Emotion regulation Flashcards
What is emotion regulation?
- how do we regulate?
Gross (1998)
the process by which individuals influence which emotions they have, when they have them, and how they experience and express their emotions
=this process enables us to have optimal level of engagement with our environment
Emotional regulation is critical to initiating, motivating and organising adaptive behaviour, and preventing stressful levels of negative emotions and maladaptive behaviour
- we upregulate and downregulate our emotions to allow us to adapt to certain social situations
POSITIVE and NEGATIVE
= influences how we interact with our environment
sleep is critical for optimal cognitive functioning and sleep deprivation can impair cognitive performance
BUT, its also critical for our emotional and mental health
–> sleep deprivation/ problems can have a more profound effect on emotional health compared to cognitive health
REM
- fragmented REM?
- role of REM
- brain networks associated with emotions?
emotion processing occurs during REM
= highly associated with emotional functioning
- fragmented REM sleep may disrupt the functioning of emotional brain networks during this stage of sleep = further emotional disturbances
Role of REM:
- increased activity of brain networks associated with emotions during REM sleep
- alterations and abnormalities in REM sleep are associated with daytime affective states
- mood disorders have been linked to alterations in REM
Brain networks associated with emotions during REM include:
- AMYGDALA and CORTICAL REGIONS (prefrontal cortex)
Sleep and emotion relationship?
Sleep influences 3 aspects of emotion?
bidirectional relationship - emotional intensity affects how we sleep BUT how well we sleep influences our emotion - sleep affects: emotion memories emotion reactivity emotion recognition
Study - Dinges et al, 1997
emotion regulation and sleep
only allow participants to sleep 4-5hrs per night for 7days
- in the period of restriction = significant decrease in emotional wellbeing
(also, the more sleep deprived you are the more likely your mood is to decrease even further)
- after sleep deprivation = recovery = increase wellbeing
- more cognitive and emotional complaints during sleep deprivation compared to baseline and recovery period
study - Walker & van der Helm, 2009
‘sleep to forget, sleep to remember model’
emotion memories and sleep
- how is emotional homeostasis maintained?
- HOW?
(emotional memories - awake vs asleep)
-sleep helps us encode emotional memories
- REM helps maintain emotional homeostasis
- emotional memories not as intense as when 1st experienced BECAUSE REM activates brain structures associated with an emotion but takes away the affective tone associated with memory (sleep = over night therapy)
more sleep = more emotional tone reduces over time (adaptive as emotional event only affects us recently after it has occurred)
HOW?
- awake = form episodic emotional memories which involve coordinated activity between the hippocampus, cortical structures and amygdala
- sleep = during REM, structures are reactivated in order to reprocess previously learned emotional experiences –> affective tone decreased during this, so emotion involved with memory is reduced
Dreams Vs Nightmares
dreams are associated with emotional regulation and are presumed to serve some kind of adaptive function
- between 75-95% dreams contain emotional content
- nightmares reflect a failure to regulate our emotions (associated with mental health disorders eg. PTSD)
Associated with a lack of emotional control, bizarre features and replay of traumatic experiences/ memories
(challenging to study as it relys on subjective recall)
Emotion reactivity and sleep study
Yoo et al, 2007
sleep deprived awake for 35 hrs, vs, control
FMRI used whilst performing emotional task
found: - control and sleep deprived showed increased activation to negative stimuli
- sleep deprived group 60% greater amygdala activity
–> extent of amygdala engagement can be influenced by a variety of connected systems, particularly proposed to exert inhibitory top-down control over amygdala
with sleep = MPFC strongly connected to amygdala (controlling/regulating it with inhibition))
without sleep = MPFC + amygdala disconnect (overactive emotional brain)
Emotion recognition and sleep
Gujar et al, 2011
assessing whether sleep can modulate our ability to recognise emotions
looking at our ability to recognise emotional expressions in the face –> fear/sad/anger/happy
- compared those who had a 90 min nap to control
found: no nap= more sensitive to negative emotional expressions (fear + angry faces)
nap group = more sensitive to positive/ happy faces
(nap group sub divded into group that achieved REM and group that didn’t)
REM nap = sig reduction in ratings towards fearful expressions, yet sig increase in rating of happy faces
no REM nap = no sig changes in sensitivity to recognising emotions
(nothing found for ‘sad’ because its less intense than fearful/ angry)
Sleep and mental health
cycle of depression
sleep cycle
Depression
effect of anti-depressants on REM
90% depressed patients report problems with their sleep
-overdreaming/ intense REM and less deep sleep = associated with depression
(less SWS = less restful state = important functions don’t occur = feel fatigued)
CYCLE of depression:
reduced serotonin –> impaired sleep pattern –> tiredness or exhaustion by morning –> depressive thinking style (feeling of anxiety and hopelessness) –> emotionally arousing rumination –> over-dreaming (REM) + less deep sleep (SWS) = TIREDNESS/ EXHAUSTION AGAIN = feeds back into cycle
Sleep cycle:
Steiger & Kimura (2010) - depression abnormalities in REM = REDUCED REM sleep latency// INCREASED REM density and time
(REM density = freq of eye movements per unit of time)
Depression:
- struggle to get into deep sleep
- REM occurs earlier and lasts longer
- less time for deep sleep
- increased density for REM (lots of dreaming = exhaustion)
Antidepressants & REM:
= they increase the time taken to get into REM = increase onset latency
- they decrease time spent in REM
neural basis of REM
serotonergic activity is high during wakefulness, decreased during NREM and becomes almost silent during REM
(REM = DECREASE SEROTINERGIC)
- REM believed to be regulated by reciprocal inhibition of REM - promoting system compromising:
1) REM-on = cholinergic neurons TURN ON REM
2) REM-off neurons = serotinergic systems & noradrenergic systems TURN OFF REM
reciprocal inhibition
= when cholinergic HIGH (REM on), serotenergic/ noradrenergic LOW (REM off)
(and vice versa)
- cholinergic neurons located in the lateral pons, and neurons located in the medial pontine reticular formation appear to be the locus for the REM-on neurons (which initiate and/ or maintain production of REM sleep)
REM = increased cholinergic activity in these regions, but at termination of REM = activity reduces greatly - REM-off neurons in medial raphe nucleus (contains 5HT neurons) in the locus coeruleus (located at the midbrain-pons junction which contains NE neurons) are highly active during waking but reduce activity during SWS and significantly decrease with initiation of REM
Depressed patients REM
REM-on and REM-off neurons appear to oscillate in a rhythmic fashion = inducing sleep/ dreaming and waking
= a continuous cycle of 90mins of REM–> non-REM sleep alteration
- in depresse individuals = depletion of serotonin (5HT) and noradrenalin (NE) = spend longer in REM as need 5HT and NE to off REM
–> so, wake depressive patients up before REM = improves emotional function (As REM is dysfunctional)
mental health and sleep disruptions
= share common pathways
- sleep disruptions may exacerbate mental illness and vice versa
so, if we stabilise sleep we may help mental illness
–> sleep disruption could be an early warning for diagnosis of mental health?
