Schizophrenia Spectrum Disorders Flashcards
Historical Context
Kraeplin (1986); described systematically- inappropriate behaviour, stereotypes motor behaviour, hallucinations
First person to conduct follow up studies of MI
Dementia praecox- early onset with deteriorating course & no recovery
Brueler (1926); coined the term schizophrenia
Disagreed that the condition was early onset & always had poor recovery
Schizo=split, phrenia= mind
Loosening of associations in thoughts or between emotions & thoughts
Schizophrenia
Severe & enduring form of psychosis
Impaired insight & reoccuring & ongoing loss of contact with reality
Much variation between individual sufferers
Psychosis
Loss of contact with reality
Disturbances in thought & language, sensory perception, emotion regulation, distortions in perception & reality which are different to those experienced by others around them
May lead to false beliefs & delusions about self & others
Effects of psychosis
Social withdrawal
Preoccupation with personal world
Often difficult to maintain/obtain job
High incidence of homelessness; 11% average, rates higher in women, young people & chronically homeless, just under half not receiving treatment
Liddle’s Tripatrite Model
Looks at which symptoms cluster together & then examine any underlying mechanism that contribute to these symptom clusters
Factor analysis of the signs & symptoms have identified 3 clusters
1) disorganised; speech, behaviour & flat or inappropriate mood
2) positive; hallucinations & delusions
3) negative; absence of activation, apathy, lack of motivation or poverty of speech
Each cluster may have different causes
Positive symptoms
Hallucinations
Delusions
Disorganised speech
Disorganised or catatonic behaviour
Negative symptoms
Flattened affect; lack of response to emotional stimuli
Poverty of speech
Apathy/avolition; lack of energy, lack of ability/interest in normal functioning
Cognitive dysfunction
Alogia; negative thought disorder (poverty of speech content & quality)
Anhedonia; inability to experience pleasure
Asociality; lack of social interaction
Cognitive deficits
Often present before onset of psychotic symptoms
May have developmental role
Poor insight, impaired attentional process & memory deficits
Disorganised symptoms
Disorganised speech
Bizarre behaviour; diverse forms, inappropriate affect
Schneider’s first rank symptoms
Audible thoughts, voices arguing/discussing/commenting, somatic passivity experiences, thought withdrawal, influenced thought, thought broadcasting, delusional perceptions, all other experiences involving volition, impulses & effect
2nd rank symptoms; other disorders of perception, sudden delusional ideas, perplexity, depresssive & euthoric mood changes, feelings of emotional impoverishment
Demographics
0.3-0.7% lifetime prevelance rate Most sufferers 15-35yrs Among top 10 cases of disability worldwide Men & women both affected 24 million sufferers worldwide Most sufferers require lifetime care
Burden of schizophrenia
Life expectancy reduced by 15 yrs
Majority of premature mortality due to CHD
risk; smoking (70%), obesity (leading to diabetes), hypertension
About 1/20 commit suicide, usually near illness onset
Increased risk (10%) of alcohol problem or drug misuse
Burden on families & carers
Widespread stigma
Cost & consequences of schizophrenia
Occupy more beds than any other psychiatric disorder
Rationalisation of resources introduces pressure to discharge patients into the community
Revolving door patients
Reinforcement of the negative stereotype of schizophrenia held by the general public
Course of psychotic illness
Group 1 (22%); 1 episode only- no impairment Group 2 (35%); several episodes with no or minimal impairment Group 3 (8%); impairment after the first episode with subsequent exacerbation & no return to normally Group 4 (35%); impairment increasing with each of several episodes with no return to normality
Delusions overview
Experienced by 75% of those hospitalised due to psychotic symptoms
Firmly held beliefs that usually involve a misinterpretation of perceptions or experiences & become fixed beliefs that are not amendable to change in light of contradictory evidence
Types of delusion
Delusions of persecution
Delusions of grandeur
Delusions of reference; natural environmental event has special meaning
Bizarre delusions; first rank e.g. abduction
Delusional misidentification; imposters
Delusions of guilt or worthlessness
Nihilistic delusions; belief that self, body, part of, other person or world doesn’t exist
Erotomanic delusions; another person, often important or famous, is in love with them
Delusions of control
Thought insertation; have to distinguish from auditory hallucinations
Thought withdrawal: thoughts taken from you
Thought broadcasting; belief that others can here thoughts
Thought block; sudden loss of train of thought
Hallucinations
False sensory experiences
Differentiate between illusions
Auditory hallucinations most common (70% experience it)
Associated with earlier age of onset
Auditory hallucinations
Vary
Running commentary, 1st/2nd person voice, group, discussing individual in critical way
Perceived as external but over time come to have insight of origin
When experienced there is neural activity in brain regions involved in speech generation & sound perception
Reality-monitoring effect; difficulties in distinguishing whether something is real or imagined
Brebion et al (2000)
Schz vs controls
Asked to remember list of self-generated or experimenter generated words
Scz more likely to list false positives
More likely to say that self-generated words were experimenter generated
Motor systems
Catalonia; severe motor abnormalities
Catatonic stupor (freezing in awkward poses)
Excitement (over-activity)
Stereotyped movements (rocking, rubbing)
Waxy flexibility (awkward positions maintained)
Disorganised thinking (speech)
Derailment/tabgeniality; sentence goes off course, unrelated topics
Word salad; unintelligible random mixture of words & phrases
Neologisms; percuiliar combinations of words or a word coined by a psychotic which is meaningless except to the coiner
Clanging/clang associations; words chosen for their sound rather than meaning
Poverty of content of speech; lack of additional, unprompted content seen in normal speech
Schizophrenia spectrum disorders
Spectrum based on a gradient of psychopathology & impairment
4 main disorders; delusional disorders, brief psychotic disorder, schizophrenia, schizoaffective disorders
Delusional disorder
One or more delusions lasting at least 1 month
Normal functioning not markedly impaired, behaviour not bizarre
Any manic or depressive episode has been brief in relation to delusional episode
Disorder is not directly attributable to use of substance or medication
Brief psychotic disorder
Sudden onset of at least one of the main psychotic symptoms
Change has to occur within 2 weeks
Associates with emotional turmoil & overwhelming confusion
Schizophrenia
At least 2 must be present; delusions, hallucinations, disorganised speech, highly disorganised or catatonic behaviour, negative symptoms
Ability to function in 1 or more major areas e.g. work markedly diminished
Continuous signs of disturbance for at least 6 months
Schizoaffective disorder
Presence of significant mood episode alongside psychotic symptoms
Delusions or hallucinations for 2 or more weeks without occurance of major mood episode
DSM-5
Raises symptom threshold; individual muse exhibits at least 2 specified symptoms
No special attribution of bizarre delusions or 1st rank auditory hallucinations (2 or more voices conversing) due to poor reliability
No longer identify subtypes of schizophrenia; dimensional scale provided instead
Psychosis spectrum
Schizotypy; continuum of personality characteristics
Schizophreniform disorder; time dependent diagnosis
Attenuated psychotic symptoms syndrome; psychosis risk syndrome, mild psychotic symptoms, poor diagnostic reliability
Psychosis proneness can be used to investigate presence of sub-clinical levels of psychotic symptoms
Schizotypal personality
Dimensional model of schizophrenia
Found with cluster A personality disorders; odd or ecentric
Pervasive pattern of social & interpersonal deficits marked by acute discomfort with reduced capacity for close relationships, cognitive or perceptual distortions & eccentricities
Superordinate factors of traits are -ve,+ve or disorganised
Subordinate factors are; ideas of reference/suspiciousness, odd or ecentric behaviour, constructed affect/no close friends, odd speech, excessive social anxiety, unusual perceptual disturbances, odd beliefs/magical thinking
Psychotic symptoms in the general population
Bentall (2007); firmly opposed to the biomedical model
Argues that no clear distinction exists between those diagnosed with mental illnesses & the well
Insists that schizotyoal existences are common
Rufus May; heading voices network
The divided self; an existential study in sanity & madness
Aimed to make madness comprehensible
Revolutionised the way we perceive mental illness
Using case studies of patients he’d worked with, Dr Laing argues that psychosis is not a medical condition but an outcome of the divided self or the tension between the 2 personas with ya (private & public)
The dangerous patient
Walsh at al (2002); violence & schizophrenia, examining the evidence
People with a diagnosis of schizophrenia are more likely than other members of the general pop to be violent
But proportion attributable to scz is small (<10%)
Co morbid substance abuse considerably increases the risk
Violence as a result of delusional beliefs is a common cause
Stress-diathesis model of causation in psychosis
Effects of stress on cortisol production may be mediating factor
Stressors; early parental factors, dysfunctional family relationships, inability to cope during adolescence
Genetic risk/prevelance
MZ twins; 48% DZ twins; 17% Siblings; 9% Parents & half siblings; 6% General pop; 1%
Genes for schizophrenia overview
Not one gene; does not follow Mendelian pattern of inheritance
DRD2 susceptibility gene
DRD2; altered D2 receptor available in areas with dopaminergic activity (striatum & cortisol regions)
SNP Rs6277; genetic variation resulting in altered risk of developing schizophrenia
Effects of genotypic variation may affect cognition; working memory, attentional processes & response inhibition
COMT susceptibility gene
COMT; regulation of dopamine metabolism at synapses
COMT Val158Met; associated with cognitive dysfunction in schizophrenia
Dopamine hypothesis
Antipsychotic drugs like chlorpromazine block DA receptors (D2); long term usage can cause parkinsons type symptoms
Amphetamine psychosis resembles schizophrenia: blocks DA transporters, exacerbates symptoms
May give added salience to cognitions (positive symptoms)
Dopamine pathways
Pathway to prefrontal cortex leads to more negative symptoms
Pathway to nucleus accumbens leads to more negative symptoms
Evidence to support the DA hypothesis
Antipsychotic drugs most effective in treating schizophrenia & dopamine antagonists
Side effects of antipsychotic drugs are similar to those seen in Parkinson’s
The drug L-dopa produces schizophrenia like symptoms in some people
Amphetamines can make psychotic symptoms worse in some schizophrenics
Evidence against the DA hypothesis
Many people with schizophrenia are not helped by DA antagonists
Symptoms subside a lot slower than would be expected if the disorder were just a neurotransmitter imbalance
Negative symptoms are not wholly treated by antipsychotics
Role of other neurotransmitters
Several psychotomimetic drugs (induce psychosis like experience) exist which act on other neurotransmitter symptoms
LSD & psilocybin act on 5HT, 5HT1 or 2a receptor agonists, newer antipsychotics act to block 5HT as well as DA
ketamine & PCP act as glutamate antagonists; glutamate is increased in frontal cortex, hippocampus & amygdala, best drug model of certain-psychotic-like experiences
Neuroanatomical changes in schizophrenia
26% increase in ventricle size
Decrease in grey matter; specific areas affected more than others (hippocampus, PFC, anterior cingulate cortex, insular cortex, white matter)
Neurodevelopmental model
Genes involved in neurodevelopment and/or environmental insults in early life lead to aberrant brain development, which in turn predisposes to the later onset of psychosis
Dominant paradigm guiding research 80’s
Schizophrenia result of abnormal brain development, secondary to genetic predisposition & early environmental factors
Ventricular enlargements don’t change, altered cytoarchitrcture & absence of gliosis all led to neurodevelopmental theory over neurodegenarative
Developmental risk factor model
Early causes; genetic, obstretric complications
Childhood vulnerability
Late causes (adolescence); life events, drug abuse
Dysplastic networks, cognitive impairment & social difficulties
Eventually psychosis
Environmental risk factors
Place/time of birth; winter, urban
Infection; flu, respiratory, rubella (high risk), poliovirus, CNS
Prenatal; famine, bereavement (high risk), flood, unwantedness, maternal deprivation
Obstetric: Rh incompatibility, hyproxia, CNS damage (v high risk), low birth weight, pre-eclampsia
Psychosocial factors
Urban poor more at risk
Culture
Increased stress in lower SES pop
Social isolation
Migration
Socio-genic hypothesis; environmental causality
Socio-selection theory; person selects environment
Thought & communication styles in families
Schizophrenigenic mothers; the way they communicate may lead to child’s psychosis
High expressed emotion in family; more likely to be sciziohrenic (criticism & hostility), particularly concealing, controlling & denying meaning
Gene x environment interactions
Occur when the effect of exposure to an environmental pathogen on health is conditional of a persons genotype (pathogenesis model)
First evidence that genotype moderates the capacity of an environmental risk factor to bring about mental health problems reported in 2002: role of genotype in cycle of violence in maltreated children
COMT genotype & cannabis use in early adolescence
Increases risk of developing psychosis & schizotypy
Sub-clinical features in development
Delayed motor milestones Speech defects, solitary Cognitive decrement Social anxiety Eventually schizophrenia
Cognitive domains affected in psychosis (willed action & working memory)
Willed action; diminished capacity to regulate willed (goal-directed) & stimulus-driven action systems
Working memory; studies of animals & of cognitive function in normal, brain-injured & schizophrenic subjects support the theory that a defect in working memory (ability to guide behaviour by representations) may be fundamental impairment leading to schizophrenic thought disorder
Cognitive domains affected in psychosis (cognitive dysmetria & deficits & biases)
Cognitive dysmetria; a disruption in neuronal circuitry produces difficulty in prioritising, processing, coordinating & responding to info, can account for broad diversity of scz symptoms
Deficits & biases; attentional processes (over/under attention) can lead to attribution am & interpersonal biases (external attributes, cognitions of persecution), deficits in their of mind & link to paranoia
Reasoning bias & delusion formation
RB; jumping to conclusions, over-adjustment of probability estimates following a single instance of disconformity evidence
Seen in people at risk of schizophrenia as well
Threat-anticipation model of persecutory delusions
4 factors important in development of cognitive biases involved in persecutory delusions
1) anomalous experiences that do not have an obvious explanation e.g. hallucinations
2) anxiety, depression & worry may cause a bias towards negative thinking & threatening interpretation of events
3) reasoning biases leading to jumping to conclusions rather than questioning
4) social factors such as isolation & trauma
Psychology of alien abduction; McNally et al (2012)
Traits associated with identifying as an alien abductee;
Experiencing sleep paralysis & hallucinations when waking
Tendency to recall false memories
High levels of absorption
New age beliefs
Familiarity with cultural narrative of alien abduction
Interpretational bias
13% of individuals hear voices
In psychosis, there is a bias towards interpreting voices as threatening, can lead to increased voice hearing
Failure in signal detection leads to interpretational bias
Increasing externalisation & controllability leads to increased developing of relationship with the voice(s)
Psychodynamic model of psychosis
Caused by regression to a previous ego state of primary narcissism
Results in loss of contact with reality
Due to cold & unnurturing parents
Behavioural model of psychosis
Role of learning & conditioning
Bizzare behaviours may arise due to operant conditioning
May be due to difficulty attending to appropriate social cues
Evolutionary model of schizophrenia
Consequence of the evolution of language
Scz individuals have less left-sided dominance for language
Scz associated with atypical patterns of lateralisation
Purported to explain more severe form of psychosis seen in makes who have increased lateralisation
The role of dopamine
One if it’s roles is to mediate the salience if environmental events
& internal representations
Dysregulated hyperdopaminergic state may lead to abberant assignment of salience to elements of ones experiences
Psychosis as a state of aberrant (non-normal) salience
Aims to link the biology, phenomenology & pharmacology in scz into a unitary framework
