top down 1 Flashcards
define emotion regulation
the ability to alter the time course, intensity or profile of our emotional responses to a situation
- all types of affect
shaefer et al 2002
prefrontal reg of amyg
method
conscious maintanence of neg emotion (make last longer
fmri: is voluntary modulation of neg emotion assoc with changes in neural activity in the amyg?
reappraise task: neg/neutral images
maintain (temporally extend) emotional response or view passively
shaefer et al 2002
prefrontal reg of amyg
results
heightened BOLD in amyg during neg maintain to neg valenced images> passive
(not for neutral)
amyg somewhat under conscious control - central component in emotion perception
oschner et al
prefrontal reg of amyg
method
fmri
attend: dont try to alter emotional response
reappraise: reappraise neg response
oschner et al
prefrontal reg of amyg
results
neural correlates of effective neg reappraisal:
- heightened LPFC/mPFC - wm/cog control
- diminished mOFC/amyg - emotional processing
mag of LPFC inversely correlate with both MOFC and amyg *mOFC small and unrelaiable(early research)
common brain regions facilitated in emotional reg tasks
mPFC dlPFC thall frontal opercular Insula (critchly - interoception) visual cortex (attention?)
johnstone
healthy vs depressed
and emotion reg
method
MDD freq characterised by inability to effectively reg onset of neg mood
fmri: med free MDD and control
pos/neg valence pics
“attend” “enhance” “suppress”
johnstone
healthy vs depressed
and emotion reg
RESULTS
healthy:
heightened left lat. PFC in down reg of neg affect:
- vlPFC + dlPFC
- affective reappraisal:
inverse relationship between (left) vlPFC and the (BLN) amyg mediated by the VMPFC - lat. PFC in emotion reapp
MDD:
- right vlPFC in neg affect down reg and absence of left
- No inverse relationship between vmPFC +amyg + no mediation with left vlPFC
- instead show a pos assoc between VMPFC and amyg
Pupil dilation:
MDD more dilation = more amyg/insula
healthy more dilation = less amyg insula
johnstone
healthy vs depressed
and emotion reg
EXPLAIN
MDD= counterproductive engagement of right > left PFC+ lack of engagement of left vlPFC in downregulation of amyg responses to negative stimuli
vmpfc inhibits amyg vi vlPFC - compromised in MDD -
inppropriate engagement of r.PFC
pupil:
inverse with pupil and amyg/insula = emotion reg
MDD ineffective/counterproductive
-PFC flexible in responses
- dlPFC/vlPFC (l>r) important in reapprial and mediated via vmPFC towards responses in subcortical circuitry that may determine ability to reg response
hartley and phelps diagram
what does is the role of the dlPFC/vlPFC proposed to play a role in in assoc with the vmPFC
dl/vlPFC connect and engage vmPFC cirtcuitry that initiates/dictates emotional response based on the vmPFCs descending subcortical connections
dl/vlPFC re-evaluate stimuli
vmPFC process hedonic value with re-eval and determine subsequent response
van reekum eye gaze
method
eye tracking and fMRI
how long loot and and where look in emotionally valent images
van reekum eye gaze
results
heightened dm/vlPFC when emotionally reg (both increase/supress response)
bilat amyg activation increase as heighten appraisal/emotional response
EYEGAZE -
change attentional focus based on regulation
- dont look at emotionally valence when decrease
- look more at emotionally valent when increase
what might van reekum suggest about the role of the dl/vlPFC beyond the vmPFC?
how might it interact in explaining anxiety?
dlPFC may have additional links to more sensory areas - and may be involved in the regulation of attention towards external in additional to internal cues
ie dlPFC may determine gaze in emotion reg in van reek
dlPFC may alter focus on the insula - thus if dysfunctional may determine someones trait anxiety - attend more on internal state when should focus away from when trying to downreg emotional responses (critchley - insula link)
right vl pfc
predominantly involved in spatial processing + the processing of threat/shock
may underpin vigilance
left vl pfc
predominantly more involved in verbal processing + emotional reg
may facilitate the capacity of individuals to control attention and to resist temptations
ascending connections from the amyg
to
ACC
m/of/dl PFC
- amyg when detect threat send signal to areas involved in exec control tasks (ie wm tasks) to aim to reorient attention
how might we regulate interference from the amyg when wm load high?
ie. in n-back
may modulate interference by heightening down regulation of emotional responses via the dl/vlPFC
clarke and johnstone
method
PFC reg of threat under high cog load.. due to:
- down reg of emotion/up reg of wm?
- passive inability to process threat due to high load (pessoa)
spatial n-back (r.pfc)
high / low wm
threat: safe or shock
clarke and johnstone
results
low wm = sig impairment in task from threat = heightened amyg
high wm = no sig impairment from threat = heightened dACC and LPFC
BUT heightened pupil dilation to threat in high wm - recog threat (not cog capacity taken up) - due to down reg or wm processes
dynamic causal modelling in determining relation between pfc and subcortical circuitry in reg of attention in threat
use correlations between patterns of activation in the brain and test models of what may give rise to diff patterns of activation
- diff options - ACC (conflict monitor/attend) may strengthen dlPFC (heighten wm) or vlPFC may inhibit amyg (emotion reg)
mot likely emotional modulation/inhibition - fits best, but not rule out wm heighten role
relation of top down control research to anxiety
like MDD, anxiety may have dysfunctinoal activation/manipulation of PFC circuitry which may make them unable to properly control ascending signals from the amyg
i. e. right > left
i. e. vmPFC impoverished descending connect to amyg
may have altered dlPFC attentional focus towards external and internal cues - may focus on insula = heightened anxiety (johnstone)
