PSYCH 415--Key terms for psychological disorders
SCHIZOPHRENIA
- positive symptoms - thought disorder, hallucinations, delusions
- negative symptoms - flattened (blunted) affect, poverty of thought, social withdrawal, deterioration in behavior (these occur in many neurological disorders)
- incidence - 1% (most common onset in adolescents and young adults age 20-30)
- heritability
- twin studies - monozygotic (MZ) twins compared to dizygotic (DZ) twins
- Gottesman & Bertelsen (1989)
- Kety et al (1968)
- congenital factors - factors present at birth but not inherited
- dopamine hypothesis (theory)
- neuroleptic drugs
- amphetamine-induced stereotypy
- Parkinsonian side effects
- dopamine pathways - nigrostriatal vs. mesolimbic and mesocortical systems
- amphetamine psychosis
- autopsy and PET scanning studies
- problems with the DA theory
- not all patients respond to neuroleptic therapy
- response to drug therapy is delayed
- tardive dyskinesia - denervation supersensitivity
- schizophrenia as a neurological disorder
- neurological symptoms
- general brain atrophy
- hippocampus
- hypofrontality - Wisconsin Card Sort Test (dorsolateral prefrontal cortex function)
- the virus theory of schizophrenia
- AIDS-related dementia
- rabies
- herpes simplex encephalitis
- influenza
- slow infections or prion disease
- lately, a lot of interest has centered on two areas of the brain
- the hippocampus
- the dorsolaterial prefrontal cortex - possible role in STM
AFFECTIVE DISORDERS
- reactive vs. endogenous depression
- unipolar vs. bipolar depression
- incidence (DSM): 20% of women and 10% of men (probably gross overestimates; book says 6%)
- heritability: 69% of MZ twins were concordant, 13% of DZ twins were concordant
- effective therapies
- traditional psychotherapy hasn't been very effective with endogenous depression
- biomedical treatments
- MAO inhibitors: iproniazid (the classic one)
- tricyclic antidepressants: imipramine (Tofranil), amitriptyline (Elavil)
- new generation antidepressants or SSRIs: fluoxetine (Prozac)
- selective norepinephrine-reuptake inhibitors: reboxetine
- lithium salts (lithium carbonate): for bipolar disorder
- electroconvulsive therapy (ECT)
- sleep deprivation
- the monoamine (or biogenic amine) hypothesis (theory)
- treatments that deplete the brain of MA cause depression: e.g., reserpine
- suicidal depression is associated with low 5-HIAA levels in CSF
- drugs successful at alleviating depressive symptoms are MA agonists
- diets that deplete 5-HT (low tryptophan diets) cause relapse
- evidence for upregulation of NE and 5-HT receptors during successful treatment
- questions
- is the DA reward system involved?
- why does it take antidepressant drugs 2-3 weeks to have a therapeutic effect?
- according to one promising theory, the key characteristic of effective treatments for endogenous depression seems to be their ability to alter beta-NE receptor sensitivity
- all effective treatments reduce sensitivity of postsynaptic beta-NE receptors
- the therapeutic response has the same time course as the change in receptor sensitivity
- reserpine makes beta-NE receptors supersensitive
- change in receptor sensitivity somehow involves the action of 5-HT neurons
- relationship of depression to circadian rhythms
- one of the most prominent symptoms of depression is disorganized sleep
- one of the most effective treatments for depression is REM sleep deprivation
- the Wu & Bunney theory - a depressogenic substance is produced during sleep
- seasonal affective disorder (SAD)
- PET scanning studies
- drug-free depressives, both those actively depressed and those in remission, show increased activity in the amygdala
- those in an episode of active depression show increased activity in the prefrontal cx.
ANXIETY DISORDERS
- obsessive-compulsive disorder (OCD)
- obsessions - persistent, irresistible thoughts
- compulsions - persistent, irresistible behaviors
- incidence - about 2%, slightly more in women than men and in young adults
- most effective treatment - drug therapy (often used in combo with behavior therapy)
- all therapeutic drugs block 5-HT reuptake: clomipramine, fluoxetine (Prozac), fluvoxamine
- antidepressants also work - but antiobsessional effects unrelated to antidepressive effects
- PET scanning studies - increase glucose utilization in: caudate nuc., cingulate gyrus, orbitofrontal cx
- after successful drug or behavioral therapy, glucose utilization in caudate and orbitofrontal cx tends to return to normal levels
- panic disorder - panic (anxiety) attacks
- incidence - 1-2%, 2X more common in women, onset in young adulthood
- a single dominant gene is suspected to confer a hereditary predisposition
- treatment - combo of benzodiazepines and behavior therapy
- PET scanning studies
- panic attacks can be induced by injection of lactic acid or inhalation of CO2
- the anterior temporal lobes "light up" - amygdala, uncus, etc.
increased glucose utilization occurs in the temporal poles of normal Ss who are experiencing anxiety, too
- general anxiety (generalized anxiety disorder)
- the role of GABA
- anxiolytic drugs are (almost) all GABA agonists: benzodiazepines, barbiturates, alcohol
- GABA-A receptor complex - gates a chloride channel
- anxiety disorders may result in chronic decrease in sensitivity - due to decreased number of benzodiazepine receptors?
- effect of prenatal diazepam (Valium) in kittens
- buspirone (Buspar) - 5-HT agonist
- anxiolytic but not sedating or ataxigenic
- acts at the 5-HT1A receptor
- role of the amygdala - local infusions of GABA antagonists prevent the anxiolytic effects of systemically administered benzodiazepines in animal experiments
Return to Psyc 415 Main Page