Articles: neuralgia.
-
Chronic neuropathic pain associated with peripheral neuropathies cannot be attributed solely to lesions of peripheral sensory axons and likely involves alteration in the processing of nociceptive information in the central nervous system in most patients. Few data are available regarding EEG correlates of chronic neuropathic pain. The fact is that effective cortical neuromodulation strategies to treat neuropathic pain target the precentral cortical region, i.e. a cortical area corresponding to the motor cortex. It is not known how these strategies might modulate brain rhythms in the central cortical region, but it can be speculated that sensorimotor rhythms (SMRs) are modified. Another potent way of modulating cortical rhythms is to use EEG-based neurofeedback (NFB). Rare studies previously aimed at relieving neuropathic pain using EEG-NFB training. ⋯ The value of EEG-NFB procedures to relieve neuropathic pain has been rarely studied. This pilot study will attempt to show the value of endogenous modulation of brain rhythms in the central (rolandic) region in the frequency band corresponding to the frequency of stimulation currently used by therapeutic motor cortex stimulation. In the case of significant clinical benefit produced by the low-β(SMR)/high-β ratio increasing strategy, this work could pave the way for using EEG-NFB training within the armamentarium of neuropathic pain therapy.
-
Patients with chronic pain often report being sensitive to pain at night before falling asleep, a time when the synchronization of cortical activity is initiated. However, how cortical activity relates to pain sensitivity is still unclear. Because sleep is characterized by enhanced cortical delta power, we hypothesized that enhanced cortical delta power may be an indicator of intensified pain. ⋯ Chemogenetic activation of GABAergic neurons in ACC enhanced EEG delta power and lowered mechanical pain thresholds simultaneously in naive mice. However, chemogenetic inhibition of ACC GABAergic neurons could not block mechanical allodynia. These results provided compelling evidence that elevated EEG delta power is accompanied with aggravated neuropathic pain, whereas decreased delta power attenuated it, suggesting that enhanced delta power can be a specific marker of rising chronic neuropathic pain and that wake-promoting compounds could be used as analgesics in the clinic.
-
We sought to refine a screening measure for discriminating a sensitized or normal sensation pain phenotype among African American adults with sickle cell disease (SCD). ⋯ The PR-Lasso offers a way to discriminate a SCD pain phenotype.
-
Individuals with pain from sickle cell disease (SCD) are often treated for nociceptive pain, but recent findings indicate they may also have neuropathic pain. PAINReportIt, a computerized version of the McGill Pain Questionnaire, provides a potential subscale that is the summed number of selected neuropathic pain quality words (PR-NNP), but it lacks construct validity. The study purpose was to ascertain PR-NNP construct validity in adults with SCD and chronic pain. ⋯ PR-NNP was moderately correlated with NPSI (r = .33, p < .001) and S-LANSS (r = .40, p < .001). Regression analysis indicated that PR-NNP and pain intensity, but not a nociceptive pain subscale, were significant predictors of NPSI and S-LANSS. Findings support construct validity of PR-NNP, which may be useful as a screening tool for neuropathic pain in patients with SCD.