Schizophrenia Flashcards
(36 cards)
1
Q
DSM-5
A
- criteria A: 2 or more of the following, at least 1 must be 1,2, 5
- 1) Delusions
- 2) Hallucinations
-3) disorganised or catatonic beh - 4) Beh symptoms (diminished emotion)
- 5) Disorganised speech
2
Q
Crow’s alternative classification system
A
- 2 types of SZ
- Type 1 pos symptoms (added) -> Hallucinations, delusions, fair prognosis, reversible, excess dopamine
-Type 2 neg symptoms (taken away) -> affective flattening, speech poverty, poor prognosis/, structural issues, irreversible
3
Q
Structural Issues - Ventricle enlargement
A
- Lateral ventricle enlargement projecting out into temporal lobes
- Jacobi + winkler -> pneumoencephalography to remove cerebrospinal fluid found 18/19 had enlarged ventricles but side effects meant it was unethical (headache, death)
-Johnstone et al First CAT scan of SZ showed large ventricles
4
Q
Ventricle enlargements - Temporal lobe
A
- crow et al-> enlargement confined to temporal horn + lobe which were predominantly on left Side of brain
- Barta et al -> relationship between left temporal gyrus size + severity of hallucinations, as gyrus volume decreases, hallucinations increase
5
Q
volume reduction- possible causes
A
- Thompson et al -> grey matter loss in adolescents with SZ parietal, temporal + frontal lobes
6
Q
Brain changes + time of onset
A
- Kemptom et al -> meta-analysis of 13 studies found ventricular dilation begins before or shortly after birth
7
Q
SZ + urbanisation
A
- Torrey + Bowler- reflecting aspects of social upheaval +stresses during industrial revolution
- most urbanised area most Sz cases
8
Q
Neural migration
A
- Bracha et Al -> neural migration responsible for fingerprints
- Fingerprints of twins with SZ very different
9
Q
FlU + SZ
A
- Medrick et dl-> those in 2nd trimester during flu epidemic more likely to dev SZ than matched controls
10
Q
Retrovirus + SZ
A
- monkey virus - Lillinoj et al found evidence for retrovirus activity in 29% of SZ patients compared with 3% of controls
-Karlsson et al (2001) found HERV-W retrovirus active in SZ patients
11
Q
DSM-5 delusions
A
- fixed beliefs
- grandeur: belief you have special power/ world figure
- persecution: belief others are plotting against them
- Thought insertion : belief others placing thoughts in head
- Broadcasting : belief own thoughts broadcasted Out loud
12
Q
DSM-5 Hallucinations
A
- Auditory: most common
- voices saying unpleasant things
visual may be of people/objects not really there
13
Q
Dopamine Hypothesis + Ampretamine
A
- Amphetamine boosts synaptic Levels of dopamine
- symptoms resemble paranoid (Type 1) SZ: auditory hallucinations, delusions, thought alienations
14
Q
treatment : Neuroleptics
A
- Delay + Deniker- first report use of chlorpromazine which had calming effect on agitation
- dopamine receptor blockage May be basis of therapeutic effects of neuroleptics
15
Q
Clinical description
A
- Lifetime prevalence is 1% + affects slightly more men
- Appears in late adolescence, early adulthood
16
Q
Avolition - Neg symptom
A
- Diminished motivation
17
Q
Asociality - Neg symptom
A
- severe impaired relationships
- want to be alone
- don’t desire close relationships
18
Q
Anhedonia - Neg symptom
A
- loss of experience/ interest of pleasure
- kring et al -> have deficit in anticipatory ( expected) pleasure but can experience pleasure
19
Q
Blunted Affect- Neg symptom
A
- Lack of outward expression of emotion
- motionless face
- flat, toneless speech
20
Q
Alogia - Neg symptom
A
- sig reduction in speech
- answer questions with 1/ 2 words
21
Q
Disorganised speech - Disorganised symptom
A
- problems organising ideas + speaking clearly
- loose associations
22
Q
Disorganised beh - disorganised symptoms
A
- inexplicable bouts agitation, act silly
- lose ability to organise beh
- catatonia - gesture repeatedly
23
Q
Brief psychotic disorder
A
- same symptoms as SZ but only last a few months
- TO diagnose SZ must last 6 months
24
Q
Genetic Influence
A
- Andreasen et al-> heritability of SZ is 0.77
25
Genetics research - family studies
-relatives of people with SZ are at higher risk
- risk increases as genetic relationship grows closer
- MZ twins 44.30 %
- DZ twins = 12.08 %
- sibling = 7.30
- children = 9.35
- Laursen et al > incidence of SZ was highest for children with both parents having SZ
26
Genetic research- Twin studies
- meta-analysis of 12 studies concluded that there is high heritability but also evidence of small but sig ENV contribution (Sullivan, Kendler)
- family + twin studies have shared + non-shared env factors
27
Genetic research- Adoption studies
- children who bio mother had SZ but were adopted eliminates effects of being reared in env with SZ
-Heston -> 10.6% developed SZ
28
Molecular genetic research
-multiple genes associated with SZ
-25 candidate genes for SZ
- one is DRD2 (werge) encodes specific D2 dopamine receptor
- genome-wide study found over 50 variation mutentions were 3x more common in SZ (McClellan)
- only some people with rare mutation have SZ
29
Dopamine Theory
- SZ related to excess activity of dopamine NT
- based on drugs effective in SZ reduce dopamine
- too simple to explain range of symptoms
-excess dopamine is related to pos disorganised symptoms
30
other NT
- MoIski et al treatment blocking serotonin 5HT2 recepter
-low glutamate found cerebrospinal fluid of SZ
- Bressan et al -> brain imaging shows decreased NMDA receptor (glutamate system)
31
Prefrontal cortex + SZ
- known to play a role in beh ( speech, emotion) that are disrupted in SZ
- MRI shows reduced grey Matter in prefrontal cortex
-dendritic spines may be lost meaning communication disisupted
32
connectivity
- SZ have less connectivity in White matter in frontal + temporal cortices -Assoc with genetic vulnerability of SZ
-less connectivity between frontparietal + Default mode networks correlated with neg symptoms
33
Excessive pruning
- cannon
-loss of synapses
- loss of necessary communication
34
treatment - medication
- Antipsychotics help some symptoms
-people who respond pos are kept on maintenance dose to continue effect
- common side effects = sedation, dizziness, blurred viSion
- extrapyramidal side effeits resemble Parkinson disease
35
Treatment- first gen antipsychotics
- first discovered
-reduce pus + disorganised
-no effect on neg
- 30 % don't respond
- common side effects: extrapyramidal (PD), drowsiness, restlessness
- chlorpromazine
36
Treatment- second -gen antipsychotics
- side effects: extrapyramidal (PD) , drowsiness, weight gain , insomnia, headache
- clozapine
- second gen more effective
- second gen produce fewer side effects
- Not very effective at reducing neg symptoms