- 6.7% pop, more common in women, diagnosed between ages 30-40

- 10% women, 4% of men

-

- Decreased volume in orbital frontal cortex, hippocampus, amygdala, basal ganglia, thalamus

- Reduced brain activity in left frontal cortex, cingulate gyrus, and basal ganglia

-Identical twins, 50% risk

- Fraternal twins, 20% risk

-Induces symptoms of depression, reduces serotonin and norepinephrine

- Even as monoamine levels increase in brain, antidepressants take 2-4 weeks to work

- Revision: Receptors less sensitive to monoamines

- Block breakdown of monoamines

- Many negative side effects

- Short half life

-Block serotonin and norepinephrine transporters and prevents reuptake

- Many Negative side effects

- Long Half Life

-Selectively block serotonin transporters

- Increase Serotonin in synapse

- Less side effects

Non Drug

- Electroconvulsive therapy (IE Shock)

- Transcranial magnetic stimulation

- Cognitive Behavior Therapy (usually in conjunction w/ other treatment)

-2.6% pop.

- Equally common in men and women

- onset about 25 years old

2 'poles'

1. Mania

2. Hypomania (depressive)

1. Inflated self-esteem

2. decreased need for sleep

3. more talkative/pressure to talk

4. flight of ideas/racing thoughts

5. distractable

6. increase in goal directed activity (hyperactive)

7. excessive and impulsive invovlement in pleasurable activities

1. Sadness

2. Social Withdraw

3. Fatigue

4. Suicidal

Affects of Bipolar on Brain structure

- Decrease in prefrontal cortex volume (planning, attention)

- Increase of activity in manic phase and decreased during depressed

- Twins: 20-75% identical

0-8% fraternal

- Certain genes do code for it

- Norepinephrine levels differ during phases

- Drugs that increase nore. alleviate depressive symptoms, including antidepressants

- Mechanism unknow, affects dopamine, glutamate, other shit

- lots of side effects

-Anticonvulsant

- Works well with rapid cyclers

-1% US pop.

- No gender difference

- Late teens/early 20s for men

- mid 20s-mid30s for women

-Don't "grow out"

Flattened Affect

- Large role

- 50% identical twins, 17% fraternal

-Hippocampus disorganized and smaller

- Influenza affects radial glial cells

- Decreased dendritic arborization in prefronta, less dendrites

- reduced thalamic & cingulate gyrus neurons

- enlarged ventricles

- Positive symptoms caused by excess subcortical dopamine

- negative symptoms caused by loss of cortical dopamine

Dopamine Hypothesis Schizo Evidence

.

1. Cocaine & amphetamines induce psychotic symptoms

2. Typical antipsychotic drugs alleviate psychotic symptoms

3. Schizos have more dopamine receptors and drugs that block dopamine receptors are effective

- Reduction of glutamate in cortex

- based on observation that PCP & Ketamine induce both positive and negative symptoms

- Cortical gluatmate reduction leads to excess dopamine in subcortical regions. Leads to positive symptoms.

- Cortical glutamate leads to loss of doapmine in cortical regions

- Block D2 dopamine receptors, make neg symptoms worse

- Motor symptoms worsen, parkinsons like

- Relieve Postive, worsen negative

- Low affinity for D2 receptors

- Primarily block serotonin receptors

- Alleviates positive and negative. But doen't entirely fix negative.