Pain
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During the past few years, the research of chronic neuropathic pain has focused on neuroinflammation within the central nervous system and its impact on pain chronicity. As part of the ERA-Net NEURON consortium, we aimed to identify immune cell patterns in the cerebrospinal fluid (CSF) of patients with herpes zoster neuralgia and patients with polyneuropathy (PNP), which may contribute to pain chronicity in these neuropathic pain conditions. Cerebrospinal fluid of 41 patients (10 herpes zoster and 31 PNP) was analyzed by flow cytometry identifying lymphocyte subsets: CD4+ (T-helper cells), CD8+ (cytotoxic T cells), CD19+ (B cells), and CD56+ (natural killer [NK]) cells. ⋯ The analysis of the individual follow-up showed a worsening of the pain condition if NK-cell frequency was low. Low NK-cell frequency is associated with signs of central sensitization (MPS), whereas high NK-cell frequency might prevent central sensitization. Therefore, NK cells seem to play a protective role within the neuroinflammatory cascade and may be used as a marker for pain chronicity.
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Endometriosis (ENDO) and interstitial cystitis/bladder pain syndrome (IC/BPS) are chronic pain conditions for which better treatments are urgently needed. Development of new therapies with proven clinical benefit has been slow. We have conducted a review of existing preclinical in vivo models for ENDO and IC/BPS in rodents, discussed to what extent they replicate the phenotype and pain experience of patients, as well as their relevance for translational research. ⋯ This analysis highlights the wide variety of models used, limiting reproducibility and translation of results. We recommend refining models so that they better reflect clinical reality, sharing protocols, and using standardized endpoints to improve reproducibility. We are addressing this in our project Innovative Medicines Initiative-PainCare/Translational Research in Pelvic Pain.
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Clinical Trial
Examination of mechanism effects in cognitive behavioral therapy and pain education: analyses of weekly assessments.
Psychosocial treatments for chronic pain produce favorable outcomes. However, we still do not know precisely by what mechanisms or techniques these outcomes are wrought. In secondary analyses of a 10-week group intervention study comparing the effects of literacy-adapted cognitive behavioral therapy (CBT) with literacy-adapted pain education (EDU) among patients with chronic pain, low-socioeconomic status, and low literacy, the Learning About My Pain trial, we examined whether pain catastrophizing was a mechanism specific to CBT. ⋯ Results suggest the existence of reciprocal influences whereby cognitive changes may produce outcome improvements and vice versa. At the same time, results from analyses of changes in slopes between pain catastrophizing and outcomes indicated that CBT and EDU were successful in decoupling pain catastrophizing and subsequent pain intensity and interference as treatment progressed. Results provide further insights into how psychosocial treatments for chronic pain may work.
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The genesis of the headache phase in migraine with aura is thought to be mediated by cortical spreading depression (CSD) and the subsequent activation and sensitization of primary afferent neurons that innervate the intracranial meninges and their related large vessels. Yet, the exact mechanisms underlying this peripheral meningeal nociceptive response remain poorly understood. ⋯ Pharmacological inhibition of astrocytic function, which ameliorated meningeal afferents' sensitization, reduced basal astrocyte calcium activity but had a minimal effect on the astrocytic calcium wave during CSD. We propose that calcium-independent signaling in cortical astrocytes plays an important role in driving the sensitization of meningeal afferents and the ensuing intracranial mechanical hypersensitivity in migraine with aura.