Offensive Anger:
Associated with a sense of control over the conflict's outcome.
Individual approaches the offender.
Linked to a leftward prefrontal EEG asymmetry.
Empathy towards the offender reduces this asymmetry as empathy diminishes hostile approach tendencies.
Defensive Anger:
Associated with a sense of helplessness regarding the conflict.
Individual tends to avoid the offender.
Linked to a rightward EEG asymmetry.
Prefrontal asymmetries in temperament and emotion studies are better explained by dimensional theories linking specific emotions to motivational axes (approach/avoidance).
Vertical Integration Models: Attempt to provide an integrative account of emotional processing across multiple levels of the nervous system, relating deeper brain regions, neocortical contributions, and bodily changes.
Fear Conditioning: A well-characterized vertical integration model.
Classical and operant conditioning principles explain how animals extract regularities indicating when/where reinforcing events occur.
Conditioning responses involving emotion, especially fear, can be rapid due to immediate consequences for survival.
Understanding fear acquisition and extinction mechanisms is crucial for treating anxiety disorders.
Rodent Studies: Provide detailed insights into neuroanatomy, neurophysiology, and molecular signaling underlying fear acquisition.
Typical Paradigm: Rats receive an auditory conditioned stimulus (CS) predicting a mild foot shock (unconditioned stimulus, US).
The testing chamber is the context.
After CS-US pairings, rats exhibit physiological and behavioral changes in response to the CS (cued fear) preparing them for threat like potentiation of startle reflexes, cessation of exploratory behavior (freezing), fight-or-flight response
Responses also occur due to contextual features (contextual fear).
Acquisition and expression of conditioned fear require the amygdala's integrity.
Rats with amygdala lesions are impaired in acquiring conditioned fear responses to cues and contexts.
The amygdala rapidly detects threats via direct thalamic input, bypassing primary sensory cortical areas.
Lateral amygdala neurons show conditioned increases in firing rates (within 15ms of CS onset) through the thalamo-amygdala pathway.
Long-term potentiation (LTP) is observed in this pathway, representing a potential electrophysiological signature of learning.
Alterations in gene expression and protein synthesis further strengthen synaptic connections for consolidating fear memories.
Activation of the rapid subcortical pathway can evoke fear reactions to simple stimuli, but its contribution to emotions in primates/humans is not fully understood.
This pathway allows crude sensory discrimination. More sophisticated perceptual analysis reaches the amygdala later via cortical pathways.
The rapid subcortical pathway may prime the amygdala for effective processing of slower cortical information.
This parallel arrangement allows faster emotional responses.
Synaptic plasticity in cortico-amygdala pathways permits long-term sensory representation alterations, facilitating future threat detection.
The amygdala is the most densely interconnected structure in the primate forebrain, influencing cognitive, sensory, and motor systems to enable behavioral adaptation to threats.
Human Studies:
Patients with amygdala damage show diminished conditioned fear responses, including reduced fear-potentiated startle and skin conductance responses (SCRs).
These deficits occur even with declarative knowledge of the learning parameters, suggesting dissociation from declarative memory.
Fear-relevant stimuli (e.g. angry faces, snakes) can be conditioned subliminally, without conscious awareness.
Neuroimaging reveals amygdala, thalamus, and anterior cingulate cortex activity during fear conditioning acquisition.
The degree of amygdala activation correlates with physiological fear learning (skin conductance amplitude).
These findings support the amygdala and related structures importance in warning of impending danger associate with threatening circumstances through activating fight-or-flight responses via downstream subcortical structures.
Revising fear responses is important when threats are no longer present.
Persistence of fear responses to non-threats is a hallmark of anxiety disorders like phobias and PTSD, termed emotional perseveration.
In fear-conditioning protocols, removing the negative reinforcer (US) changes the CS’s fear value, leading to fear extinction.
Fear Extinction:
Depends on the ventromedial prefrontal cortex (vmPFC).
vmPFC damage impairs extinction, while normal fear acquisition remains.
vmPFC influences amygdala activity suppressing responses and reducing behavior.
In humans, vmPFC damage causes difficulty reversing stimulus-reinforcer relationships, and fMRI activity in this region correlates with retention of extinction behavior.
Clinicians target pharmacological agents to mimic or augment these effects in anxiety disorder patients.
Hippocampus' Role:
Given its role in spatial processing and declarative memory, the hippocampus mediates contextual fear conditioning.
Hippocampal lesions impair fear responses to context but spare responses to discrete cues.
Amnesia patients with hippocampal damage lack contextual details about conditioning while exhibiting SCRs to a discrete CS.
Hippocampus contributes similarly to emotional and nonemotional learning, making it inappropriate to consider it specifically dedicated to emotional processing.
The Smatic Marker Hypothesis: Antonio Damasio's theory explains how the brain and body signal affective information to guide everyday decision making.
vmPFC contains indexes that link factual knowledge and bioregulatory states associated with an event.
When encountering a related event prior triggers somatic markers including autonomic, endocrine, and musculoskeletal changes that constitute emotion.
The vmPFC triggers reactivation of the somatosensory pattern describing the appropriate emotion through connections to emotion-eliciting structures, like the amygdala.
This can occur directly through a body loop expressing the appropriate visceral response, or indirectly stimulating the somatosensory pattern in the insula and somatosensory cortex without evoking physical changes known as an "as if" loop.
By evoking these somatosensory patterns, reasoning and decision-making processes are constrained to options qualitatively marked as good or bad.
These somatic markers serve as a heuristic rule of thumb for efficient optimal decisions without elaborate logical weighing of utility.
Reactivation of emotional states facilitates logical reasoning, and without this guidance everyday decisions are more costly.
This hypothesis relies on feedback from the body (or body representations) in generating emotional states, like James's theory.
Iowa Gambling Task: Experimental evidence supports some aspects of the theory.
Participants choose cards from four decks with differing monetary gains/losses to maximize profit.
Decks A & B yield larger short-term rewards but larger occasional punishers, leading to long-term losses (disadvantageous).
Decks C & D yield smaller short-term rewards, but smaller punishers leading to higher long-term gains (advantageous).
Healthy subjects tend to stop choosing from high-risk decks and reap rewards, but vmPFC patients continue selecting from risky decks and losing endowments.
During risky deck selection, healthy subjects exhibit an SCR a somatic marker for risky actions, while vmPFC patients do not.
vmPFC patients compromise their ability to learn from somatic markers, leading to non-optimal choices and poor decisions.
Insula plays a key role in monitoring the physiological state of the organism (interoception) and storing visceral/skeletomotor representations of emotional states, reinstated during decision-making.
Insula is an evolutionarily older cortical region lying hidden beneath the confluence of frontal and temporal lobes.
A posterior-to-anterior gradient in the insula provides a pathway for homeostatic regulation.
The posterior insula receives ascending information from pain and temperature pathways via the ventromedial thalamus, and parallel input from cranial parasympathetic nerves.
This information feeds to the mid-insula, where it is integrated with exteroceptive input from somatosensory cortices and limbic regions like the amygdala.
In primates, the anterior insula contains another level of integration with anterior cingulate cortex, orbitofrontal cortex, and dorsolateral prefrontal cortex.
The complex rerepresentation of body state that informs decision making and conscious awareness of motivational/affective state results at each station.
Evidence supporting the insula's role:
Activity correlates with heartbeat detection ability.
Anterior insula activation during fMRI correlates with subjective experience of temperature changes applied via a thermal probe to the hand.
Insula damage can dampen cravings for cigarettes in smokers, other patients lose their ability to appreciate music.
The role of body feedback plays an important effect on emotion in complex cognitive functions
When consciously describing their affective state (e.g. "How do you feel?") humans use verbal labels (e.g. happiness, sadness).
Whether specific emotions evoke unique autonomic or neural signatures is unanswered.
Dimensional theories suggest emotional categories emerge from a two-dimensional space formed by crossing axes of arousal and valence/approach and avoidance.
Hemispheric asymmetry models find signaling of different valences across hemispheres (positive emotions in left, negative in right).
Most individuals don't show strong EEG asymmetries, and neuroimaging studies failed to find a clear dichotomy between positive and negative affect signaling using spatially refined hemodynamic measures.
Categorical theories support neural specialization for discrete emotions in limbic and paralimbic regions.
Insula appears important for disgust, is often linked to nausea/ the vomiting reflex
Patients with damage to this are impaired in recognizing disgust in vocal/facial recognition
Neuroimaging confirms insula and other areas such as the facial expression of disgust.
The amygdala has been specifically linked to fear through studies on fear conditioning and facial expression processing, especially when viewing the eye region
Recent meta-analytic studies pooling data from hundreds of articles find no obvious markers of discrete emotions: instead, involvement of structures depends on task, emotion intensity, and other factors.
This challenges neural correlates of emotion categories and has led some researchers to abandon neuron notions.
Neuroscientists now implement novel approaches like multivariate statistics revealing complex patterns of neural and autonomic activity differentiating emotions.
Emotion categories may be "read out" by activity pattern combinations that are differentially weighted across emotions.
An analytic solution to the Cannon-Bard criticism that autonomic indices may be too undifferentiated to discriminate specific emotions results.
Such approaches may validate psychological theories and depend on further refinement, integration of theories, and advanced neuroscientific methods.
Processing emotionally significant sensory information is prioritized.
This can be automatic (involuntary detection) or voluntary (attentional bias).
Experiments examine whether masked emotional stimuli elicit autonomic responses that modulate ERP/ hemodynamic responses.
Brief presentations of fear-inducing stimuli elicit amygdala activity and skin conductance responses, even without conscious awareness.
Phobias and PTSD exaggerate these responses, underscoring covert contribution to anxiety disorder.
Perceptual awareness can be limited by rapid presentation (RSVP).
Detection of the second word is impaired with an attentional blink
*However, emotionally arousing words can be detected at shorter lag times by overriding capacity-limited perceptual mechanisms (requires the amygdala)
*Connections between amygdala/ sensory cortices also provide by which emotion can influence perception.
*A study of extrastriate responses to fearful expressions reduces enhanced activity seen in fusiform gyrus/occipital cortex.
lthough emotional stimuli elicit fast responses, other cognitive functions are recruited to further evaluate and initiate behavior.
*A first step in attention is to first alert to the emotional trigger by engaging the autonomic nervous system
*Limbic regions influence attentional processing to influence the basal forebrain cortex through modulatory action of the amygdala.
*The interfaces of the prefrontal cortex and anterior cingulate link limbic areas to the dorsal frontoparietal attentional network.
*Mayberg theorizes emotional balance. The anterior regulate medial/orbital balance processing at the expense of short behavioral goals.
We recall the emotional and personally meaningful events and are markers of life's shared by family through memories.
Unexpected tragedies leave emotional trace called "scars on the mind"
The term memory was introduced on all the vivid details of episodes.
Neurobiologist James posits that events enhance memory by regulating storage on information using memory modulation.
*The arousal dimmension is neuromodulatory with memory regions influenced through the amygdala, other regions on the direct axonal projects and indirectly using stress hormones from bloodstream.
*HPA axis and glucocorticoid, acute administration generally enhances retention while hormonal action effects through the consolidation due.
Administration on blocks the emotional narrative that effects memory
*Memory modulation is also seen from fmri scan emotional versitions and is greater to regions in emotional than to the neutral
Vertical integration models: Fear modification
*Just as fear mandates mandates changes in emotional response, but also revise
The ventral meidal cortex with amygdala is critical
*Stress is complex term referring to physiological changes, during short to long terms stress will increase the chance
The brain through adrenal and hormone in HPA access.
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