psyc 372 final

psychotherapy advantages

treats root cause, long-term coping skills, helps build support & connection, reduces risk of relapse if drug issue

psychotherapy disadvantages

it can take long, emotionally challenging, progress is not linear, cost & access barriers

advantages of pharmacology

faster symptom relief, regulates brain chemistry, widely available, can be life-saving

disadvantages of pharmacology

side effects, finding discontinuation symptoms, not effective for everyone

key differences

-pharmacology is faster than psychotherapy

-psychotherapy treats root cause

-pharmacology has side effects, psychotherapy doesn’t

-psychotherapy is best mild-moderate depression

-pharmacology is best for moderate-severe depression

-pharmacology is easier to access than psychotherapy

common effects of pharmacology & psychotherapy

paroxetine & interpersonal psychotherapy normalized PET scans 12 weeks post treatment

paroxetine

bilateral normalization in prefrontal cortex

interpersonal psychotherapy

right side of the prefrontal cortex

both pharmacology & psychotherapy

normalization of activity in anterior cingulate gyrus & left temporal lobe

implications of using both pharmacology & psychotherapy

more effective treatment, faster stabilization, lower risk of relapse, better engagement in theory

are psychotherapy & pharmacology mutually exclusive?

-no, but can be used separately

-each approach targets diff aspects of depression

-lot of treatment plans include one or other

mood changes (anxiety, depression, etc)

normal but sometimes emotions can be overwhelming, unrealistic, and mess with everyday lives

DSM-5

diagnostic & statistical manual (used for diagnosing mental disorders)

what population of american’s meet criteria to be diagnosed with mental disorder?

50%

Major depressive disorder (MDD)

aka unipolar depression, debilitating condition characterized by overwhelming sadness, feelings of worthlessness, and loss of interest in pleasurable activity

what percent of hospitalizations is from MDD

70%

what percentage of suicides from MDD

40%

prevalence of MDD

United States: 20% lifetime prevalence (14.7% of men, 26.1% of women)

demographics of MDD

-women are more likely to have than men

-diff symptoms in men (rage, aggression, substance abuse) than women (sadness, guilt, hopelessness)

-diagnosed more frequently in younger people

genetic causes of MDD

children of parents with depression are 4x more likely

psychological causes of MDD

stressful life events, beck’s negative cognitive triad, learned helplessness

beck’s negative cognitive triad

negative views about world = negative views about future or negative views about oneself

social causes of MDD

poverty, trauma, drug use, lack of social support

monamine theory (neurochemistry causes)

suggests that depression is caused by low levels of serotonin, dopamine, norepinephrine

support for monoamine theory

-drugs that increase monoamines can increase mood

-drugs that decreases them can lower mood

-autopsy study suggest reduced monoamine levels in suicide victims

evidence against this theory

-no proof depressed individuals have lower monoamine levels

-no correlation between serotonin levels & depression severity

-antidepressant raise monoamines within hours, mood increase takes weeks

neuroanatomy causes of MDD

smaller volumes of hippocampus, basal ganglia, thalamus, etc, overactive stress, chronic inflammation

neurogenic theory

integrates previously disparate findings (stress, imaging, neurochemistry, treatment)

neurogenic theory is based on two changes of thinking

1. existing neurons repair & remodel themselves

2. neurogenics (hippocampus & frontal cortex)

loss of cellular plasticity

-hippocampal neurons among most sensitive to stress-induced damage

-high glucocorticoid levels damage hippocampus & reduce hippocampus neurogenesis, dendritic branching & spines

-MRI scans show reduced hippocampal volumes in depressed patients

depression & altered stress hormones

-hypersecretion of corticotropin-releasing factor (CRF) by hypothalamus

-elevated cortisol levels

-early life trauma can alter setpoint of HPA, permanently hyperresponsive

-antidepressants & ECT decrease CRF in depressed patients

Brain-derived Neurotropic factor (BDNF)

-BDNF central during brain development, cellular survival & synaptic changes

-Low BDNF responsible for loss of dendritic brances & spines

-chronic stress reduces BDNF in rats hippocampus

-chronic antidepressants administer increases BDNF in animals & humans

BDNF & depression

-BDNF levels in blood decreased in patients, antidepressants reverse

-BDNF levels correlated with depression & severity

-reduced expression of frontal lobe & hippocampal BDNF in people who committed suicide

-BDNF increased by antidepressants after several weeks

neurogenic hypothesis

drugs may exert their effects by increasing growth & survival of newly formed neurons in hippocampus

symptoms of MDD

sadness, loss of interest in activities, guilt/anxiety, low self-esteem, lack of motivation, changes in appetite/weight, insomnia, thoughts of suicide or death

diagnosing MDD

DSM-5, at least 5 or more symptoms (persist for at least 2 weeks)

prevalence of antidepressant drug

more than 30 antidepressants available, 1 of 3 most common prescribed drugs, in 2019 13% of people used antidepressant in last month

monoamine oxidase inhibitor (MAOI)

inhibits enzymes that breaks down serotonin, dopamine, norepinephrine, etc

tricyclic antidepressants (TCA)

blocks reuptake of serotonin & norepinephrine, blocks post-synaptic acetylcholine, norepinephrine & histamine receptors

selective serotonin reuptake inhibitors (SSRIs)

blocks reuptake of serotonin

atypical/mixed action antidepressants (SNRIs)

most block reuptake of serotonin & norepinephrine

side effects of MAOI’s

wine & cheese effect

wine & cheese effect (dietary restriction)

dairy (cheese, unpasteruized milk), meat (liver, canned meats), breads/grains (homemade yeast breads, crackers with cheese), veggies (sauerkraut, avocado, banana), alcohol (red or white wine, beer, champagne)

side effects of TCA

cardiotoxic (low therapeutic index, TCA’s lethal at doses) (fatalities occur at approximately 3-10x normal dose)

SSRIs & SNRIs

fewer side effects than older antidepressants

most common side effects of MDD treatment

dizziness, headache, dry mouth, weight gain, sleep disruption & s*xual dysfunction (36-70% SSRIs)

MAOI & Tyramine

MAOI induced build up of tyramine: severe increase in blood pressure, heart attack, stroke, potentially fatal

Amitriptyline & doxepin

sedating & then useful for treating agitation & insomnia

despiramine & nortriptyline

stimulant effect useful for treating motivational issues

serotonin discontinuation syndrome (wtihdrawal)

SSRIs can be dependent but not addictive

60% show on abrupt SSRI discontinuation

onset within days, lasts 3-4 days (fluoxetine is onset after 2 weeks)

“FINISH” symptoms (for SSRI withdrawal)

Flulike symptoms (fatigue)

Insomnia (sleep disturbances)

Nausea (GI symptoms, vomiting)

Imbalance (dizziness)

Sensory disturbances (sensation of electric shock)

Hyperarousal (anxiety, agitation)

serotonin syndrome

high doses or when SSRI combined with other serotonergic drugs

last 24-48 hours after discontinuation

potentially fatal

greatest risk with paroxetine (most potent at transport)

symptoms of SSRI syndrom

cognitive alterations (disorientation)

behavioral alterations (agitation)

autonomic nervous system (fever)

neuromuscular activity( (muscle spasms)

efficacy of treatments for MDD

meta-analyses found SSRIS are slight effective in severe depression, but not more effective than placebo for mild depression

efficacy of antidepressants

50% of patients will respond (50% with partial response, 33% with full remission)

efficacy vs. placebo (antidepressants vs. placebo)

comparisons are usually vs. single drug

full remisson vs. partial vs. placebo

antidepressants often have similar efficacy to psychotherapy

place effects occur before drug effects, at less than 4 weeks

placebos have been found to have antidepressant effects (Niacin)

antidepressants during pregnancy

14% of pregnant women take antidepressants

SSRIs linked to spontaneous abortion, preterm birth, low birth weight

untreated depression can have negative outcomes

fetal effects of antidepressants

challenging to study the effects, mixed results & growing concerns

suicidality in children & adolescents

increased risk of suicidal thoughts

FDA warning 2-4% increase

2 years number using antidepressants decreased & number of suicides increased (22% in adolescents & 33% in young adults)

clinical considerations for treatment emergent suicidal thoughts

appropriate monitoring of patients

adjust doses

adding cognitive therapy

consider alternative treatments (ECT)

electroconvulsive therapy (ECT)

shocks sent through brain

quicker so used with severely suicidal patients

may increase norepinephrine, dopamine & serotonin