Psychiatric disorders Flashcards
anhedonia
lack of ability to experience pleasure
alogia
reduce conversation
positive symptoms
shouldn’t be there, but it is
negative symptom
should be here but isn’t
Schizophrenic Brain
- Large ventricles (medial temporal lobe, hippocampus)
- Hippocampus- cognitive symptoms, decreased volume and disorganized
- Large loss of grey matter in teen years (especially in parietal association cortex/temporal memory cortex)
- Hypofrontality- reduced dendritic synaptic spines and activity
Test schizophrenic activity for frontal lobe activity
lack inhibitory control
card sorting
Antipsychotics
affinity for D2 dopamine receptors, helps positive symptoms, higher affinity, lower does symptoms
Dopamine hypothesis support
- Neuroleptics developed as anesthetics but help + symptoms by blocking D2 receptors
- Parkinson’s paradox
- Amphetamine induced psychosis (PCP), schizophrenics have more dopamine receptors
Evidence against Dopamine hypothesis
- Atypical antipsychotics, atypical high affinity for serotonin, but just as effective in symptom relief
- No different in symptom relief
- Atypical have no motor side effects
Medication for negative symptoms
Depression meds
Odd since increased serotonin = psychosis
and decreased = depression
Glutamate hypothesis:
PCP causes symptoms by blocking transmission at NMDA receptors.
Schizophrenia underactive glutamate receptors
Evidence: Mice engineered to have fewer NMDA receptors have some symptoms, but selective NMDA agonists produce seizures so hard to use
DISC gene
KO in mice, schizophrenic symptoms
Depression brain
hyperactivity frontal lobes, amygdala,
decreased blood flow in temporal regions
thinner cortex in RH
MAO inhibitor
inhibits monoamine oxidase
no monoamine breakdown
Problem: increases bp
Tricyclic/Heterocyclic/2nd gen
inhibit uptake of monoamines
SSRIs
only block serotonin reuptake
Dexamethasone Suppression Test
Depressed people don’t show blockage. Gives high cortisol so it should result in negative feedback
Depression Sleep
longer sleep onset Frequent REM. but less overall, shorter REM immediately Little or no time in Stage 3 or 4, no SWS Wake up in night frequently
Less extreme bipolar
cyclothymia
Dysthymia- mild depression
Bipolar Brain
Large ventricles, more manic episodes
atypical antipsychotics helps with manic phase
Lithium treatment
Decrease brain activity, treats manic phase to break cycling.
Increase BDNF neurotrophic growth factors
increase grey matter
Fear in amygdala: Projects to what areas
- Hypothalamus
- Periaqueductal grey matter
- Diffuse modular systems
Hypothalamus projections from amygdala
HPA activation, cortisol release
Sympathetic Nervous System: increase blood pressure.
Periaqueductal Grey matter projections from amygdala
Avoidance behavior
Diffuse Modular Systems projections from amygdala
Increase vigilance
Anxiety: 2 targets and why
Amygdala: activates HPA
Hippocampus: responds to cortisol feedback (glutatmate) and inhibits HPA.
Treat Anxiety: DRUG
benzodiazepine: GABA agonist
More receptive to GABA, increase Cl-, main inhibitory neurotransmitter.
OCD treatment
Drugs that inhibit serotonin reuptake
Increase serotonin
Extreme OCD treatment
Cingulotomy: surgical disruption of cingulate cortex
Anterior cingulate: oh shit center
Lower threshold
Tourette’s
decrease in somatosensory/motor cortex activity. Motor activity- areas in the face. Increase in D2 dopamine receptor activity due to greater density of receptors in caudate nuclei of BG
PTSD
rests threshold for traumatic event
- Old system (Brainstem), activate at lower threshold
- Amygdala: fear conditioning.
Most effective PTSD treatment
Extinction training, CTB. not erasing it, form new memories that overtime become dominant.
