Neuroinflammation and comorbidity of pain and depression

Walker, A.K.; Kavelaars, A.; Heijnen, C.J.; Dantzer, R.

doi:10.1124/pr.113.008144

Cited by 460Tryptophan and brain disordersPain Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration Mechanisms

Neuroinflammation and comorbidity of pain and depression

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Walker, A.K., Kavelaars, A., Heijnen, C.J., Dantzer, R.·2014·Pharmacological Reviews

DOI 10.1124/pr.113.008144PMC PMC3880465

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Abstract

Comorbid depression and chronic pain are highly prevalent in individuals suffering from physical illness. Here, we critically examine the possibility that inflammation is the common mediator of this comorbidity, and we explore the implications of this hypothesis. Inflammation signals the brain to induce sickness responses that include increased pain and negative affect. This is a typical and adaptive response to acute inflammation. However, chronic inflammation induces a transition from these typical sickness behaviors into depression and chronic pain. Several mechanisms can account for the high comorbidity of pain and depression that stem from the precipitating inflammation in physically ill patients. These mechanisms include direct effects of cytokines on the neuronal environment or indirect effects via downregulation of G protein-coupled receptor kinase 2, activation of the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase that generates neurotropic kynurenine metabolites, increased brain extracellular glutamate, and the switch of GABAergic neurotransmission from inhibition to excitation. Despite the existence of many neuroimmune candidate mechanisms for the co-occurrence of depression and chronic pain, little work has been devoted so far to critically assess their mediating role in these comorbid symptoms. Understanding neuroimmune mechanisms that underlie depression and pain comorbidity may yield effective pharmaceutical targets that can treat both conditions simultaneously beyond traditional antidepressants and analgesics.

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Comorbidity between chronic pain and psychological distress in clinical practice is higher than 60%.
“comorbidity between chronic pain and psychological distress in clinical practice is higher than 60% (Walker et al., 2014).”
From A systematic review of cognitive behavioral therapy-based interventions for comorbid chronic pain and clinically relevant psychological distress (2023) · cites this paper as Walker et al., 2014
The Introduction reports that chronic pain and depression co-occur at a prevalence of 30–60%, not higher than 60%. It describes high prevalence in clinical settings but gives no clinical figure above 60%; the paper also discusses depression rather than psychological distress broadly. (LLM, conf=0.88)
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Chronic pain frequently co-occurs with clinically relevant psychological distress.
“Chronic pain frequently co-occurs with clinically relevant psychological distress.”
From A systematic review of cognitive behavioral therapy-based interventions for comorbid chronic pain and clinically relevant psychological distress (2023) · cites this paper as Walker et al., 2014
One proposed mechanism is that proinflammatory cytokines stimulate indoleamine 2,3-dioxygenase in glial cells, converting tryptophan to kynurenine, which is then transformed into neurotoxic quinolinic acid in the brain.
“one hypothesis postulates that proinflammatory cytokines stimulate indoleamine 2,3-dioxygenase (IDO) in glial cells to convert tryptophan to kynurenine which is transformed into the neurotoxic quinolinic acid inside the brain (Müller and Schwarz, 2007;Walker et al., 2014).”
From A Review of the Relationship between Proinflammatory Cytokines and Major Depressive Disorder (2014) · cites this paper as Walker et al., 2014

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Authors: Walker, A. K., Kavelaars, A., Heijnen, C. J., & Dantzer, R.
Affiliations: The University of Texas MD Anderson Cancer Center (US)
ORCID: Walker, A.K.
Kavelaars, A.
Heijnen, C.J.
Dantzer, R.
Venue: Pharmacological Reviews
Publisher: Elsevier BV
Published: 2014-01
Volume: 66
Issue: 1
Pages: 80-101
ISSN: 0031-6997 (ISSN-L)
DOI: 10.1124/pr.113.008144
PMC: PMC3880465
OpenAlex: W2138452800
Cited by: 460
References: 190
Citations by year: 2026: 24 · 2025: 40 · 2024: 34 · 2023: 34 · 2022: 44 · 2021: 53 · 2020: 50 · 2019: 46 · 2018: 29 · 2017: 42 · 2016: 25 · 2015: 31 · 2014: 8
FWCI: 1.52
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Pharmacological Reviews (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Neurological Disorders and Stroke (R01NS074999, R01NS073939)
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: depression, chronic pain, pain-depression comorbidity, neuroinflammation, neuroimmune mechanisms, cytokines, G protein-coupled receptor kinase 2, indoleamine 2,3-dioxygenase, kynurenine metabolites, tryptophan metabolism, glutamate, GABAergic neurotransmission, sickness behavior, chronic inflammation, physical illness
MeSH terms: Animals, Brain, Depression, Humans, Inflammation, Pain, Comorbidity

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Neuroinflammation and comorbidity of pain and depression

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