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Chapters 21/22: Attention and Mental Illness AFFECTIVE DISORDERS…
Chapters 21/22: Attention and Mental Illness AFFECTIVE DISORDERS
Disorders of Mood (Affective Disorders)
Bipolar disorder
cycling mood changes - from extreme highs (mania) to extreme lows (depression)
Mania
persistent, abnormally elevated mood
grandiosity; decreased need for sleep
racing thoughts, increased talkativeness
impulsive behaviors, rapid onset
hypomania: increase in efficiency, creativity
Types
Type I
mania w/ or w/o extreme depression
Type II
hypomania w/ extreme depression
Treatment for Bipolar disorder
lithium
stabilizes mood, negative side effects
antipsychotics
(DA receptor antagonists) help control MANIA
antidepressants
DO NOT HELP treat bipolar depression
psychosocial therapy
Major depression
severe symptoms that interfere with one's ability to work, sleep, study, eat, and enjoy life
cognitive difficulties
overeating or appetite loss
fatigue and decreased energy
suicide ideation/suicide attempts
feelings of hopelessness, pessimism
feelings of guilt, worthlessness, helplessness
insomnia, early-morning wakefulness OR excessive sleeping
Treatment for depression
cognitive behavioral therapy
efforts to overcome negative thought processes
Antidepressant pharmacotherapies
tricyclics
monoamine oxidase inhibitors
SSRIs and SNRIs (for serotonin and norepinephrine)
Ketamine (hallucinogenic glutamate agonist): rapid improvement, long term value is unclear
ECT (electroconvulsive therapy) of temporal lobes: used when SUICIDE RISK IS HIGH
Deep brain stimulation
stimulate anterior cingulate, recruits inhibitory neurons to reduce activity
electrodes left in place with battery-operated stimulator for constant stimulus
Biological Basis of Affective Disorders: monoamine hypothesis
mood disorders arise from DEPLETED levels of serotonin and norepinephrine (monoamine neurotransmitters)
antidepressants ELEVATE levels of serotonin, norepinephrine, and/or dopamine in synapse
MAO inhibitors
enhance NE and 5-HT action by PREVENTING enzymatic destruction
Tricyclics
enhance NE and 5-HT action by BLOCKING reuptake
SSRIs
enhance 5-HT action by BLOCKING reuptake of 5-HT
Limitations of monoamine hypothesis
drugs require LONG TIME to achieve clinical efficacy
they DO NOT WORK in up to 40% of patients
Pituitary hormones
a way for psychiatrists to get a glimpse of brain function
many pituitary hormones are controlled by monoamines
hormonal marker of depression: ACTH, which controls RELEASE OF CORTISOL
the pituitary hormone that is abnormal in depression: baseline cortisol or ACTH
ACTH is high in depressed patients
Neurohormonal hypothesis replaces the monoamine hypothesis
hypothalamus is regulated by same monoamines implicated by effective drugs
hypothalamus is related to cardinal symptoms: sleep, appetite, hormones, libido
central acting CRH mimics depression (loss of appetite and libido, increased arousal and anxiety)
Stress and HPA Axis
Hypothalamus responds to levels of cortisol
Cortisol has negative feedback on brain
cortisol: when released into bloodstream, cortisol prepares us for stress by mobilizing energy reserves and suppressing immune system
depressed patients have high cortisol all the time
loss of negative feedback in depressed patients
HPA Dysfunction and Depression
Onset: often after extremely stressful events
HPA anomalies
elevated cortisol
enlarged adrenals
excess brain CRH: elevated CRH in CSF
Role of hippocampus
Abundant cort receptors in hipposcampus
cortisol binds to receptor for a long time in depressed patients
activation of cort receptors NORMALLY leads to feedback inhibition of HPA
hippocampal lesions: prolonged stress responses (why there's so much cortisol in HPA)
antidepressants INCREASE cort receptors in hippocampus
Biological Basis of Affective Disorders: diathesis-stress hypothesis
diathesis = genetic predisposition
depressed patients exhibit hyperactivity of HPA axis
elevated cortisol
elevated CRH
enlarged amygdala
reduced volume of hippocampus (less negative feedback)
Environment factors and negative feedback
human health benefits from touch
those who received maternal care as babies had
more cort receptors as adults
less CRH in hypothalamus
reduced anxiety
newborn tactile stimulation
activates serotonin in hippocampus
creates long-lasting expression of cort receptors in hippocampus
Biological Basis of Mood: Anterior Cingulate Cortex
increased resting state activity in depressed patients
increased activity during autobiographical recall of sad event
decreased activity after successful treatment of depression
anterior cingulate cortex has connections with amygdala and hippocampus