Schizophrenia

• Effects thought processed and ability to determine reality
• May experience one episode, or have persistent episodes, and people respond differently to treatment - some live 'normal' lives whilst others remain disturbed
• Type I Schizophrenia - acute type, categorized by positive symptoms + better recovery prospect
• Type II Schizophrenia - chronic type, characterized by negative symptoms + poorer recovery prospect
• 1% of people suffer worldwide (between 24 and 55 million people) - most common mental disorder
• Inaccurate stats because of disagreed criteria for diagnosis
• Diagnosis occurs when at least 2 symptoms present for at least 1 month + reduced social functioning present - DSM 5 (USA) + ICD-10 (produced by WHO)
• Chronic onset scz - become increasingly disturbed through gradual withdrawal + loss of motivation over long period
• Acute onset scz - symptoms appear suddenly, after stress/trauma
• Most common between ages 15-45 (males show earlier onset)

• Behaviours concerned with loss of touch from reality
• E.g., hallucinations and delusions
• Occur in acute, short periods, with normal periods in between
• Respond well to medication 

Schnider (1959) detailed first-rank symptoms, subjective experiences based on patient's verbal reports:

• Passivity experiences and thought disorders - thoughts and actions under external control (aliens) + thoughts are inserted withdrawn and broadcast to others
• Auditory hallucinations - insulting and obscene voices in their head, providing commentary, or discuss behaviour, anticipate thoughts and repeat thoughts out loud - occur with delusions
• Primary delusions - delusions of grandeur, believing they are someone important + later they become delusions of persecution where they think someone wants to hurt them

• Behaviours concerned with disruption of normal emotion and actions
• Occur in chronic longer-lasting episodes
• More resistant to medication
• Suffers most likely cannot function effectively in society e.g., relationships/work

Slater and Roth (1969) added 4 symptoms observed from behaviour:

• Thought process disorders - wander off point, invent new words, muddle words, stop mid-sentence etc. + excessively brief answers and minimal elaboration
• Disturbances of affect - appear uncaring, display inappropriate emotional responses e.g., laughing at bad news
• Psychomotor disturbances - adopt frozen 'statute like' poses, exhibit tics and twitches and repetitive behaviour e.g., pacing
• Avolition - inability to make decisions, lack enthusiasm and lose interest in socialisation, affection, and personal hygiene

• Concerned with consistency of symptom measurement + affects diagnosis in 2 ways:
• Test-retest - clinician makes same diagnosis on separate occasions from same info
• Inter-rater reliability - different clinicians make same diagnosis of same patient

Read et al (2004)

• Test-retest reliability only had 37% concordance rate - 1970 study showed when 194 British and 134 US psychiatrists made diagnosis based on case info, 69% Americans diagnosed scz but only 2% British did - never fully reliable

Beck et al (1962)

• 54% concordance rate of diagnosis on 153 patients, whilst this increased to 81% according to Soderberg et al (2005) using DSM - more reliable over time and Nilsson et al (2000) found only 60% concordance rate using ICD - DSM more reliable

Reliability of scz disorder (81%) superior of that of anxiety (63%) + superior to scz validity

Reliability has increased as classification systems updated

Classifications allows a common language  - better disorder understanding + treatments

• Concerned with accuracy of diagnosis - scz should be separate to all other disorders
• Validity is assessed by:
• Reliability - must be reliable to be valid (first step to assessing validity)
• Predictive Validity - if successful treatment is given, diagnosis seen as valid
• Descriptive Validity - patients should differ in symptoms from people with other disorders
• Aetiological - all patients should have same cause of disorder

Mason et al (1997)

• Tested 4 classification systems over 13 years using 99 patients to find modern systems had higher predictive validity  - improved over time

Baille et al (2009)

• 154 British psychiatrists had differing views on cause of scz (other than genetics, substance abuse and biochemical abnormalities) - aetiological validity is low

Kendall & Jablensky (2007) - diagnostic categories justifiable as they give a framework to investigate experiences to gain better understanding and treatments

Predictive validity argued to be low - different sufferers have large range of symptoms

Being labelled with scz has long-lasting negative effects, which is unfair when diagnoses made with very little validity

Incidence of scz is 1% and OCD is 3% but scz co-morbid with OCD is much higher than probabilities suggest - scz validity low as not a completely separate disorder

Rosenhann (1973)

• investigate how situational factors affect diagnosis - sane confederates went to mental health professionals and said that had a hallucination 
• said they heard unclear, unfamiliar and same-sex voices saying 'empty', 'hollow', and 'thud' - when on ward they stopped pretending symptoms and made observations - only discharged when convinced staff they were sane
• diagnosed 11 with scz and 1 with manic depression - av. stay was 19 days and real patients detected sanity - CANNOT ALWAYS DETECT SANE + INSANE PEOPLE SO DSM FLAWED

• One or more additional disorders occur with scz, causing confusion as to what is being diagnosed

Sum et al (2006)

• 32% of 142 hospitalised schizophrenics had additional disorders

Buckley et al (2009)

• 50% schizophrenics had co-morbid depression, 15% panic disorder, 29% PTSD, and 23% OCD, as well as 47% diagnosed with substance abuse

High levels of co-morbid disorders led to such co-morbidities are sub-types of disorder

Biggest problem in diagnosis is differentiating it from bipolar disorder - mood changes and mania and depression often don't meet bipolar criteria for separate diagnosis

Substance abuse makes reliable and valid diagnoses hard to achieve 

• Concerns tendency to over-diagnose some cultures as suffering from scz e.g., people in Britain of Afro-Caribbean descent (more likely to be confined to secure hospitals due to perception of them being more dangerous)
• Higher stress levels from ethnic minority experiences e.g., poverty and racism contribute

McGovern and Cope (1977)

• 2/3 patients detained in Birmingham's hospitals were 1st and 2nd generation Afro-Caribbeans

Whaley (2004)

• Cultural bias seen as mean reason for scz among black Americans (2.1%) being higher than white Americans (1.4%)

Rack (1982) says in some cultures it is normal to see and hear deceased loved ones - grieving

Cochrane & Sashidharan (1995) say racism and social deprivation bound to effect mental health, but clinicians wrongly attribute behaviour to ethnicity

• Disagreement over gender prevalence rate - belief was males + females equally vulnerable 
• Clinicians (most men) have misapplied criteria to women + may be 50% more male, sufferers
• Clinicians ignore males tend to suffer more negative symptoms + more substance abuse
• Females have better recovery rate and lower relapse rate
• Clinicians ignore different predisposing factors giving different vulnerable points in their life
• First onset occurs earlier in males than females - 18-25 in males but 25-33 in females
• 2 peaks for males - 21 and 39 but 3 for females - 22, 37, and 62

Lewin et al (1984) -- If clearer criteria applied, there would be fewer female sufferers - supported by Castle et al (1993) who found when more restrictive criteria used, men incidence double that of women

Kulkarni et al (2001) -- Female sex hormone estradiol effective in treating scz in women when combined with antipsychotic therapy, suggesting unconsidered predisposing factors

Difference in ages may be related to different stressors in life, and changes in menstrual cycles

Different diagnostic considerations between genders - validity doubts as scz as its own disorder

Difference in ages at which scz develops suggests different types of scz - questions validity

• Symptoms often found to be similar to those of other disorders e.g., bipolar where depression and hallucinations are common symptoms
• Symptom overlap can occur with autism and cocaine intoxication

Konstrantareas and Hewitt (2001)

• Compared 14 autistic patients and 4 scz sufferers and found no one with scz had autism symptoms but 7 autistic patients had scz symptoms

Ophoff et al (2011)

• Assessed genetic material from 50,000 participants to find 7 gene locations associated with scz, 3 of which were linked to bipolar - genetic overlap between disorders

Genetic overlap may mean therapies can be developed to treat disorders simultaneously

Grey matter of brain can be examined - scz patients have decreased grey matter but not bipolar

Ketter (2005) reports misdiagnosis due to symptom overlap leads to treatment delay, leading to condition worsening and suicide

• Scz seen as being transmitted through genes (not a single gene so increases vulnerability)
• Research includes twin studies/adopted family concordance rates  + gene mapping

Gottesman and Shields (1976)

• Reviewed 5 twin studies and concordance rate was 75-91% between MZ twins with severe scz - Torrey et al supported this when they found if one MZ twin had scz there was a 28% chance other developed it

Kety and Ingraham (1992)

• Prevalence rates 10x higher in genetic relatives than adoptive  (environmental factors less impact)

Scz Working Group of Psychiatric Genomics Consortium (2014) analysed DNA of 36,989 scz patients and 113,000 non scz patients and found 128 genetic variations at 108 locations on chromosome (lots expressed in tissues involving immunity) - link between immune system and scz

Twin studies suggest genetic factor but ignore environment, social class and socio-psychological factors

Concordance rates should be 100% if genes were pure cause - heritability between 11 and 58% in MZ twins

Gene mapping allows high risk individuals to be identified but causes ethical and socially sensitive concerns

• Dopamine linked to onset - increases rate of firing neurons enhancing neuron communication
• Synder (1976) says too much dopamine release leads to scz
• Theory developed when antipsychotic drug worked by reducing dopamine activity and dopamine-releasing drug L-dopa causes symptoms in non-schizophrenics (LSD does same)
• Genetic factors linked to faulty dopaminergic systems in scz sufferers
• Davis et al (1991) updated theory as high dopamine is not found in all sufferers and clozapine drug has little dopamine-blocking activity but is an effective treatment
• High dopamine in mesolimbic dopamine system = positive symptoms
• High dopamine in mesocortical dopamine system = negative symptoms 
• NT glutamate involved as there is reduced function of NMDA glutamate receptor in scz patients - dopamine receptors restrict glutamate release

Kessler et al (2003)

• PET and MRI scans found schizophrenics had higher dopamine receptor levels in basal forebrain etc. + cortical dopamine levels differed to those of non-scz patients

Javitt (2007)

• Phencyclidine and ketamine induce symptoms in non-scz by blocking transmission at NMDA-type glutamate receptors -> abnormal dopamine system function

No consistent evidence that dopamine levels differ between sufferers and non-sufferers

Theory doesn't explain why recovery is slow when neuroleptic drugs affect dopamine instantly

Biochemistry differences could be an effect rather than a cause 

Over-simplistic as other NTs may be involved in scz development

• Brain abnormalities associated with development
• Research includes post mortems, non-invasive methods e.g., fMRI (compared to non-scz)
• Consider whether abnormalities are a genetic cause or effect - compared with non-scz family members and if same found then genetic
• Research focussed on enlarged ventricles (fluid-filled gaps between brain areas) - associated with pre-frontal cortex damage which has been linked to negative symptoms of disorder

Li et al (2010) --Meta-analysis of fMRI studies found scz had limited activation of bilateral amygdala + right fusiform gyri compared to non-scz - explains difficulty in facial emotion processing 

Boos et al (2012) -- MRI scans on 155 scz, 186 of non-scz siblings and 122 non-related scz to find scz-patients had decreased grey matter density + cortical thinning - suggests effect not due to genetics

Non-schizophrenics found with enlarged ventricles and not all sufferers have enlarged ventricles

Consideration must be given to environmental factors e.g., substance abuse (influence tissue)

Patients who don't respond to treatment may not do so because of structural brain damage

• Maladaptive relationships and communication patterns cause stress which influences scz development
• Parents of schizophrenics display 3 types of dysfunctional characteristics
• High levels of interpersonal conflicts (arguments)
• Difficulty in communicating with each other
• Being excessively critical of children
• Bateson et al (1956) came up with phrase 'double bind' to explain contradictory situations where parents give verbal message but exhibit opposite behaviour 
• Leads to negative reaction of social withdrawal and flat effect (lack of emotional expression) to avoid double bind situations
• Another feature is expressed emotion (EE) where families constantly exhibit criticism and hostility and exert a negative influence - causes relapse and positive symptoms of persecution

Tienari et al (2004)

• Level of scz in adopted families who were biological children of scz-mothers was 5.8% in those adopted by healthy families compared to 36.8% fo children in dysfunctional families

Kavanagh (1992)

• Reviewed 26 EE studies finding mean relapse rates of those who returned to live in high EE family was 48% compared with 21% who lived with low EE families - further supported by Butzlaff and Hooley (1998) who performed meta-analysis of 26 studied to find relapse rates were 2x higher in those who returned to high EE environments

Family dysfunction theory supported therapies which focus on lowering EE in families, showing lower relapse rates than other therapies

Research into EE suggests that family dysfunction plays large role in scz maintenance

Having a schizophrenic in the family can be stressful so could be effect rather than cause

Fails to explain why all children in schizophrenic families do not go on to develop scz

• Focus on maladaptive thought processes being central feature
• Beck and Rector (2005) proposed model combining interaction of neurobiological, environmental, behavioural and cognitive factors 
• Brain functioning abnormalities seen to increase vulnerability to stressful experiences leading dysfunctional beliefs and behaviours
• Cognitive deficits occur where sufferers have problems with attention, communication and information overload
• Sufferers unable to deal with inappropriate ideas e.g., misperceiving voices in their head as people speaking to them rather than it being their 'inner voice' like most people
• Delusions occur due to active cognitive bias (irrational thoughts) e.g., believing they are being persecuted
• Hallucinations understood by biased information processing, while cognitive deficits referred to as 'alien control symptom' - external people have influence over thoughts and behaviour
• Negative symptoms occur due to use of cognitive strategies to control high levels of mental stimulations experinced
• Sufferers may experience more emotion than they display as not expressing emotion is a method used to control levels of internal emotion experienced

Bowie and Harvey (2006)

• Reviewed evidence to find cognitive impairments are core feature of scz, affecting attention, memory, verbal learning, and executive functions
• Impairments pre-date onset disorder+ found throughout course of illness - supported by fact that effective therapies reduce cognitive defects

Takahashi et al (2013)

• Compared electrical brain activity of 410 schizophrenics and 247 non-scz exposed to auditory tones to find ability to detect tone changes severely limited in scz patients - may explain cognitive defects as tone of voice changes are considered as complex information that tend to suggest emotion changes etc.
• May also explain auditory hallucinations and delusions

Accounts for positive and negative symptoms

Combined with other explanations to provide fuller understanding of causes and maintenance 

Cognitive theories don't explain what led to cognitive dysfunction so cannot explain causes

• Maladaptive ways of thinking plays role in cognitive explanation
• Humans use metacognition (cognitive monitoring of own thought processes and identification of errors in that processing) - schizophrenics experience metacognitive dysfunction
• Allows people to view mental state + wishes and intentions of others to make sense of world
• Metacognitive dysfunction affect executive functioning, higher cognitive processes that manage other cognitive and behavioural processes
• Can lead to impairments in goal-directed behaviour, attention, memory, inhibition of inappropriate responses and motor control of body

Joshua et al (2009)

• Hayling Sentence Completion Test to compare 39 scz with 40 bipolar patients + 44 healthy controls to find scz patients had slower responses + suppression of inappropriate responses

Brune et al (2011)

• Reviewed 20 years evidence to report many symptoms result from poor metacognition especially self-reflection and empathising with others

Highlighting of metacognition shows treatments need to focus on improving metacognitive abilities to be successful

Garety et al (2001) believes scz best understood by linking different explanations, with dysfunctional though processing being a vital one

Research suggest DTP occurs before onset of disorder so is not an effect

Research shows links to memory impairments are limited - only specific areas (CE of WMM)

• Anti-psychotic drugs are prime treatment - chlorpromazine introduced in 1952 - tablet, syrup, inject
• Enables many to live relatively normal life outside institution - dampen symptoms not cure
• Divided into typical antipsychotics (1st gen) and atypical psychotics (2nd gen)
• Atypical drugs introduced as they were supposedly more effective and had less side effects 
• Hallucinations and agitation reduce in few days and delusions in few weeks - lots of progress in 6 weeks
• Patients take several types before finding best one, and some patients take one dose, and others regular ones to prevent symptoms reappearing
• Sizeable minority who do not respond
• Anti-psychotics used as combination therapy - reduce symptoms so CBT has better effect
• Reduce dopamine production by blocking receptors that absorb dopamine (reduce positive symptoms)
• Typical antipsychotics also affect other NT systems (cholinergic, serotonergic mechanisms) - can cause side effects such as dry mouth, urinary problems, constipation and visual disturbances
• Long term leads to 15% developing tardive dyskinesia (TD) causing uncontrollable muscle movement around mouth e.g., lip smacking and jaw swinging - can be permanent condition
• Atypical drugs introduced in 1990s act on serotonin and dopamine systems affecting negative symptoms
• Unknown exactly how they work, but incur reduced TD levels but can cause weight gain, increased risk of stoke, blood clots, diabtes and sudden cardiac death

Lieberman et al (2005)

• Examined effectiveness of typical and atypical antipsychotics in treating 1432 chronic schizophrenics
• 74% patients discontinued use due to intolerable side effects - rates similar between both 

Schooler et al (2005)

• Found both typical and atypical effective in treating scz with 75% patients experiencing at least 20% symptom reduction - 55% taking antipsychotics relapsed but only 42% did in typical treatments
• Side effects fewer with antipsychotics implying atypical drugs superior

Antipsychotics effective, and cheap to produce and administer

Relapse rates of 40% in first year and 15% after that - due to side effects and reduced QOL

Side effects

Widespread use of antipsychotics fuelled by powerful influence of production companies who make enormous profits from increased use

• Beliefs, expectations and cognitive assessments of self, environment and nature of personal problems  affect how individuals perceive themselves and others 
• Looks at how problems are approached and how successful people are in coping and achieving goals
• CBT changes maladaptive thinking and distorted perceptions seen as underpinning disorder - to modify hallucinations and delusions
• CBT more affective after antipsychotics given - undertaken every 10 days for 12 sessions to identify and alter irrational thinking
• Drawings used to display links between thoughts actions and emotions - understanding where symptoms originate can reduce anxiety levels 
• One approach is personal therapy (PT) - detailed evaluation of problems + experiences, their triggers and consequences, and coping strategies 
• Coping techniques include intrusive thought distractions, challenging their meanings, changing amount of social activity to distract from low moods, and relaxation techniques
• Small groups or individuals
• Taught to recognise small signs of relapse
• Rational Emotive Behaviour Therapy (REBT) teaches people they must live with emotional instability
• Muscle relaxation techniques detect gradual anger build-ups and relaxation skills applied to control 

Zimmerman et al (2005)

• Meta-analysis of 14 studies between 1990 and 2004 involving 1484 participants to find CBT significantly reduced positive symptoms and was especially beneficial with short term acute schizophrenic episodes - more effective in certain circumstances 

Jauhar et al (2014)

• Meta-analysis of 50 studies conducted over last 20 years to find small therapeutic effect on symptoms - small effect disappeared when only studies using blind testing considered - questions effectiveness

CBT and antipsychotics are effective treatment supporting combined treatments

Practioner training is essential as they must give unconditional positive regard, empathy and honesty

Fewer side effects but more expensive

Not suitable for those who do not trust practitioners 

Trower et al (2004) found it made hallucinations seem less of a threat - coping mechanism not treatment

• Aka Family-Focussed Therapy
• Psychotherapy based on altering relationship and communication patterns in dysfunctional families
• Whole family involved - become support network
• Main aims include
• Improve positive and reduce negative communication forms
• Increase tolerance levels and decrease criticism levels
• Decrease guilt and responsibility for causing illness among family members 
• Therapists regularly meet with patients and families who talk openly about symptoms, behaviour and progress with treatments and how the illness affects them
• Family members taught to support each other - given specific role in rehabilitation of patient
• Emphasis on openness and boundaries drawn and a part of informed consent 
• Given for set time (9months-1 year)
• Reduces symptoms and allows family to develop skills that can continue after therapy 

Pilling et al (2002)

• Performed meta-analysis including 18 family therapy studies with 1467 patients, finding it has smallest number of relapses and lowest number of hospital readmissions, as well as highest medication compliance 

McFarlane et al (2003)

• Reviewed evidence to find family therapy results in reduced relapse, symptom reduction and improved family relationships so increased patient well-being

Useful for patients who lack insight into illness or cannot coherently speak about it as family can assist

Younger people who live at home with family can benefit

Family members may be reluctant to share sensitive information as it may reopen family tensions - some members may not want to admit problems

Very expensive combination of family therapy and drug therapy

• Behaviourist therapeutic approach where tokens awarded for desirable behaviour
• Introduced in 1970s and used mainly with long-term hospital patients, enabling them to leave and live relatively normal life
• Aimed at changing negative symptoms.g., low motivation, poor attention and social withdrawal
• Uses OC principles where reinforcements given when desired behaviour shown e.g., self care/socialising
• Tokens later exchanged for goods or privileges 

Dickerson et al (2005) -- Reviewed 13 studies of token economy finding it useful when combined with psychosocial and drug therapies - specific benefits not identified so srea for future research 

Silverstein et al (2009) -- Schizophrenics in community have trouble doing jobs when paid monthly due to distant rewards but engage readily when short-term reward present i.e. token economy - real life application

Patients become more independent and active, as well as less violent when in therapeutic environments

Flexibe and tailored to meet individual needs

Work best in unison with other treatments so not treatment in itself 

Desired behaviour dependent on being reinforced, which is not further showed outside institution

• Best to perceive scz as developing through several factors and view treatment combinations as best
• Encompasses diathesis-stress model where scz perceived as resulting as biology and environment
• Episodes worsened when environmental stressors combine with biological diathesis (vulnerability)
• Research shows scz has biological component with several genes increasing vulnerability 
• Genetic factors linked to faulty dopaminergic systems and abnormal NT functioning
• Genes do not cause disorder but increase likelihood that stressors can trigger an episode 
• Psychological triggers include
• Family dysfunction, substance abuse, critical life events etc.
• Cognitive deficits and dysfunctional thoughts seen as being due to scz rather than causes of triggers

Walker (1997)

• Schizophrenics have higher cortisol levels - related to severity of symptoms with stress related increases in cortisol levels heightening genetic-influenced abnormalities in dopamine transmission, triggering onset of disorder

Barlow and Durand (2009)

• Family history of scz indicated genetic link, coupled with being part of dysfunctional family elevated risk of scz development - supports diathesis stress model

Differential susceptibility hypothesis extends to include positive environments - when living with loving family, reduces chances of scz development 

Not clear how risks contribute to diatehsis stress interaction for a particular person as it differs between individuals 

Genes cannot determine outcomes alone, they need specific environments to express themselves

• Combination of treatments is most effective
• Which combination affected by individual needs and circumstances - antipsychotics given first so psychological treatments can be mire effective 

Sudak (2011) -- Antipsychotic drugs combined with CBT strengthens adherence to drugs as CBT gives rational insights into benefits

Morrison and Turkington (2014) -- Drug treatment plus CBT produced better rates pf symptom reduction and relapse than alone

Treatment combination effective as cognitive therapies address disordered thinking, allowing behavioural therapies to tach functional social skills

Expensive combination but more cost-effective in long run

Scz often has biological and psychological components so combined treatments deal with both

Receiving CBT can cause side effects to be interpreted in delusional manner causing mistrust