The A* Students Handbook (c)

AQA A PsychologyPsya4:

Schizophrenia

AQA A

June 2015/16 Spec

Saj$Devshi$+$www.loopa.co.uk$A*$Psychology$Revision

2nd Edition

A* Model Essay Answers

Hello..1Write your model answers over and over until you can do them from memory

Hello,Firstly thank you for purchasing my book for AQA Psychology and the Psya4 Schizophrenia topic (2nd edition). A bit about me: My name is Saj Devshi and I was a private student that self-taught myself AQA Psychology from 2011-2012 and I received my certificate in January 2013 achieving an A* Grade. The certificate you can view on my website which I will post at the bottom - You can also get my other A* model essay answers from there too for the other topics for AQA Psychol-ogy. I achieved an A* grade overall scoring two As in Psya1 and Psya2 as well as 100% in both my A2 exams (Psya3 and Psya4) My final score was 373/ 400 ums points. (You only needed 90% in A2 and 320 ums for an A* grade). So basically I didnt just beat the boundary - I abso-lutely smashed it. How did I do it? It wasnt easy and I am by no means some savant genius. I made great notes and essays that simplified things for me as I had no teachers and it is these notes I share with you now to help you with this topic. Self-teaching myself AQA Psychology from the ground up has given me a unique and strong foundation in grasping the concepts. I am by no means the oracle but I understood enough that I was able to work completely inde-pendently without support and create such good, concise essays. Since 2012 thousands of stu-dents across the UK (as well as abroad where these exams are also taken) have downloaded my books to support their revision. These books will help cut down revision time as all the es-says are made concisely and clearly for people to follow. Im confident these essays will serve you well as they did me for AQA Psychology.If your curious to know more about me you can visit my website at http://www.loopa.co.uk There it tells you more about me, how I self-taught myself as well as contact me directly for help and advice as well as get books on the other topics and papers too.You can get plenty more free resources by liking my Facebook page and following me on twit-ter below - My Facebook page: http://www.facebook.com/aqapsychologyFollow me on twitter here too: https://twitter.com/SajDevshi

Again thank you for your support and I wish you the very best in your exams! Now - Lets get this show started..

Overview of this book..This book covers paper 4 which is also known as Psya4 and specifically the Schizophrenia topic. This book breaks down the specification itself for the Schizo-phrenia topic and then presents to you all the dierent chapters you are expected to know. These are then broken down into the possible essay questions that can be asked and this is where this book helps you - every single possible essay question in the exam for Psya4 Schizophrenia is pro-vided within this book with my proven model A* essays that helped me get 100 ums for Psya4.

The answers in this book are by no ways the definitive answers and there are vari-ous ways that students can answer the possible questions. I merely present one such way which worked for myself.

A good first question is how do I write a model essay answer?

From my experience there are many routes to writing the essay answers and this is not set in stone.

The most important thing I found in achieving high marks was making it clear for examiners where each of the sections are.

For instance for big essay questions you will find that you will have about 8 Marks for an outline and 16 Marks for evaluation of sorts.

Therefore I have found it useful to structure my essay answers with 8 marks worth of the-ory followed by 16 marks worth of Research, evaluation and IDA (issues, debates & ap-proaches)

The way I answered questions is covered in this book and is as follows:

Outline theory

Research studies supporting the theory - Research studies criticising the theory

Evaluation with strengths and weak-nesses of the theory and studies (and how the weaknesses of the studies im-pact the theory)

Issues, debates and approaches (mini-mum of 2 in each essay)

I tend to stick to this throughout my schizo-phrenia model answers.

With big essay based questions you have to make sure you put sufficient information for the marks shown.

It is possible questions can be smaller in which case less detail is required however for the full essay questions there must be suffi-cient detail.

I have tried to cover this in the model answers by ensuring their is sufficient detail for each of those sections.

You may find that I have written too much and it is likely you wont need to remember every

2

single bit of each section to still get full marks as the focus is on quality rather than quantity.

Personally I didn't want to disappoint by leav-ing the answers short on detail so I have de-cided to put more information rather than risk putting less.

One thing that was vital in Psya3 was includ-ing Issues, Debates and Approaches in your evaluations to reach the top bands in scores.However for paper 4 this is not the case and the use of IDAs is more optional - However you can still use them for evaluation points to score marks and I will include them as they are an easy way to score 16 marks worth of evaluation. Therefore I defi-nitely recommend using them at every oppor-tunity to pick up easy marks for evaluation if your struggling. A good method to use IDA points is to remember the word GRENADE. Each letter represents an IDA - here let me show you:! ! G = Gender Bias! ! R = Reductionism! ! E = Ethical Issues! ! N = Nature vs Nurture! ! A = Animal Studies! ! D = Determinism! ! E = Eurocentrism/EthnocentricThere is a good post and video about these on my website here:http://www.loopa.co.uk/aqa-psychology-level-issues-debates-approaches/

The image above is a little small but you should be able to zoom in if your on a tablet. If not click the link I pasted just before as it takes you to a video and bigger sized im-age of the one above.

Gender Bias

Is there gender bias?

Has most the studies Involved men? Or women?

How might the theory/study not apply to both genders?

How might the other gender behave differently? Why?

What does this mean for the original theory?

Reductionism

Is the theory reductionist and too simplistic?

Is there something more complex going on?

What else could be happening?

This may actually mean what then?

How does this affect the theory?

Ethical Issues

What ethical issues exist?

Is the research/theory socially sensitive?

How could it affect society?

How could it hinder society?

What are the implications?

Nature vs Nurture

Does this theory support nature (and genes)?

3

Is there evidence for nurture and the environment?

Are they both interacting in some way?

How does this affect the theory?

Animal Studies

Were animals used?

Were they subjected to physical/emotional harm?

Is this morally right?

Why might animal studies HELP us?

Why cant we generalise results to humans?

How might this affect the theory basing results on ani-mals?

Determinism vs Free Will

Is the theory too deterministic in assuming there is no control?

When is this not true?

How does free will factor in and conscious thought?

Can we hold people responsible when they have no con-trol?

What are the implications for society if so?

When does free will come in?

Eurocentrism

Is the theory/studies based in one culture?

How do other cultures differ?

Are we generalising one cultures values and behaviour to others?

Why might this affect the theory?

What are the implications for the theory?

Does the theory lack wider generalisation due to this?

4

The Psya4 Specification

5

What you have above is the specification for PSYA4 and specifically the first selection of topics you can choose from.On the left box it has the disorders ranging from Schizophrenia, Depression, Phobic Disorders and Obsessive compulsive disorder.On the right box it lists all the possible questions they can ask in relation to our chosen disorder - the question can be phrased in various ways to throw you o but ultimately they will all be asking one of those possible questions.As we have chosen Schizophrenia - the questions will look something like this:

Clinical Characteristics of Schizophrenia Issues surrounding the classification and diagnosis of Schizophrenia including reliability

& Validity Biological explanations for Schizophrenia Psychological explanations for Schizophrenia Biological Therapies for Schizophrenia (evaluation focuses on whether its eective or ap-

propriate) Psychological Therapies for Schizophrenia (again evaluation is heavily focused on

whether the therapy is eective or appropriate)

Sometimes the question can be asked as a plural. What this means is it may ask for Explanations of schizophrenia (be it Psy-chological or biological). The important thing to note is the letter S at the end of explanationS

Memorising Your Answers & Acronyms..Memorising your model answers is going to be pretty much your hardest task.People have various ways in which to do it and it is entirely up to you.For myself; I personally employed 2 methods;One was through the use of Acronyms and made up words to memorise all the various studies.I used the same system I created in Psya3 and applied it to paper 4.Here is an example as previously mentioned in my last book;For example for the question on How Genes Affect Aggression - I remembered the phrase MHBC.Each letter would stand for a researchers name and study related to the question.M=Mcguffin H=Hutchings B=Brunner C=Caspi et al.It is in essence a form of chunking that we learnt about for paper 1 in AS.With enough practice I found this worked quite well and in the exam I was able to learn and master all the topics this way by simply remembering certain letters and words.The second method I found that helped was practice, practice and practice writing and re-writing the model answers over and over again.This may sound overly simple but it has proved to be by far the most effective way to memorise the model essay answers consider-ing the huge amount of content you will need to learn.It is very boring I know and by the end of it my arm was about to drop off but achieving a good grade comes at a price.

I spent every available moment I had con-stantly going over the model answers until I could do them from memory.Eventually I found I was able to recall all the essay answers through simply remembering the acronyms which in turn would trigger my memory for the model answers themselves.------

I will list my acronyms used for Schizophrenia but feel free to create your own if you struggle and make it work for you - i simply adjusted them to phrases I liked to remember myself.

The theory is usually the only part you need to know from the top of your head without as-sistance but this should be much easier as you should be understanding the topic your writing about and the theory behind it; for ex-ample if your writing the theory element for biological explanations for Schizophrenia - you should know how to explain how its either genes or neurotransmitters such as dopamine causing it.

The acronyms are used to recall the strange research and what they actually carried out which may be harder to recall.

This should hopefully trigger your memory for the rest of the evaluation we will be memoris-ing too once you have had enough practice as you will be able to tell whether something is missing or not.

Right, enough small talk - lets go onto the an-swers themselves..

7

The Model Answers 2 The first model answer is on outlining the clinical characteristics of Schizophrenia (updated with DSM 5). It is the shortest essay and thus no acronyms are used. Its unlikely to be a big essay question and highly likely to be an outline type of ques-tion ranging from 4-8 marks I would imagine. Never the less I have given you a de-

tailed answer and its unlikely you need to know it all in such detail but here it is any-way. You can shorten it with the key details any way you wish depending on the mark allocation.

Clinical Characteristics Of SchizophreniaUnder the new DSM 5 Diagnosis; Schizophrenia requires two or more of the following symptoms be-ing apparent for a one-month period:

Criterion A)

Positive symptoms: are symptoms that occur in excess of normal functions such as:

-Delusions Bizarre beliefs that are not real, para-noid, fearful of persecution, inflated beliefs about the persons power and importance.

-Experiences of Control- Belief they are under the control of an external force; god or aliens, spirits that have invaded their mind.

-Hallucinations- Bizarre unreal perceptions of the environment; Hearing voices, seeing things that are not there, even smelling things.

-Disordered thinking Feeling of thoughts being inserted or withdrawn from ones mind. Other cases a person may think their thoughts are being broad-cast to others. Incoherent or loose speech.

Negative Symptoms: are those that appear to re-flect a diminution or loss of normal functions - these include:

-Aective flattening: Reduced range and intensity in expressing emotions such as facial expressions, tone of voice, eye contact and body language.

-Alogia: Speech is not fluent or productive with sparse replies or there is a lack of speech. Re-sponses may be slurred too or trail o into a whis-per. This is believed to show blocked or slowed down thought processes.

-Avolition: Literally translates to poverty of will - A lack of drive or motivation to pursue meaningful goals or socialize is apparent. The person may sit still for long periods of time - This may sometimes be confused with disinterest.

In addition to this one of the symptoms must be delusions, hallucinations or disorganised speech with continuous disturbance persisting for 6

months which includes at least one month of symp-toms.

Additionally subtypes are no longer identified as clinicians found patients symptoms changed from one subtype to another and overlapped which blurred the distinctions among the 5 subtypes, de-creasing their validity.

Criterion B) - Social/Occupational dysfunction: For a significant portion of time one or more major areas of functioning such as work, relationships or self-care or markedly lower than the level prior to onset.

Criterion C) Duration: Continuous signs of the dis-turbance persist for at least a 6 month period.

Criterion D) Exclusion of mood disorders with no major episodes of depression or elation have oc-curred concurrently with the psychotic symptoms

Criterion E) Exclusion of known organic causes: the disturbance is not due to the direct eects of drugs or a brain disorder

9

Issues with the Classification of Schizophrenia Including Reliability & Validity

WMR-BSRC

Whaley-Mojtabi-Rosanhan/ Bentall-Schneider-Ross-Copeland

Reliability is the extent to which psychiatrists can agree on the same diagnoses when inde-pendently assessing patients.

In parts of the world the DSM diagnostic tool is used while other parts may use the ICD tool to diagnose Schizophrenia.

Issues with reliability first arise as both these tools have dierent diagnostic criterias; for example the DSM 4 tool previously recog-nised 5 sub-types of Schizophrenia while the ICD tool recognised 7 subtypes. Although now updated, this means diagnosis was not consistent between dierent parts of the world dependent on the tool being used - this means one country may have diagnosed someone as normal while another place with the same symptoms may see them as Schizo-phrenic. Therefore there is a clear cultural bias dependent on which identification tool is being used and where the individual is in the world highlighting how inconsistent diagnosis actually is.

This raises clear issues of validity highlighting how Schizophrenia is evidently not under-stood well enough to diagnose accurately.

This has huge consequences for those diag-nosed as this can lead to them being stigma-tised and mistreated raising ethical con-cerns.

A person can also only ever be classed as a Schizophrenic in remission and not cured meaning such a label may stay with them af-fecting other areas of life (Employment, so-cial interaction with people and how they are perceived) raising further ethical issues.

There is also no physical cause that can be conclusively measured for Schizophrenia and a great deal of emphasis is placed on the pa-tients ability to report the symptoms which may not always be accurately described (pos-sibly due to schizophrenia) further hindering reliability of diagnosis.

Relying on patients reporting symptoms there-fore makes objective diagnosis dicult.

Also interpretation of symptoms is subjective and down to the person doing the diagnosis so a great deal of importance is placed on the individuals ability in diagnosis which may vary between health professionals. Therefore skill, experience and knowledge further aect reliability and diagnosis.

Whaley et al demonstrated this and found Inter-rater reliability between health profes-

10

sionals as low as 0.11. in diagnosis. This means when independently assessing pa-tients, the diagnosis was rarely consistent between them meaning the DSM tool ap-pears to be unreliable in accurately and consistently diagnosing Schizophrenia.

Also the diagnostic criteria in DSM states only one symptom is required if delusions are bizarre however even this is dicult to consistently agree on as Mojtabi found; When 50 senior psychiatrists in the US were asked to dierentiate between bi-zarre and non-bizarre delusions, they produced inter-rater reliability correlations of only 0.40 suggesting even this diagnos-tic requirement lacks sucient reliability to distinguish between schizophrenic and non-schizophrenic symptoms. Therefore attempting to use bizarre as a means to diagnose schizophrenia is reductionist and simply an attempt to overs-simplify something we do not fully understand.

Rosanhans famous study highlighted the unreliability of diagnosis for Schizophrenia further. Normal people presented them-selves to psychiatric hospitals in the US claiming to hear voices. They were all diag-nosed as having Schizophrenia and admit-ted. Throughout their stay none of the hos-pital sta recognized they were actually normal highlighting the unreliability of diag-

nosis for Schizophrenia raising serious ethi-cal issues.

In a follow up study Rosanhan called hos-pitals informing them he would be sending in fake patients however none were really sent. This resulted in an apparent 21% detection rate.

This further highlights how diagnosis meth-ods are unreliable meaning current under-standing of Schizophrenia is insucient and lacking validity.

Reliability and Validity are linked together and if health practitioners cannot conclu-sively agree who has Schizophrenia, this raises the question of what it actually is (Va-lidity) and whether our understanding of it is sucient.

Bentall et al conducted a comprehensive review of research into the symptoms, causes and outcomes of Schizophrenia and concluded that Schizophrenia was not a useful scientific category.

Schneider developed the First Rank symp-toms that he believed distinguished Schizo-phrenia from other disorders e.g. delusions of being controlled, the belief that thoughts are being broadcast, hearing hallucinatory voices.

11

The belief was that the existence of these first rank systems would make diagnosis more reliable and thus more valid.

However issues with validity arise as such symptoms overlap with other disorders such as depression and bipolar disorder. Ellason & Ross point out that people with dissociative Identity disorder (DID) actually have more Schizophrenic symptoms than people diagnosed with it.

This raises issues of Comorbidity as symp-toms may appear to fit in with Schizophre-nia however may be due to a combination of other illnesses that resemble it making diagnosis unreliable and treatment dicult.

If we do not accurately know what Schizo-phrenia is we cannot suciently treat it.

In the same way people diagnosed with Schizophrenia rarely share the same symp-toms, likewise there is no evidence to sug-gest they share the same outcomes.

Research suggests that the outcomes for patients diagnosed with Schizophrenia var-ies with only 20% recovering their previous level of functioning, 10% achieving signifi-cant and lasting improvement and 30% showing some improvement with intermit-tent relapses.

A diagnosis of Schizophrenia therefore has little Predictive validity as some people never appear to recover from the disorder while others may do. We cannot fully un-derstand why this is and this highlights ex-actly how reductionist our tools in identifi-cation are as we clearly do not understand the disorder or why it varies from one indi-vidual to another.

Further issues arise as we are still unclear as to what causes the disorder and various explanations exist meaning classification; diagnosis and even treatment all become dicult. Explanations vary from biological to psychological and without knowing what causes it; it is dicult to fully classify what we are dealing with and treating it.

Copeland et al highlighted cultural dier-ences in diagnosis and how this varies greatly between countries. Giving a de-scription of a patient to US psychiatrists and British Psychiatrists; 69% of those from the US diagnoses the patient with Schizophrenia while only 2% of british psy-chiatrists did.

Therefore dierences exist in what people expect symptoms to look like and this cre-ates highlights further issues in diagnosis and cultural bias as behaviour in one country may be seen as relatively normal

12

within the context of that culture but possi-bly a symptom of schizophrenia in another country/culture.

Next we move onto Biological Explana-tions for Schizophrenia..

13

Biological Explanations Of SchizophreniaThe Dopamine Hypothesis - DIJH

The Dopamine Hypothesis

DIJH

Davis-Iverson-Javitt-Healy

Dopamine is one of the many dierent neu-rotransmitters that operate in the brain.

The Dopamine Hypothesis states that mes-sages from neurons that transmit dopa-mine fire too easily or too often leading to the characteristic symptoms of schizophre-nia.

Schizophrenics are thought to have abnor-mally high levels of D2 receptors on receiv-ing neurons resulting in more dopamine binding and thus more neurons firing.

Dopamine plays a key role in guiding atten-tion so disturbances in this process may well lead to the problems related to atten-tion, perception and thought found in peo-ple with Schizophrenia.

The key role of Dopamine was highlighted by 3 sources of evidence: AAP

Amphetamines Amphetamine drugs are dopamine agonists and increase levels of dopamine in the synapses. Large amounts of Amphetamines can cause the characteristic symptoms of Schizophrenia such as Hallucinations and delusions.

Anti-Psychotic Drugs Although there are many dierent types of antipsy-chotic drugs; they all have one thing in common they look to block dopamine ac-tivity in the brain.

By doing this, Antipsychotics have been found to eliminate symptoms such as Hal-lucinations & delusions.

Parkinsons Disease Low levels of Dopamine are found in those suering from Parkinsons disease. Drugs taken to increase this resulted in such individuals developing Schizophrenic symptoms high-lighting a link between excess dopamine and Schizophrenia.

Davis updated the original theory arguing it to be too reductionist and simplistic be-cause high levels of dopamine were not found in all schizophrenics and modern

14

anti-psychotic drugs such as Clozapine work eectively against the disorder yet have very little dopamine blocking activity.

New theories suggest high levels of dopa-mine in the Mesolimbic dopamine system are associated with positive symptoms of schizophrenia while high amounts in the Mesocortical system are associated with negative symptoms.

Other research has focused on the neuro-transmitter Glutamate as reduced function of the NMDA Glutamate receptor is found in Schizophrenics. Glutamate release is in-hibited by Dopamine receptors and it may be the two are involved and not necessar-ily Dopamine alone.

Iverson reported post-mortems on Schizo-phrenics found excess levels of Dopamine in the limbic systems suggesting Dopa-mine to be involved in the disorder. How-ever dierences in biochemistry of Schizo-phrenics could just as easily be an eect rather than a cause of Schizophrenia there-fore conclusions cannot be drawn from causal relationships.

Javitt found that Glycine, a glutamate ago-nist reversed the symptoms of Schizophre-nia is rats supporting the Glutamate theory and its involvement with Schizophrenia

suggesting Dopamine alone is not in-volved.

However studies with animals cannot be generalised to humans due to the huge dif-ference in anatomy.

Healy argued pharmaceutical companies were keen to see the Dopamine Theory promoted as it allowed them to make huge profits from manufacturing antipsychotic drugs that inhibit Dopamine for profit.

Second generation Atypical drugs look to reduce serotonin as well as Dopamine and such drugs have been found to be better in treating Schizophrenia compared to typi-cal varieties suggesting dopamine alone is not the sole cause and other neurotransmit-ters and factors also need to be included.

A major problem for the dopamine hypothe-sis is that drugs used to actually reduce do-pamine levels can actually increase them as the body attempts to compensate for the sudden deficiency.

Research in to post-mortems of schizo-phrenics has shown that those with ele-vated levels had taken antipsychotics just prior to death.

15

Those with normal dopamine levels had not taken any medication and this goes against the Dopamine hypothesis.

Drugs designed to reduce dopamine levels work eectively after a few hours yet it takes many weeks for patients to have fewer schizophrenic symptoms.

This suggests although dopamine may be involved; it may only be one of the many links in the chain that causes the disorder.

Neuroimaging and PET scans have al-lowed researchers to investigate dopamine activity more accurately than previous methods. However as of yet no link has been found to suggest excess dopamine activity in the brain occurred with Schizo-phrenics.

The following evaluation point below can be used in both biological explana-tions:

An evolutionary approach may fit better in explaining Schizophrenia supporting bio-logical explanations. The disorder has been found even in the most remote of tribes and Price et al suggested this could be explained through evolutionary explana-tions. They proposed the schizophrenic personality could have acted to help split tribal communities when they reached a

large size to deal with less resources. The disorder creates charismatic individuals which would then facilitate the splitting of groups. This would have been through the schizoid traits such as bizarre beliefs, hallu-cinations and delusions of ones own impor-tance helping influence unhappy group members to leave their group. However with evolutionary explanations we cannot prove or disprove this scientifically which undermines this biological explanation.

16

Biological Explanations: GeneticsEvidence for genetics playing a role in schizophrenia comes from family studies, twin studies as well as adoption studies.

With family studies researchers look to identify whether biological relatives are more likely to be aected by Schizophre-nia than non-relatives. As relatives share a higher proportion of similar genes, if schizo-phrenia had a genetic basis it would be more apparent in closely related family members and research findings have sug-gested this to be case. Those more closely related to suerers have been shown to be more at risk themselves suggesting a ge-netic basis. Kendler et al found first de-gree relatives were 18 times more likely to be at risk than the general population. This lends support to the theory that genetics may be involved in schizophrenias onset.

With twin studies identical twins who share 100% of their genes are compared to non-identical twins who share only 50%. Both sets of twins would share simi-lar environments allowing for the role of nurture to hopefully be discounted. Higher concordance rates among identical twins for Schizophrenia would suggest a genetic contribution. Research findings have supported such findings with identi-cal twins more likely to develop schizophre-

nia than non-identical. Joseph et al found that when comparing identical twin stud-ies, they had a concordance rate of 40% while non-identical twins had 7.4%. This higher concordance rate would present a strong argument for genetic factors.

In adoption studies, adopted children with biological parents suering from schizophrenia are compared to a control group of adoptees with non-schizophrenic parents. The aim here is to help separate the role of nature (genes) and nurture (the environment) in Schizophrenias develop-ment when those related are reared apart. Tienari et al found that out of 164 adopted children whose mothers had been diagnosed with schizophrenia, 6.7% of chil-dren also shared this diagnosis compared to only 2% out of 197 children with non-schizophrenic mothers. This supported the role of genes influencing the onset of schizophrenia.

One major flaw for twin studies is the as-sumption that the environment shared be-tween identical and non-identical twins are the same. Joseph et al highlighted how identical twins are more inclined to be treated similarly and be seen as one per-son therefore sharing the exact same envi-ronment. This could also be used to ex-

17

plain the higher concordance rates as be-ing due to environmental factors (nur-ture) rather than necessarily genes alone (nature). Also the fact that even though identical twins share 100% of the genes, concordance rates remain at 40% and not 100% suggesting the environment still plays a huge mitigating role in schizophre-nias onset. It may be that the diathesis-stress model applies here with both na-ture (genes) and nurture (the environment) interact and with the right amount of envi-ronmental triggers and stressors, a genetic vulnerability for schizophrenia may be acti-vated.

Also non-identical twins are more likely to be treated as individuals and two separate people due to dierent appearances and therefore the lower concordance rates be-tween them may be explained due to dier-ences in the environmental influence (nurture) rather than necessarily genes and nature. This may also be used as an explanation for why non-identical twins who share 50% of their genes have much lower concordance rates highlighting a strong case for the environment.

With adoption studies it may well be that adopting parents are influenced by selec-tion bias. Such studies assume the selec-tion of children is equal between parents

who choose to adopt children with schizo-phrenic parents and those without. This may not be the case as in countries such as the US and Denmark, potential adopt-ing parents are told of any disorders suf-fered by the biological parents such as schizophrenia. This may in turn influence their decision to adopt children skewing the results.

Wahlberg et al re-examined the same data from Tienari et als adoption studies finding only children who are reared in fami-lies with poor communication were at in-creased risk of developing schizophrenia highlighting possible methodological problems into heredity studies. This raises some issues; firstly the fact that Schizo-phrenia is still not fully understood may mean that it is being incorrectly identified with children who simply have poor com-munication skills. This could be due to en-vironmental factors (social learning) af-fecting this ability. There is clear issues of validity and reliability when were attempt-ing to explain this due to genetics when in truth it may simply be that researchers are mistakenly interpreting poor communica-tion skills as part of Schizophrenic symp-toms. Also the fact that the diagnostic crite-ria is continually updated and changed means research where studies have sup-

18

ported a genetic basis such as Tienari et als may become invalidated as our under-standing of the disorder increases. This possibility is supported by Kety et als study which found no cases of full schizo-phrenia among first degree relatives of adopted children identified with a schizo-phrenia spectrum disorder. Most studies finding schizophrenia being apparent in adopted children and their biological par-ents would not have done so without broadening the definition to include non-psychotic schizophrenic spectrum disor-ders. This suggests methodical issues in such studies undermining the genetic ba-sis for Schizophrenia.

With family studies the higher rate of Schizophrenia among those more closely related could also be explained due to psy-chological factors such similar learning en-vironments resulting in similar behaviour which may in turn be interpreted as schizo-phrenic symptoms. Therefore such expla-nations proposing genetics as the cause is open to crticism.

Using genes to explain Schizophrenia is re-ductionist as clearly genes are not the only factor influencing its onset. This is highlighted by the fact that even identical twins have less than 50% concordance rates. Therefore the onset of schizophrenia

is far more complex than simply due to ge-netics and attempting to oversimplify it through biology would limit our progress in attempting to identify the true causes be-hind it such as environmental triggers.

Such theories are also deterministic in as-suming biological pre-disposition could lead to schizophrenias onset when this is clearly not the case. If identical twins with the exact same genetic makeup can dier in being diagnosed with schizophrenia even biology cannot fully determine the dis-orders onset and it is deterministic to as-sume

Supporting evidence for schizophrenia be-ing caused by genetics comes from brain-scans of suerers. Torrey et al found that schizophrenics have ventricles in the brain that are 15% larger than non-schizophrenics. Bornstein et al found those with larger ventricles displayed nega-tive symptoms of schizophrenia and en-larged ventricals may be linked to poor brain development. This may in cause schizophrenia with poor brain develop-ment being due to genetics supporting this explanation. However it could well be that enlarged ventricles are the result of suer-ers having schizophrenia rather than the cause themselves. Therefore we cannot be

19

certain of cause and eect with such find-ings.

The following evaluation point below can be used in both biological explana-tions (Dopamine & Genetics)

An evolutionary approach may fit better in explaining Schizophrenia supporting bio-logical explanations. The disorder has been found even in the most remote of tribes and Price et al suggested this could be explained through evolutionary explana-tions. They proposed the schizophrenic personality could have acted to help split tribal communities when they reached a large size to deal with less resources. The disorder creates charismatic individuals which would then facilitate the splitting of groups. This would have been through the schizoid traits such as bizarre beliefs, hallu-cinations and delusions of ones own impor-tance helping influence unhappy group members to leave their group. However with evolutionary explanations we cannot prove or disprove this scientifically which undermines this biological explanation.

20

Psychological Explanations Of SchizophreniaThe Behaviourist Explanation..

The Behaviourist Explanation

SUTLAMK

Sche-Ullman-Tarrier-Liberman-Azrin-Meehl-Kazdin

One psychological explanation of Schizo-phrenia is the behaviorist explanation which does not see Schizophrenia as a mental disorder with a physical cause but rather as a learned condition through clas-sical conditioning, operant conditioning or from the principles of social learning the-ory and learnt behaviour.

Operant conditioning may be involved with people being reinforced (rewarded) for ab-normal behaviour and thus learning bizarre

behaviors. Additionally bizarre behaviour may be rewarded due to the attention it brings with an increase in such behaviour eventually leading to psychosis.

Alternatively, retreating to an inner world may be rewarding as an escape from real-world pressures, leading to such people being labelled as Schizophrenic and then behaving so as to meet the requirements of the label.

There is some Correlational support for such with studies finding those most likely to be diagnosed with Schizophrenia come mostly from working class backgrounds where pressures are likely to be the high-est. However with correlational data we

21

I chose to do something which many people would find actually quite odd. I chose to go with the behaviorist explanation for Schizophrenia as opposed to other more popular psy-chological explanations.The reason for this was it is still in the specification as an acceptable explanation however it is heavily overlooked as most people accept that it carries little weight as an explanation itself - quite frankly its poor.This was actually the reason why I chose it - with it being such a poor explanation it leaves it very open to being torn apart in the evaluation section.The theory of it is something were also very familiar with involving conditioning which is something we have already extensively learnt about from AS level hence its something thats familiar and easy to understand the dissect.........

cannot be sure of cause and eect and other factors may be contributing.

People doing the diagnosing tend to be of a higher social class themselves and bias is possible where cultural dierences in be-haviour mistaken for symptoms of schizo-phrenia.

Behaviourist approaches to Schizophrenia explain the tendency of Schizophrenia run-ning in families in social learning terms, as being merely a result of observing and imi-tating aected family members.

Once diagnosed such a theory proposes that Schizophrenic behaviour is then unin-tentionally reinforced through the special attention paid by those around them which explains how the behaviour may then be maintained.

Sche reported that people behaving bizarrely come to be aware of their label of Schizophrenic and then fulfill this by play-ing the role of the mentally ill person, per-haps inadvertently at first but later voluntar-ily.

Therefore a group of actually short-lasting symptoms come to be stabilised through self-consciousness and rearmation by others, as a career of mental illness.

Ullman and Krasner reported that sta in hospitals reinforced Schizophrenic behav-iour in their patients by paying more atten-tion to those who displayed characteristics of the disorder supporting Sches theory. The patients saw that if they disobeyed and played up, the sta would give greater attention and the behaviour becomes rein-forced through operant conditioning this way as the reward for such behaviour was greater attention.

However this could also be a way for genu-inely ill patients with an actual physical dis-order to gain more support from hospital sta due to this underlying cause.

Tarrier et al found that suerers randomly assigned to behavioural intervention treat-ments had lower relapse rates than those receiving more regular treatments suggest-ing a behavioural component to the onset of the disorder played a role.

Liberman reported that children may learn to be Schizophrenic by being reinforced for bizarre responses to inappropriate stim-uli and such reinforcements lead to even more bizarre behaviour and eventually psy-chosis. This attempts to explain how very bizarre behaviour may form through a vi-cious circle of reinforcement with strange behaviour increasing for greater attention.

22

Another way of assessing the validity of the behaviourist approach is looking at how eective treatments are for the disor-der; for Behaviourist approaches the treat-ments involve token economies which are under the assumption that behaviour that is learnt through reinforcement can be un-learnt in the same way through reinforcing desirable behaviour instead.

In token economies rewards or tokens are given that can be exchanged for de-sired goods every time patients display de-sired behaviour.

Azrin et al found token economies worked well in increasing desirable behaviour while reducing undesirable behaviour.

The desired behaviour was at its highest when reinforcements for it were highest and lowest when reinforcement was low-est.

This suggests that there is a behavioural element in the maintenance of the schizo-phrenic behaviour and some validity in the explanation.

However this behaviourist element may be better suited in explaining the maintenance rather than the formation of the disorder.

Meehl et al dismissed the behaviourist ex-planation citing extreme behaviour pa-tients have gone to with self-injury and irra-tional behaviour citing one example who kept his finger up his own back passage to stop thoughts escaping stating such behaviour is too extreme to be simply brought about simply by being labelled a schizophrenic or the reward of attention.

Kazdin et al also argued that treatments based on the behavioural explanation merely masked the problem and did not deal with the actual cause of the behaviour as when token economies were removed from patients, the undesired behaviour re-turned which suggests the validity of the behavioural explanation is flawed and other elements must be at work beyond the behaviour being simply learnt.

The behaviour explanation cannot also ex-plain why suerers display such similar be-haviours and symptoms without ever hav-ing experienced such behaviour before or witnessing it and having no opportunity to learn it or why the behaviour tends to oc-cur in late adolescence or early adulthood.

The biological approach has also shown links in respect to genetic causes through higher concordance rates between closely related family members and also identical

23

twins in comparison to control groups again suggesting the behavioral approach is flawed and lacks credibility when com-pared to other biological explanations which have greater evidence.

The Success of anti-psychotic drugs that lower dopamine levels also highlights how such behaviour may not simply be down to learning but biological factors. If it was learning, one might argue people would simply continue to behave the same rather than choose to be normal after having taken the drugs.

A Diathesis-Stress Relationship may exist between biological and Psychological causes; some may be more genetically pre-disposed to develop the disorder if cer-tain psychological stressors trigger its on-set and its possible both psychological and biological elements play a role.

The behaviourist explanation could be ar-gued to be reductionist as it portrays peo-ple as simply Stimulus response ma-chines with little ability for conscience thought to control or manage their symp-toms.

The explanation could also be argued to be Deterministic as it ignores the role of free will people have in controlling their own behaviour.

24

Psychological Explanations:Cognitive Explanations

Cognitive explanations may not necessar-ily rule out genetic or biological causes however see faulty thoughts as the cause for schizophrenic symptoms such as disor-dered thoughts and hallucinations rather than a symptom.

One explanation suggests the role of atten-tion being involved with schizophrenics struggling to focus or filter out irrelevant in-formation from the senses resulting in them becoming overwhelmed with sensory information they cannot interpret. This would then cause them to experience a world very dierent to normal people. Sup-port for this comes from laboratory stud-ies which have shown people with schizo-phrenia struggle with tasks that require them to pay attention to some stimuli while ignoring others.

Helmsley proposed a breakdown between stored memories and new incoming infor-mation occurring. Stored information is used to create schemas allowing people to interpret the world and situations how-ever schizophrenics may not have these schemas activated. This may be due to a breakdown in cognitive processes which

then causes an overload of sensory infor-mation as schizophrenics struggle to iden-tify what to attend to or ignore. The result is delusional thoughts which are then inter-preted as originating externally rather than from memory.

Another explanation proposed by Frith sees schizophrenia arising due to prob-lems with information processing and meta-representation. This is the ability to reflect on thoughts, experience as well as central control which is the ability to sus-pend automated responses and act on conscious intent. Positive symptoms such as delusions are believed to be linked with problems in meta-representation and an inability to distinguish internal thoughts and external speech. Negative symptoms such as disorganised thinking are thought to be linked to problems in central control and an inability to distin-guish between behaviour due to conscious intent or automatic response.

Problems with attention which have been identified in lab studies could be argued to be symptoms rather than a cause of schizophrenia and we cannot infer cause

25

This essay is ideally used alongside another in a question that asks for explanations (requiring 2). If your asked to outline one or one or more stick to the behaviorist expla-nation as it is more extensive and easier to grasp and recall.

and eect due to this. It may be that a con-founding variable such as a biological cause is causing these psychological prob-lems. For example enlarged ventricles have been associated with negative symp-toms and these would then lend support for genetic explanations and undermine the cognitive explanation.

Schizophrenia is still not fully understood and Garety et al argued that it is best un-derstood by combining dierent explana-tions such as the psychological with the biological. The cognitive explanation may be the link between the two chains high-lighting the role of nature (biology) and nur-ture (cognitive processes).

Kane et al argued that including cognitive impairment within the diagnosis criteria for schizophrenia would help improve the cur-rently poor reliability in diagnosis of the dis-order. This could then help in creating more targeted treatment through cognitive enhancement being the primary goal.

Frith conducted a study giving schizo-phrenics and non-schizophrenics a task in-volving two choices. They were tasked with predicting the next playing card in a deck with either a red or black response. Schizophrenics tended to produce predict-able patterns of responses such as RRRR

or RBRBRB. Non-schizophrenics pro-duced more random responses and this suggested suerers tended to struggle in generating responses with spontaneous ac-tions. This supports Friths theory that negative symptoms may be caused by a lack of central control.

Although Friths theory has provided a comprehensive framework that explains many of the symptoms of schizophrenia, the research is far from conclusive. Critics argue his theory continues to be purely speculative until proven and the theory is seen as reductionist as it discounts the role of nurture and the environment play-ing a role in schizophrenias development.

Becker et al reported support for Helmsleys theory through studying neu-ronal circuits within the limbic system within schizophrenics. They were seen to struggle to integrate moment-to-moment sensory input with stored memories sup-porting Helmsleys cognitive explanation. The distress that then resulted would lead to increased dopamine production which then further influenced the functioning of these brain areas. This suggests a link be-tween cognitive as well as biological fac-tors and a combined approach is evidently more suited to understanding schizophre-nia.

26

Biological Treatments For SchizophreniaAnti-Psychotic Drugs

Biological Treatments for Schizophrenia

Anti-Psychotic drugs

DVHR-L JL

Davis-Vaughn-Hill-Ross / Leucht-Jeste-Liberman

The prime treatment for Schizophrenia is the use of anti-psychotic drugs; the first anti-psychotic was Chlorpromazine which was introduced in the 1950s and very quickly had a major eect by enabling many schizophrenics to live normal lives outside of mental institutions.

Conventional anti-psychotic drugs such as Chlorpromazine are dopamine antagonists and work by arresting dopamine produc-tion through blocking the D2 receptors in synapses that absorb dopamine and thus reducing the positive symptoms of the dis-order.

Chlorpromazine does not cure the patient of schizophrenia but instead dampens the positive symptoms such as hallucinations and thought disturbances down to a level

where a regular degree of functioning be-comes possible.

Antipsychotics can be taken in tablet form, syrup or injection and can be divided into first generation (typical) and second gen-eration (atypical) varieties.

Atypical anti-psychotics introduced in the 1990s such as Clozapine work by acting upon serotonin as well as dopamine pro-duction systems and aect negative symp-toms of the disorder such as reduced emo-tional expression. Although atypical drugs are perceived as having fewer side-eects, it is not always known specifically how they aect the brain to alleviate symptoms.

Some suerers only have to take a course of anti-psychotics once, while others have to take regular doses in order to prevent schizophrenic symptoms reappearing. There is also a sizeable minority of people who do not respond to drug treatment at all.

Davis et al performed a meta-analysis of over 100 studies that compared antipsy-chotics with placebos finding drugs to be more eective, with over 70% of suerers

27

NOTE: When evaluating treatments you al-ways answer it based on how appropriate-ness and eectiveness.

treated with antipsychotics improving in condition after 6 weeks while fewer than 25% percent improved with placebos, sug-gesting antipsychotics have a beneficial ef-fect.

However one of the studies in Davis et als review was by Vaughn and Le, who found that antipsychotic medication did make a significant dierence but only for those living with hostility and criticism in their home environment. In such condi-tions, the relapse rate for those on medica-tion was 53% but for those in the placebo condition the relapse rate was 92%.

For individuals living in more supportive en-vironments however there was no signifi-cant dierence between those on medica-tion and placebos (12% relapse and 15% relapse).

This shows that the environment people are surrounded by is very important and high amounts of hostility and criticism ap-pears to be linked with higher relapse rates and environmental factors need to also be considered when deciding on the appropri-ateness of drug therapies.

Supportive home environments yielded the best results regardless of being on medication or placebos which suggest drug therapies are most eective when cer-

tain environmental conditions are not al-ways ideally suited.

Hill et al highlighted another concern for conventional anti-psychotics; the side-eects, one of which is Tardive dyskinesia which results in uncontrollable movements of the lips, face, hands and feet. About 30% of people taking antipsychotic drugs develop Tardive Dyskinesia and it is irre-versible in 75% of cases therefore this needs to be considered when considering the appropriateness of drug therapies.

Therefore ethical concerns arise and in one particular case in the US; a Tardive Dyskinesia suerer sued on the grounds of inhumane treatment due to the side-eects of the drugs. Some argue a cost/benefit analysis of conventional drugs would likely result in more negatives.

Ross & Read also argue that being pre-scribed medication reinforces the view that there is something wrong with you with patients.

This, they argue prevents the individual from thinking about possible stressors that might be a trigger for their condition in turn reducing their motivation to look for possi-ble other solutions beyond drug therapies that might alleviate stressors and suering.

28

-Reductionist - as patients are reinforced to believe that they have less control over their disorder when in fact CBT treatments have been found to help hugely in daily functioning.

The introduction of the new atypical anti-psychotics raised expectations for the out-comes possible with medication.

A meta-analysis of studies by Leucht et al revealed however that the superiority of atypical drugs over conventional anti-psychotics was only marginal and only slightly more eective.

The claim the atypical antipsychotics are more eective in dealing with negative symptoms of Schizophrenia was also found to only be slightly more eective in Leuchts study.

One of the main claims of atypical drugs was that side eects such as Tardive Dyski-nesia was less likely.

This claim was supported by a study by JESTE et al which found people on con-ventional anti-psychotics had rates of 30% for Tardive Dyskinesia after 9 months while those on atypical antipsychotics had only 5%.

Therefore Atypical anti-psychotics may be more appropriate in the treatment of schizophrenia because of the fewer risks of side eects which means patients are more likely to continue their medications and therefore see more benefits.

Liberman also conducted a study compar-ing conventional anti-psychotic use and atypical anti-psychotics and found from a study of over 1400 people; 74% discontin-ued their treatments due to the side eects from both drugs however for dierent rea-sons.

First generation drugs were given up due to muscular disorders while atypical sec-ond generation drugs given up due to weight gain and metabolic eects.

This suggests if atypical drugs are to be prescribed more due to lower side-eects; other aspects of life would also need to be recommended to be changed such as di-ets and levels of exercise to better manage the side eects to allow patients to con-tinue treatment increasing the benefits of use.

The benefit of anti-psychotics in the treat-ment of Schizophrenia is that they are rela-tively cheap to produce and easy to admin-ister. They have found to have hugely bene-ficial eects on suerers allowing many to

29

live normal lives outside of mental institu-tions. In the UK, through the use of drugs less than 3% of people live in hospitals on a permanent basis when previously this was much higher for those with Schizo-phrenia.

There is also recent evidence however that even second generation atypical drugs in-cur serious other side-eects such as the reduction in white blood cells which can lead to infection and even death.

Due to this blood tests are required regu-larly for white blood cell count and this is another reason why atypical drugs tend to be prescribed after conventional drugs are tried first due to the high risks of infection or illness.

Biological treatments can also be consid-ered deterministic in assuming Schizophre-nia is caused completely due to a biologi-cal cause. In truth research suggests psy-chological factors and environmental fac-tors also play a role in its onset and mainte-nance and simply taking a pill to deal with it is also reductionist as it provides a simple way of managing the symptoms but ignores other stressors that contribute.

30

Biological Treatment For Schizophrenia: ECT

An early biological treatment for schizo-phrenia was electroconvulsive therapy (ECT). ECT was first used by Cerletti un-der the false assumption that inducing an epileptic fit would remove the disorder as researchers believed epilepsy and schizo-phrenia could not co-exist. Although proven not to be the case it has proven to be more eective than placebos in some studies although not as eective as drug treatments.

With ECT electrodes are placed on the scalp with one on the non-dominant side of the brain above the temple and another in the middle of the forehead. The patient is also injected with a barbiturate to ensure they are unconscious and a nerve blocking agent to paralyze the muscles to prevent contraction and possible fractures during the treatment. An electric current is then passed between the electrodes in small bursts to induce a seizure. Seizures can last up to one minute aecting the whole brain and a course of ECT consists of two to three treatments a week for up to 12 treatments. ECT is generally used when other treatments have failed however to

this day it is not fully understood how ECT aects schizophrenia or the brain to pro-duce results.

Tharyan et al reviewed 26 studies involv-ing treating schizophrenia with ECT. The conclusion drawn was it appeared to be ef-fective in the short-term and also better than having no treatment however anti-psychotic drugs were more eective and therefore more appropriate. It may there-fore be that ECT is most appropriate in pa-tients which are not responsive to alterna-tives such as anti-psychotic drug medica-tion and as a last resort. This assumption and ECTs use is further supported by Tang et al who found ECT to be eective in treating schizophrenics who did not re-spond to antipsychotic medication sug-gesting it may be appropriate as a last re-sort and eective in providing some relief to patients. Further research by Tharyan has found that ECT was eective when combined with drug medications such as antipsychotics. This suggests ECT alone may provide limited results but when com-bined with other treatments it may be more

31

This essay is ideally used alongside another in a question that asks for explanations (requiring 2). If your asked to outline one or one or more use the essay on anti-psychotic drugs as it is more ex-tensive.

eective in producing a more rapid reduc-tion in schizophrenic symptoms.

Fisk oered a possible explanation for why ECT may be eective in some cases but not others. Reviewing clinical literature he concluded that ECTs success rate varied from 60-80% but it was only this eective when treating certain categories of schizo-phrenia. As schizophrenia is not fully under-stood and has many subsets; it is possible ECT is more appropriate and eective when targeting specific forms of schizo-phrenia.

A major criticism of ECT as a treatment is the therapy is still not fully understood and why it works for some but not others. With-out knowing how it aects patients it poses a huge risk especially since the treat-ment may be causing damage which we are not even of aware of yet.

In the short-term it can also cause distress for patients as they suer confusion, mem-ory loss, brain damage and even death. In 1% of cases cumulative severe memory loss may also occur which increases with more treatments raising ethical concerns as to its appropriateness.

However others argue it is no more danger-ous than minor surgery with a death rate of 1 in 10000 approximately and the poten-

tial benefits such as recovery from a debili-tating disorder such as schizophrenia is worth the risk.

The use of ECT as a treatment is reduc-tionist as were attempting to treat a disor-der through an oversimplified method such as running a current through someones brain, a procedure we do not fully under-stand the complexities of. It may well be that the treatment is likely to lead to longer term side aects that we do not fully under-stand possibly due to schizophrenic symp-toms masking these in some patients. It may well also make the disorder worse for those whom it doesn't work for over the longterm. Therefore this raises serious ethi-cal issues as to whether we should be car-rying out treatments that may actually cause more harm for the patient. Also those suering from Schizophrenia are un-likely to be able to give informed consent in some cases due to their disorder it raises ethical issues whether health profes-sionals should be allowed to suggest such a treatment when this is the case.

32

Psychological Treatments For SchizophreniaBehavioural Therapy (Token Economies)

Token Economies

Aylon-Kazdin-Sultana-Ost-Upper-Baddeley

AKSOUB

One psychological treatment for Schizo-phrenia is behaviour modification therapies which assume Schizophrenia is acquired through learning processes, either through classical or operant conditioning, and can be eradicated and replaced with adaptive behaviours in the same way.

One example of a behaviour modification therapy is the use of Token Economies which is a technique in which a change in behaviour is achieved by means of tokens awarded for displaying desired behaviours (operant conditioning) thus reinforcing the desired behaviour.

These reinforces are provided immediately after the desired behaviour which can then

be exchanged later for goods or privileges by patients.

The technique has been used especially with long-term institutional patients to pre-pare them for transfer into the community.

The technique has proven successful in changing negative symptoms of schizo-phrenia like poor motivation, poor attention and social withdrawal. This has also the benefit of nursing sta also viewing pa-tients more positively.

Additionally the undesirable behaviour can also be removed by removing any reinforc-ers that maintain it and restructuring the en-vironment so the undesirable behaviour is no longer reinforced allowing token econo-mies to reinforce desired behaviours.

This treatment assumes the behaviour can then be carried on and maintained once learnt more permanently.

The approach has its roots in a study re-ported by Ayllon et al. They were asked to

33

Again here I have chosen a therapy thats under-used and ignored but is acceptable in the specification; Token Economies.The reason for this is the same as before; its so ridiculous that its easy to remember (Conditioning) and easy to tear apart as a therapy.

visit a hospital where sta were finding it dicult to get withdrawn Schizophrenic pa-tients to eat regularly and noticed sta had to coax patients into eating.

They believed the special attention paid to such resistant patients was reinforcing their behaviour (the reward/reinforcement was the special attention) and decided to change hospital rules.

For example if patients did not arrive on time for dinner they would be locked out and also to gain entry they would need to pay one penny. Sta were no longer al-lowed to interact with patients either thus removing any chance of them gaining at-tention and reinforcement for the behav-iour.

To earn the pennies for entry they would need to display desired behaviours.

They found this to be a huge success re-sulting in patients displaying more desired and functional behaviours in the hospital. The desired behaviour was highest when reinforcements were imposed for behav-iour and lowest when they were not.

The token economy also had a positive ef-fect on patient and sta morale with pa-tients being less apathetic and irresponsi-

ble whist sta also became more enthusi-astic in their jobs.

Ayllon and Azrin refined this further to form what we now know as the token economies.

Several other studies have confirmed the eectiveness of token economies and it is generally accepted that it is eective in pro-ducing a variety of behaviour changes at least in a setting where tokens are given.

Sultana et al conducted a review of token economy regimes over s 15year period finding that they did reduce negative symp-toms in Schizophrenic patients although it was unclear if these behavioural changed were maintained beyond the treatment pro-gramme.

Ost et al treated 12 Schizophrenics with token economy regimes for 8 months find-ing positive changes in behaviour. Of the 5 patients discharged, none had been re-admitted in the 1-year follow-up suggest-ing that behavioural changes can be main-tained after treatment ends in the short-term.

Upper et al found that weight gain associ-ated with the use of Antipsychotics could be addressed with token economy re-gimes and Schizophrenics were able to

34

achieve a target of 3 pounds of weight loss a week. However the sample size was very small making it dicult to generalise re-sults. This does suggest a combination of drugs and token economies may be eec-tive and appropriate in managing the side-eects of anti-psychotics.

However Kazdin et al claimed that the to-ken economies do not lead to permanent change and that once the rewards are re-moved, the undesirable behaviours return to their initial level.

Token economy systems are only eective if given straight after the desired behaviour has occurred. The longer the interval be-tween the behaviour and token the less likely that learning will take place. Addition-ally the method is most eective if tokens can be exchanged for a variety of rewards as if they remain the same, satiation oc-curs and the behaviour decreases in fre-quency.

For these practical reasons it may be di-cult to maintain eciently.

Another factor that aects token econo-mies is intelligence of patients and it is gen-erally accepted it is best suited for patients of Schizophrenia with limited intellectual capacity. Therefore it may not be as eec-tive in patients with greater intelligence

and some might even argue degrading in essence regardless treating people in a pa-tronising way.

Various issues have been raised about the appropriateness of token economies. For example tokens will eventually have to be replaced by other social reinforces both within and outside the therapeutic setting. This is achieved by gradually weaning the person o tokens in the therapeutic set-ting or some other community live-in ar-rangement where more social reinforcers can be used.

Unfortunately this does not always occur and studies find that there have been high relapse rates for discharged individuals.

Baddeley also argued token economies lead to token learning. This means that people might only indulge in behaviour if they are directly reinforced for it.

Whilst this might be eective within thera-peutic settings, Baddeley argued this was unproductive in real world settings where rewards are not always possible.

One of the major issues with the appropri-ateness of token economies is that they only focus on the observable aspects of Schizophrenia and critics argue that token economies do not address the underlying

35

causes and simply masks them rather than addressing them.

Another factor on appropriateness of to-ken economies is the ethical issues it raises. Some critics have claimed it exer-cises authoritarian control and dehuman-ises patients and eectively brainwashes them.

It has also been suggested the therapy ma-nipulates people and deprives them of their freedom and it is the therapist that is controlling the actions of patients rather than themselves trying to seek insight into their own Schizophrenia.

Also as the Token Economy system does not address the underlying cause of Schizophrenia but merely masks it; it may not be appropriate on economic grounds either due to the high cost of stang and supply of appropriate reinforcers as well as constructing suitable environments.

Also the treatment could be argued to be reductionist as it oversimplifies the cure for schizophrenia as merely achieving desired behaviours through a process of operant conditioning. In truth it only deals with the symptoms and not the cause and portrays humans as simple stimulus response ma-chines ignoring the role of free-will they have and the ability for conscious thought.

It is also deterministic in assuming all be-haviours can be controlled this way and are due to purely learnt behaviour that can be simply unlearnt.

Biological treatments may be more eec-tive and appropriate as anti-psychotics for example have resulting in less than 3% of Schizophrenics being housed in hospitals due to their eectiveness and relatively cheap costs in comparison to such Token economies with cost far more.

36

Psychological Treatments: CBT

CBT is the main psychological treatment used in treating schizophrenia and it works by modifying delusional beliefs and halluci-nations within suerers. CBT assumes it is these delusional beliefs which cause schizophrenia. These may occur due to in-correct interpretations the suerer has of the world around them, themselves, other people, maladaptive thinking or distorted perceptions on how to approach problems and goals. The aim of CBT is to help the patient identify these faulty and distorted beliefs and address them.

Patients may be encouraged to think back to when their schizophrenic symptoms first started to help them get a better idea of how they developed. Other methods may see them use self-talk to challenge any de-lusional beliefs or voices they may hear and how they could test their validity. Draw-ings may be used to display links between the suerers thoughts, actions and emo-tions using the ABC model helping them understand where symptoms may be origi-nating from to alleviate any anxiety. One form of CBT is Personal Therapy (PT) which looks at detailing the problems, ex-periences, triggers and consequences as well as potential strategies suerers could

use to cope. This may involve helping pa-tients cope with intrusive thoughts and voices through distraction, learning to chal-lenge the meaning of intrusive thoughts through self-talk, increasing/decreasing so-cial activity to help distract the patient from troublesome moods as well as relaxa-tion techniques. Patients can also be taught to recognize signs of potential re-lapses before they build up into schizo-phrenic symptoms again.

McGorry et al found CBT was eective when comparing two samples of patients at high risk of having a schizophrenic epi-sode receiving dierent treatments. After 6 months 36% of patients receiving psycho-therapy developed schizophrenia while only 10% of those receiving CBT and drug therapy developed the disorder. This sup-ports the use of CBT as an eective form of treatment.

However it is questionable whether it is ap-propriate as the lower rate could have ac-tually been mainly due to the drugs re-ceived rather than CBT itself. Therefore the drug therapy administered may have been a confounding variable with results with CBT having little to no aect potentially. In

37

Use this essay in a question that asks for two treat-ments. In a question that asks for one, or one or more use Token economies

addition to this it could be argued that CBT may merely help mask the disorders symptoms better by teaching functional behaviour. Therefore the root underlying cause may remain. CBT could therefore be argued to be reductionist as it attempts to oversimplify schizophrenia down to cogni-tive thought processes when evidence strongly suggests a biological origin which remains ignored. The disorder is also deter-ministic in assuming that behaviour can be so easily controlled through simply CBT. In truth it may only be eective with people with milder forms of schizophrenia and enough level of insight and awareness into their own thinking to actually address this. Not all patients will be able to use CBT as they may lack the intelligence, in-sight or their symptoms are too severe and chaotic to control. Some studies have found that age may well be a factor with CBT less appropriate for older patients compared to younger as they may not en-gage as well.

Trower et al conducted a study of CBTs eectiveness finding it did not reduce symptoms such as hallucinations however it helped patients see them as less of a threat and help them see they had greater control and outranked the voices. Pa-tients also displayed less positive and negative symptoms and reported a better

quality of life overall. This suggests al-though CBT is not as eective as drug therapies, it is still eective in helping pa-tients manage their symptoms better.

It is questionable whether CBT is appropri-ate however when it appears to reduce cer-tain schizophrenic symptoms. It may well be that patients being able to express their symptoms allows them to gain greater at-tention and support e.g. more medication. Such behaviors may be safety behaviors and encouraging patients to reduce these through CBT may not necessarily mean they experience their symptoms with any less distress but rather they are forced to mask them reducing the possible support they may receive. This raises ethical con-cerns especially if CBT is denying patients treatment for suering they may be experi-encing as they are taught instead to mask them in silence. This alone may make the treatment inappropriate.

Other studies have found training is essen-tial in ensuring CBTs eectiveness with practitioners needing to show respect and unconditional positive regard with the pa-tient. Other studies have found empathy to be a key determinant with Rathod et al finding non-afro caribbean practitioners were less eective in using CBT with Afro-caribbean patients highlighting this need

38

References, Copywrite and credit..

xxxix

Its dicult for me to attribute the exact references for my answer as they have evolved so much over time and have been phrased and rephrased until they resemble what they are now.Any resemblance to any other materials or books will be purely coincidental and care has been taken to insure no part of these model answers have been copied directly from anywhere; there is only a limited number of ways to describe the same facts hence there may appear to be some slight overlap.

The main books used for referencing and which would be highly recommended for purchase to better your un-derstanding are:

The Complete Companion 2nd/3rd Edition by Cara Flanagan & Mike Cardwell.

Collins Psychology AQA A2 4th Edition by Mike Cardwell, Liz Clark, Clare Meldrum & Alison Wadeley.

Psychology A2 For AQA Hodder Education by John-Mac Lawton, Richard Gross and Geo Rolls.

Various internet searches (DSM 5 for example).

These books were all invaluable in their own ways to better my understanding and I would recommend look-ing in dierent ones to understand the theory of the answers better yourself.

It is always better and easier to memorise things you understand so do not rely on this book completely; it is simply to aid your learning only on top of your main text books.

I hope this book proves useful and with practice and preparation you will do well.

I want to thank everyone for their support in this book, my website and my other books. In the future I have various ideas on making A level Psychology more accessible to everyone and it is only possible with your sup-port.

Any questions, concerns please email me on: Sajdevshi@gmail.com

Thank you again,-Saj

www.loopa.co.uk - A* Psychology Revision