Schizophrenia Flashcards
Positive symptoms of sz (appear in addition to ordinary symptoms)
Hallucinations- perceptual sensory experiences that in reality don’t exist.
Delusions- disturbances in thought content, irrational beliefs commonly linked to paranoia. Grandeur, Persecution, Control.
Disorganised speech- derailment (shifts themes), Incoherence (meaningless words put together), Repeat sounds.
Negative symptoms of sz (Thoughts beh taken away from psyche when ill)
Avolition (apathy)- lack of drive, reduced motivation to carry out activities.
Speech poverty- reduction in amount and quality of speech.
Affective flattening- poor range of emotional expression, lack of sensitivity.
What are the 2 ways of measuring reliability in sz?
Inter-rater: Whether 2 independent assessors give similar diagnosis of same person independently.
Test-retest: Whether tests used to deliver diagnosis (DSM and ICD) are consistent over time allowing a clinician to make the same diagnosis on separate occasions.
Inter-rater reliability evidence
+Classification systems seem to have become more reliable, Carson (91) claimed DSM-3 meant Psychiatrists now had a reliable classification system leading to much greater agreement over who did and didn’t have sz.
+Soderberg et al (05)- 81% agreement using DSM.
+Jakobsen et al (05)- tested ICD-10 reliability as 100 Danish patient were tested finding a concordance rate of 98%.
- -However, Whalley (01)- found IR correlations as low as +0.11.
WOR
Test-retest reliability evidence
+Wilks et al (03)- gave 2 alternate forms of cognitive screening test to sz patients in intervals of 1-134 days. Test reliability was high at 0.84 correlation.
+Osario et al (2019)- excellent TR reliability of +0.92 when using DSM5.
-Read et al (2004)- reported TR reliability of only 37% suggesting not fully reliable.
Describe the cognitive approach to sz
Focuses on role of mental processes and that sz is caused by “faulty thinking” and abnormal info processing which disrupts normal thought processing.
Sz is associated with several abnormal cog processes:
- Cognitive deficits- Impairments in thought processes (perception, memory, attention).
- Cognitive biases- Selective attention, when ppl notice, pay attention to or remember certain info better than other.
- Dysfunctional thought processing.
schema
What is Hemsley’s model of cognitive deficits and biases? (1993)
He perceived a breakdown in relationship between memory and perception in szs meaning schemas are not activated.
Therefore, szs can’t make sense of context. They experience difficulties processing visual and auditory info and don’t understand what info needs attention and what should be ignored.
They **can’t filter out irrelevant **sensory info so become overwhelmed with data which results in delusional thinking and disorganised beh.
2 kinds thought process dysfunction
What is Frith’s dysfunctional thought processing? (1992)
2 kids of dysfunction thought processing:
Meta-representation: Szs fail to meta represent meaning they can’t distinguish external speech from internal thoughts. They misattribute their thoughts to the outside world (hallucinations, when person hears voices it’s actually their inner speech being misinterpreted.)
Central control: Szs are unable to supress automatic responses while performing deliberate actions instead. Leads to positive symptoms of disorganised speech.
Yellowless
+RWA (cog explanation to Sz)
Yellowless et al (2002)- produced a machine that produced virtual hallucinations (e.g. telling you to kill yourself) to show szs their hallucinations weren’t real.
Success of (CBTp) provides support for the role cognitions have in causing Sz. NICE (2014)- meta-analysis found consistent evidence that when compared w antipsychotic medication CBT was more effective in improving social functioning.
Suggests understanding cognitive deficits of Sz helps create effective treatments.
-Negative and positive symptoms not equally explained (cog explanation to Sz)
Not a full explanation given as only some symptoms are explained (can only explain hallucinations and delusional thinking).
Not as effective in explaining symptoms like avolition (states they emerge due to stratergies used to control mental stimullation)
Therefore cog explanation of Sz is only a partial one.
Buckley
Factors affecting validity (comorbidity)
-Buckley et al (2009)- Comorbid depression occurs in 50% Szs, 23% OCD, 29% PTSD, 47% substance abuse.
-Jeste et al (1996)- Szs with co-morbid conditions are often excluded from research yet form the majority of patients. Research may not be applicable to majority of Szs.
Factors affecting validity (Symptom overlap)
-Ellason and Ross (1995)- Ppl w DID (dissasosiative identity disorder) have more first rank symptoms than Szs.
-Sz is not pathognomonic (does not have distinct symptoms) so is hard to differentiate from other disorders.
Studies in genetic explanations for sz
Gottesman large scale family study: Children w 2 sz parents have 46% concordance, one parent (13%), siblings (9%).
Joseph, twin studies: Pooled data from all sz twin studies prior to 2001, MZ (40%) concordance, DZ (7%) concordance.
Tienari et al, adoption studies: Large scale Finland study. If bio parents had Sz greater chance of getting Sz (6.7%) compared to control group (2%).
Ripke et al, candidate genes: Found 108 seperate genetic variations associated with Sz risk. Sz likely polygenic.
What can we conclude from genetic explanations of Sz?
+Strong evidence that genetics are a risk factor, relevant genes have been found to be associated with Sz.
-Concordance not 100% for Mzs, Can’t find specific gene so we can’t help to cure, involves huge number of genes which each make a small contribution.
What are typical antipsychotic drugs?
- Conventionals
- Combat +ve symptoms
- Dopamine antagonists (block receptors)
- Bind tightly to dopamine receptors (particulary D2 in mesolimbic pathway)
- Between 60-75% of D2 receptors must be blocked
- E.g. Chlorpromazine, haloperidol
What are Atypical antipsychotic drugs?
- Newer, second generation (fewer side effects, produce faster outcome)
- Combat +ve symptoms as well as helping -ve symptoms.
- Have lower affinity and occupancy for dopamine receptors as they bind and then dissociate allowing for anti-psychotic effect without motor side effects.
- Also acts on seratonin and glutamate receptors (useful for suicidal and -ve symptoms)
- E.g. Clozapine
Are typical antipsychotics effective?
+Revolutionary treatment: Rapidly reduced most disturbing symptoms (decreasing time in hospital) allowing patients to live relatively normal life.
+ Relapse rates are lower: Thornley et al studies comparing Chlorpromazine to placebo (control conditions), 13 studies w 1121 ptts showed Chlorpromazine was associated w better overall functioning and reduced symptom severity.
Are typical antipsychotics appropriate?
-Side effects:
Serious side effects including tardive dyslexia (involuntary facial movements). This is a side effect in 30% of antipsychotics and is irreversable in 75% of these cases (Hill 1986).
Neuroleptic malignant syndrome (NMS) is the most serious side effect where drug blocks dopamine action in the hypothalamus. Can lead to high temp, delirium, coma and can be fatal. 0.1-2% frequency.
Are atypicals effective?
+Supporting evidence of effectivness: Meltzer (12)- Clozopine more effective than typicals. Effective in 30-50% of cases where typical antipsychotics have failed.
-Ctradictory evidence of atypicals: Crossley et als meta-analysis found no sig diff in effectivness. (did note diffs in side effects- Atypicals, more weight gain wheras typicals, extrepyramidal effects).
-Healy (12): evidence for effectivness has flaws as most studies only show short-term effects, evidenec has been published multiple times (exaggerating the size of evidence base for antipsychotics), easy to demonstrate +ve effects due to powerful calming effect.
