schizophrenia Flashcards
classification of schizophrenia AO1
according to DSM-5- for diagnosis of sz, 2 of following symptoms must be present for at least a month, 1 being positive
POSITIVE- (experiences that are in addition to normal experiences)- hallucinations (additional sensory experiences e.g. seeing distortions in objects or hearing voices), delusions (irrational beliefs about themselves or the world e.g. the gov is out to get me)
NEGATIVE- (loss of normal experinces and abilities)- avolition (lack of purposeful, willed behaviour. no energy, socialability, affection or attempt at personal hygiene), speeh poverty (brief verbal communication style. loss of quality and quantity of verbl responses.)
biological explanation for schizophrenia AO1
GENETIC- genes code for biological processes- neural structure and biochemistry- not one single sz gene but a collection of gene locations that are associated w a higher risk of developing sz- disorder is polygenic
concordance rates are higher in families than found in general pop- the closer the related the higher the concordance rate- due to the increased genetic similarity
NEURAL CORRELATES- the variations in neural structure and biochemistry that are correlated with an increased risk of developing sz
THE DOPAMINE HYPOTHESIS- symptoms of sz are due to too much/imbalance of dopamine across the brain- excessive amunts in speech cnetres (broca) lead to auditory hallucinations- lower levels in areas like frontal cortex are linked to -ve symptoms
enlarged ventricles have also been correlated with sz
biological explanations for sz AO3
(-) claiming sz is biologically determined due to genetics and neurochemistry may make sufferers feel disempowered when diagnosed and passively reliant on drug therapies- cognitive soft determinist perspective suggests clients can reconstruct irrational mental processes, empowering sufferers to control their disorder actiely
(+/-) explaining sz as the basic cellular and chemical level has the advantage of the scientific prinicple of parsimony- has also led to highly effective drug therapies HOWEVER taking a biologically reductionist approach fails to consider evidence for psychological causes of sz
(-) diathesis stress approach more likely to be valid than biology alone- suggests the root cause is a biological/genetic weakness (diathesis) however an environmental stressor must be present.
psychological explanation for schizophrenia AO1
FAMILY DYSFUNCTION- sz symptoms are due to the interpersonal relationships within family- schizophrenogeric mother- paranoid delusionsresult from the influece of a cold, rejecting and controlling mother and a passive father- atmosphere of stress triggers psychotic thinking
double bind theory-due to mixed messages, feels unable to do the right thing- disorganised thinking and paranoi
expressed emotion- verbal interactions, exaggerated involvement indicating the sufferer is a burden via self-sacrifice
critism & control of the sufferers behaviour and physical, verbal, emotional hostility towards the sufferer= rejection
COGNITIVE EXPLANATIONS- the ability the process thoughts is dysfuntional- attention deficit theory- a faulty attention system cannot filter preconscious thought and gives too much significance to the info that would usualyy be filtered- causes +ve symptoms
psychological explanation for schizophrenia AO3
(+) meta analysis of 27 studies- found that relapse into sz is significantly more likely in families w issues w expressed emotion
(-) socially sensitive- suggests family causes sz- likely to cause additional stress and enxiety
(-) evidence in this area is correlational- could be argued that having a schizophrenic child is what caused the family dysuntion
drug therapy for sz AO1
ANTIPSYCHOTICS- medication used to control symptoms of psychosis e.g. delusions and hallucinations- pill or injection
TYPICAL ANTIPSYCHOTICS- 1st gen drug therapy used since 1950s, less popular due to severe side affects + only treat +ve symptoms. e.g. chlorpromazine- work as dopamine antagonists- reuce dopamine activity by blockingdopamine receptors at synapse- reduce +ve symptoms e.g. hallucinations and delusions- side effects= dry mouth, confusion, tardive dyskinesia
ATYPICAL ANTIPSYCHOTICS- 2nd gen drug therapy (1970s+) e.g. clozapine- block dopamine receptors but also act on others such as serotonin- adress negative and positive symptoms and side effects are less severe e.g. weight gain- less likely to cause involuntary movements
drug therapy for sz AO3
(+) cheap, qucik and easy compared to things such as CBT
(+) meta analysis of 212 studies- found drug treatment of symptoms was more effective than a placebo- shows drugs that target dopamine system are effective in reducing symptoms
(-) drugs only treat the symptoms not the cause
CBT to treat sz AO1
assumes sz results from dysfunctional thought processes
ABC(DE) model by ellis- therapists role is to identify and challenge irrational beliefs by logically disputing the reality of the faultycognitions (delusions), then cognitively reconstructing those beliefs into alternatives
reality testing- process in which the patientcan demonstrate that their irrational thoughts arent real
CBT to treat sz AO3
(+) no side effects
(-) high cost- train professionals
(-) drop out rates are high
family therapy to treat sz AO1
attempts to improve the home situation of person w sz - family dysfuntion can increase risk of relapse into sz
treatment is family centred- to change whole familys behaviour
family educated on symptoms and devlops techniques to reduce conflict, stress and improves communication
family therapy to treat sz AO3
(+) found that those w standard outpatient care- 50% relapsed by 9 months, 8% relapsed who recieved family therapy but after 2 years this increased to 50% but 75% with standard out patient care
(-) not a cure for the disorder- tries to manage symptoms and reduce chance of relapse
(-) problematic practical issues- length of therapy- often takes up to a year- drop out rate high
token economies to treat sz AO1
designed to make behaviour more manageable within a hospital to prepare long stay patients for transfer into the community
based on skinners op conditioning- tokens used as +ve reinforcement
patients immediately rewarded when they show a predefined target behaviour
tokens exchanged for somthing else
behaviours progressively changed with tokens first given for smallchanges in behaviour towards the ideal
token economies to treat sz AO3
(+) dickerson found that when reviewing the fndings of 13 studies - token economies can effectively improve adaptive behaviour of ppl with sz
(-)dont directly treat symptoms of sz- they only attempt to manage
-ve symptoms e.g. poor motivation, poor attention- usig skinarian principles can be seen as degrading- same treatment as used with rats
interactionist approach for sz AO1
suggests that the development of sz is due to the combined effects and interaction of biological and social factors and treatment more effective when compining bio/cog therapy
DIATHESIS STRESS MODEL- psychological concept that a disorder is due to the interction between a predisposed vulnerability (diathesis) and an environmental trigger later in life (stressor)
diathesis in sz- considered genetic vulnerability potentially resulting in a dopamine imbalance
stressors in sz- -ve environmental eperiences such as family dysfunction- emotional event triggers the disorder
importance in treating sz- suggest both biological andpsychological aspect to sz so treatment would combine psychologica and biological treatments
interactonist approach to explaining sz AO3
(+) positive real life application- treatment
(-) determining causal stress is dificult
(+/-) diathesis for sz is no longer considered single gene- its olygenic- includes vulnerabilities like emotional trauma acting as a diathesis by altering neurological development
