Schizophrenia Flashcards
Positive and negative symptoms
Positive symptoms (excess or distortion of normal functions) Delusions, hallucinations, disorganised speech, disorganised or catatonic behaviour.
Negative symptoms (reduced or loss of normal functions) Flattened affect, alogia (poverty of speech), apathy.
Delusions
Firmly held but erroneous beliefs involving misinterpretations of perception or experiences.
75% of hospitalised patients with psychotic disorder.
Problems integrating perceptions/experience with knowledge/history
Biased information processing.
Types of delusions
Persecution – being spied upon/persecuted/in danger.
Grandeur – having fame or power.
Control – thoughts/feelings/actions are controlled by external forces.
Reference – external events are referencing the individual.
Nihilistic – some aspect of themselves or world has ceased to exist.
Hallucinations
Sensory experience that isn’t actually present.
Auditory most common - voices commanding/commentating.
Visual 2nd common - abstract (colours) or specific (person).
Tactile – skin tingling.
Olfactory – smells.
Gustatory – unusual tastes of food.
Can be aware that hallucinations are not real.
Disorganised speech
- Derailment – quick jumps in conversation between topics.
- Tangentiality – answers questions with unrelated answers.
- Neologisms – Made-up words.
- Word Salad – no link between words or phrases.
- Poverty of content.
- Clanging – thinking driven by sounds and creation of logical connections based on these.
Disorganised or catatonic behaviour
Catatonic stupor - decrease in reactivity to the environment.
Catatonic rigidity – maintaining rigid, immobile postures.
Catatonic negativism – resisting attempts to be moved.
Catatonic excitement or stereotypy – purposeless and excessive motor activity consisting of simple, stereotyped movements.
Negative symptoms
Affective flattening – limited or no emotion.
Anhedonia – inability to react to pleasurable events.
Alogia – lack of verbal fluency, brief replies to questions.
Avolition – unable to carry out goal-orientated activities.
Must not be attributable to other factors.
Stages of schizophrenia
Late teens-mid-30s.
1: Prodromal - 5 years duration.
Slow deterioration from normal to delusional/dysfunctional functioning
Withdrawal, shallow emotion, decrease personal care & responsibility
2: Active
Full-blown psychotic symptoms emerge.
3: Residual
Positive symptoms cease.
DSM
Two or more. 1 month period (less if treated).
One must be 1), 2) or 3)
1) Delusions
2) Hallucinations
3) Disorganised Speech
Grossly disorganised or catatonic behaviour
Negative symptoms (e.g. avolition)
OLIFE rating scale
Four sub-scales used for diagnosis:
- Unusual Experiences - “Strange shapes in the dark?”
- Cognitive Disorganisation - “Speech hard to understand?”
- Introvertive Anhedonia – “Has dancing seemed dull to you?”
- Impulsive Nonconformity - “Do you stop to think things through?”
Prevalence and importance
0.3 - 0.7% lifetime prevalence.
Variation across race/gender/cultures.
Peak onset early to mid-20s males, late 20s females
Suicide, harm from violence to self or others, substance misuse.
Genetics
Siblings – 7%
DZ – 12%
MZ – 44%
MZ treated more similarly than DZ (shared environment).
Gottesman, McGuffin & Farmer (1987)
10 times more likely if first degree relative has disorder.
Adoption studies
Children reared apart from first-degree relatives with psychotic symptoms more likely to develop schizophrenia than controls.
21% more likely to have a relative with disorder.
Genetic x Environment
Predisposition is inherited.
No single gene.
“Perfect storm” of genetic predisposition and life events.
Dopamine Hypothesis
Neurotransmitters enable communication between brain cells.
Excess dopamine causes schizophrenia.
Dopamine receptors too sensitive – messages sent too often and too easily.
Dopamine thought to control and guide attention.
Evidence for dopamine hypothesis
- Anti-psychotics reduce dopamine activity, block receptors.
- Side effects like Parkinson’s symptoms = low dopamine.
- Parkinson drugs to raise dopamine cause psychotic symptoms.
- Amphetamines - raise dopamine, high doses cause symptoms.
- Brain imaging - high dopamine in the brains sufferers.
- Post-mortem - high dopamine and number receptors in sufferers.
Problems with dopamine hypothesis
Only associated with positive symptoms.
Antipsychotics only effective for positive symptoms.
Antipsychotics take 6 weeks to work, yet block dopamine in hours.
Modern drugs little effect on dopamine but inhibit serotonin.
Neurochemical interactions may be key.
Brain abnormalities
Smaller brain size Larger ventricles (control cerebral-spinal fluid)
Cause not consequence as:
Structural changes prior to first psychotic episode.
Brain abnormalities in 1st-degree relatives with no symptoms
Abnormal brain development in 2nd/3rd trimester of pregnancy.
General:
Frontal Lobes (movement, problem solving, planning, willpower)
Temporal Lobes (hearing, memory, emotion, language, taste/smell)
Basal Ganglia (motor movements)
Cerebellum (muscular activity)
Schizophrenia:
Frontal Lobes (cognitive, memory/attention, blunted affect, social withdrawal).
Temporal Lobes (auditory hallucinations and thought disorder)
Basal Ganglia (executive tasks and goal-directed activity)
Cerebellum (verbal ability and narrative memory)
Psychodynamic
Freud – Primary Narcissim
Regression to oral stage - preoccupation with the self.
Caused by cold/un-nurturing parents.
Regression = loss of reality.
Thought/communication withdrawal - self-centred focus
Hallucinations/Delusions - re-establish “contact” with reality
Schizophrenogenic Mother – rejecting, distant, demanding, dominate
Conflicting messages = child withdrawing from reality
Problems -no evidence of sufferers having this type of mother.
Behavioural theories
Ullman & Krasner (1975)
Bizarre behaviours learned through operant reinforcement
Learn to attend to irrelevant cues due to poor family functioning
Bizarre behaviour gets attention/reward - reinforcing it
Reinforcement and extinction
Ayllon, Haughton & Hughes (1965)
Female sufferer rewarded for carrying a broom
Two (unaware) psychiatrists asked to give opinions
Described as a ritualistic magical behaviour, where the broom probably represents 1) a child 2) a phallic symbol or 3) sceptre
Ayllon (1963) – Extinction of behaviour
Female patient who insisted on wearing layers of excess clothing (25Ibs) only allowed to enter cafeteria if she weighed 2Ibs less than the previous day.
Normal dressing exhibited within 14 weeks.
Cognitive theories - Attentional processes
Attentional processes, attributional biases and TOM deficits
Attentional processes
Inability to associate relevant events/making irrelevant associations
Overattention to irrelevant aspects of environment.
Deficits in orienting response & highly distractible on cognitive tasks.
Cognitive theories - TOM deficit
Ability to understand own and others mental states.
Frith (1992) – deficit in inferring beliefs/attitudes/intentions of others
Corcoran et al (1997) – jokes involving inferring the mental state of others difficult to understand.
Cognitive theories - Attributional bias
Bias attribute negative event to external, positive to internal causes
Excessively stable/global attributions to negative life events.
Explains high incidence of reports of persecution in sufferers.
Cognitive theories - information processing
Morrison (2001)
Bias labelling cognitive intrusion as threatening. Leads to negative mood and physiological arousal.
Freeman et al (2002)
Four factors contribute to emergence and maintenance of delusions:
1) Hallucination/delusion with no obvious explanation
2) Anxiety, depression & worry creating negative bias
3) Reasoning bias that seek to find evidence for delusion.
4) Social factors such as isolation
Sociocultural factors
Diathesis-Stress
Sociogenic hypothesis – low economic classes experience more life stressors such as unemployment, poor education, crime and poverty.
Bjern et al. (2004) – immigration a risk factor
Social-selection theory - Intellectual/behavioural/motivational problems cause downward drift towards unemployment and poverty and low socio-economic status. Accounts for sufferers from high socioeconomic families.
Social Labelling theory – symptoms are influenced by diagnosis:
Others behave differently toward them.
Sufferer plays into it and behaviour defined as symptoms.
8 normal individuals infiltrated a hospital claiming to have symptoms.
(Rosenhan, 1973)
Family influence
Double-Bind Hypothesis (Bateson et al., 1978)
Conflicting messages in childhood = difficulty interpreting environment and social withdrawal.
Communication Deviance (CD) – communication that would be difficult for ordinary listeners to follow and understand.
Wahlberg et al (2004) – CD a stable characteristic in families of sufferers and a predictor in adopted children.
Expressed emotion (EE)
Amount of emotion displayed between people/family.
Stems from findings where patients returning to family home more likely to relapse.
Hostile/critical environments - sufferer shown intolerance in strategies for coping with their symptoms.
High EE - predictor of relapse.
Prefrontal lobotomy
Severs pathways between the frontal lobes and lower brain
For particularly disruptive or violent patients
More passive
Fatality rates high
Intellectual and emotional capacity severely affected
Drugs
1st line of treatment 40s/50s
Developed when antihistamines calmed patients before surgery
Antipsychotics or Neuroleptics
Typical (older)/Less typical (targeted)
Suppress symptoms rather than cure
Low motivation, dry mouth, blurred vision, dizzy, low blood pressure
Tardive Dyskinesia - 1/5 patients - resembles Parkinson’s.
Atypical (recent)
Less relapse, side effects and broader effect.
Block excessive dopamine and serotonin activity in the brain.
Psychological treatments
Social skills training, CBT.
Personal Therapy
Life challenging upon release from hospital
1. Group or individual teaching
2. Identify signs of relapse
3. Relaxation techniques
4. Identify inappropriate responses and learn adaptive ones
5. Identify inappropriate and dysfunctional thinking
6. Deal with negative feedback & conflict resolution
7. Medication routine compliance
Family intervention
Reduce levels of EE and CD
Teaching families about the diagnosis, symptoms
Nature of medication and how to help the sufferer to comply
Signs of relapse and how to deal with them
Identify problems and solve them as a family
Blame avoided
Modelling, counselling and behaviour training
Reduces risk of relapse, increase social functioning, more effective longer it continues.
DSM Schizophrenia Spectrum & Psychotic disorders
Delusional Brief Psychotic Schizophreniform Schizophrenia Schizoaffective Substance/Medication induced Unspecified catatonia
