Research Topic

The Role of Neuroinflammation in Chronic Pain Development and Maintenance

About this Research Topic

Pain that resolves quickly (acute) is a commonly experienced and evolutionarily conserved mechanism of survival. Chronic pain, which may persist for years, is associated with inflammatory diseases, peripheral and central neuropathies, cancer, and idiopathic conditions, and is a distinct and debilitating ...

Pain that resolves quickly (acute) is a commonly experienced and evolutionarily conserved mechanism of survival. Chronic pain, which may persist for years, is associated with inflammatory diseases, peripheral and central neuropathies, cancer, and idiopathic conditions, and is a distinct and debilitating condition that affects 25% of European adults. The burden of chronic pain is enormous in terms of suffering, disability, health care and social and economic cost. Currently available medicines for treating chronic/neuropathic pain states, which include anti-inflammatory compounds, opioids, antidepressant and anticonvulsant drugs, are often unsatisfactory. Also, such therapies usually possess adverse effects. Thus, there is an urgent need to understand the fundamental mechanisms of chronic pain development to improve therapies.

Different chronic (i.e. neuropathic) or inflammatory injuries to nervous system trigger structural and functional changes in the peripheral or central sensory circuits, resulting in behavioral dysfunctions, such as hyperalgesia and allodynia, and neuropsychiatric comorbidities. A part from the cause, chronic pain is maintained in part by central sensitization and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is driven by neuroinflammatory processes in the peripheral and central nervous system. Characteristic features of neuroinflammation are 1) activation/proliferation of resident glial cells; 2) infiltration of peripheral immune cells 3) release of inflammatory mediators. Indeed, the overproduction of proinflammatory cytokines and chemokines, and other mediators, are thought to be responsible for neuronal sensitization, at both spinal and brain levels, with subsequent maintaining of pain. Changes in neurotransmitters and neuromodulators (i.e. neuropeptides, glutamate, GABA, NO and neurotrophic factors) contribute to the neural plasticity induced by chronic pain and the complex central sequelae.

In this Research Topic, which will comprise both Original Research articles (in vitro, animal or clinical studies) and Reviews, we invite researchers to discuss the behavioural, and biomolecular mechanisms activated by chronic pain states with a particular attention dedicated to the recent evidence exploring the pathways promoting neuroinflammation. A further important topic to consider will be the emerging pharmacological targets for reversing aberrant pain behaviors activity in these neural circuitries may contribute to pain relief and to improve some negative affective states.


Keywords: Chronic pain, neuroinflammation, allodynia


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Submission Deadlines

16 December 2020 Manuscript
15 February 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

16 December 2020 Manuscript
15 February 2021 Manuscript Extension

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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