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• W4229017801 abstract "Offset analgesia is defined by a dramatic drop in perceived pain intensity with a relatively small decrease in noxious input. Although functional magnetic resonance imaging studies implicate subcortical descending inhibitory circuits during offset analgesia, the role of cortical areas remains unclear. The current study performed task-based and connectivity analyses to elucidate the cortical correlates of offset analgesia using functional near infrared spectroscopy (fNIRS). This study was approved by the University of Pittsburgh IRB. After providing informed consent, twenty-four healthy volunteers (18-50 years old) underwent fNIRS scanning at rest and then during offset (OS) and control (Con) heat stimuli applied to the forearm. NIRS data were collected with a head probe targeting bilateral frontal and somatomotor cortices (NIRx NIRSport2). Pain intensity was recorded continuously on a computerized visual analogue scale (COVAS, Medoc). NIRS data were preprocessed and analyzed in NIRS Toolbox, a free analysis package based in Matlab. After controlling for non-neural hemodynamic responses in superficial tissues, widespread increases in cortical oxygenated hemoglobin concentration were observed, reflecting cortical activation during heat pain. OS – Con contrasts revealed deactivations in bilateral medial prefrontal cortex (mPFC) and bilateral somatosensory cortex (SSC) associated with offset analgesia. Right dorsolateral prefrontal cortex (dlPFC) showed activation only during OS. Functional connectivity analyses are ongoing. These data demonstrate opposing cortical activation patterns during offset analgesia and support a model in which right dlPFC underlies ongoing evaluation of pain intensity change. With predictions of decreasing pain intensity, right dlPFC activation likely inhibits ascending noxious input via subcortical pathways resulting in SSC and mPFC deactivation. This study identifies cortical circuitry underlying offset analgesia and introduces the use of fNIRS to study pain modulation in an outpatient clinical environment. Grant support from NIGMS T32GM075770 (BA), NIBIB R01EB028248-01 (TH), the Virginia Kaufman Endowment Fund in the form of a Pitt CTSI competitive research grant (BA, HS, AW, TH), and the International Anesthesia Research Society in the form of the Mentored Research Award (BA). Offset analgesia is defined by a dramatic drop in perceived pain intensity with a relatively small decrease in noxious input. Although functional magnetic resonance imaging studies implicate subcortical descending inhibitory circuits during offset analgesia, the role of cortical areas remains unclear. The current study performed task-based and connectivity analyses to elucidate the cortical correlates of offset analgesia using functional near infrared spectroscopy (fNIRS). This study was approved by the University of Pittsburgh IRB. After providing informed consent, twenty-four healthy volunteers (18-50 years old) underwent fNIRS scanning at rest and then during offset (OS) and control (Con) heat stimuli applied to the forearm. NIRS data were collected with a head probe targeting bilateral frontal and somatomotor cortices (NIRx NIRSport2). Pain intensity was recorded continuously on a computerized visual analogue scale (COVAS, Medoc). NIRS data were preprocessed and analyzed in NIRS Toolbox, a free analysis package based in Matlab. After controlling for non-neural hemodynamic responses in superficial tissues, widespread increases in cortical oxygenated hemoglobin concentration were observed, reflecting cortical activation during heat pain. OS – Con contrasts revealed deactivations in bilateral medial prefrontal cortex (mPFC) and bilateral somatosensory cortex (SSC) associated with offset analgesia. Right dorsolateral prefrontal cortex (dlPFC) showed activation only during OS. Functional connectivity analyses are ongoing. These data demonstrate opposing cortical activation patterns during offset analgesia and support a model in which right dlPFC underlies ongoing evaluation of pain intensity change. With predictions of decreasing pain intensity, right dlPFC activation likely inhibits ascending noxious input via subcortical pathways resulting in SSC and mPFC deactivation. This study identifies cortical circuitry underlying offset analgesia and introduces the use of fNIRS to study pain modulation in an outpatient clinical environment. Grant support from NIGMS T32GM075770 (BA), NIBIB R01EB028248-01 (TH), the Virginia Kaufman Endowment Fund in the form of a Pitt CTSI competitive research grant (BA, HS, AW, TH), and the International Anesthesia Research Society in the form of the Mentored Research Award (BA)." @default.
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• W4229017801 date "2022-05-01" @default.
• W4229017801 modified "2023-09-23" @default.
• W4229017801 title "Cortical Activity During Pain Relief: A Functional Near-infrared Spectroscopy Study of Offset Analgesia" @default.
• W4229017801 doi "https://doi.org/10.1016/j.jpain.2022.03.161" @default.
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