These are interlinked. According to medicalapproach in order to diagnose a specificdisorder, we need to distinguish one disorder from another. By identifyingclusters of symptoms that occurtogether and classifying this as one disorder.Diagnosis is possible by identifying symptoms and decidingwhen a disorder a person has. Two majorsystems for classification of mentaldisorderICD-10 and DSM-5. DSM-5 system one of the so called positivesymptoms must be present fordiagnosis, whereastwo or morenegativesymptoms are sufficientunderICD.
Positive symptoms
These are additional experiencesbeyondthose of ordinaryexistence including hallucination and delusions. Hallucinations are usualsensory experiences and can be related to events in the environmentbutothers aren't. For example, hearingvoices ether talking or commenting on person, oftencriticising. Also seeing people or animalsthataren'tthere.
Negative symptoms
Involve loss of usualabilities and experiences e.g speech poverty and Avolition. Speech poverty-characterised by changes in patterns in speech, seen as anegative symptom as theemphasis is on thereduction in theamountandquality of speech in schizophrenia. Nowadays though more emphasis is placed on speech disorganisation in which speechbecomesincoherent or the speaker changes topic-midsentence. This is classified in DSM-5 as positivesymptom of schizophrenia whilst speech poverty remians a negative symptom.
Positive symptoms
Also known as paranoia, common onesinvolve being an importantpolitical, historical figure like Jesus or Napoleon.
Delusions also commonlyinvolvebeingpersecutedperhaps by government or aliens or superpowers. Another class of delusions is concern of thebody- person may believe they are underexternal control, delusions canmake person behave in ways that makesense 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 calledapathy, finding it difficult to begin or keep up goal directedactivity e.g actions performed in order toachieve a result. People with schizophrenia often have often sharplyreduced motivation to carry out a range of activities.Andreasen 1982- identified 3 signs ofavolition- poorhygiene and grooming , lack of persistence in work/educationandlackofenergy.
Another strength
Good reliability- means consistency, psychiatric diagnosis is said to bereliable when different diagnosing cliniciansreachsame diagnosisforsame individual - inter rater reliability.
One limitation- Low validity
One waytoassessvalidity is criterionvalidity. Cheniaux 2009- hadtwopsychiatristsindependentlyassess the same100clients using ICD-10 and DSM-IVcriteria and foundthat68 were diagnosedwithSZunder the ICDsystem and 39 under DSM. This suggests thatSZ is eitherover-orunderdiagnosedaccording to the diagnosic system. Either way this suggeststhat the criterionvalidity is low.
Another limitation- Co-morbidity with other conditions
If conditionsoccurtogether a lot of the time then this questions validity of theirdiagnosis and classificationbecause they mightactually be a singlecondition. 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 forclassificationbecause it means SZ may not exist as a distinct condition, and this is problem fordiagnosis as at leastsomepeople diagnosed with SZ may have unusual cases of conditions, depression
Another limitation- Gender bias in diagnosis
Since the 1980s, menhavebeendiagnosedwithSZmorecommonlythanwomen (Fischer2017). One possibleexplanation for this is thatwomen are lessvulnerablethanmenperhapsbecause of geneticfactors. But it seemslikely that woman are underdiagnosedbecause they havecloserrelationships and hencegetsupport- Cotton 2009.
Leads to women with SZ functioning betterthanmen.
This underdiagnosis is genderbias and meanswomen may notthereforebereceivingtreatment and services that maybenefitthem.
Another limitation- Symptoms overlap with other conditions
There's considerable overlap between symptoms of SZ and symptoms of otherconditions. E.g. both Bipolar disorder and SZ involve positive symptoms- delusions and negativesymptoms-avolition.
Terms of diagnosis, it means that SZ is hard to distinguish from bipolar.
As with co-morbidity, symptomoveralpmeans that SZmay not exist as adistinct 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-riskof SZ increases in linewithgenetic similaritytorelativewiththecondition. E.g. someone with auntwithSZhas2%chance of developingit,9%ifsibling, 48% if identicaltwin.Hasgood support forthe importance ofgenesin SZ.
Role of mutation-SZcanalsohavegeneticorigininabsenceoffamily historyofthedisorder, oneexplanation- is mutation in parental DNA, canbecausedbyradiation, poison.
Candidate genes-Appearsthatnumber of genesareinvolved i.e. SZ is polygenic, themostlikelygeneswouldbethosecodingforneurotransmittersincludingdopamine.
Ripke 2014-combinedprevious data fromgenome-wild studies. I.e. thoselookingatwholehumangenomeasopposedtoparticulargenesofSZ.
The geneticmake-up of 37000peopleasopposeddiagnosis of SZwascompared to 113,000controls, 108separategeneticvariationswereassociatedwithincreasedriskofSZ
Research hasidentifiedsomeneuralcorrelates i.e. brainstructuresorfunction.Bestknown is neuralcorrelateistheneurotransmitterdopamine.
The originalhypothesiswasbasedon the discoveryofdrugsused to treatSZcausedsimilar to thosewithParkinson'sdisease, associatedwithlowDAlevels, thereforeSZmightberesultofhighlevels of DA (hyperdopaminergia)insubcorticalareasinbrain. E.g. anexcessofDAreceptorsinpathwaysfromthesubcortextoBroca'sareamayexplainspecificsymptomsofSZsuchaspovertyofspeechorauditoryhallucinations.
Neural explanation (2)
Davis1999-proposedaddition of corticalhypodopaminergia i.e. abnormallylowDA in brain'scortex, this toocanexplainsymptomsofSZ.
E.g. lowDA in theprefrontalcortex (responsiblethinking) couldexplaincognitiveproblems i.e. negativesymptomsofSZ.
Has alsobeensuggestedthatcorticalHYPDMAleadstosubcorticalHYPDMA - so bothhighandlowlevelsofDAindifferentbrainregionsarepartoftheupdatedversion.
So it seemsthatbothgenetic variations and early experiences of stress, bothpsychologicalandphysical, makesomepeoplemoresensitivetocortical Hypodopaminergiaandhencesubcortical hypodopaminergia
Evaluation of Genetic basis- One strength
Research support- familystudiessuchasGottesmanshowthatrisk increaseswithgenetic similarityto a familymemberwithSZ.
Adoption studiessuch as Pekka Tienari 2004-showthatbiological kidsofparentswithSZareatheightened riskeven if theygrow up in anadoptive family.
A recent twin study by Hilker 2018-showed a concordance rateof33% foridentical twinsand7%- nonidentical
Dopaminehypothesis is evidenceforacentralroleofglutamate.
Post-mortemandlive scanningstudieshaveconsistentlyfoundraisedlevelsoftheneurotransmitterglutamate in severalbrain regionsofpeoplewithSZ, severalcandidate genes for SZarebelievedtobeinvolvedinglutamateproductionorprocessing.
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 stoptheirusewithout the return of symptoms. Other people may requireantipsychotics for life or else face their likelihood of a recurrence of SZ.
Antipsychotics can bedivided into typical and newer atypical drugs.
Typical antipsychotics
Been around since1950'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 muchsmaller and for mostpeoplethedosage is graduallyincreased to a maximumof 400-800 mg.
Typical prescribeddoses have declined over thelast50years (Liu2009.)
Sedation effect
Sedation effect- as well as havingantipsychoticpropertieschlorpromazine is also an effectivesedative, believed to berelated to itseffect on histaminereceptors but not fullyunderstoodhow this leadstosedation.
Chlorpromazine if oftenusedtocalm people not onlywithSZ but also with otherconditions.
This has oftenbeendone when patients are firstadmitted to hospitalsandare very anxious .
Syrup is absorbed faster than tablets so it tendsto be givenwhenchlorpromazine is used for its sedativeproperties.
Dopamine antagonists
Strongcorrelationbetweenuse of TA likeCLPM and the dopmaine hyothesis.
Typical ones (Chloropromazine) work by actingasantagonists in dopaminesystem.
Antagonists-chemicalswhichreduceaction of neurotransmitter.
Dopamine antagonists work by blockingdopaminereceptors in synapses in brain, reducingaction of dopamine.
According to dopaminehypothesis of SZ this dopamie-antagonisteffectnormalisesneurotransmission in keyareas of brain, reducinghallucinations.
Atypical antipsychotics (ATA)
Used since1970's- aim indevelopingnewer antipsychoticswastomaintain /improveupontheeffectiveness of drugs in suppressing symptoms of psychosis, minimise side effects of drugsused.
There are a range of ATA antipsychotics and theydon't all work in the same way and in fact we don't know how some of themwork.
Clozapine
First trialled in theearly1970's, waswithdrawn for while in 1970's follwingdeaths of somepatients from a bloodcondition.
But in 1980's- was discovered to be moreeffectivethanTypical ones and clozapine was remarketed as treatmentforSZ to be used whenothertreatmentsfailed.
Still used in this way today and peopletaking it haveregularblood tests toensure they aren'tdevelopingAgranulocytosis, because of its potentiallyfatalsideeffectsclozapineisn'tavailable as aninjection.
Daily dosage is little lowerthanfor 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 helpsimprovemood and reducedepression and anxiety in patients and that may improve cognitive functioning.
The mood-enhancingeffects of clozapine mean that it's sometimes prescribed when person is considered at high risk of suicide.
This is moreimportant as 30-50% people with SZ attemptsuicide 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, serotoninreceptors.
It binds more strongly to dopaminereceptors than clozapine and thereforeeffective in much smallerdoses than mostANP.
One strength of antipsychotic drugs
Largebody of evidencetosupport idea thatbothtypicalandATAANParemoderatelyeffectiveintacklingsymptomsofSZ.
Datafrom13trialswithtotal of 1121pptsshowedCPLMwasassociatedwithbetteroverallfunctioning, reducedsymptomsseveritycomparedtoplacebo.
Also evidenceforbenefitsofATAANP, Meltzer2012- conluded thatclozapinemoreeffectivethantypicalANP, other ATA ANP, it's effective in 30-50% of treatment-resistant cases, wheretypicalANPfailed.