Chapter 14: Emotion and Stress Flashcards

1
Q

What is an Emotion?

A

Emotions are subjective experiences that arise spontaneously and unconsciously in response to internal and external events.

Physiological response and conscious feeling.

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2
Q

Expression & Recognition of Emotion

A

Arousal
Approach / Avoidance
Communication

The Yerkes-Dodson Law

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3
Q

The Yerkes-Dodson Law

A

The Yerkes–Dodson law is an empirical relationship between arousal and performance, originally developed by psychologists Robert M. Yerkes and John Dillingham Dodson in 1908. The law dictates that performance increases with physiological or mental arousal, but only up to a point.

The graph of Arousal Level (y) vs. Performance (x) is bell-shaped.

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4
Q

Facial Expressions

A

Facial nerves control the muscles involved in facial expression.

–Cranial nerve VII: superficial muscles attached to skin
–Cranial nerve V: deep muscles attached to bones of head

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5
Q

Facial nuclei

A

–Located in pons nuclei near midline.
–Upper 1/3 of face receives bilateral input.
–Lower 2/3 of face receives contralateral input only.
–Hemispheric stroke may impact muscle tone in lower face on one side.

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6
Q

Neural Control of Facial Expression

A

Right Hemisphere Cortical Damage.

Voluntary smile: sideways
Spontaneous: normal

Volitional facial paralysis

Two pathways control expression:

  • Voluntary: motor cortex input
  • Involuntary: subcortical (BG)
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7
Q

Neural Control of Facial Expression:

Parkinson’s Disease

A

Parkinson’s disease

Emotional facial paralysis
Two pathways control expression
- Voluntary: motor cortex input
- Involuntary: subcortical Basal Ganglia

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8
Q

Emotions are Universal

A

Paul Ekman: small number of universal emotions.

  • Happiness, sadness, anger, fear, disgust, surprise.
  • Expressed by 42 facial muscles.

Children’s capacity for emotional expression:
Blind infants express emotions (e.g. social smile) at the same time as sighted infants
Infants protest separation from mothers at the same time across cultures

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9
Q

Cultural Contributions to Expression

A

Cultures influence how expressive we are in group situations.

–American students are about as expressive when alone as when in a group of strangers
–Japanese students are more expressive when alone than when in a group of strangers

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10
Q

Individual Differences in Emotion

A

Kagan: Temperament differs at birth.
–Babies that are highly reactive to environmental stimuli may develop anxiety disorders later in life
–Low responders may develop antisocial behaviors later in life

Psychopaths are extremely non-responsive, possibly leading to lack of empathy;
Low amygdala activation.

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11
Q

Three Theories of Emotion

A

–James-Lange Theory
–Cannon-Bard Theory
–Schacter-Singer Theory

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12
Q

James-Lange Theory

A

Specific pattern of autonomic arousal (bodily response) leads to specific conscious emotion.

Emotion can be induced by the corresponding bodily responses

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13
Q

Schacter-Singer Theory

A

Physiological arousal contributes to emotion’s intensity, while identity of emotion is based on cognitive appraisal.

Subjects injected with adrenaline or placebo:
–In absence of “appropriate explanation” for arousal participants manipulated into emotional experience
–Informed vs. ignorant subjects paired with euphoric or irritable companion
–Ignorant subjects attributed physiological arousal to presence of companion.

This theory has the most support right now.

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14
Q

Complexity of Emotion

A

Physiological feedback may not be necessary, but adds intensity.
–Patients with spinal cord injury have full range of emotions, though muted.

Conscious appraisal may not be necessary, but allows for identification of appropriate response
–Disgust vs. pride

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15
Q

Biological Correlates of Emotion

A

Complex interacting physical responses that combine activation of ANS, amygdala, cingulate cortex, and cerebral cortex

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16
Q

The Limbic System

A

that combine activation of ANS, amygdala, cingulate cortex, and cerebral cortex

Cingulate Cortex
Corpus Callosum
Thalamus
Hippocampus
Amygdala
Hypothalamus
17
Q

The Amygdala

A

Stimulation: produces fear & anxiety

Damage: difficulty identifying fear & anger expressions
Input: sensory cortices, ACC, hippocampus

Output: frontal & temporal lobes, BG, hypothalamus

18
Q

Kluver-Bucy Syndrome

A

bilateral temporalobectomy.

  • Decreased emotional reactivity
  • Hyper-orality: putting random things in mouth
  • Hyper-sexuality
19
Q

The Amygdala

A

Stimulation: produces fear & anxiety

Damage: difficulty identifying fear & anger expressions
Input: sensory cortices, ACC, hippocampus

Output: frontal & temporal lobes, BG, hypothalamus

Imaging: more active when viewing expressions of fear.

Bilateral damage to the amygdala impairs ability to associate neutral and aversive stimuli.

20
Q

Fear Conditioning

A
Information related to CS and US can enter amygdala directly through thalamus or indirectly through cortex
Lateral Nucleus (La): site of CS-US association
Central Nucleus (Ce): expression of CR
21
Q

Anterior Cingulate Cortex

A

Role in emotion, attention, cognitive processing, consciousness.
–Serves as gateway between limbic structures and PFC
–Active when we express emotion
–Damage may be implicated in psychopathy
–Same regions activated by physical and emotional pain
–Right ACC larger in people who score high in harm avoidance

22
Q

The Cerebral Cortex

A

Clinical observations of frontal lobe damage—e.g., Phineas Gage

  • Difficulty making and executing plans
  • Reduced emotionally, esp. fear and anxiety
23
Q

Emotional lateralization of The Cerebral Cortex

A
  • Left hemisphere damage: depression
  • Right hemisphere damage: surprisingly cheerful

Look left, right hemisphere processes emotional facial expression better and faster.

24
Q

Stress

A

unpleasant and disruptive state resulting from the perception of danger or threat

25
Q

Stressors

A

sources of stress, can be physical or psychological

26
Q

General Adaptation Syndrome (GAS)

A
  1. Alarm Stage: The stressor upsets homeostasis or cellular balance.
  2. Resistance Stage: The Body fights back by adjusting to the stress.
  3. Exhaustion Stage: Rest permits enhanced adaption.
    No Rest= overtraining, injury, lack of adaption

Dome-Shaped Graph of the Stages

27
Q

Two major systems mediate most components of the stress response

A

SNS activation raises Catelcholamines.

HPA activation raises Cortisol.

28
Q

Stress Hormones

A
Sympathetic Nervous System:
1. Norepinephrine (Noradrenaline)
2.  Epinephrine (adrenaline)
–Increase output from heart
–Liberate glucose from muscles for additional energy

Hypothalamic Pituitary Axis:
Cortisol
–Increases energy by converting proteins to glucose, increasing fat availability, and increasing metabolism
–Long-term energy increase for sustained stress

29
Q

Sympathetic Nervous System (SNS)

A

Walter Cannon (1929):
–Stressors lead to SNS activation
–Adrenal medulla releases 2 Catecholamines: adrenaline and noradrenaline
–The resulting increases in heart rate, blood flow, and respiration rate help the person deal with the stressful situation

30
Q

Hypothalamic-Pituitary-Adrenal (HPA) Axis

A

Higher cognitive centers identify specific stimulus as a stressor.
Sensory information also travels to the amygdala, which identifies danger.
The amygdala sends information to the hypothalamus (PVN) via the stria terminalis.
The paraventricular hypothalamus (PVN) releases corticotrophin-releasing hormone (CRH), which affects the anterior pituitary.
The anterior pituitary releases adreno-corticotropic hormone (ACTH).
In response to ACTH, the adrenal glands release cortisol.
Cortisol influences many neurons in the brain, increasing the release of several neurotransmitters.

31
Q

HPA Axis: Negative Feedback

A

The hippocampus contains receptors for glucocorticoids, such as cortisol.
When the hippocampus binds cortisol, it acts to inhibit CRH release by the hypothalamus
With less CRH, less ACTH and cortisol will be released

The Amygdala stimulates CRH release in the PVN.

32
Q

Stress and Health – Hippocampus

A

Cortisol increases the amount of calcium entering neurons—too much can be neurotoxic.

Neurons in the hippocampus are particularly vulnerable to stress, impacting negative feedback of stress response

33
Q

Cellular Changes in Response to Stress

A

The Hippocampus dendrites atrophy and neurogenesis is inhibited.

Thr Amygdala dendrites hypertrophy.

34
Q

Stress and Health - Immunity

A

Acute stress may be beneficial; it increases immune system activity, increasing number of immuno-responsive cells

Chronic or prolonged stress compromises the immune system.

Catecholamines and cortisol are immunosuppressive; they suppress the activity of lymphocytes (white blood cells) and affect the production of cytokines (antibody-recognizing cells).

Consequently, people experiencing chronic stress are more vulnerable to disease.

35
Q

Stress and Health - Cardiovascular

A

The cardiovascular system is particularly vulnerable to stress.
–Stress increases blood pressure, and prolonged high blood pressure can damage the heart or cause a stroke.

“During the Siege of Leningrad, BP increased dramatically. The effect of that siege combined with its starvation conditions cast a long lasting effect on cardio health. Even 50 years later, survivors of the Leningrad siege had increased BP and increased mortality from cardiovascular disease.” (Sparen P, et al., 2004)

36
Q

Stress and Health

A

Whether stress has a negative impact on health depends on a variety of factors, including social support, personality, and attitude.

Attitudes about stress and a sense of control may influence health.

37
Q

Cannon-Bard Theory

A

Autonomic arousal and identification occur simultaneously and independently.