task 2 Flashcards
The emotionally motivated brain
What are two brain pathways that are
assumed to be most importantly involved in experiences of (threat-related) emotions? LeDoux
- the thalamo-amygdala route –> early conditioned fear resposne if the sensory input signals threat
- tha thalamo-cortico-amygdala pathway –> complex analysis of imput and delivers slower conditioned emotional response
Why 2 brain pathways?
- proposed by LeDoux
- -> one set of circuits for generationg conscious feelings; involving cortical areas
- -> produces anxiety
- -> another set for behavioral and physiological responses to threats; involving subcortical areas such as amygdala; largely UNconscious
- -> produces fear
What ‘different’ brain pathways/processes are involved in
emotional responsiveness vs conscious experience of fear (emotions)?
THE INNATE FEAR CIRCUIT VIEW
Circuitry of anxiety
- -> conscious (but not correctly interpreted
- -> responses about uncertain threats
- -> BNST (bed nucleus of the stria terminalis)
Circuitry of fear (Fear-circuit hub)
- -> Behavioral and physiological responses
- -> conscious
- -> certain about threats
- -> Amygdala
ONLY AMYGDALA & BNST ARE SUFFICIENT ENOUGH TO REACH CONSCIOUSNESS
How are these pathways
involved in anxiety disorders?
l
Does LeDoux see the amygdala as the centre of explicit emotional
experience? What (implicit) processes does he think underlie conscious emotional experiences?
-> The amygdala contributes to fear indirectly but is NOT an innate fear center out of which fear percolates
- > And the BNST is NOT itself responsible for the experience of anxiety
- > but instead is a key part of an innate defense circuit that detects and processes uncertain threats
- subjective feelings of fear or anxiety are not products of subcortical circuits underlying defensive responses,
- but instead depend on the same circuits that underlie any other form of conscious experience—namely, circuits in the so-called higher-order association cortex that are responsible for cognitive processes such as attention and working memory
- -> lPFC
Why is fear not what causes threat responses?
fear –> due to higher order association cortex
threat repsonses –> not dependent o cortex
–> subjective feeling of fear and anxiety are NOT products of subcortical circuits underlying defense responses
–> defensive behaviors and physiological responding are not reliable indicators of subjective fear in humans (also why you cant compare humans to animals)
Why can people without an amygdala still feel
fear?
bc of the second pathway?
-figure out what the figure means
(great amygdala responsiveness to
negative pictures (vs fixation cross) in
PTSD patients
siehe the brain structures involved in PTSD
How to explain higher amygdala responsiveness to negative stimuli in anxiety disorder patients? -> responsiveness
-Medial cortical areas down-regulate the amygdala in healthy humans and this capacity is weakened in people with anxiety disorders
Neuroimaging studies investigating anxiety disorders employ a symptom provocation paradigm. They contrast a negative
emotional condition (e.g., pictures of feared objects or situations) with a neutral or positive condition to elicit anxiety-specificbrain activity, and then compare activity in anxiety disorder patients with healthy controls. Such studies consistently show
hyperactivity of the amygdala during symptom provocation that is related to the experienced symptoms of fear
Almost all anxiety disorders show enhanced activation in the fear network during symptom provocation
Which brain areas/cirvcuits are involved in the ‘aversive conditioning network’?
- amygdala, insula, and ACC are part of an aversive
conditioning network
amygdala:
- codes salience or relevance or value
- involved in fear and emotion
Insula:
- central structure for emotion processing, subjective feelings, and interoceptive awareness
ACC:
- approach and avoidance and fear learning
–> anxiety disorder patients show hyperactivity of the amygdala during symptom provocation that is related to the experienced symptoms of fear
Why is it a Two-system model?
Global workspace theory
Higher-oder theory
–> bc of the 2 differnet pathways with 2 differnet brain structures as the “center” (not literally though) of it?
includes…
Global workspace theory
–> subjective experience emerges through widely distributed reentrant circuitry, with prefrontal areas
Higher-order theory
–> subjective experience arises from a more delimited circuitry, involving a prefrontal hub, which supports thoughts about lower-order information
–> WM and attention may support consciousness BUT WM is not enough to reach consciousness
–> The two-system view, which treats fear and anxiety as cognitively generated conscious experiences, fear and anxiety as cognitive generated experiences, which only bevome conscious after the neocortex is involved (PFC)
Animals and consciousness
not necessarily suggesting that animals lack conscious experiences, but rather that it is problematic to draw inferences about conscious experiences, and thus problematic to use words like fear and anxiety, when describing animal behavior and physiology
How does the aversive conditioning network function in patients with anxiety disorders?
PTSD - amygdalar hyperactivity - hypoactivity in the medial prefrontal cortex and anterior cingulate cortex --> reduced top-down regulation of fear and fear extinction - reduced hippocampal activity
OCD
- striatal dysfunction leads via direct and indirect pathways to inefficient thalamic gating, which results in
hyperactivity within the orbitofrontal cortex and ACC
- Orbitofrontal hyperactivity is associated with the occurrence of intrusive
thoughts
- hyperactivity within the ACC is considered to reflect unspecific anxiety arising from these thoughts
- Compulsions
are assumed to be performed to activate the striatum, achieve thalamic gating, and therefore neutralize intrusive thoughts and
anxiety
- limited evidence for a prominent role of the amygdala in this disorder
–> although Amygdala hyperactivation in patients was found during OCD related symptom provocation and during presentation of unrelated aversive stimuli
–> This hyperactivation in OCD patients may
reflect general emotional hyperarousal rather than OCD-related anxiety
