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Year 2 - Theme 3 > Schizophrenia: Neurobiology and treatment > Flashcards

Schizophrenia: Neurobiology and treatment Flashcards

1
Q

Percentage risk of schizophrenia in monozygotic twins

A
  • Up to 50%
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2
Q

Genetic risk of schizophrenia

A
  • 1% general population
  • Partial penetrance(interaction of genes and environment)
  • Likely to be polygenic - multiple susceptibility genes
  • Presence of these and environmental factors triggers schizophrenia
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3
Q

What does the genetics of schizophrenia overlap with

A
  • Overlaps with the genetics of autism and other neurodevelopmental disorders
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4
Q

Environmental causes of schizophrenia at birth

A
  • Obstetric complications
  • Prenatal infection
  • Nutritional deficiency
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5
Q

Environmental causes of schizophrenia during adolescence

A
  • Adverse life events
  • Substance abuse
    (cannabis use - 6x risk)
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6
Q

Structural changes in the brain in schizophrenic patients

A

• Ventricular enlargement
• Reduced brain volume (less gray matter)
(temporal lobes, frontal lobes, subcortical structures)
Cytoarchitectural differences in cortex and hippocampus
- Gray matter loss: 1. Synaptic pruning + 2. Increased myelination

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7
Q

What is paracingulate sulcus morphology associated with

A
  • Hallucinations
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8
Q

Neurodevelopmental model of schizophrenia

A
  • During adolescence, grey matter is lost(pink), which may speed up in early-onset schizophrenia
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9
Q

Dynamic changes in male and female teenagers with schizophrenia

A
  • A consistent pattern of progressive grey matter loss, in parietal, frontal, and temporal cortices, is observed in independent groups of male and female patients
  • A single pattern is observable in both boys and girls, supporting the anatomical specificity of the findings
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10
Q

dIPFC significance in healthy volunteers and schizophrenics

A

Increase in activity in dIPFC seen in healthy volunteers. Absent in schizophrenics

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11
Q

What is pruning and why is it relevant to schizophrenia

A
  • Pruning is a sort of clean-up job conventionally thought to eliminate weak synapses and leave strong ones
  • In schizophrenia, it was suspected, the pruning process hacked away indiscriminately, knocking out strong synapses along with weak ones
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12
Q

Normal neurodevelopmental model of schizophrenia

A
  • Proliferation
  • Migration
  • Arborization(circuit formation)
  • Myelination
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13
Q

Functional changes of the auditory cortex activation during hallucinations

A
  • Auditory cortex activation during hallucinations(fMRI evidence)
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14
Q

What are oscillations in the brain

A
  • Important organisers of brain activity, plasticity and connectivity(maturation)
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15
Q

What is neuronal synchrony

A
  • Well-timed coordination and communication between neural populations
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16
Q

When do high frequency oscillations and synchrony emerge

A
  • Emerge during the transition from adolescence to adulthood
  • Differences in neural oscillations and synchrony between controls and patients with schizophrenia
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17
Q

What is hypofrontality

A
  • State of decreased cerebral blood flow in the prefrontal cortex of the brain
  • Hypofrontality is symptomatic of several neurological medical conditions such as schizophrenia, ADHD, bipolar disorder and major depressive disorder
18
Q

Neurophysiology summary in schizophrenics

A
  • Hypofrontality
  • Hyper-excitable sensory cortex
  • Abnormal neural oscillations
19
Q

Features of typical antipsychotic(neuroleptic) drugs

A
  • D2 receptor antagonists

- Prevent positive symptoms

20
Q

Which is a more potent antipsychotic, chlorpromazine or haloperidol

A
  • Haloperidol is more potent than chlorpromazine
21
Q

Examples of DA agonists

A
  • Cocaine, amphetamine, L-dopa can(in large doses) cause positive symptoms of schizophrenia(eg psychosis)
  • These drug-induced psychoses can be treated with the D2 antagonist antipsychotic drugs
22
Q

Which dopamine receptors are Gs coupled

A

D1 and D5

23
Q

Location of D1 receptors

A
  • Caudate putamen NAcc

- Olfactory tubercle

24
Q

Location of D5 receptors

A
  • Hippocampus

- Hypothalamus

25
Q

Which dopamine receptors are Gi coupled

A

D2, D3 and D4

26
Q

Location of D2 receptors

A
  • Caudate-putamen NAcc

- Olfactory tubercle

27
Q

Location of D3 receptors

A
  • Olfactory tubercle
  • Hypothalamus Medulla
  • NAcc
  • Cerebellum
28
Q

Location of D4 receptors

A
  • Frontal cortex
  • Amygdala
  • Midbrain
29
Q

What are extrapyramidal side effects caused by

A
  • Typical antipsychotics
30
Q

Examples of extrapyramidal side effects caused by typical antipsychotics

A 
Parkinsonian-like symptoms (inhibition of DA action in Caudate) (slow movement, lack of facial expression) followed by 
Tardive dyskinesia (slow, faulty movements) (upregulation of D2 receptors- supersensitivity - need to keep upping the dose)
31
Q

Atypical antipsychotics

A

(e.g. clozapine - more selective to D4 - beneficial effects without EPS (plus actions at other receptors - 5HT receptors)

32
Q

Typical vs atypical antipsychotics

A

• Atypical antipsychotics can work in patients resistant to typicals
• Atypicals do not have same extra-pyramidal side effects (lower activity at D2 receptor)
Clozapine activity mainly at D4 receptors (also binds D3, D1, D2, D5)
5HT receptors improves positive and negative symptoms

33
Q

Side effects of atypical antipsychotics

A

side effects - weight gain, sedation, hypersalivation, tachycardia, hypotension, neutropenia (needs to be watched - blood tests)

34
Q

Examples of other atypical antipsychotics

A

Risperidone, Olanzapine - differing affinities for receptor subtypes, varying levels of side effects.

35
Q

What is PCP(phencyclidine, angel dust)

A
  • Causes many positive, negative and cognitive symptoms of schizophrenia
  • NMDA receptor antagonist
36
Q

Effects of PCP treatment in animal studies to model schizophrenia

A

1) NMDA antagonism in PFC - less glutamergic firing to VTA GABA neurons
2) Less GABAergic inhibition of VTA-NAcc DA neurons
3) Greater DA release in NAcc
4) Less activation of VTA-PFC DA neurons - less glu- hypofrontality

37
Q

Effect of dopamine agonists or boosting drugs

A
  • Cause psychosis
  • Action in nucleus accumbens(and amygdala)
  • Glutamate antagonists(PCP) positive + negative + cognitive symptoms
  • Action PFC(feedback to DA system - hyperactive in NAcc - hypoactive in PFC)
38
Q

Effect of atypical antipsychotic drugs on DA activity in PFC and in NAcc

A
  • Increase DA activity in PFC

- Decrease DA in NAcc

39
Q

Effect of typical antipsychotics on neurocognitive deficits

A
  • No effect
40
Q

Effect of atypicals on neurocognitive deficits

A
  • Some improvement

- eg, increase verbal fluency

41
Q

Neurocognitive deficits of schizophrenia

A
  • Lower IQ
  • Attentional deficits(eg stroop test)
  • Working memory(eg Wisconsin Card Sorting Test)
  • Planning and information processing deficits

Year 2 - Theme 3 (9 decks)

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