The Corticolimbic Circuit: Disorder Flashcards
how we approach learning about disorders
(image of blind scientists trying to identify the elephant, while they touch different parts) “it’s a wall, it’s a spear, etc.” Each are right to an extent, but don’t have an understanding of the whole
lumper or splitter?
lumper, these things don’t happen in isolation
externalizing disorders
untreated distress, usually manifests itself as disruptive behavior
internalizing disorders
inward directed distress (depression, PTSD, etc.)
thought disorder
can’t keep track of information, distanced from world/ reality
how is the amygdala associated with disorders of the corticolimbic system?
usually greater amygdala activity at rest is correlated with severity of depression
major depressive disorder
a mood disorder, a sustained disturbance in predominant internal emotional experience
major depressive disorder and amygdala activity
greater amygdala activity at rest is correlated with severity of depression
what else is activated during MDD?
- greater activity in the anterior insula
- greater activity in the dorsal anterior singulate cortex
- greater activity in the pulvinar
- dACC hyperactivity
why hyperactivity in insula in MDD?
greater subjective awareness of the physiological changes
why hyperactivity in dACC in MDD?
may reflect emotional conflict in patients struggling to maintain normal relationship in face of depressive mood
- conflict monitoring
MDD and hyperactivity of the PFC
- lower vmPFC activity
- higher activity in dmPFC
failure of vmPFC to integrate signal of amygdala leads to over-attempts to regulate by the dmPFC (creates futile attempts and poor communication)
correlation between the strength of amygdala and the mPFC
less functional connectivity between amygdala and mPFC leads to a greater severity of depression (negative correlation)
treatment of amygdala
- therapy and pharmacology
SSRI treatment
proven to lower amygdala activity and thus increase functional connectivity
CBT treatment
(cognitive behavioral therapy)
greater amygdala activation to hearing negative words, but have a lesser response to them after treatment
DBS treatment
(deep brain stimulation)
- last resort treatment
electrodes are implanted deep in patients brains and targets the medial PFC
- sometimes stimulation can normalize functioning of the circuit
- but if you turn off the therapy, people will usually experience symptoms again
predictor of depression
family history of depression, high childhood anxiety
why hyperactivity of amygdala in depression?
usually anxious early in life, so a big part of neuroticism is anxiety, which makes people have a greater sensitivity to stressful life experiences
amygdala activity in GAD, MDD and both
MDD: high
GAD: elevated
both: slightly elevated
vmPFC activity in GAD, MDD and both
MDD: very low
GAD: low
both: low
anxiety disorder and BNST
found that high trait anxiety is associated with higher BNST activity
(*remember, BNST can maintain background awareness so amygdala can respond to immediate threats)
panic disorder activation
(not actually that common, but panic attacks are)
increase activity in insula over feelings of discomfort and then increase amygdala response before having a panic attack
(STUDY: showed them sad faces and experienced it while in scan)
specific phobia activation
most elevated amygdala and insula activation over SAD and PTSD
(because most acute, super afraid of one thing)
what is specific phobia?
conditioning in the absence of extinction
effects of exposure therapy
when you slowly expose them to stimulus, it reduces amygdala activity and insula activity massively (creating an extinction memory)
more activation in vmPFC and normalizes the dysfunction patterns between dmPFC and vmPFC
PTSD symptom severity
associated with….
- higher amygdala activity
- lower dmPFC activity
- lower hippocampal formation activity
STUDY of twins and PTSD (one went into combat and the other didn’t)
found that in the extinction memory was low vmPFC and high amygdala in PTSD twin
and in the recall memory was low vmPFC and low amygdala in PTSD twin
STUDY of military medics in Israel (required to serve)
military-related PTSD makes people more susceptible to combat-related stress, which may be reflected in impairments in the ability of HF and vmPFC to effectively regulate the amygdala hyperactivity when facing the stressor
how can PTSD be generalized experiences too?
STUDY of people after Boston marathon bombing
Hippocampal formation (contextualizes our experiences) can reduce the experience of PTSD, a greater amygdala activation leads to a greater response in general
what is antisocial personality disorder?
adult manifestation of conduct disorder.
- reactive aggression when provoked
- intermittent explosive disorder
what does ASPD look like in the brain?
diminished connection between the amygdala and vmPFC and amygdala hyperactivity
what is a distinguishing characteristic between people with ASPD?
how much sensitivity and emotionality they have for other people (especially as a result of their actions)
- more practice aggression
what is intermittent explosive disorder?
hypersensitivity to threat and greater levels of reactive aggression
- failure to effectively regulate response through the PFC
what is the response of people with intermittent explosive disorder to seeing angry expressions (STUDY)?
greater trait anxiety is associated with higher reactive anger
what is autism spectrum disorder?
kind of its own disorder, not internalizing, not externalizing, or thought
- its a developmental disorder
Dr. Temple Grandin
one of the first with autism to actually describe it themselves
- describes it as vigilant and wary of fear (somewhat of an animal whisperer, especially of cows)
- historically people with autism were seen as having lower IQ and intelligence
ASD and angry expressions STUDY
- found that they mostly focused their attention on people’s mouths and not their eyes
- but found hyperactivity in moments they looked at their eyes
why don’t people with ASD look at other’s eyes?
HYP: don’t want to look at eyes as a compensatory response to hyperactivity
- less habituation than with healthy people
when is there amygdala hypoactivity in Major Depressive Disorder?
amydala response to sad expressions more in MDD and happy expressions more in healthy individuals
when is there amygdala hypoactivity in ASPD?
(people with greater CU–callous and unemotional traits, less emotionality for other people)
- less response to distress in others
what does amygdala hypoactivity look like in CU in ASPD?
(in response to fear and sad expressions)
- less response to fear expressions
- less connectivity between amygdala and vmPFC
why do ASD and high CU both not look at eyes?
amygdala hyperactivity versus hypoactivity driving behavior
what is psychopathy?
superficial appearance of sanity
why psychopathy a thing?
no fear conditioning response
- don’t association of fear between CS and US
- little brain activity in response to fear
- less activity in dmPFC and amygdala
psychopathy and the self-report psyopathy test
lower amygdala activity for lower interpersonal score
lower amygdala activity for lower lifestyle score
what is williams syndrome?
chromosomal abnormality (microdeletion on long arm of chromosome 7)
- deletes protein molastin (cortical connective tissue)
- creates elfin like facial features
what is the social profile of people with williams syndrome?
greater pull for social interactions
- no stranger danger
how does the amygdala contribute to greater prosocial behavior in william’s syndrome people?
- greater response to happy expressions
- less response to fear expressions (so more likely to approach strangers)
(opposite of healthy people)
do people with william’s syndrome have fear?
yes just not to other people
- amygdala reaction to non-social responses to threat
why are people with william’s syndrome so friendly?
- very language oriented
- affective state language (emotional of characteristics)
- more langauge use (engagement of prefrontal cortex) –> drives inhibition of amygdala
