Schizophrenia

• Diagnosis and classification of Schizophrenia

  These are interlinked. According to medical approach in order to diagnose a specific disorder, we need to distinguish one disorder from another. By identifying clusters of symptoms that occur together and classifying this as one disorder. Diagnosis is possible by identifying symptoms and deciding when a disorder a person has. Two major systems for classification of mental disorder ICD-10 and DSM-5. DSM-5 system one of the so called positive symptoms must be present for diagnosis, whereas two or more negative symptoms are sufficient under ICD.
• Positive symptoms 


  These are additional experiences beyond those of ordinary existence including hallucination and delusions. Hallucinations are usual sensory experiences and can be related to events in the environment but others aren't. For example, hearing voices ether talking or commenting on person, often criticising. Also seeing people or animals that aren't there.
• Negative symptoms


  Involve loss of usual abilities and experiences e.g speech poverty and Avolition. Speech poverty- characterised by changes in patterns in speech, seen as a negative symptom as the emphasis is on the reduction in the amount and quality of speech in schizophrenia. Nowadays though more emphasis is placed on speech disorganisation in which speech becomes incoherent or the speaker changes topic-mid sentence. This is classified in DSM-5 as positive symptom of schizophrenia whilst speech poverty remians a negative symptom.
• Positive symptoms


  Also known as paranoia, common ones involve being an important political, historical figure like Jesus or Napoleon.

  Delusions also commonly involve being persecuted perhaps by government or aliens or superpowers. Another class of delusions is concern of the body- person may believe they are under external control, delusions can make person behave in ways that make sense to them but seem bizarre to others. Although vast majority of people with delusions are not aggressive and more like victims but some delusions can lead to aggression.
• Negative symptoms 


  Avolition- sometimes called apathy, finding it difficult to begin or keep up goal directed activity e.g actions performed in order to achieve a result. People with schizophrenia often have often sharply reduced motivation to carry out a range of activities. Andreasen 1982- identified 3 signs of avolition- poor hygiene and grooming , lack of persistence in work/education and lack of energy.
• Another strength


  Good reliability- means consistency, psychiatric diagnosis is said to be reliable when different diagnosing clinicians reach same diagnosis for same individual - inter rater reliability.
• One limitation- Low validity

  One way to assess validity is criterion validity. Cheniaux 2009- had two psychiatrists independently assess the same 100 clients using ICD-10 and DSM-IV criteria and found that 68 were diagnosed with SZ under the ICD system and 39 under DSM. This suggests that SZ is either over-or underdiagnosed according to the diagnosic system. Either way this suggests that the criterion validity is low.
• Another limitation- Co-morbidity with other conditions

  If conditions occur together a lot of the time then this questions validity of their diagnosis and classification because they might actually be a single condition. SZ is commonly diagnosed with other conditions, e.g. one review found half of those diagnosed with SZ also had a diagnosis of depression or substance abuse

  This is problem for classification because it means SZ may not exist as a distinct condition, and this is problem for diagnosis as at least some people diagnosed with SZ may have unusual cases of conditions, depression
• Another limitation- Gender bias in diagnosis


  Since the 1980s, men have been diagnosed with SZ more commonly than women (Fischer 2017). One possible explanation for this is that women are less vulnerable than men perhaps because of genetic factors. But it seems likely that woman are underdiagnosed because they have closer relationships and hence get support- Cotton 2009.

  Leads to women with SZ functioning better than men.

  This underdiagnosis is gender bias and means women may not therefore be receiving treatment and services that may benefit them.
• Another limitation- Symptoms overlap with other conditions


  There's considerable overlap between symptoms of SZ and symptoms of other conditions. E.g. both Bipolar disorder and SZ involve positive symptoms- delusions and negative symptoms- avolition.

  Terms of diagnosis, it means that SZ is hard to distinguish from bipolar.

  As with co-morbidity, symptom overalp means that SZ may not exist as a distinct condition and that even if it does it's hard to diagnose, so both of classification and diagnosis are flawed
• Final limitation

  Some symptoms of SZ - hearing voices. E.g. Afro societies, voices may be attributed to communication from ancestors.

  Afro living in UK, 10x likely to receive diagnosis as white British people, although people living in African countries aren't, ruling out genetic vulnerability.

  Most likely the explanation- culture bias in diagnosis of clients by psychiatrists from different cultural background.

  This appears to lead to an over interpretation of symptoms in black British people. (Escobar 2012).

  Means they may be discriminated against culturally biased diagnostic system
• Bio explanations SZ- genetic basis

  Family studies- risk of SZ increases in line with genetic similarity to relative with the condition. E.g. someone with aunt with SZ has 2% chance of developing it, 9% if sibling, 48% if identical twin. Has good support for the importance of genes in SZ.

  Role of mutation- SZ can also have genetic origin in absence of family history of the disorder, one explanation- is mutation in parental DNA, can be caused by radiation, poison.

  There's positive correlations between parental age, risk of SZ, increasing - 0.7% fathers under 25, 2% fathers over 50- Brown 2002.
• Genetic basis of SZ

  Candidate genes- Appears that number of genes are involved i.e. SZ is polygenic, the most likely genes would be those coding for neurotransmitters including dopamine.

  Ripke 2014- combined previous data from genome-wild studies. I.e. those looking at whole human genome as opposed to particular genes of SZ.

  The genetic make-up of 37000 people as opposed diagnosis of SZ was compared to 113,000 controls, 108 separate genetic variations were associated with increased risk of SZ

  SZ - aetiologically heterogeneous, as different studies have different CG- (genetic variation)
• Neural correlates of SZ

  Research has identified some neural correlates i.e. brain structures or function. Best known is neural correlate is the neurotransmitter dopamine.

  The original hypothesis was based on the discovery of drugs used to treat SZ caused similar to those with Parkinson's disease, associated with low DA levels, therefore SZ might be result of high levels of DA (hyperdopaminergia)in subcortical areas in brain. E.g. an excess of DA receptors in pathways from the subcortex to Broca's area may explain specific symptoms of SZ such as poverty of speech or auditory hallucinations.
• Neural explanation (2)

  Davis 1999- proposed addition of cortical hypodopaminergia i.e. abnormally low DA in brain's cortex, this too can explain symptoms of SZ.

  E.g. low DA in the prefrontal cortex (responsible thinking) could explain cognitive problems i.e. negative symptoms of SZ.

  Has also been suggested that cortical HYPDMA leads to subcortical HYPDMA - so both high and low levels of DA in different brain regions are part of the updated version.

  Current versions of the dopamine hypothesis try to explain the origins of abnormal DA function.
• Neural explanation (2)

  So it seems that both genetic variations and early experiences of stress, both psychological and physical, make some people more sensitive to cortical Hypodopaminergia and hence subcortical hypodopaminergia
• Evaluation of Genetic basis- One strength

  Research support- family studies such as Gottesman show that risk increases with genetic similarity to a family member with SZ.

  Adoption studies such as Pekka Tienari 2004- show that biological kids of parents with SZ are at heightened risk even if they grow up in an adoptive family.

  A recent twin study by Hilker 2018- showed a concordance rate of 33% for identical twins and 7%- non identical

  Shows that some people are more vulnerable to SZ as a result of their genetic make up.
• One limitation of genetic basis

  Environ fac increase risk of SZ, include bio, psycho influences.

  Bio Factors: birth complications- Morgan 2007, smoking-rich cannabis in teenage years.

  Psycho risk factors- childhood trauma which leaves them more vulnerable to adult mental health problems in general but now evidence for particular link with SZ.

  Study- 2017 Nina, 67% people with SZ, related psychotic conditions reported at least one childhood trauma as opposed to 38% matched group with non-psychotic mental health problems.

  Means genetic factors alone can't provide complete explanation for SZ.
• One strength of Neural explanation- Evidence of dopamine


  The idea that dopamine is involved in SZ.

  First amphetamines increase DA and worsen symptoms in people with SZ and induce symptoms in people without- Curran 2004.

  Second, antipsychotic drugs reduce DA activity and also reduce the intensity of symptoms- Tauscher 2014

  Third, some candidate genes act on the production of DA or DA receptors.

  This strongly suggests that dopamine is involved in the symptoms of SZ
• One limitation of neural basis- Glutamate

  Dopamine hypothesis is evidence for a central role of glutamate.

  Post-mortem and live scanning studies have consistently found raised levels of the neurotransmitter glutamate in several brain regions of people with SZ, several candidate genes for SZ are believed to be involved in glutamate production or processing.

  Means that an equally strong case can be made for a role for other neurotransmitters.
• 
  

  Psychological explanations of SZ- Family dysfunction

  The schizophrenogenic mother- Reichmann 19480 proposed psychodynamic explanation for SZ based on accounts she heard from her patients about their childhood.

  Fromm-Reichmann noted that many of her patients spoke of a particular type of parent- schizophrenogenic mother.

  According to her se is cold, rejecting and tends to create a family climate characterised by tension and secrecy.

  Leads to distrust that later develops into paranoid delusions (beliefs of being persecuted by another person.) and ultimately SZ.
• Family dysfunction (2)

  Double-bind theory: Bateson 1972- agreed family climate is important in development of SZ but emphaisised role of communication style within family, developing child regularly finds themeselves trapped in situations where they fear doing wrong thing.

  But receive mixed messages about what this is, feel unable to comment on unfairness of situation. When they 'get it wrong', child is punished by withdrawal of love.

  Leaves them understanding of the world as confusing and dangerous.

  Baeston said was neither main type of communication in family member, just a RF.
• Family function (3) Expressed emotion


  The level of emotion, particularly negative emotion expressed towards patient by their carers who often family members, contains:

  Verbal criticism of patient occasionally accompanied by violence.

  Hostility towards patient including anger,rejection.

  Emotional overinvolvement in life of the patient, including needless self sacrifice.

  These high levels of expressed emotion directed towards patient are serious source of stress for them.

  Primarily an explanation for relapse in patients with SZ.
• Family dynsfunction (3) expressed emotion


  But also has been suggested that it may be source of stress that can trigger onset of SZ in person who is already vulnerable.

  E.g. genetic make-up.
• Cognitive explanations

  Dysfunctional thinking- Sz is associated with several types of dysfunctional thought processing and these can provide possible explanations for SZ as whole.

  Sz is caharcterised by disruption to normal thought processing- can see this in many of its symptoms.

  Reduced thought processing in Ventral striatum is associated with negative symptoms, whilst reduced processing of info in temporal and cingulate gyri associated in hallucinations.

  This lower-than- usual level of info processing suggests that cognition is likely to be impaired.
• Cognitive explanations (2)

  Metarepresentation dysfuction- Frith 1992- identified two kinds of dysfunctional thought processes. The first is metarepresentation, the cognitive ability to reflect on thoughts, behaviour.

  Allows us insight into our own intentions and goals, also allows us to interpret actions of others.

  Dysfunction in metarepresentation would disrupt our ability to recognise our own actions and thoughts as being carried out by ourselves rather than someone else

  This would explain hallucinations of hearing voices, delusions like thought insertion.
• Cognitive explanations (3)

  Central control dysfunction- Frith identified issues with the cognitive ability to supress automatic responses while we perform delibrate actions.

  Speech poverty and thought disorder could result from inability to suppress automatic thoughts and speech triggered y other thoughts.

  E.g. people with SZ tend to experience deraliment of thoughts because each word triggers associations and the person cannot suppress automatic responses to these.
• Evaluation on family dysfunction- One strength

  Research support- Evidence linking family dysfunction to SZ.

  Indicators of family dysfunction include insecure attachment and exposure to childhood trauma, especially abuse.

  According to John Read 2005- adults with SZ are disproportionally likely to have insecure attachment especially type C and D.

  Also reported that 69% women, 59% men with SZ have history of physical, sexual abuse.

  2017 study Morkved- most adults with SZ reported at least one childhood trauma, mostly abuse.

  Strongly suggests FD makes people more vulnerable to SZ.
• One limitation of Family dysfunction

  Poor evidence base for any of the explanations.

  Although there's plenty of evidence supporting idea that childhood family-based stress is associated with adult SZ, there's almost none to support importance of traditional family-based theories e.g. schizophrenogenic mother and double bind.

  Both of these theories are based on clinical observation of patients and informal assessment of the personality of mothers of patients but no systematic evidence.

  Means family explanations haven't been able to account for the link between childhood trauma and SZ.
• One strength of Cognitive explanations

  Research support- evidence for dysfunctional thought proccessing.

  Stirling 2006- compared performance on range of cognitive tasks in 30 people with SZ and control goup of 30 without SZ.

  Tasks include the Stroop task- ppts have to name the font-colours of colour-words, so have to surpress the tendency to read words aloud.

  As predicted by Frith's central control theory- people with SZ took longer- over twice as long as average- to name font-colours

  Means that the cognitive processes of people with SZ are impaired.
• One limitation of cognitive explanations

  A proximal explaantion- only explains proximal origins of symptoms.

  CE for SZ are proximal explanations as they explain what's happening now to produce symptoms- as distinct from distal explanations which focus on what initially caused the condition.

  Possible distal explanations are genetic, FD explanations.

  What's currently unclear, not well-addressed is how genetic variation/ childhood trauma might lead problems with metarepresentation or central control.

  Means cognitive theories on their own only provide partial explanations for SZ.
• Biological therapy for SZ

  Some people can take a short course of antipsychotics then stop their use without the return of symptoms. Other people may require antipsychotics for life or else face their likelihood of a recurrence of SZ.

  Antipsychotics can be divided into typical and newer atypical drugs.
• Typical antipsychotics 


  Been around since 1950's- include chloropromazine which can be taken as tablets, syrup, injection.

  If taken orally it is administered daily up to maximum of 1000 mg, although initially doses are much smaller and for most people the dosage is gradually increased to a maximumof 400-800 mg.

  Typical prescribed doses have declined over the last 50 years (Liu 2009.)
• Sedation effect

  Sedation effect- as well as having antipsychotic properties chlorpromazine is also an effective sedative, believed to be related to its effect on histamine receptors but not fully understood how this leads to sedation.

  Chlorpromazine if often used to calm people not only with SZ but also with other conditions.

  This has often been done when patients are first admitted to hospitals and are very anxious .

  Syrup is absorbed faster than tablets so it tends to be given when chlorpromazine is used for its sedative properties.
• Dopamine antagonists 


  Strong correlation between use of TA like CLPM and the dopmaine hyothesis.

  Typical ones (Chloropromazine) work by acting as antagonists in dopamine system.

  Antagonists- chemicals which reduce action of neurotransmitter.

  Dopamine antagonists work by blocking dopamine receptors in synapses in brain, reducing action of dopamine.

  Initially when person begins taking CLPM dopamine levels build up but its production- reduced.

  According to dopamine hypothesis of SZ this dopamie-antagonist effect normalises neurotransmission in key areas of brain, reducing hallucinations.
• Atypical antipsychotics (ATA)

  Used since 1970's- aim in developing newer antipsychotics was to maintain /improve upon the effectiveness of drugs in suppressing symptoms of psychosis, minimise side effects of drugs used.

  There are a range of ATA antipsychotics and they don't all work in the same way and in fact we don't know how some of them work.
• Clozapine

  First trialled in the early 1970's, was withdrawn for while in 1970's follwing deaths of some patients from a blood condition.

  But in 1980's- was discovered to be more effective than Typical ones and clozapine was remarketed as treatment for SZ to be used when other treatments failed.

  Still used in this way today and people taking it have regular blood tests to ensure they aren't developing Agranulocytosis, because of its potentially fatal side effects clozapine isn't available as an injection.

  Daily dosage is little lower than for CLPM, 300 -440mg a day.
• Clozapine (2)


  Clozapine binds to dopamine receptors in the same way that CLPM does, but its acts on serotonin and glutumate receptors.

  Believed that this action helps improve mood and reduce depression and anxiety in patients and that may improve cognitive functioning.

  The mood-enhancing effects of clozapine mean that it's sometimes prescribed when person is considered at high risk of suicide.

  This is more important as 30-50% people with SZ attempt suicide at some point.
• Risperidone


  More recently developed ATA psychotic, been around 1990's, developed to produce a drug as effective as clozapine but without its serious side effects.

  Like CLPM, risperidone can be taken in form of tablets,injection that lasts around 2 weeks.

  In common with other ANP small dose is initially given, this is built up to typical daily dose- 4-8mg, maximum- 12mg.

  Like clozapine, Risperidone believed to bind to dopamine, serotonin receptors.

  It binds more strongly to dopamine receptors than clozapine and therefore effective in much smaller doses than most ANP.
• One strength of antipsychotic drugs

  Large body of evidence to support idea that both typical and ATA ANP are moderately effective in tackling symptoms of SZ.

  Thornely 2003- reviewed studies comparing effects of CLPM to control conditions.

  Data from 13 trials with total of 1121 ppts showed CPLM was associated with better overall functioning, reduced symptoms severity compared to placebo.

  Also evidence for benefits of ATA ANP, Meltzer 2012- conluded that clozapine more effective than typical ANP, other ATA ANP, it's effective in 30-50% of treatment-resistant cases, where typical ANP failed.