Chapter #15: Emotions, Aggression, and Stress Flashcards
Emotion
subjective mental state
-distinctive behaviors
-feelings
-involuntary physiological changes (ex. rapid heartbeat, tears, blush = caused by autonomic nervous system)
facilitate social contact and learning
Range of human emotions
-core set of emotions (6-8) (degrees of intensity)
-Emotion is communicated through verbal
communication (words, tone of voice) and
non-verbal communications (body language,
facial expressions)
Universal facial expressions of emotion
-Facial expressions provide emphasis and context for verbal communication to your audience
-ex. anger, sadness, happiness, fear, disgust, surprise, contempt, embarassment
Human emotions - biological and cultural influences
-Agreement about meaning of most facial expressions
-Happiness is most agreed upon
-Non-literate groups had less agreement with disgust and surprise
Individual variability
- reactivity (measured in 4 month old infants)
-Low reactivity (~40% infants)
-High reactivity (~20% infants) - High reactive children are biased to become
-Timid, shy, cautious in unfamiliar situations (risk averse)
-Greater risk for anxiety disorders
-Exaggerated amygdala response - Low reactive children are biased towards being
-outgoing, spontaneous, and fearless
Circuit #1: Medial forebrain bundle
Intra-cranial self stimulation
-Operant conditioning
-Stimulation of brain region may be reinforcing or aversive
-Reinforcement may, or may not, correlate with subjective pleasure
Circuit #2: Papez Circuit - Limbic System
-Negative emotion elicited by stimulating limbic system
-Lesion overactive amygdala:
o increased social affiliation
o decreased anxiety
o increased confidence
-Central amygdala = hub for
anxiety, stress, fear, addiction
Kluver-Bucy Syndrome and the Medial Temporal Lobe
-Dramatically lessened fear and aggression
-Blunted affect
-Hyperorality
-Hypersexuality
-Visual agnosia
-Monkey lost its fear of snakes → early signs that the amygdala is involved in these responses
Amygdala - A part of the Medial Temporal Lobe
Patient S.M.
-Developed fearlessness in childhood
-Outgoing, but few good friends
-Confronts risk
-Normal nervous system responses
-brain scan reveals calcium deposits that have destroyed cells in her amygdala
Patient S.M. examples
-Fearless in risky social situations
-Unafraid of spiders/snakes
-No (or very low) normal sympathetic nervous system response to normally fear-evoking stimuli
-Has little social fear or sense of personal space
-Can, however, exhibit panic in physiological challenges (panic attacks) (external threats and internal threats)
External Threats
can be detected by the amygdala (patient S.M
cannot detect these)
Internal Threats
detected by brainstem
Amygdala Crucial to unlearned fear
-Low road allows for immediate responses
-High road allows for higher level cognitive
processing (PFC allows for observational fear
learning)
Different emotions activate
different brain regions
Brain regions activated by sadness
-anterior cingulate cortex
-posterior cingulate cortex
-insula
-dorsal pons
Brain regions activated by happiness
-right posterior cingulate cortex
-left insula
-left anterior cingulate cortex
Brain regions activated by fear
-midbrain
-orbitofrontal region of prefrontal cortex
Brain regions activated by anger
-pons
-left anterior cingulate cortex
Stress response
-initial response to stress
-sympathetic nervous system
1. norepinephrine released from adrenal medulla (direct input from hypothalamus)
2. fast
-Hypothalamus Pituitary Adrenal (HPA) axis
1. Cortisol released from adrenal cortex
2. Slow
Autonomic Nervous System
Sympathetic (fight or flight)
→ Norepinephrine
Parasympathetic (relax)
→ Acetylcholine
** Sympathetic and Parasympathetic
nervous systems often oppose each
other **
HPA Axis - A stress responsive system
HPA = Hypothalamus – Pituitary – Adrenal
The adrenal cortex/adrenal gland secretes
steroids, including glucocorticoids
Cortisol is a glucocorticoid hormone that
prepares the body to deal with stress
→ Increases blood glucose
→ Promotes metabolism
→ Suppresses inflammation
Individual Differences
Early stressful experiences can
allow for later resilience
→ Stress immunization
More significant early life stress
→ Greater stress responses
→ Learning deficits
→ Long-lasting changes in brain steroid receptor expression (epigenetic regulation)
Negative Affect
experiences world in negative terms
-Higher levels of distress, anxiety, dissatisfaction
-Low subjective sense of well-being
Genetic risk
many genes contribute to susceptibility to negative affect disorders
chronic, lower grade stressors increase risk for
anxiety disorders or depression
General Adaptation to Stress Theory Steps
- Alarm
- Resistance
- Exhaustion
Alarm
body mobilizes to confront threat
Resistance
body actively copes with threat
Exhaustion
if threat continues the body’s resources become depleted
General Adaptation to Stress Theory
-Chronic stress produces excess alarm and resistance
-Contribute to development of negative affective
disorders
Anxiety Disorders
- Generalized Anxiety Disorder
- Obsessive-compulsive Disorder
- Panic Disorder
- Posttraumatic Stress Disorder
- Social Anxiety Disorder
Generalized Anxiety Disorder
chronic anxiety, exaggerated tension
Obsessive-compulsive Disorder
recurrent unwanted thoughts (obsessions) and/or repetitive behaviors (compulsions)
Panic Disorder
unexpected, repeated episodes of intense fear and physical symptoms
Posttraumatic Stress Disorder
memories of unpleasant event produce same intense visceral arousal
Social Anxiety Disorder
overwhelming anxiety and excessive self-consciousness in everyday social situations
PTSD involves
-hippocampus atrophy
-PTSD patients have smaller hippocampi (HPC)
→ Does stress shrink HPC to produce PTSD?
→ Are smaller HPC a risk for developing PTSD?
What kind of fear does PTSD involve?
learned fear
Fear Conditioning
-Tone is associated with mild electrical shock
-Eventually tone alone elicits “freezing” response
-If tone has a regular pattern, animal will habituate
-Chronic, unpredictable stressor (tone) will continue to elicit “freezing”
Original Trauma Activates
- alarm stress systems
-Subsequent stressors produce heightened alarm stress response - amygdala
Acute neurochemical responses to PTSD
-Locus Coeruleus (norepinephrine)
-Ventral tegmental area (dopamine)
-Endogenous opioids
-Corticotropin-releasing hormone
How is the amygdala activated during trauma?
-reciprocal interactions may facilitate encoding and retrieval of traumatic memories
-triggers traumatic memory via the amygdala
What happens over time with traumatic memories?
Over time, traumatic memory associations and
physiological response are strengthened
What is depression?
Unhappy mood, loss of interests, energy and appetite, difficulties with concentration, restless
agitation
Brain changes - Depression
→ Greater brain activity in PFC and amygdala
- Persists after depression period is over
- Electroconvulsive therapy
→ Smaller hippocampus
→ Reduced monoamine transmitter activity
- Serotonin, norepinephrine, dopamine
- Selective serotonin reuptake inhibitors (SSRIs)
Co-morbidity
when two disease traits co-occur at a frequency that is higher than expected based upon the base rates of the two, alone
Therapeutics for depression and anxiety
-Also, SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors:- Cymbalta, Effexor, Pristiq)
-ElectroConvulsive therapy
-Ketamine – NMDA receptor antagonist
-Cognitive Behavioral Therapy
Criticisms of medical treatments of depression and anxiety
-Non medical treatments (CBT) work
-Placebo effects
-Medications are not effective in some people
