of biological treatments

A

-evidence for its effectiveness –> Thornley et al (2003) –> reviewed studies comparing the effects of taking chloropromazine to control conditions who received a placebo. 1121 ppts thought chloroproamzine had association with better overall functioning and reduced symptom severity. Relapse rate was also lower in 512 participants

-Metzler (2012) –> Clozapine is effective 30-50% of treatment resistant cases where typical antipsychotics have failed

48
Q

limitations of biological treatments

A

-Serious side effects –> The short-term side effects of typical antipsychotics are relatively mild (e.g. agitation and weight gain), whilst the long-term risk include tardive dyskinesia (characterised by involuntary contraction and relaxation of the facial muscles) and neuroleptic malignant syndrome (NMS). NMS is 7 characterised by fever, altered mental states, muscle rigidity and autonomic dysfunction and is thought to be caused by dopamine receptor blockage or central nervous system infections. These side effects are not offset by atypical antipsychotics, where agranulocyotis remains a serious concern for those taking Clozapine, whose state must be continually monitored using blood tests. Therefore, a cost-benefit analysis should be carried out to consider whether the benefit of symptom reduction outweighs the cost of side effects for each specific patient.

-depends on the dopamine hypothesis and the patient themself –> higher than usual levels of activity of dopamine in the subcortex of the brain For example, if antipsychotics appear to alleviate symptoms by reducing the action of dopamine, this makes sense considering the original dopamine hypothesis i.e. hyperdopaminergia in the subcortex. However, this action is not in line with the revised version of the dopamine hypothesis, which suggests that abnormally low levels of dopamine in the cortex are responsible for symptoms. Therefore, a further reduction in dopamine levels should make symptoms worse, and not better. This paradox has caused some to question the validity of the use of antipsychotics, as well as the accuracy of the dopamine hypothesis as an explanation for schizophrenia.

-Despite there being a range of evidence supporting the use of typical (Thornley et al, 2003) and atypical antipsychotics (Meltzer, 2012), these studies still suffer from problems of validity, as suggested by Healy (2012). For example, since Chlorpromazine has particularly powerful sedative effects, then this suggests that studies reviewing the effectiveness of antipsychotics in terms of symptom reduction may actually be measuring how calm and functional the patient appears to be - simply suppressing the symptoms is not a way of controlling them, and so such studies may lack validity due to not accurately assessing the actual effectiveness of antipsychotics in treating the proximal cause of SZ. Secondly, drug companies are selective about what type of information they publish: many focus on the short-term benefits as opposed to the long-term risks, and use inappropriate control groups, such as patients suffering from withdrawal symptoms as they have stopped taking their medication. This distorted focus brings into question, yet again, the validity of research into the effectiveness of antipsychotics.