Topic 10 - Emotion

guest lecture with Seth Winward

What is an emotion?

something of the body and of the mind

can be looked at as an evolved phenomenon that maximizes survival (evolutionary perspective) for reward-and-punishment circuits - conditioning

neural overlap between emotion and conditioning, but can’t all be conditioning since that’s not under conscious control

James-Lange Theory

says emotion is just a conditioned response

core idea is when we perceive some external stimulus and the feeling is perceived by somatosensory cortex, that’s where the subjective experience of emotion comes from

the response IS the emotion - we are sad BECAUSE we cry, we are angry BECAUSE our face gets red and not the other way around

Arguments about James-Lange Theory

evidence for:

• pure autonomic failure: peripheral NS degenerates over time so patients can’t modulate physiological process via ANS - emotional bluntness

• facial feedback hypothesis: mood will change by making an emotional expression suggesting emotional experience is caused by physical experience 

• botox cases: people with facial botox tend to report less intense emotional experiences after getting it

evidence against: 

• quadriplegic cases: can’t feel anything lower than the injury but still have regular emotional experiences

• capgras syndrome: rare delusion in which people believe their family members have been replaced by imposters

  • physical damage prevents visual info from going to amygdala and hypothalamus and patient still has emotional response to parents and is scared of those seen as imposters

Cannon-Bard Theory

physiological change and associated emotion happen simultaneously

thalamus is where subjective emotion is processed and that is sent to the body and somatosensory cortex

based on animal neurophysiology where they would remove entire branches of the ANS without causing any change in emotional behaviours

• removing cortex including somatosensory areas increased emotional behaviour which he attributed to removal disinhibiting activity in thalamus

Two-Factor Theory

Schachter and Singer induced physiological arousal with epinephrine injection with a different description of how the injection will make them feel

• one group got accurate description

• one got no description

• one got wrong description

• control group got no epinephrine and no description

talked to experimenter after injection who would either act rude or pleasant

researchers found people no explanation for how they felt were more likely to report their emotional state as same as experimenter - participants had same physiological processes attributed this to completely different emotions based on surrounding context

• two-factor theory says stimulus is perceived and autonomic response happens

• cognitive appraisal of physiological sensations gives rise to subjective emotional experience

Two-factor theory says …

our emotions are influenced by both our physiological state and the context of the environment surrounding us

Subcortical Areas

limbic system is a primarily subcortical circuit that gets input from association and entorhinal cortex → cingulate gyrus and hippocampus respectively

• limbic system is getting both sensory information and information from memory

after cingulate gyrus and hippocampus → amygdala → hypothalamus (other signals go through fornix and into mamillary bodies and the anterior thalamic nuclei)

hypothalamus → prefrontal cortex for basic emotional response → fornix, anterior thalamus, amygdala project back to cingulate gyrus which makes a loop

limbic system is NOT universal emotion center but is still important for emotion

Limbic System

subcortical structures are evolutionarily ancient and are not unique to humans, mostly in autonomic unconscious emotional responses

Kluver-Bucy syndrome: diminished fear response, low aggression, and no aversion to danger

• was first seen in rhesus monkeys after bilateral lesions to medial frontal lobe (includes amygdala)

Amygdala and Fear Learning

amygdala is highly connected to other areas of brain and has receptors for neurotransmitters and hormones and has many nuclei

fear conditioning involves changes to lateral amygdala cells even if signals come from different brain regions like auditory cortex for loud noise and visual cortex for light - lateral amygdala cells react the same way

signals get projected from lateral to central amygdala then hypothalamus, etc for responding to stimulus

emotional conditioning doesn’t work without central amygdala

Severing pathway to lateral hypothalamus interferes with ___ fear response but not ____ fear response.

autonomic; behavioural

when LeDoux used fear conditioning paradigm with different brain areas - lateral hypothalamus and periaqueductal gray

when connection between central amygdala and lateral hypothalamus is severed, rates had appropriate behavioural fear response (freezing) but not autonomic response like no increased BP

therefore amygdala is not one-size-fits-all and different pathways are involved in different aspects of emotion

PAG in Brainstem

rats that got PAG lesions - when presented with conditioned stimulus, BP increased as you would expect for a healthy rat but without the behavioural response and autonomic parts of fear response 

this shows that even tho behavioural and conditioned responses have amygdala, they have two separate pathways

• amygdala is a choke point for fear processing, not fear center

3 Stages of Emotion

1. sensory processing - visual info comes to eyes and is sent to thalamus

2. low road (subcortical) - goes to amygdala for FAST unconscious response to dangerous stimulus → hypothalamus for sympathetic branch of ANS → HR increases, BP increases, muscles contract

3. high road (cortical) - conscious pathway through cortex where first thalamus info is processed from V1 → amygdala and cortical areas to think about your next move

Lesions to the Human Amygdala

patient SM had full complete bilateral lesions and specifically did not have subjective experience of fear and physiological responses to scary things were extremely blunted

• couldn’t recognize fearful faces, draw a fearful face but was fine for other emotions

• positive emotional responses were normal

• no sense of personal space, doesn’t recognize situations as dangerous until too late (less situational awareness)

Cortical Role in Emotion

• perception of emotion (interpretation)

• expression of our own emotional state in face and tone

• internal, subjective experience of our own emotions

purposes of this could be:

• immediate response to a stimulus

• influencing social behaviours such as tone of voice

• communicating intent - emotions function as social behaviours e.g. giving someone a dirty look

• subjective feelings - internal state of feeling something

Perception of Emotion

right lateral fissure is important for perceiving prosody and tone of voice

aprosidia: inability to comprehend someone’s tone of voice

Ekman faces are those that have the most universal emotions (anger, happiness, sadness, surprise, fear, disgust) - cross-cultural indicators of emotional states that are easily perceived and recognized by healthy participants

Prosopagnosia does not affect _____.

perception of facial expressions - even though they cannot identify whose faces are making those expressions

amygdala damage patients have difficulty recognizing all the basic emotions, especially fearful

• amygdala damage patients don’t focus on eyes the way healthy people do

• instructing people to attend to the eyes increases ability to recognize fearful faces back up to the level of a healthy participant

Expression of Emotion

RH has a dominance for emotional expressions so right side damage has difficulty perceiving others’ emotions and expressing their own

left side of the face is perceived as more expressive since contralateral control

• with chimera stimulus, you see each side of the face mirrored to make its own face

• participants rate faces made of two left halves as more emotionally intense than either the original faces or the faces of the two right halves

• negative emotions are judged asymmetrically (left side is seen as more intense)

• positive emotions tend to be judged symmetrically

Innate vs. Voluntary Expression

innate facial expressions are automatic in response to real emotion

voluntary facial expressions are consciously produced for any number of reasons

volitional facial paresis: difficulty in voluntary facial expression but can still do the innate ones in the case they are feeling the emotions, damage to motor cortex and subcortical connections

• happens as damage to motor cortex and its connections, especially the parts of hypothalamus that are connected to cranial nerves

voluntary and innate expressions rely on different face nerves; the nerves in volitional paresis do NOT connect to Duchenne’s muscle, which is always involved in a genuine smile

emotional facial paresis has opposite symptoms

Emotional Facial Paresis

participants have no difficulty doing voluntary facial expressions but not when they are really experiencing emotion

damage to prefrontal cortex, thalamus, subcortical white matter in frontal lobe → connected to Duchenne’s muscle which is paralyzed

Expression of Prosody

affective prosody = emotional tone → perception and expression of this are localized to cortical areas surrounding the lateral fissure in the right hemisphere

propositional prosody is for semantic information

• left hemisphere could be for propositional prosody, or for just language production areas incorporating prosodic cues that are processed in the right hemisphere

Experience of Emotion

Damasio and colleagues: studied patterns of neural activation for sadness, happiness, anger, fear

• used PET scans to investigate neural activity

• participants lie in scanner and remember emotionally intense moments of their lives with emotionally natural recollection of a regular day

• used skin conductance, HR, and self-reports to confirm emotional response

Experience of Sadness

significant activation:

• Bilateral anterior insula

• Anterior cingulate cortex

• Right basal forebrain

• Right OFC

• Dorsal pons

significant deactivation in posterior cingulate cortex

Experience of Happiness

significant activation:

• right posterior cingulate

• right anterior cingulate

• left insula

• left SII

significant deactivation in left anterior cingulate

basically the reversed pattern for sadness, and is lateralized

Experience of Anger

significant activation:

• pons and midbrain

• left anterior cingulate

• right insula

significant deactivation in bilateral SII and right orbitofrontal cortex

Experience of Fear

significant activation in midbrain and left insula

significant deactivation:

• right SII

• hypothalamus

• bilateral orbitofrontal cortex

Valence and Arousal

valence: positiveness or negativeness of emotional state

arousal: how strongly you feel positive or negative

right hemisphere is specialized for negative affect, left for positive

• widespread LH damage → emotional lability (mood swings with little to no control over emotions)

• widespread RH damage → euphoric indifference (very happy when it is not appropriate)

Mood Disorder Symptoms

• adynamia: flat affect from lack of modulation of emotional expression (can be positive or negative emotions)

• anhedonia: loss of pleasure from normally pleasurable things

have similar profile of symptoms, differentiated by whether actual emotional state matches

Depression Overview

defining symptoms are anhedonia, chronic sadness, hopelessness

other common symptoms:

• changes in appetite

• insomnia

• lethargy

• cognitive deficits like biasing memory and attention towards negative interpretations of things

• low self-esteem

• suicidal ideation

Depression and the Brain

• dIPFC hypoarousal, disconnected from ACC so doesn’t regulate activity

• subgenual cingulate cortex is hyperactive, involved in regulating body functions during rest

• hemispheric asymmetries - right is more active, less decreased in left frontal lobe

• amygdala activation persists in response to negative stimuli

• ventral striatum hypoarousal

• hippocampus is less active for encoding positive stimuli

Anxiety Overview

includes phobias, generalized anxiety, OCD, PTSD

key dimensions are anxious apprehension (worrying) and anxious arousal (panic) such as activation of sympathetic NS

Anxiety and the Brain

• hyperactive amygdala since fear response to specific triggers compared to controls

• HC smaller in PTSD since flashbacks and memory loss comes from stress hormones that are released that destroy HC tissue

• ventromedial prefrontal cortex hyperactive to threat so doesn’t regulate amygdala as well

• ACC overactive at rest and during threat since it monitors action

• anxious apprehension associated with left frontal cortex therefore speech centers

• anxious arousal associated with posterior right cortex