Psychopathology Flashcards
DSM and heritability
40-50% heritable for depression, 75-80% bipolar, height is 90%. Heritability is accentuated when environment is the same for everyone. Reasonable reliability but questionable validity. Phenomenology does not appear to map onto biology. Currently defined psychological disorders likely involve several sub-disorders. Diagnostic heterogeneity. Considerable comorbidity between disorders. Call for cells to circuits to symptoms classification system. 1952- Freudian, 1968, 1980 - poor reliability before this one (III), no more classification based on causes, just defining the phenotype. But then realizing phenomenology is not mapping onto etiology or pathophysiology (just looking at self-reported symptoms, underlying thing may not relate to presentation of symptoms).
Future Directions
RDoC. NIH not funding DSM classifications but research with brain, using biology to understand symptoms. RDoC- not studying things as homogeneous constructs, focuses on neural circuits and relationships to specific symptoms (agnostic about DSM classification). Expecting that identifying syndromes based on pathophysiology will eventually be able to improve outcomes.
What is depression?
Deficits in positive emotion. Can have over 200 combos of criteria to have depression.
What are anxiety disorders?
Fear disorders: phobias, panic attacks and panic disorders. General distress/anxious misery: GAD. GAD more aligned with depression than other anxiety disorders, GAD is more like depression generally too, so it maybe is more of a depressive disorder.
Threat-circuitry in depression and anxiety
Depression and anxiety are associated with elevated amygdala activation, insula, and anterior cingulate cortex (detecting conflict and violating expectation). Anxious people look for these violations, detecting things when off-track (like expressions to indicate disinterest in a conversation). Depression and anxiety markers are the same.
Bed nucleus of the stria terminalis
Amygdala associated with immediate response to fear but BNST associated with more diffuse anxiety and worry. Amygdala more punctuated moments, and this is more chronic negative mood. Related to cortisol. Elevated threat circuitry in anxiety and depression, same in brain.
Reward circuitry in depression and anxiety
Ventral striatum, nucleus accumbens, caudate, and putamen all part of basal ganglia. Unipolar depression associated with reduced positive/reward affect. Ventral striatum not as active (low positive emotion), harder time engaging in reinforcement learning. fMRI reward paradigm: probing ventral striatum, attenuated activation during reward tasks with depression, remission from depression - still reduced circuitry, so state-independent marker. Meta-analysis with decreased activity in ventral striatum. Depression: decreased reward circuitry, increased threat. Ahendonia - diminished interest in pursuing rewards, goals, or engaging in pleasurable activities. Decreased activity in ventral striatum associated with anhedonia but not general distress.
Bipolar disorder def.
Presence of mania and depression. Mania: amplification of goal-directed emotion, too much energy, mild levels of hypomania are positive but associated with poor decisions. Mania itself is awful. Disorder of energy and not positive emotion.
Reward hyper-responsivity and bipolar disorder
Hypersensitivity to reward: risk for mania. Excessive increase in approach affect reflected in hypomanic symptoms. Excessive goal-directed activity, increased energy, psychomotor agitation. Elevated self-reported reward sensitivity. In same study as with the depression people (fMRI study), show more activity in ventral striatum (neurological opposite), those in remission have risk factor of this. Also potentially too sensitive to losses too (depressive portion). You don’t see that heightened activation when depressed though. Left lateral OFC - depression to mania regardless of state. You also see these things in people at risk, suggests a preexisting risk factor rather than a consequence. They have too much reward and too much threat.
Reward/pleasure circuitry in anxiety
Anxiety associated with intact/maintained reward-related brain function. Summary: reward-related brain function as a biological marker for differential risk for depression, bipolar disorder, and anxiety. Amygdala may mark a host of illnesses (common risk factor), lots of illness. Different disorders have different subneural circuits.
Executive/cognitive control circuitry in depression and anxiety
PFC. Depression and anxiety associated with reduced activity in PFC, especially lateral (explicit emotion regulation area). If you give them simple tasks like put the digits in order, they have a harder time activating the PFC. Could be that the PFC is important for depression or depression hijacks working memory. DLPFC - cognitive control and emotion regulation.
Emotion regulation and negative affect in depression
When healthy controls use their prefrontal cortex to dampen negative emotions, they are successful. When depressed individuals do this, they actually generate more negative emotion. Depressed individuals upregulate negative emotion. Looking at happy face: healthy - OFC and amygdala relationship, elevated amygdala and positive response - induction of happiness. Depression - more depressogenic chatter, an ideal discrepancy, negative experience around the positive (comparison) mediated by cingulate cortex. Depression down-regulation of positive emotions. Deficits in amygdala and ventral striatum may be because of PFC, mediated by uncinate fasiculus (people with depression have reduced activity here). Excessive anxiety, fear, neuroticism, and behavioral inhibition involves too much amygdala activation during fear acquisition and too little top-down regulation of amygdala by vmPFC during fear extinction.
Neuroscience of psychopathy
Psychopathy: lack of remorse, callousness/lack of empathy, glibness/superficial charm, grandiose sense of self-worth, and pathological lying. Psychopathy single best predictor of recidivism.
Psychopathy and amygdala low-fear hypothesis
Individuals with CU style (psychopathy) have reduced amygdala activation to fear stimuli. Limited fear conditioning in the amygdala.
Psychopathy - low fear and high reward sensitivity and low empathy
Blunted amygdala to fear and hyper ventral striatum to reward cues. Skin conductance - an index of arousal and anxiety.
Antisocial PD
ASPD associated with elevated impulsivity, disregard for rights of others, incarceration/unemployment. Psychopathy associated with reduced fear and blunted emotional reactivity, ASPD is characterized by elevated amygdala responsivity and heightened emotional reactivity. Brains hijacked by negative emotion - overwhelming PFC which would otherwise put the brakes on behavior.
Schizophrenia
Neurodevelopmental perspective: requires normative brain maturation for symptoms to emerge. Some of the pathophysiology of schizophrenia is in the PFC which hasn’t yet matured in younger kids. Typically see it emerge at 18-22. Excessive neurodegeneration over course of life. Dopamine perspective: Schizophrenia associated with increased dopamine signaling in salience processing regions. People with psychosis start to ascribe salience to irrelevant stimuli. Secondary to poor prefrontal control of striatal reward processing. Antipsychotics (affecting dopamine), PCP, increased dopamine synthesis. If you give Parkinson’s patients L-Dopa (precursor to dopamine) increases risk of psychosis. PCP increases dopamine and is linked to risk of psychosis. Increased dopamine synthesis in schizophrenia.
