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Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...

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Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder

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Published on: June 23, 2023

Alcohol dependence as a chronic pain disorder.

Mark Egli¹, George F Koob, Scott Edwards

¹Division of Neuroscience and Behavior, National Institute on Alcohol Abuse and Alcoholism, NIH, DHHS, Bethesda, MD 20892-9304, USA. megli@mail.nih.gov

Neuroscience and Biobehavioral Reviews

|September 15, 2012

Summary

Alcohol dependence may stem from disrupted pain pathways, influencing misuse and withdrawal. This review explores the link between pain neurobiology and alcohol use disorders.

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Development of Recombinant Proteins to Treat Chronic Pain

Development of Recombinant Proteins to Treat Chronic Pain

Published on: April 11, 2018

Area of Science:

Neuroscience
Psychiatry
Addiction Medicine

Background:

Pain neurocircuitry and neurochemistry are implicated in various diseases like migraine, fibromyalgia, depression, and PTSD.
Aberrant neurobiological substrates of pain are increasingly recognized as critical in disease pathology.

Purpose of the Study:

To explore the hypothesis that alcohol dependence arises from aberrant pain neurobiology.
To examine the influence of alcohol analgesia and hyperalgesia on alcohol misuse and dependence.
To investigate the overlap in neuroanatomical sites and genetic links between pain transmission and alcohol dependence.

Main Methods:

Review of existing evidence on pain neurobiology and alcohol dependence.
Examination of neuroanatomical sites involved in negative emotional states and pain transmission.
Consideration of genetic factors linking pain and alcohol dependence.

Main Results:

Evidence supports the hypothesis that alcohol dependence is linked to dysregulated pain neurobiology.
Neuroanatomical sites for negative emotions in alcohol dependence are also involved in pain transmission.
Chronic pain conditions may functionally alter these overlapping neural substrates.

Conclusions:

Alcohol dependence may be a pathology arising from aberrant pain neurobiological substrates.
An allostatic load model is proposed, where stressors dysregulate neural substrates, leading to pain states integral to alcohol dependence and comorbidities.
This framework integrates alcohol intoxication/withdrawal, trauma, and injury in the development of sensory and affective pain states.