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Seminowicz, D.

Publications and source records attributed to Seminowicz, D..

3 recordsLinked to original sources

Cortical 6-9 Hz Oscillation are a Reliable Biomarker of Persistent Pain in Rats

Neural biomarkers of chronic pain offer a potential tool for improving the speed of diagnosis and delivery of treatment for this devastating disease. Here, we tested the hypothesis that pain states are associated with distinct changed in cortical brain waves. We induced neuropathic orofacial pain in female rats by chronic constriction injury of the infraorbital nerve (CCI-ION). In most animals, this resulted in lasting reductions in mechanical sensitivity thresholds, and in lasting increases in facial grimace scores. We recorded electrocortigraphy (ECoG) signals over the neocortex of these rats, before and after CCI-ION, and analyzed these signals with a novel, spectral modelling approach. Consistent with our hypothesis, power in the 6-9 Hz bandwidth of the ECoG was differentially modulated in animals displaying signs of chronic pain. Specifically, development of mechanical hypersensitivity correlated with a decrease in 6-9 Hz power. Furthermore, we show that changes in the power of this oscillation after injury, obtained at the individual animal level, provide a more sensitive marker of pain presence than do traditional between animal comparisons of post-injury oscillatory power. Identification of animals demonstrating chronic-pain behaviors was more accurate when estimates of post-injury oscillatory power were compared against each animals own pre-injury baseline than when compared against post-injury power estimates from animals not developing chronic pain. These results highlight the need for establishing individual-specific, "pain-free" baselines from which oscillation disturbances can be measured and which may constitute a reliable, low-cost approach not only for diagnosing chronic pain, but also for identifying individuals likely to transition from acute to chronic pain.

neuroscience↗

Prolonged tonic pain in healthy humans disrupts intrinsic brain networks implicated in pain modulation

Neural mechanisms of ongoing nociceptive processing in the human brain remain largely obscured by the dual challenge of accessing neural dynamics and safely applying sustained painful stimuli. Recently, pain-related neural processing has been measured using fMRI resting state functional connectivity (FC) in chronic pain patients. However, ongoing pain-related processing in normally pain-free humans remains incompletely understood. Therefore, differences between chronic pain patients and controls may be due to comorbidities with chronic pain. Decreased FC among regions of the descending pain modulation network (DPMN) are associated with presence and severity of chronic pain disorders. We aimed to determine if the presence of prolonged tonic pain would lead to disruption of the DPMN. High (10%) concentration topical capsaicin was combined with a warm thermode applied to the leg to create a flexible, prolonged tonic pain model to study the FC of brain networks in otherwise healthy, pain-free subjects in two separate cohorts (n=18; n=32). We contrasted seed-based FC during prolonged tonic pain with a pain-free passive task. In seed-based FC analysis prolonged tonic pain led to enhanced FC between the anterior middle cingulate cortex (aMCC) and the somatosensory leg representation. Additionally, FC was enhanced between the pregenual anterior cingulate cortex (pACC), right mediodorsal thalamus and the posterior parietal cortex bilaterally. Further, in the seed-driven PAG network, positive FC with the left DLPFC became negative FC during prolonged tonic pain. These data suggest that some altered DPMN FC findings in chronic pain could partially be explained by the presence of ongoing pain.

neuroscience↗

Sensorimotor peak alpha frequency is a reliable biomarker of pain sensitivity

Previous research has observed that individuals with chronic pain demonstrate slower alpha band oscillations (8-12 Hz range) during resting electroencephalography (EEG) than do age-matched, healthy controls. While this slowing may reflect pathological changes within the brain that occur during the chronification of pain, an alternative explanation is that healthy individuals with slower alpha frequencies are more sensitive to prolonged pain, and by extension, more susceptible to developing chronic pain. To formally test this hypothesis, we examined the relationship between the pain-free, resting alpha frequency of healthy individuals and their subsequent sensitivity to two experimental models of prolonged pain, Phasic Heat Pain and Capsaicin Heat Pain, at two testing visits separated by 8 weeks on average (n = 61 Visit 1, n = 46 Visit 2). We observed that the speed of an individuals pain-free alpha oscillations was negatively correlated with sensitivity to both prolonged pain tests and that this relationship was reliable across short (minutes) and long (weeks) timescales. Furthermore, we used the speed of pain-free alpha oscillations to successfully identify those individuals most sensitive to prolonged pain, which we also validated on data from a separate, independent study. These results suggest that alpha oscillation speed is a reliable biomarker of prolonged pain sensitivity with the potential to become a tool for prospectively identifying pain sensitivity in the clinic.

neuroscience↗