Pain
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Lamina I of the dorsal horn, together with its main output pathway, lamina I projection neurons, has long been implicated in the processing of nociceptive stimuli, as well as the development of chronic pain conditions. However, the study of lamina I projection neurons is hampered by technical challenges, including the low throughput and selection biases of traditional electrophysiological techniques. ⋯ Although we were able to confirm the nociceptive involvement of this group of cells, we also describe an unexpected preference for innocuous cooling stimuli. We were able to characterize the thermal responsiveness of these cells in detail and found cooling responses decline when exposed to stable cold temperatures maintained for more than a few seconds, as well as to encode the intensity of the end temperature, while heating responses showed an unexpected reliance on adaptation temperatures.
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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.
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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.