• 1) “Fast response” by norepinephrine/epinephrine
• released via the sympathetic nervous system (SNS)
o Effects within seconds, but only lasts minutes (fast-acting & short-term)
o Prepares body for sudden burst of activity
2) “Slow response” by cortisol (the main glucocorticoid) released via the hypothalamic-pituitary-adrenal (HPA) axis
o Activated in minutes to hours and may last hours
o Prepares body for longer-lasting adaptations (occurs later & longer-lasting)
• Cortisol - Restores energy that has been expended
• Shuts down systems not immediately needed to deal with stressor
• Inhibits reproductive system
• Inhibits slow-wave sleep
cortisol. This in turn may (a) inhibit the immune and reproductive systems (libido, reproductive hormones); (b) cause appetite/weight gain and glucose intolerance; and (c) increase the risk for depression, anxiety, and cognitive dysfunction
The NMDA-glutamate receptor is hypothesized to be the major central biological flaw in schizophrenia
(a) hypoactivity of the mesocortical pathway, resulting in cognitive, negative and affective symptoms; and (b) hyperactivity of the mesolimbic pathway, resulting in positive symptoms.
o Cognitive/executive symptoms/signs are the strongest predictor of real-world functioning in patients suffering form schizophrenia
interpreting social cues and may have distortions in social judgment and reasoning partially because (a) their amygdalae are hyperactive when viewing neutral faces, (b) their amygdalae are hypoactive when viewing scary faces, and (c) they suffer dysconnectivity between emotion and goal-directed behavior.
identify early, subclinical, or pre- symptomatic patients w/ schizophrenia.
o Low “level” of 5-HT system is associated with increased “negative affect.”
o Dysphoria, rumination, guilt/disgust, worthlessness, loneliness, fear/anxiety, irritability, hostility, suicidality
o Particularly affects prefrontal cortex, amygdala, hypothalamus.
o Low “level” of DA system is associated with decreased “positive affect.”
o Dysphoria, anhedonia, loss of motivation & enthusiasm, apathy, anergia or psychomotor retardation, impaired attention & cognition, decreased self-confidence
o Particularly affects prefrontal cortex, nucleus accumbens, basal ganglia, hypothalamus
o Low “level” of NE system is associated with increased “negative affect” and decreased “positive affect.”
an anxiety disorder or a mood disorder.
unstable “out-of-tune” circuits, resulting in inefficient information processing during both manic and depressive episodes.
being unipolar depression (i.e., major depressive disorder) is a serious mistake.
dysfunction of circuits that involve the amygdala; and worry and obsession are associated with dysfunction of circuits that involve the cortex, basal ganglia (striatum), and thalamus.
depression, mania, or anxiety even when these affect other body systems in addition to the CNS.
intense and phasic DA firing in the mesolimbic pathway shortly after taking the drug or engaging in the behavior and hypofunction of the mesolimbic pathway during withdrawal (DA deficit).
(a) neuroplastic changes with the DA reward circuit down-regulating (tolerance) and the compulsive (habit) circuit getting stronger, (b) craving caused by classical conditioning to associated stimuli, and (c) associative learning/conditioning.
why the benefits of drug rehab programs often do not last unless there is follow-up treatment designed to offset this effect.
• Associative learning/conditioning — Drug effects & withdrawal become linked w/ cues & mood states
• A major factor in the “failure” of many in-patient drug rehab programs, unless there is sufficient follow-up treatment designed to offset this effect
* The “amyloid cascade hypothesis”
frontotemporal lobar degeneration (“frontotemporal dementia”) is associated w/ primarily executive dysfunction and changes in mood and behavior.
severe memory and other cognitive impairments in addition to emotional, behavioral, or perceptual abnormalities.
a medical workup (H&P, labs, neuroimaging) and neuropsychological assessment.
Dr. Burke clearly expressed his belief (and supported that belief with many examples)
that psychiatric sx’s that occur during neurological or other medical illnesses/conditions are often due to the pathology of the illnesses/conditions and not just psychological reactions to having such illnesses/conditions. However, there may also be psychological reactions superimposed on the primary sxs.
review past medical records and recommend a current medical evaluation (unless a recent one within the last several months has already been performed).
• Neuropsychological assessment, including being the best technique/method for predicting real-world functioning after a CNS injury
• Cognitive inflexibility and perseveration may occur with dysfunction of the dorsolateral prefrontal cortex (DLPFC).