Week 11 Lecture 11 - Schizophrenia (DN) Flashcards Preview

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60

Neurodevelopmental animal model

could be born early but disorder doesn't manifest

Lesion in rats
changed in PFC only in adolescence
credence to idea that developmentally specific avenues at which abnormalities express themselves

61

How have late brain developmental factors have been suggested to play a role in the development of Schizophrenia?

Late brain developmental factorsmay also play an impt role
peak age onset = late teens/early adulthood
SYNAPTIC PRUNING - born with all neurons
scan age 5 = lots of grey matter (abundance of connections)
overtime = lots of blue (pruned back, use it or lose it)
areas of frontal lobe are last to develop
IDEA: is in S that there is an abnormality in this pruning process, i.e., there is an acceleration of this process(maybe too much pruning going on)

62

Summarise the early predisposition/later maturational processes explanation for developing Schizophrenia?

Basic Model:
Early insult > predisposes > interacts with later maturational processes (pruning) > leads to onset of disorder
all interacts with genes & environment

Neurodevelopmental > Affective Continuum
No clean-cut off between Schiz & Affective, but where you are on the continuum will determine the disorder you end up getting

comb. of genetic vulnerability & environmental impact on your brain circuits
125:00

63

Give brief timeline for development of antipsychotics

1950's - Antihistamines
Paul Charpentier: developed Chlorpromazine (Thorazine) later effective in treating S
by 1990 - over 40 antipsychotics introduced
Late 50's, early 60's:Extra-pyramidal side effects (EPS) > Motor problems
1960's - Clozapine - few EPS side effects & helped treatment-resistant patients - although led to heart problems, agranulocytosis
still used today, but heavily monitored
Clozapine then led to atypical antipsychotic drugs which reduce psychotic symptoms with few EPS (but have other side effects, weight gain, high blood pressure etc)

64

what was the Catie trial?

compared the efficacy of 1st and 2nd generation drugs
found 2nd gen atypical just as effective
both types of drugs 70% discontinued use coz of side effects

2nd phase
Clozapine more effective in more severe cases

MAIN POINT: no real difference in efficacy, difference is in side effects

65

1. How do antipsychotic drugs act?
2. What kind of symptoms do they effectively treat?
3. What is the time course of treatment?

1. all anti-psychotics act by blocking D2 receptors
2. Only effective in treating positive symptoms
- ineffective for negative & cognitive symptoms
- ineffective in 30% patients
3. treatment is ongoing, with maintenance doses

66

What difference has been found in treatment responders compared to treatment non-responders?

Treatment responders have elevated Dopamine level in Striatum

maybe there is a Dopaminergic form of Psychosis (responsive to treatment)
and another form of Psychosis that is not responsive

135:30ish

67

What was found in a study that looked at rate of exposure to antipsychotics & rate of change in grey matter?

Volumetric changes across a range of brain areas were more severe in medicated group compared to non-medicated

this is not causative
although a recent meta-analysis showed correlation between brain volume change & antipsychotic
but no correlation between brain volume change & illness duration, so it could be due to medication exposure (remains unclear)
monkey studies have mimicked this



136:40

68

What are some psychosocial therapies for Schizophrenia?

CBT - focussed on reappraising &/or managing symptoms
Social/skills training
Occupational placement
Cognitive remediation

in combination with pharmacological therapy they do tend to reduce relapse rates

69

Targeted brain stimulation

Trans-cranial magnetic stimulation
auditory hallucination (temporal - wernickes area) - stimulate this area to change its function

70

SUMMARY

*Schizophrenia is an evolving concept - human arbitrary construct
*Current criteria may describe multiple diseases (which may benefit from different treatments)
*Arises from complex interactions: multiple genetic risk factors interacting with environment to impact brain development
*Dopamine dysregulation plays critical role - but upstream causes may be variable/distinct (maybe treating upstream causes could be more effective)
*Current treatments: generally only treat positive symptoms (so we need treatments for negative symptoms & cognitive deficits)
*Psychosocial interventions in combination with medication can help reduce relapse