Term
| What are some candidate endophenotypes that may increase risk of pt from schizo spectrum to schizo? |
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Definition
| working memory, sensory motor gaiting, glial cell abnormalities, oculomotor fuctioning |
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Term
| What are the postulated pre-morbid predictors of schizophrenia? |
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Definition
| social functioning, organizational ability, interest in physical activity, individual autonomy, and intellectual fuctioning |
|
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Term
| is there a large genetic component? |
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Definition
| yes--offspring of dual mating is about 40%. MZ = 50% |
|
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Term
| Does paternal age matter? |
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Definition
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Term
| What is the startle response? |
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Definition
| When I bang on a desk, you startle. But a prepulse of clappiong should reduce the startle. However, in pts with schizophrenia, there is much less reduction with the prepulse, they will continue to startle. |
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Term
| Do SZ have the same startle response? |
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Definition
| No--they do not have a reduced startle response with a prepulse. |
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Term
| In the hippocampus, what do schiz pts have a reduction of? |
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Definition
| dysbindin-1 and VGluT-1 in hippocampal formation |
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Term
| What are possible environmental factors? |
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Definition
| season of birth (birth in late winter/early spring increases risk, probably becasue of exposure to the Flu), nutritional deficiency, viral infection (flu) |
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Term
| What is the possible neurobiological hypothesis? |
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Definition
Primary lesion in prefrontal cortex (PFC)
- genetic and intrauterine environmental factors
- aberrant GABAergic circuitry |
|
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Term
| When you see a primary lesion in the PFC? |
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Definition
* PFC normally comes “on-line” in adolescence
- PFC function required to handle stress in adolescence
- Stress becomes overwhelming, triggering psychosis
- The PFC defect manifests as negative symptoms |
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Term
| What does a PFC deficit cause? |
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Definition
* PFC deficit causes excessive mesolimbic activity
- Excess limbic DA transmission produces positive symptoms
* Aberrant mesolimbic activity may engender
- neuroplastic processes such as sensitization
- neurotoxic effects |
|
|
Term
| According to this hypothesis, what causes negative symptoms? positive symptoms? |
|
Definition
the PFC defect manifests as negative symptoms and
- Excess limbic DA transmission produces positive symptoms |
|
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Term
| in the PFC, what genese might you see a difference in? |
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Definition
| Presynamptic machinery, GLUT, GABA |
|
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Term
| What circuitry might be f-ed up? |
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Definition
|
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Term
| Explain the "genetic disorder of synapse." |
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Definition
| there is cellular neuropathy interacting with dysregulated dopaminergic transmission (with possible influence from deffective COMT) that creates cognative and other trait features AS WELL AS psychotic symptoms respectively |
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Term
| What are the 2 neurotransmitter associated with Schiz? |
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Definition
| dopamine and glut/NMDA glut receptor |
|
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Term
| What is the dopamine hypothesis? |
|
Definition
A deficit may result in a psychotic state.
D2 receptor binding correlates with antipsychotic
efficacy of medications;
Psychostimulants (amphetamine, cocaine) mimic
positive psychotic symptoms |
|
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Term
| what is the GLut Hypothesis? |
|
Definition
NMDA glutamate receptor antagonists (PCP, ketamine)
mimic both positive and negative symptoms of an
acute schizophrenic break.
NMDA receptor blockade at the level of thecortical
interneuron can lead to glutamatergic hyperactivity
in associate pyramidal cells.
Increased glutamate activity can lead to neurotoxic and
neuroplastic effects (and to a hyperdopaminergic state). |
|
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Term
| What does this mean in terms of Tx? |
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Definition
| Reversal of PCP effects by a Glut agonist have some effect. |
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Term
|
Definition
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Term
| Why do you need to medicate to prevent relapse? |
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Definition
| when you are psychotic, you destroy brain tisssue (so the more the relapses, the more the destruction)--and antipsychotics reverse this. |
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Term
| What abnormal neuronal synchrony is seen? |
|
Definition
| no production of brain activity necessary to distinguish btw square and no square. |
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|
Term
|
Definition
Pathogenesis:
Strong component of genetic susceptibility;
Probable environmental insult during gestation;
Onset in early adulthood during time of synaptic refinement;
Multiple non-specific structural & functional abnormalities;
Deficit in cortical synaptic function (interneurons?) gives rise to
failures in cortical integration, cognition, motivation;
Resulting increase in subcortical DA function gives rise to
episodic positive symptoms |
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