SCHIZOPHRENIA Flashcards
1
Q
What is the prevalence of schizophrenia, and how is it characterised?
A
- Schizophrenia > lifetime prevalence of 1%
- characterised > by diverse range of clinical symptoms > forming a heterogeneous clinical picture.
2
Q
What is the economic impact of schizophrenia compared to other health conditions?
A
Schizophrenia imposes enormous economic burden on society, surpassing the combined cost of all cancers in the United States (Thaker and Carpenter, 2001).
3
Q
What is Dementia Praecox?
A
- Dementia Praecox : describe a disorder characterised by psychotic symptoms accompanied by a progressive early cognitive decline
- term defined by Emil kraepelin > distinguished between Dementia Praecox and Manic depression
4
Q
how did Eugen Bleuler describe what is schizophrenia?
A
- describes failure to integrate feelings, thoughts, memories, perceptions into coherent whole
- 4 A’s > loosening of associations, inappropriate effect, ambivalence and autistic behaviour
5
Q
what are the symptoms of schizophrenia?
A
- positive > hallucinations, delusions, thought disorder & bizarre behaviour
- negative > flat affect, logia, apathy, attention disorder
- negative symptoms associated w/ poorer premorbid adjustment> poorer performance on cognitive tests & response to treatment
6
Q
what is meant by positive symptoms of schizophrenia?
A
- make themselves known by their presence > delusions, hallucinations or thought disorders
- thought disorder > disorganised, irrational thinking
- hallucinations > typically auditory > hearing voices but can also be visual
7
Q
what is meant by delusions?
A
- positive symptom
- beliefs that are contrary to fact
- delusions of Persecution > false beliefs that others are plotting & conspiring against oneself
- delusions of Grandeur > false beliefs in ones power & importance > one has godlike powers or special knowledge no one else has
- delusions of Control > related to delusions of persecution > person believes they’re being controlled by others by radar or radio receiver implanted in their brain
8
Q
what are cognitive deficits for understanding schizophrenia?
A
- refer to impairments in various cognitive functions or mental processes that can affect perception, attention, memory, reasoning, and problem-solving
- they are present years before first clinical symptoms
- predict outcomes more reliably than clinical symptoms
- increasingly recognised as important target for therapeutic interventions
- Study of cog deficits helps understanding complex genetic & neurophysiological aspects of schizophrenia.
9
Q
what are the DSM-5 criteria for schizophrenia?
A
- two or more symptoms lasting at least 1month
- delusions, hallucinations, disorganised speech, abnormal psychomotor behaviour
- negative symptoms (blunted affect, avolition, ascociality)
- functioning in work, relationships or self care have declined since onset > signs for at least 6m
10
Q
what are the phases of symptoms for schizophrenia?
A
- Prodromal Phase: Early signs emerge, e.g.> subtle behavioural changes & social withdrawal
- Acute Phase: Pronounced symptoms like hallucinations & delusions become active
- Stabilisation Phase: Symptom severity lessens; medication and interventions aim to stabilise the individual.
- Residual Phase: Lingering symptoms persist but are less intense, with potential cognitive deficits.
11
Q
what are the risk factors of schizophrenia?
A
- heritability > biological disorder that is heritable > twin studies & genetic risk = increases susceptibility
- environment >epidemiological studies (study of distribution & causes of diseases in populations), examine freq of diseases in groups of ppl in diff environment & correlate diseases freq w/ factors in these environment > schiz related to environmental factors; seasons of birth (winter birth), viral epidemics, population density, prenatal malnutrition, maternal stress & substance abuse
12
Q
what was the AESOP study?
A
- epidemiology : the aetiology & ethnicity in schizophrenia & other psychoses ( AESOP) study
- compared first incidence of psychosis over 2yrs in 3 centres> incidences of diagnosis > greater in South ldn compared to Bristol & Nottingham = effects of environment
- 3 fold increased incidence of psychoses in black minority ethnic group compared to white British
13
Q
what Is the vulnerability stress model in relation to schizophrenia?
A
- combination of genetic vulnerability and environmental stressors contributes to the onset of the disorder
- Genetic predisposition and certain life events interact, with the interplay surpassing a threshold leading to the manifestation of schizophrenia symptoms.
14
Q
what is the dopamine hypothesis?
A
- 1960 > link between dopamine & Parkinson’s disease
- dopamine hypothesis suggests positive symptoms of schizophrenia are causes by overactivity of DA synapses
- chlorpromazine developed as antihistamine in France > calming effect = suggested use of psychosis treatment = started research into use for schizophrenia
15
Q
what do antipsychotic drug side effects suggest about role of dopamine?
A
- act by modulating dopamine neurotransmission, specifically by blocking dopamine receptors
- chlorpromazine > antagonises dopamine activity by binding & blocking domaine receptors
- amphetamine & cocanine = dopamine agonists & produce psychosis
16
Q
what are the problems with medication associated with dopamine hypothesis?
A
- neg & cognitive symptoms are not alleviated by classical antipsychotic drugs
- typical drugs cause parkinsonian side effects (temporary) but patients who receive long term treatment = tardive dyskinesia
- atypical drugs =. less likely to have extra-pyramidal side effect & more likely they reduce positive symptoms + neg ones
17
Q
what are extrapyramidal side effects?
A
- most schiz drugs cause extrapyramidal side effects > nerves & muscles controlling movement & coordination
- resemble some of symptoms of Parkinson’s disease : trade dyskinesia > repetitive & involuntary movements or tics, symptoms may appear months or years after taking drugs > after drug stopped =. symptoms can sometimes persist
18
Q
what are typical and atypical medication?
A
- typical = block mainly D2 receptors & mainly effective for positive symptoms
- atypical neuroleptics act on various neurotransmitters >clozapine acts on D2, D4 and serotonin receptors but only some bindings to D2
- neuroleptics act quickly on synapses but don’t alleviate symptoms for weeks > initial increase in firing followed by decrease at time when neuroleptics effect come to play
19
Q
what are striatal dopamine levels and schizophrenia?
A
- correlates w/ severity of symptoms & neurocognitve dysfunction (verbal fluency)
- Elevated dopamine activity in the striatum > excess is associated with positive symptoms, and antipsychotic medications often target dopamine receptors in the striatum
20
Q
what is the relationship between dopamine in the mesolimbic system?
A
- Dysregulation of dopamine in the mesolimbic system > linked to reinforcement and reward expectations
- this abnormal dopamine activity = reinforce inappropriate behaviours, incl > delusions
- Antipsychotic medications target this dopamine dysregulation to alleviate positive symptoms in individuals with schizophrenia.
21
Q
what is the role of the prefrontal cortex in schizophrenia?
A
- weinberger > negative symptoms of schizophrenia = caused by hypofrontaity > decreased activity of frontal lobes
22
Q
what causes abnormal frontal activity?
A
- dopamine > agonists e.g. cocanine & amphetamine = postive sympto,ms
- NMDA > ketamine & PCP = postive & negative symptoms > inhibiting NMDA = decreases dopamine utilisation
- GABA > defects in inhibitory GABAergic transmission in dIPFC disrupts neural activity = cog defects e.g. working memory
23
Q
what is the role of NMDA receptor in antagonists?
A
- PCP (phencyclidine) & ketamine are both NMDA receptor antagonists = they block the activity of the NMDA receptors in the brain > This blockade results in disruptions in glutamate neurotransmission> induce positive, negative, and cognitive symptoms similar to schizophrenia
