Psych 2 - Psychiatric Disorders

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Dopamine theory of SZ, casused by what

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caused by Excess Dopamine

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first anti psychotic medicine

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THORAZINE

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Dopamine theory of SZ: caused by excess DA.
○ Evidence:

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1) Drugs that block DA receptors (neuroletpics or antipsychotics) reduce symptoms

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but caused side effects

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PARKINSON's Symptoms, tardive dyskinesia and newer drugs have less of this

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Tardive dyskinesia

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involuntary repetitive movements, lip smacking, etc.

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Parkinson's symptoms

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slow movement, DEFECIT OF DOPAMINE

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Tardive Dyskinesia

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○ A side effect of neuroleptic meds
○ Stereotyped involuntary movements particularly of the face and jaw (sucking, lip smacking , darting of the tongue)
○ Purposeless quick uncontrolled movements o f the arms and legs
○ Irreversible

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Problems with DA theory

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1) DA antagonists block DA right away, but symptoms don’t abate for weeks
§ One hypothesis: therapeutic effects requires slow neural change - decrease in firing of DA neurons
2) Most older DA antagonists work on positive symptoms, not negative.
§ One hypothesis: case with positive symptoms - excess D2 activity and helped by neuroleptics. Cases with mostly neg. symptoms = brain damage not help.
3) Newer Neuroleptics (clozapine) act on > than DA receptors (serotonin also) and still help with symptoms
4) Known brain damage, but not linked directly to DA pathway problems
§ Smaller cortex, larger ventricles
§ Decreased activity in frontal lobes (from imaging studies) and trouble on WCST
§ No known structural damage to DA circuits in brain; no ongoing degeneration.
□ There is a larger ventricles but it has nothing to do with the dopamine pathways.

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reactive depression

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reaction to bad event much causes symptoms of major depression.

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Endogenous

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no apparent trigger

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Unipolar affective disorder

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no mania (60% of depression) females 2x men (6% incidence overall)

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Bipolar-affective disorder

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depression with mania (high-energy, impulsive (40% of depression); no sex differences (1% incidence overall).

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Monoamine theory - theory -

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depression caused by under activity of 5HT and NE synapses

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Diathesis - stress model

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inherited predisposition for depression PLUS stressor early in life = hyper sensitized for rest of life for depression.

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ACTH

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adrenocorticotropic hormone,

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explain the process

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SO CRH releases into the anterior pituitary gland which releases ACTH in to the adrenal gland and coritsol in to the bloodstream, which causes physiological changes supporting "flight or flight" responses.

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tricyclic antidepressants

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block reuptake of NE and 5HT; may have troublesome side effects (dry mouth, rapid heartbeat, etc)

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Selective serotonin reuptake inhibitors =

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e.g. prozac, zoloft, paxil, increase 5HT activity in brain (ALSO SNRI's - block NE some drugs are both NE and 5HT agonists (effexor),
a. These increase serotonin in the brain.

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Lithium chloride

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especially effective, in treating bipolar disorder but side effects.

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ECT and TMS -

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or more resistant cases.
a. IT IS BEST TO USE DRUGS AND COGNITIVE THERAPY
b. But people will still recover from it just using drugs.
c. Sometimes doctors give placebos, and give strong report in recovery.
d. ECT and TMS only used for extreme cases.

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Prozac is a

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Selective Serotonin Reuptake Inhibitor

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Prozac blocks the reuptake

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of serotonin, thus increasing the activation of serotonin receptors.

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ECT

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electroconvulsive therapy - very effective but some confusion /memory loss. Require general anesthesia.

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TMS

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transcranial magnetic simulation) - newer treatment, promising studies. No known side effects, no anesthesia required.