DESCRIBE AND EVALUATE THE CLASSIFICATION AND DIAGNOSIS OF SCHIZOPHRENIA

AO1

CLASSIFICATION OF SCHIZOPHRENIA

 SCHZOPHRENIA: a PSYCHOTIC DISORDER involving a BREAK in REALITY which involves a disruption of

COGNITION and EMOTION, which affects LANGUAGE, THOUGHT, PERCEPTION and SENSE OF SELF
 2 MANUALS : ICD 10 AND THE DSM5
 DSM-5: ONE of the POSITIVE features (delusions or hallucination or speech disorganisation)
 ICD-10: TWO or MORE NEGATIVE FEATURES and recognises SUBTYPES of SCHZOPHRENIA e.g. PARANOID
SCHIZOPHRENIA = powerful DELUSIONS and HALLUCINATIONS but few other + HEBEATRNIC
SCHIZOPHRENIA = DISTURBANCE of MOVEMENT, leaving the sufferer IMMOBILE or OVERACTIVE

POSITIVE SYMPTOMS

 HALLUCINATIONS: they SEE, HEAR, TASTE or EVEN FEEL something that ISN’T REALLY THERE – HEARING
VOICES or imagining PEOPLE/ANIMALS/DISTORDED FACIAL EXPRESSIONS
 DELUSIONS: IRRATIONAL BELIEFS e.g. being an important figure – beliefs that have NO BASIS in reality and
ACT in a way that makes SENSE TO THEM

NEGATIVE SYMPTOMS

 AVOLITION: finding it DIFFICULT to perform ACTIVITIES that are GOAL-ORIENTED e.g. poor hygiene, lack of
energy and inconsistency in work/education
 SPEECH POVERTY: REDUCTION in the AMOUNT and QUALITY OF SPEECH e.g. slurred speech or a delay in
the sufferer’s verbal responses during a conversation

AO3

 RELIABILITY: (CONSISTENCY) INTER-RATER RELIABLITY: the extent to which DIFFERENT ASSESSORS/TWO or

MORE MENTAL HEALTH PROFESSIONALS AGREE on the ASSESSMENTS/SAME DIAGNOSIS (DIAGNOSTIC
RELIABILTY) – CHENIAUX ET AL: 2 psychiatrists INDEPENDENTLY diagnose 100 patients using the DSM + ICD
= POOR INTER-RATER RELIABILITY (1ST – 26 w/ DSM + 44 w/ ICD AND the other – 13 w/ DSM + 24 w/ ICD)
 VALIDITY: the extent to which we are MEASURING what we WANT to measure – the number of VALIDITY
ISSUES  measured through the CRITERION VALIDITY; do different ASSESSMENT SYSTEMS arrive at the
SAME DIAGNOSIS – CHENIAUX ET AL: MORE likely to be diagnosed with ICD – either an OVER-DIAGNOSES
with ICD or UNDER with the DSM = LOW VALIDITY + NOT STANDARDISED
 SYMPTOM OVERLAP: SCHIZOPHRENIA + BIPOLAR DISORDER involve POSITIVE SYMPTOMS like DELUSIONS
and NEGATIVES like AVOLITION – questions the VALIDITY – under the ICD, the patients may be diagnosed
as a SCHIZOHRENIC but under the DSM may be diagnosed with BIPOLAR DISORDER
 CULTURAL DIFFERENCES: LUHRMAN ET AL: interviewed 60 adults diagnosed with SCHIZPHRENIA, 20 in
GANA, INDIA AND THE US – each were asked about the VOICES they heard. A person who claimed that he
was HOD ON EARTH would be considered DELUSIONAL in WESTERN SOCIETY but in INDIA is a spirit
medium who is the HUMAN INCARNATION of a HINDU GOD
DESCRIBE AND EVALUATE BIOLOGICAL EXPLANATIONS OF SCHIZOPHRENIA

AO1

THE GENETIC BASIS OF SCHIZOPHRENIA

 SCHIZOPHRENIA RUNS IN THE FAMILY: GREATER GENETIC SIMILARITY between FAMILY MEMBERS
associates with the LIKELIHOOD of BOTH DEVELOPING SCHIZOPHRENIA – 100% GENES with MONOYGOTIC
and 50% SIBLING  GOTTESMAN: shows the link through META-ANALYSIS of 40 studies = IDENTICAL
TWINS: 48% / DIZYGOTIC: 17%
 CANDIDATE GENES: POLYGENIC ( not determined by a SINGLE gene – 108) and AETIOLOGICALLY
HETEROGENEOUS (DIFFERENT COMBINATIONS of factors can lead to different conditions)  RIPKE ET AL:
LARGE-SCALE combining PREVIOUS DATA from ‘GENOME-WIDE’ (a complete set of DNA) studies of
schizophrenia, compared genetic makeup of 37,000 patients and 113,000 CONTROLS = 108 genes
associated with HIGHER RISK

DOPAMINE HYPOTHESIS

 NEUROTRANSMITTERS – brain’s CHEMICAL MESSENGERS

 HYPERDOPAMINE in the SUBCORTEX: ORIGINAL VERSION, HIGH levels of ACTIVITY of DOPAMINE in the
SUBCORTEX e.g. EXCESS of DOPAMINE RECEPTORS in the BROCA’S AREA (speech production)
 HYPODORAMINERGIA in the CORTEX: MORE RECENT, GOLDMAN-RAKIC ET AL show how LOW LEVELS in
the PRE-FRONTAL (thinking and decision-making) create NEGATIVE SYMPTOMS

NEURAL CORRELATES OF SCHIZOPHRENIA

 The MEASUREMENT of the STRUCTURE of the BRAIN that CORRELATE with an EXPERIENCE
 NEGATIVE SYMPTOMS: AVOLITION (loss of MOTIVATION) + MOTIVATION involves the ANTICIPATION of
the REWARD and the VENTRAL STRIATUM is believed to be involved with this  JUCKEL: LOWER LEVELS of
activity than in the CONTROLS and saw a NEGATIVE CORRELATION between ACTIVITY LEVELS in the V.S
and THE SEVERITY OF OVERALL NEGATIVE SYMPTOMS
= ACTIVITY in the V.S is a NEURAL CORRELATE
 POSITIVE SYMPTOMS: ALLEN ET AL scanned BRAINS of PAITIENTS and compared to CONTROL GROUP =
LOWER ACTIVATION LEVELS in the SUPERIOR TEMPORAL GYRUS and the ANTERIOR CINGULATE GYRUS in
the HALLUCINATION GROUP = MORE ERRORS
= LOW activity in these areas is a NEURAL CORRELATE OF AUDITORY HALLUCINATIONS

AO3

 MULTIPLE SOURCES OF EVIDENCE: GROTTESMAN: genetic similarity and shared risk of schizophrenia,
ADOPTION STUDIES (TIENARI ET AL): children of SUFFERERS are STILL at a HIGH RISK even if adopted into
FAMILIES WITH NO HISTORY
 THE CORRELATION-CAUSATION PROBLEM: DOES the UNUSUAL activity in the region of the brain CAUSE
the SYMPTOM or OTHER EXPLANATIONS? e.g. correlation with V.S + negative symptoms – could be
something in the V.S or the negative symptoms CAUSING the LESSER INFORMATION in the V.S
 PSYCHOLOGICAL ENVIRONMENT: ENVIRONMENT FACTORS have an important role like psychological ones
– FAMILY FUNCTIONING DURING CHILDHOOD – probability of getting schizophrenia, even if you are a
MONOZYGOTIC TWIN, is 50%
 MIXED EVIDENCE FOR DOPAMINE HYPOTHESIS: DOPAMINE AGONISTS like AMPHETAMINES = INCREASE
LEVELS of DOPAMINE and ANTI-PSYCHOTIC DRUGS = DECREASE of DOPAMINE levels = important role
BUT some say it doesn’t provide a full explanation  RIPKE ET AL: some genes code for production of
OTHER NEUROTRANSMITTERS = others, like GLUTAMATE, are important
DESCRIBE AND EVALUATE PSYCHOLOGICAL THEORIES OF SCHIZOPHRENIA

AO1

FAMILY DYSFUNCTION

 THE SCHIZOPHRENIC MOTHER  FROMM-REICHMANN: based on the ACCOUNTS she heard from her
PATIENTS about their CHILDHOODS, noted that many spoke of a particular parent – SCHIZOPHRENIC
MOTHER or ‘SCHROPHRANIA-CAUSING’ is COLD, REJECTING and CONTROLLING and develops a FAMILY
CLIMATE that is filled with TENSION and SECRECY = DISTRUST then PARANOID DELUSIONS then
SCHIZOPHRENIA
 DOUBLE-BLIND THEORY  BATESON ET AL: emphasises the role of COMMUNICATION STYLE in the family
– THE DEVELOPING CHILD finds themselves TRAPPED in situations where they FEAR doing the WRONG
THING, BUT received MIXED MESSAGES about what this is, and fell UNABLE to COMMENT on the
UNFAIRNESS of the SITUATION or SEEK CLARIFICATION – when they ‘GET IT WRONG’, the child is
PUNISHED by WITHDRAWAL OF LOVE = leaves them with the understanding that the world is CONFUSING
AND DANGEROUS + this is reflected in the SYMPTOMS like DISRGANISED THINKING AND PARANOID
DELUSIONS = COMMUNICATION is a RISK FACTOR
 EXPRESSED EMOTION AND SCHIZOPHRENIA: is a level of EMOTION (MAINLY NEGATIVE) expressed
towards a patient by their CARERS like VERAL CRITICISM of the PATIENT (sometimes with violence),
HOSTILITY towards the patient (inc. ANGER and REJECTION) and EMOTIONAL OVER-INVOLVEMENT in the
life of the patient (inc. NEEDLESS SELF-SACRIFICE) = HIGHER STRESS FOR THE PATIENT – explanation for
RELAPSE or an ONSET for someone that is VULNERABLE

COGNITIVE DYSFUNCTIONS

 FOCUSES on the role of the MENTAL PROCESS AND associates with several types of abnormal information
processing
 REDUCED PROCESSING in the VENTRAL STRIATUM is associated with the negative symptoms and reduced
processing of information in the TEMPORAL and CINGULATE GYRI are associated with HALLUCINATIONS
 FRITH ET AL: 2 TYPES of DYSFUNCTIONAL THOUGHT PROCESSING –
- METAREPRESENTATION: ability to REFLECT ON THOUGHTS and BEHAIOUR = able to know or own
INTENTIONS and GOALS and INTERPRET THE ACTIONS OF OTHERS  DYSFUNCTION: disrupt our ability
to recognise our actions and thoughts as being carried out by OURSELVES rather than SOMEONE ELSE
= HALLUCINATIONS of VOICES and DELUSIONS
- CENTRAL CONTROL: ability to SUPRESS AUTOMATIC RESPONSES while we perform DELIBERATE
ACTIONS INSTEAD  DISORGANISED SPEECH + THOUGHT DISORDER could result in this as it is
triggered by OTHER THOUGHTS
AO3

 SUPPORT FOR FAMILY DYSFUNCTION AS A RISK FACTOR: READ ET AL: reviewed 46 studies of CHILD ABUSE
and SCHIZOPHRENIA and concluded 69% of ADULT WOMEN in-patients with a diagnosis of schizophrenia
HAD A HISTORY OF PHYSICAL or SEXUAL ABUSE or BOTH in CHILDHOOD, for men it was 59% =INSECURE
ATTACHMENTS  SCHIZOPHRENIA
BUT the schizophrenia may have DISTORTED PATIENTS’ RECALL of CHILDHOOD EXPERIENCES = low
VALIDITY – there is PROSPECTIVE EVIDENCE but not HIGH AMOUNTS and the RESULTS are INCONSISTENT
 WEAK EVIDENCE FOR FAMILY-BASED EXPLANATIONS: NO EVIDENCE to support the evidence of the
SCHIZOPHRENIC MOTHER or DOUBLE-BLIND – they are BASED ON CLINICAL OBSERVATIONS and EARLY
EVIDENCE involved with assessing the PERSONALITY OF THE MOTHERS = NOT VALID
AND led to PARENT-BLAMING – ALREADY suffered through seeing their child’s struggle into
SCHIZOPHRENIA and they are now going through FURTHER TRAUMA
 STRONG EVIDENCE FOR DYSFUNCTIONAL INFORMATION PROCESSING: STIRLING ET AL compared 30
PATIENTS with SCHIZOPHRENIA with 18 NON-PATIENT CONTROLS on a range of COGNITIVE TASKS inc. the
STROOP TEST ( name the INK COLOURS of the colour words – SUPRESSING the IMPULSE to READ THE
WORDS) = PATIENTS took TWICE as long as the CONTROL
BUT IT DOESN’T say anything about the origins of the FAULTY COGNITIONS causing the SYMPTOMS
 EVIDENCE FOR BIOLOGICAL FACTORS IS NOT ADEQUATELY CONSIDERED: could be that BOTH BIOLOGICAL
AND PSYCHOLOGICAL FACTORS can separately produce the SAME SYMPTOMS, where both outcomes are
both SCHIZOPHRENIA – the DIATHESIS-STRESS MODEL where the diathesis may be BIOLOGICAL or
PSYCHOLOGICAL
DESCRIBE AND EVALUATE ANTIPSYCHOTICS AS A TREATMENT FOR SCHIZOPHRENIA

AO1

TYPICAL ANTIPSYCHOTICS

 CHLORPROMAZINE = taken as TABLETS, SYRUP or INJECTION – most dosages go up to 400mg to 800mg

 STRONG ASSOCIATION between CHLORPROMAZINE and the DOPAMINE HYPOTHESIS
 They work as ANTAGONISTS which BLOCK DOPAMINE RECEPTORS in the SYNAPSES of the brain,
REDUCING the action of DOPAMINE
 Initially dopamine production BUILDS UP but then it is REDUCED, IT NORMALISES NEUROTRANSMISSION
in KEY AREAS of the brain – REDUCING SYMPTOMS like hallucinations
 CHLORPROMAZINE is also an EFFECTIVE SEDATIVE – related to its effect on HISTAMINE RECEPTORS – used
to CALM PATIENTS, not only with SCHZOPHRENIA, but with other CONDITIONS

ATYPICAL ANTIPSYHOTICS

 created to MAINTAIN/IMPROVE the EFFECTIVENESS of the rugs and to MINIMISE SIDE EFFECTS
 CLOZAPINE – when REMARKETED it showed to be MORE EFFECTIVE than TYPICAL ANTIPSYCHOTICS and to
be used when other treatments FAILED
PEOPLE take a BLOOD TEST REGULARLY to check that they are NOT DEVELOPING AGRANULOCYTOSIS
(what it caused initially before the remarket)
CLOZAPINE is NOT used as an INJECTION due to its FATAL SIDE
CLOZAPINE binds DOPAMINE RECEPTORS TOGETHER but also acts on SERETONIN and GLUTAMATE
RECEPTORS = BETTER MOOD AND LOWERS DEPRESSION and ANXIETY as well as INCREASING COGNITIVE
FUNCTIONING
it is usually used when they are considered at HIGH RISK OF SUICIDE – 30% TO 50% of patients at some
point
 RISPERIDONE – MOST RECENT, developed as an attempt to be as effective as CLOZAPINE but WITHOUT
THE SIDE EFFECTS
 RISPERIDONE is believed to BIND DOPAMINE and SERETONIN RECEPTORS and binds them to dopamine
receptors MORE STRONGLY than CLOZAPINE = more EFFECTIVE and there is EVIDENCE it leads to LESS SIDE
EFFECTS
AO3

 EVIDENCE FOR EFFECTIVENESS: THORNLEY ET AL: REVIEWED studies comparing the effects of
CHLORPROMAZINE to CONTROL CONDITIONS using a PLACEBO – data from 13 TRIALS with 1121
PARTICIPANTS showed that CHLORPROMAZINE was associated with BETTER OVERALL FUNCTIONING and
LOWER SYMPTOM SEVERITY – data from 3 TRIALS with 512 PARTICIPANTS showed that the RELAPSE RATE
was also lower for CHLORPROMAZINE
ATYPICAL ANTIPSYCHOTICS – MELTZER: concluded that CLOZAPINE is MORE EFFECTIVE than TYPICAL
ANTIPSYCHOTICS and other typical antipsychotics – effective in 30% - 50% of treatment-resistant cases
where typical antipsychotics have failed // OTHER STUDIES compared CLOZAPINE and others like
RISPERIDONE but results have been INCONCLUSIVE, due some patients responding BETTER TO ONE THAN
ANOTHER
 SERIOUS SIDE EFFECTS: TYPICAL ANTIPSYCHOTICS – DIZZINESS, AGITATION, SLEEPINESS, STIFF JAW,
WEIGHT GAIN and ITCHY SKIN and long-term use – TARDIVE DYSKINESIA = caused by DOPAMINE
SUPERSENSITIVITY and includes INVOLUNTARY FACIAL MOVEMENTS like grimacing, blinking and lip-
smacking  MOST SERIOUS = NEUROLEPTIC MALIENANT SYNDROME – as the drug stops dopamine action
in the HYPOTHALAMUS – HIGH TEMPERATURE, DELIRIUM and COMA and can be FATAL (0.1% TO 2% of
people due to dosage)
ATYPICAL were developed to STOP SIDE EFFECTS and were generally succeeding BUT side effects STILL
EXIST in those taking CLOZAPINE so they have a BLOOD TEST to alert doctors of AGRANULOCYTOSIS (blood
condition)
 USE OF ANTIPSYCHOTICS DEPENDS ON THE DOPAMINE HYPOTHESIS: LOTS of EVIDENCE to show that the
ORIGINAL HYPOTHESIS ISN’T FULLY COMPLETE (what antipsychotics rely on) as in SOME PARTS of the
brain the DOPAMINE LEVELS are TOO LOW – if true then it’s NOT CERTAIN how antipsychotics
(ANTAGONISTS) help with SCHIZOPHRENIA. In our MODERN UNDERSTANDING, ANTIPSYCHOTICS
SHOULDN’T WORK
 PROBLEMS WITH THE EVIDENCE FOR EFFECTIVENESS: HEALY: some successful trials have had their data
published MULTIPLE TIMES, EXAGGERATING the evidence for POSITIVE EFFECTS and because they have
CALMING EFFECTS, it is easy to show that they have some positive effects on patients – NOT the same as
saying they really reduce the severity of psychosis + MOST PUBLISHED studies assess SHORT-TERM
BENEFITS rather than LONG-TERM and compare patients who keep taking ANTIPSYCHOTICS with those
SUFFERING WITHDRAWAL (having just stopped taking them)
DISCUSS THE USE OF PSYCHOLOGICAL THERAPIES AS TREATMENT FOR SCHIZOPHRENIA

AO1

CBT

 identify IRRATIONAL THOUGHTS and CHALLENGE them through an ARGUMENT or DISCUSSION in 5 to 20

sessions
 this helps the patient make sense of their THOUGHTS and SYMPTOMS and showing them that their
symptoms are UNLIKEY to be TRUE
 LOWERS ANXIETY but doesn’t IRRADICATE the SYMPTOMS of DELUSIONS, PARANOIA and
HALLUCINATIONS

FAMILY THERAPY

 improves THE QUALITY of COMMUNICATION and INTERACTION between MEMBERS = lowers STRESS in
the FAMILY to STOP A RELAPSE and lower EXPRESSED EMOTION
 PHAROAH ET AL: family therapy – LOWERS the STRESS of CARING for the RELATIVE, INCREASES the ability
to ANTICIPATE and SOLVE PROBLEMS, LOWER ANGER and GUILT and IMPROVES FAMILIES’ BELIEFS =
MORE LIKELY to comply to MEDS

TOKEN ECONOMY

 ESPECIALLY for those in PSYCHIATRIC HOSPITALS for LONG PERIODS who develop BAD HYGIENE or remain
in pjs
 DOESN’T CURE but does improve the QUALITY of LIFE and to be SOCIALLY ACCEPTABLE
 TOKENS = disc for DESIRABLE BEHAVIOUR, REINFORCEMENT and OPERANT CONDITIONING – should be
done IMMEDIATELY and they have SECONDARY REINFORCERS like SWEETS, CIGS AND MAGS, SERVICES
and PRIVILEDGES

AO3

 IMPROVES QUALITY OF LIFE NOT CURE: CBT – make sense and challenge symptoms / FT – lowers stress in
the family / TE – behave more socially acceptable = DOESN’T CURE LIKE DRUG THERAPIES
 ETHICAL ISSUES: helps those ONLY with MILD SYMPTOMS, NOT SEVERE = DISCRIMINATION + CBT
interferes with PATIENT’S PARANOIA – what point does it interfere with the individual’s FREEDOM OF
THOUGHT
 EVIDENCE OF EFFECTIVENESS: PHAROAH: reviewed evidence of FT and found MODERATE evidence to
show therapy gave a DROP IN READMISSION BUT ONLY VERY EFFECTIVE when with DRUG THERAPIES and
the evidence is INCONSISTENT + QUALITY = WEAK
 QUALITY OF EVIDENCE: SMALL SCALE – professionals compared patients BEFORE and AFTER TREATMENT =
POSITIVE BUT often LACK A CONTROL GROUP and NOT BEING RANDOMLY ALLOCATED
DESCRIBE AND EVALUATE THE INTERACTIONIST APPROACH TO BOTH EXPLAINING AND TREATING SCHIZOPHRENIA

AO1

DIATHESIS-STRESS MODEL – ORIGINAL

 DIATHESIS = VULNERABILITY / STRESS = NEGATIVE PSYCHOLOGICAL EXPERIENCE

 MEEHEL’S MODEL: ENTIRELY GENETIC through a SINGLE ‘SCHIZOGENE’ = a SCHIZOTYPIC PERSONALITY
which has the characteristic that it is SENSITIVE to STRESS
WITHOUT THE GENE: NO AMOUNT of STRESS can lead to SCHIZOPHRENIA
CARRIERS of the GENE: CHRONIC stress through CHILDHOOD and ADOLESENCE

DIATHESIS NOW

 NO SINGLE GENE (RIPKE ET AL) and involves PSYCHOLOGICAL TRAUMA (INGRAM + LUXTON)
 TRAUMA = DIATHESIS  READ ET AL: NEURODEVELOPMENT model that shows that EARLY TRAUMA
ALTERS the DEVELOPING BRAIN especially CHILD ABUSE etc.
e.g. HYPOTHALAMIC-PITUITARY ADRENAL (HPA) can become OVER-ACTIVE and MORE VULNERABLE

STRESS NOW

 ANYTHING that RISKS TRIGGERING SCHIZOPHRENIA – MOST RECENT research concerned factors such as
CANNABIS = INCREASES STRESS BY 7 TIMES

TREATMENT

 ANTI-PSYCHOTIC MEDS + PSYCHOLOGICAL THERAPIES (CBT)

 TURKINGTON ET AL: PERFECTLY POSSIBLE to believe in BIOLOGICAL CAUSES and practice CBT BUT needs
INTERACTIONALIST MODEL and is not possible with a PURELY BIOLOGICAL APPROACH
 In BRITAIN: is standard to have a combination of the two // USA: had a CONFLICT and SLOWER ADAPTION
to this approach

AO3

 DON’T KNOW EXACTLY HOW IT WORKS: LOTS of EVIDENCE of underlying VULNERABILITY and STRESS AND
know that it may lead to SYMPTOMS BUT DON’T understand the MECHANSMS by which the symptoms
APPEAR
 SUPPORT FOR THE EFFECTIVE OF TREATMENT : TARRIER ET AL: 315 patients were RANDOMLY ALLOCATED
to a MEDS + CBT group, MEDS + SUPPORTIVE COUNSELLING group or a CONTROL group (just MEDS) =
COMBINATIONS showed LOWER SYMPTOMS levels
 ORIGINAL IS OVER-SIMPLE: MULTIPLE GENES = HIGHER VULNERABILITY – NO SINGLE ‘SCHIZOGENE’ and
STRESS can be more than DYSFUNCTIONAL PARENTING  NEW: DIATHESIS – EARLY TRAUMA and GENES +
STRESS - CANNABIS
 EVIDENCE OF ROLE OF THE VULNERABILITY AND TRIGGERS: TIENARI ET AL: GENETIC VUL and PARENTING
STYLE (trigger) – ADOPTED from 19,000 FINNISH mothers with SCHIZOPHRENIA between 1960 + 1979 –
assessed CHILD REARING STYLE and tested with CONTROL without a GENETIC RISK = had HIGH CRITICISM
and LOW EMPATHY within their parenting style in the GENETIC RISK GROUP