PSY290 - Lecture 10: Emotion and Psychiatric Disorders

why have emotions?

why have emotions?

• adaptive and tied to specific behaviors

  • fear and survival responses

  • anger and defensive/attack responses

  • face of disgust is good for getting rid of toxic or spoiled food

• facilitate decision-making in cases where time is short, information is lacking and options available are ambiguous

• the ability to control emotions (emotional regulation) is related to mental health and job performance

physiology of emotion

• in part through the autonomic nervous system

• changes in organ function (heart rate, breathing, skin conductance)

• effects are rapid and involuntary

  • person you love walks in the door and your heart starts beating fast, you didnt initiate that it happened involuntary

• sympathetic (heart beat faster) vs parasympathetic (heart beat slower)

how many emotions are there?

• varying theories (early estimates from 6 to 8 core emotions)

• in the real world, the “pure” emotions are rare

• most emotional expressions are likely hybrids

• 6 core emotional states (simple theory)

  • readily identifiable facial expressions

  • tell mood by face

• things are more complicated than this

  • composites of the 6

  • like happy + sad: happy eyes, sad mouth

  • mixed states like bittersweet

  • these intersectional expressions are more common

emotions are innate

• the facial and physical expressions accompanying emotion are generally consistent across cultures and do not require experience (biologically hard-wired)

  • similar expression in individuals who are blind

  • everyone makes similar and can tell the similar expressions

• facial expressions are involuntary are associated with a different neural system (basal ganglia)

  • impaired in Parkinson’s disease

  • arise quickly

  • automatic emotional state like an uncomfortable smile

  • associated with a specific network

• physical expressions are adaptive and could have been selected for over time

  • clenched fists in anger to prepare for a fight

  • wrinkling of nose in disgust

voluntary/involuntary expressions

• ‘fake smile’ (voluntary) from a ‘real smile’ (involuntary)

• of the two muscles involved in a real smile (orbicularis oculi for the eyes + zygomaticus major for the mouth) one is difficult to contract voluntarily

  • in a fake smile, look at the eyes

• different system, impaired by frontal cortex damage

lying

• lying is associated w/many physical responses:

  • inappropriate smiling, nervous laughter, stiff upper body, infrequent nodding, less hand gestures, swinging feet, lack of eye contact

• there is also verbal (“um” and “ah”) while trying to meet cognitive demands of lying

  • cannot multitask

• lack of details in lies; cannot tell story backward in time

• physiological changes (due to activation of the ANS) which can be measured via polygraph

  • certain state of arousal that goes with lying

the polygraph

• at best, 80 - 88% accuracy

• not fondly viewed by the legal community

• many people show physiological changes just because theyre aroused

• so called lie detector

• maybe use an fMRI to predict lying

  • this isnt practical + so expensive

  • we dont have the data to support thats better either

theories on the origin of emotions

james-lange theory, cannon-bard theory, and modern view

james-lange theory

• perception of environmental stimuli

• feeling is an interpretation of unique physiological circumstances

• if this were true, each emotion should have a unique physiological state that can be distinguished by the person

• however, the physiology of most emotions is similar

cannon-bard theory

• separate pathways by which we get emotional states and physiological responses

• if this were true, emotion should be intact even if the ability to create physiological states was lost (eg spinal cord injury)

• however, emotions are often reduced in intensity in such cases (particularly positive emotions)

the modern view

emotion is a product of complex, reciprocal influences of the brain, nervous system and perception on each other

what parts of the brain are important?

limbic system and amygdala

the limbic system

• neural basis of emotion

• collection of brain areas that are interconnected

• lower order animals

  • been around for ages and increased in complexity

• simple theory but good enough

the case of phineas cage

frontal cortex injury is associated w/ pronounced behavioral changes, such as impulsivity, inappropriate social behavior and irritability (quick to anger)

• this suggested a role of the cortex in inhibiting emotion

the discovery of sham rage

• cats in which the removal of the cortex were hostile to all stimuli

  • also supported a role of the cortex in inhibiting emotion

• this behavior, termed sham rage, was absent in animals with hypothalamic damage

  • suggested a role of the hypothalamus in creating emotion

Kluver-Bucy syndrome

• hyperorality, hypersexuality, repeated investigation of familiar objects and no fear

• caused by damage to the anterior temporal lobe

• removal of the amygdala alone generates similar symptoms

• suggested a role of the amygdala in creating emotion

• more arousal

hypothalamus and amygdala role

amygdala is early, hypothalamus is immediately after in creating emotion

frontal cortex role

regulating emotion

case study: amygdala lesion in SM

• difficulty expressing fear and recognizing fear in others

• processed facial expressions in others differently

  • predictable pattern of eye movements

  • eye - eye nose mouth and back up

  • people with amygdala damage dont show this same pattern

• inappropriate social distancing

• abnormal behaviors

the amygdala: more than just fear

• many positive emotional states + experiences involve amygdala activation

• the role is complex

• be mindful of reverse inference errors in fMRI studies

unlearned (innate) fear in humans

• some scientists have argued that humans have only a few innate fears (eg heights, loud noises, approaching objects, snakes + spiders)

• this is the case for animals too

• most scientists believe that the majority of our fears are learned

simple fear circuit

• fast route AND a slow route

• hippocampus is necessary for contextual fear conditioning

• the amygdala is necessary for fear in general

mouse experiment

• fear to the context (blue box) is more elaborate

  • needs hippocampus

• fear to the tone (bell) is less elaborate

• all forms of fear conditioning amygdala is necessary

the prefrontal cortex

adjustment to the circuitry to reflect the environmental circumstances

PFC in emotion (including fear)

• connected to the amygdala; can inhibit it

• can prevent learned fear and other emotions (emotion regulation)

• connectivity between the amygdala and prefrontal cortex is plastic and modified by experience, particularly stress

• the ‘loss’ of prefrontal cortex control can lead to a loss of control over emotions (emotional dysregulation)

can we ‘overcome’ learned fear?

• yes! fear is not forever

• some fears we acquire early in life can become impractical later

• animals have a mechanism to limit the expression of fears that are no longer relevant

• extinction is a gradual reduction in a CR (eg fear) to a CS (eg context) following repeated presentations of the CS alone (eg context w/no shock)

  • blue box with no shock hundreds of time, blue box is no longer associated with fear

• extinction involves the PFC

neural mechanisms of extinction

in humans, the ventromedial prefrontal cortex (vmPFC) may be critical to establishing extinction

extinction is not likely forgetting

but a form of learning wherein we suppress previously acquired behaviors

after extinction, part of fear remains

reinstatement, spontaneous recovery, renewal

reinstatement

one CS-UCS repairing brings back full CR

spontaneous recovery

time-dependent recovery of CR to CS (no CS-UCS repairing required)

renewal

extinguish CR to CS in one context (green box), still have CR to CS in other contexts (eg purple box)

stress

can be viewed as a feeling of tension resulting from the perception of demanding circumstances (stressors), we can view stress through a psychological or a physiological lens

what makes a stressor

Novelty - something new you have not experienced before

Unpredictability - something you had no way of predicting

Threat to the ego - your competence as a person is called into question

Sense of control - you feel you have little or no control over the situation

common stressors

• many types, differ in severity and prevalence

• according to this data, the major stressors are work, money and the economy

• reasons can differ by year and by demographic

  • several studies suggest higher levels in Gen Z

stress levels and health

• measured by multiple stress scales

  • Social Readjustment Rating Scale (SRRS)

  • Daily Hassle Scale (DHS)

  • Perceived Stress Scale (PSS)

• stress is predictive of both physical and mental health

• many psychological disorders are precipitated by or exacerbated by stressors

• the most remarkable example is depression

  • risk is strongly related to frequency of stressors

• cumulative stress

  • stressors add together

what if stress if frequent?

risk for mental disorders increases with the frequency of stressful life events, stressors are cumulative

changes in emotion w/stress

• chronic stress in particular is associated with changes in emotion and risk for mental health disorders

• part of the negative effects of chronic stress may be due to changes in the brain

• many of the brain areas affected (hippocampus, amygdala and prefrontal cortex) are involved in emotional regulation and responding to stressors

chronic stress effects on neurons

here, the neurons of stressed animals show less branching (though the effects are complex and can vary)

the brain is vulnerable to stress, stress alters the stress network which leads to stress effecting you more in the future

starting with stress

stress —> hypothalamus —> pituitary gland —> adrenal gland —> cortisol (negative feedback loop)

as cortisol increases then it will shut off cortisol so it doesnt get too high

how does this inhibition of stress occur?

one area that may be involved: the hippocampus

controlling stress with glucocorticoid receptors

• cortisol binds to GRs in hippocampal cells

• GR-sensitive cells then prevent further cortisol release + terminate the stress response

• lower GR expression prevents this stress regulation and increases anxiety

• to reduce stress: more receptors is useful

• hippocampus is effected by high levels of cortisol

chronic stress + cortical thinning

• in veterans with post-traumatic stress disorder (PTSD), there is cortical thinning proportional to symptom severity

• effects greatest on the frontal lobe + temporal lobe

• more stress —> more thinning

hippocampus under stress

smaller in depression, size is negatively correlated w/number of depressive episodes and cortisol levels

animal model: social defeat

analogous to ‘bullying’, associated w/higher cortisol, lower testosterone, smaller testes + shorter lifespans

experiment: mouse high school model

• take a small mouse and put it with a large mouse

• fight will happen

• small mouse will be afraid

• put them in cages they cant touch but they can see each other

• produces a stress response

• higher cortisol, lower life spans

animal mode: CIS

CIS = chronic intermittent stress

most intense + popular model

depression

• loss of interest or pleasure in activities normally enjoyed (eg anhedonia)

• decreased energy (eg fatigue)

• feelings of guilt or low self-worth

• disturbed sleep, appetite and activity

• inability to concentrate

• thoughts of suicide

types of depression

• unipolar depressive disorder

  • major depressive disorder (chronic)

  • major depressive episodes (acute but often recurrent)

• biopolar disorder

• post-partum depression

• dysthymia

• seasonal affective disorder

neural features of depression

brain region

• hippocampus: volume decrease

• orbitofrontal cortex: volume decrease, activity increase

• anterior cingulate cortex: volume decrease

• amygdala: activity increase

compound

• 5-HT/serotonin: concentration decrease

• noradrenaline: concentration decrease

• gamma-aminobtyric acid (GABA): concentration decrease

• cytokines: concentration increase

• cortisol: concentration increase

diagnosing depression

• though depression has physiological and anatomical features, these features are not used in diagnoses

• diagnosis requires a trained professional (eg doctor, psychologist, psychiatrist)

• patient answers questions about their health

• diagnostic criteria from the DSM are used

• tests may be done to exclude other health problems (with similar symptoms (eg thyroid issues)

theories of depression

1. monoamine hypothesis

2. neurogenesis hypothesis

3. neuroendocrine hypothesis

4. neuroinflammation hypothesis

5. GABA/glutamate hypothesis

the monoamine hypothesis

decrease monoamine —> decrease mood

1. experimental depletion of 5-HT and other monoamine, produces depression-like behavior

2. low levels of monoamaine metabolites in depression

   1. not seeing a lot of serotonin so we can assume serotonin levels are not as high

3. tryptophan depletion can trigger depression in vulnerable individuals

   1. less serotonin being made in your brain

   2. increased risk of depression

4. drugs for depression affect monoamine signalling

   1. SSRIs

treating depression w/drugs

• most drugs modify monoamine transmission

• selective serotonin reuptake inhibitors (SSRIs)

• monoamine oxidase inhibitors (MAOis)

• tricyclic antidepressants (TCAs)

problems with monoamine theory

• antidepressants sometimes increase anxiety (so-called ‘jitterness syndrome’)

• SSRIs are not always effective

  • ~> 30% of patients do not respond to SSRIs

• though SSRIs increase serotonin levels immediately, mood is not improved for weeks

  • serotonin alone is probably not the cause or the cure

  • drugs dont work for everyone so it cannot be the sole reason

• more complicated than just assuming that a single thing explains depression

• need for alternative theories

alternative SSRI mechanisms

• one theory is that depression is not related to monoamine levels per se, but a secondary process triggered by monoamines

• for example, SSRIs may improve mood by inducing monoamine-dependent remodeling of the brain

• in particular, SSRIs might facilitate the production of new neurons in the brain (adult neurogenesis)

neurogenesis and depression

• further evidence suggests that neurogenesis may be implicated in the behavioural response of animals to antidepressants

• time course of neurogenesis aligns with time course for antidepressant efficacy (~4 - 6 weeks)

• antidepressants facilitate hippocampal neurogenesis in animals

• preventing hippocampal neurogenesis attenuates several behavioral effects of antidepressants

• when you block neurogenesis, drugs dont work as well

• one theory wont explain everything, they can cover parts though

treatment of depression

• treatable in ~70 - 80% cases

• main barrier is access to care (eg lack of funds, accessible professionals)

  • problem for less wealthy countries + low income individuals

• another barrier is intent to seek help (both self + societal stigma)

• common treatments include psychotherapy, cognitive behavioural theory and drugs (best for moderate/severe cases)

antidepressant controversy

ongoing debate about over-prescription (for off-label use and mild depression) and withdrawal

other methods of treatment for depression

• transcranial magnetic stimulation

  • rapidly growing in popularity

  • quick, cost-effective

  • less side effects

• ketamine

  • rapid effect, reserved fro severe cases

  • side effects not yet understood

  • newer

• meditation

  • small effect, but accessible with few risks

for treatment-resistant cases of depression

• electroconvulsive therapy

  • usually over frontal lobe

  • side effects include confusion + memory loss (largely transient)

• cingulotomy

  • psychotherapy

    • very severe depression, irreversible, severely debilitating, no other option

  • removal of the anterior cingulate

  • also used in the treatment of OCD + pain disorders

• deep brain stimulation has been suggested, but is not common

related to depression, we have…

• anxiety is related to amygdala activity; damage to the amygdala profoundly affects anxiety

• inhibiting the amygdala (ie w/GABA) reduces anxiety; increasing GABA activity may help treat anxiety

  • some anti-anxiety drugs increase GABA receptor activity, as does alcohol

• however, the most commonly prescribed anti-anxiety drug uses a different pharmacological mechanism

bipolar disorder

• episodes of depression and elevated mood

  • during elevated mood

    • the individual feels extremely energetic, happy and or irritable

  • they may experience reduced need for sleep and make poor decisions with little regard for consequences

• ~1% of the population

• one of the most costly disorders worldwide (top 10)

  • economic costs estimated to be $45 billion in the US

  • freq results in absenteeism

• risk of suicide and self harm is high

• neural mechanisms poorly understood

BP and creativity

• BP is more common in creative professionals + individuals with an arts education

• the genes involved in creativity may also be linked to genes regulating mental health (genetic correlation)

bipolar disorder treatments

• there are many possible treatments for bipolar disorder, including lithium, valproate, anticonvulsants and antipsychotics

• lithium is probably the most commonly employed treatment with the best results for long-term use

  • mechanisms not well understood

schizophrenia

• positive, negative and cognitive symptoms

• prefrontal cortex and hippocampus affected

• abnormalities in dopamine signalling

• treated either with conventional antipsychotics or atypical antipsychotics

personality disorders

• inflexible patterns of behavior that lead to distress in a wide variety of cases

• emerge in adolescence with other personality traits

• difficult to reliably diagnose

• less researched than other conditions

• borderline personality disorder, narcissistic personality disorder, antisocial personality disorder (ASPD)

psychopathic personality

• includes a constellation of traits: guiltless, manipulative, charming, callous, self-centered

  • aware of problematic behavior

  • often poor self control and low empathy

• research is difficult to do (privacy concerns), biased in nature (focuses on individuals who are incarcerated)

mechanisms of personality disorder

• argued to be a form of NDD

• early trauma/exposure to violence + brain damage (OFC) and poor parental relationship are risk factors

• genetic risk factors also exist

  • personality disorders and psychopathic traits are heritable

  • MAO (warrior gene) and 5-HTTLPR (serotonin) may be involved

• brain changes in ASPD:

  • reduced function, volume and connectivity in the FC + amygdala

low arousal theory

• inappropriate ANS reactivity

• chronic state of “stimulus hunger” (characteristic of ADHD, may be involved in ASPD)

• indicators of emotional state abnormal in ASPD

  • low resting heart rate and electrodermal activity

  • abnormal response to threatening stimuli

    • back off vs fight response

• may affect inability to learn from punishment