PAIN REGULATORY DYSFUNCTION IN CHRONIC PAIN

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Specific Aim 1: To examine the role of alpha-2 adrenergic mechanisms in mediating the inverse relationship between resting BP and acute pain sensitivity in pain-free normotensive humans. If alpha-2 adrenergic mechanisms contribute to the inverse BP/acute pain sensitivity relationship, selective pharmacological blockade of alpha-2 adrenergic receptors should significantly attenuate this relationship. Specific Aim 2: To determine whether changes in alpha-2 adrenergic function contribute to chronic pain-related alterations in the relationship between resting BP and acute pain sensitivity. Based on prior work, it is expected that the chronic pain sample will display significant alterations (reversal) in the BP/acute pain sensitivity relationship relative to pain-free controls. If impairments in alpha-2 adrenergic inhibitory activity associated with chronic pain contribute to these alterations, a significant interaction is expected such that alpha-2 blockade will significantly attenuate the BP/pain sensitivity relationship in pain-free controls, but will have little effect on this relationship in the chronic pain group. Specific Aim 3: To determine whether changes in baroreceptor sensitivity contribute to alterations in the relationship between resting BP and acute pain sensitivity in chronic pain patients relative to pain-free controls. If diminished baroreceptor sensitivity associated with chronic pain mediates the BP/pain sensitivity alterations across chronic pain and pain-free control groups, it is expected that statistical control of spontaneous baroreceptor sensitivity variance will substantially attenuate between-group differences in the BP/pain sensitivity relationship. Specific Aim 4: To determine whether chronic pain-related activation of pain facilatory pathways contributes to alterations in the relationship between resting BP and acute pain sensitivity in chronic pain patients relative to pain-free controls. If central nociceptive sensitization associated with chronic pain mediates the BP/pain sensitivity alterations across chronic pain and pain-free control groups, it is expected that statistical control of central sensitization (degree of temporal summation) variance will substantially attenuate between-group differences in the BP/pain sensitivity relationship.