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Alcohol dependence as a chronic pain disorder
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Dysregulation of pain neurocircuitry and neurochemistry has been increasingly recognized as playing a critical role in a diverse spectrum of diseases including migraine, fibromyalgia, depression, and PTSD. Evidence presented here supports the hypothesis that alcohol dependence is among the pathologies arising from aberrant neurobiological substrates of pain. In this review, we explore the possible influence of alcohol analgesia and hyperalgesia in promoting alcohol misuse and dependence. We examine evidence that neuroanatomical sites involved in the negative emotional states of alcohol dependence also play an important role in pain transmission and may be functionally altered under chronic pain conditions. We also consider possible genetic links between pain transmission and alcohol dependence. We propose an allostatic load model in which episodes of alcohol intoxication and withdrawal, traumatic stressors, and injury are each capable of dysregulating an overlapping set of neural substrates to engender sensory and affective pain states that are integral to alcohol dependence and comorbid conditions such as anxiety, depression, and chronic pain.
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“For example, rodent models of alcohol withdrawal have reliably observed hyperalgesia in multiple pain assays (Gatch et al., 1999;Gatch, 2009;Egli et al., 2012).”
From Drug Addiction: Hyperkatifeia/Negative Reinforcement as a Framework for Medications Development (2021) · cites this paper as Egli et al., 2012
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“As with opioids, although acute alcohol administration in animal studies may confer analgesic effects, abstinence from chronic alcohol consumption produces hyperalgesia (Gatch et al., 1999;Gatch, 2009;Egli et al., 2012).”
From Drug Addiction: Hyperkatifeia/Negative Reinforcement as a Framework for Medications Development (2021) · cites this paper as Egli et al., 2012
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Self-citationMorgan, A., Adank, D. N., Johnson, K., Blunt, E., & Patel, S. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.02.15.480609 · Cited by 1
Corticotropin-Releasing Factor Signaling at the Intersection of Pain and Opioid Addiction
McGinn, M. A., & Edwards, S. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-800213-1.00083-3
Self-citationBlanton, H. L., Bergeson, S. E., Morgan, D. J., & Guindon, J. (2019) · Elsevier eBooks · doi:10.1016/b978-0-12-813125-1.00023-4
Metadata
- Authors
- Egli, M., Koob, G. F., & Edwards, S.
- Affiliations
- National Institutes of Health (US)
- Scripps Research Institute (US)
- Corresponding author
- Egli, Mark
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2012-11
- Volume
- 36
- Issue
- 10
- Pages
- 2179-2192
- ISSN
- 0149-7634 (ISSN-L)
- PMC
- PMC3612891
- OpenAlex
- W1996880759
- Cited by
- 347
- References
- 233
- Citations by year
- 2026: 19 · 2025: 32 · 2024: 34 · 2023: 27 · 2022: 26 · 2021: 39 · 2020: 45 · 2019: 27 · 2018: 16 · 2017: 18 · 2016: 24 · 2015: 17 · 2014: 16 · 2013: 7
- FWCI
- 1.38
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (AA008459, AA012602, AA006420, AA007456, AA020608)
- National Research Service Award (AA018250)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- alcoholism, chronic pain, hyperalgesia, neurochemistry, alcohol withdrawal, traumatic stress, anxiety comorbidity, comorbid depression, affective pain
- MeSH terms
- Alcoholism, Amygdala, Catechol O-Methyltransferase, Chronic Disease, Humans, Neural Pathways, Prefrontal Cortex, Receptors, Opioid, mu, Chronic Pain
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