Hyperkatifeia is used here as a framework for understanding intensified negative emotional and motivational withdrawal states in addiction. The review positions it as a driver of compulsive drug seeking through negative reinforcement.
First-pass extracted concept
hyperkatifeia
Candidate: concept label1 source documents5 linked claims
Live refresh every 5sNext refresh in 5s
Aliases
negative emotional/motivational state during withdrawal
Extracted Explainers
What the tool is doing
What problem it solves
What it does not solve
Evidence Snippets
This review focuses on neurochemical/neurocircuitry dysregulations that contribute to hyperkatifeia, defined as a greater intensity of negative emotional/motivational signs and symptoms during withdrawal from drugs of abuse in the withdrawal/negative affect stage of the addiction cycle.
Supporting Sources
Linked Claims
Addiction can be organized into three stages with corresponding dysfunction domains and brain-region associations.
Quoted textsource-backed
Compulsive drug seeking that is associated with addiction is hypothesized to follow a heuristic framework that involves three stages (binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation) and three domains of dysfunction (incentive salience/pathologic habits, negative emotional states, and executive function, respectively) via changes in the basal ganglia, extended amygdala/habenula, and frontal cortex, respectively.
Neurochemical and neurocircuit dysregulations in addiction are hypothesized to shift hedonic state from homeostasis to an allostatic negative set point.
Quoted textsource-backed
Such neurochemical/neurocircuitry dysregulations are hypothesized to mediate a negative hedonic set point that gradually gains allostatic load and shifts from a homeostatic hedonic state to an allostatic hedonic state.
Hyperkatifeia is a withdrawal-associated negative emotional and motivational state that contributes to compulsive drug seeking through negative reinforcement.
Quoted textsource-backed
This review focuses on neurochemical/neurocircuitry dysregulations that contribute to hyperkatifeia, defined as a greater intensity of negative emotional/motivational signs and symptoms during withdrawal from drugs of abuse in the withdrawal/negative affect stage of the addiction cycle. Hyperkatifeia provides an additional source of motivation for compulsive drug seeking via negative reinforcement.
Neurobiological targets for hyperkatifeia include extended-amygdala circuitry with within-system and between-system neuroadaptations across stress and antistress transmitter systems.
Quoted textsource-backed
Neurobiological targets for hyperkatifeia in addiction involve neurocircuitry of the extended amygdala and its connections via within-system neuroadaptations in dopamine, enkephalin/endorphin opioid peptide, and γ-aminobutyric acid/glutamate systems and between-system neuroadaptations in prostress corticotropin-releasing factor, norepinephrine, glucocorticoid, dynorphin, hypocretin, and neuroimmune systems and antistress neuropeptide Y, nociceptin, endocannabinoid, and oxytocin systems.
Medications and behavioral therapies that reset brain stress, antistress, and emotional pain systems toward homeostasis are proposed as promising targets for addiction treatment development.
Quoted textsource-backed
Based on preclinical studies and translational studies to date, medications and behavioral therapies that reset brain stress, antistress, and emotional pain systems and return them to homeostasis would be promising new targets for medication development.