Unfortunately, the increase in PPT was transient in that it decreased, with no regard to the treatment, during the fifteen minutes that were post-intervention. Aboodarda and colleagues postulated that the most likely explanation for the reduced PPT is possibly the effect heavy tissue massage had on the central pain-modulatory systems. To be more specific, the pressure of the massage provided an analgesic effect via the gate theory of pain, or the ascending pain inhibitory system. The transmission of ascending pain information could have been altered by the activation of thick myelinated ergoreceptor nerve fibers (through percutaneous proprioceptor and mechanoreceptor activation), which in turn fomented a descending inhibitory effect thereby allowing pain perception modulation. A second possible explanation for the mechanism of pain modulation is the diffuse noxious inhibitory control (DNIC), or a descending anti-nociceptive pathway, also called counter-irritation. DNIC is typically induced by nociceptive stimuli that begins in the spinal cord and ascends to the brain, where pain transmission is inhibited monoaminergically, thereby reducing perception of pain not only in local sites but also in distant sites. Lastly, the increase in PPT could be caused by the control of parasympathetic reflexes by the autonomic nervous system, possibly contributing to the release of stress from the myofascial via relaxing/inhibiting/releasing of the strain located in the smooth muscle that is embedded in the soft
Unfortunately, the increase in PPT was transient in that it decreased, with no regard to the treatment, during the fifteen minutes that were post-intervention. Aboodarda and colleagues postulated that the most likely explanation for the reduced PPT is possibly the effect heavy tissue massage had on the central pain-modulatory systems. To be more specific, the pressure of the massage provided an analgesic effect via the gate theory of pain, or the ascending pain inhibitory system. The transmission of ascending pain information could have been altered by the activation of thick myelinated ergoreceptor nerve fibers (through percutaneous proprioceptor and mechanoreceptor activation), which in turn fomented a descending inhibitory effect thereby allowing pain perception modulation. A second possible explanation for the mechanism of pain modulation is the diffuse noxious inhibitory control (DNIC), or a descending anti-nociceptive pathway, also called counter-irritation. DNIC is typically induced by nociceptive stimuli that begins in the spinal cord and ascends to the brain, where pain transmission is inhibited monoaminergically, thereby reducing perception of pain not only in local sites but also in distant sites. Lastly, the increase in PPT could be caused by the control of parasympathetic reflexes by the autonomic nervous system, possibly contributing to the release of stress from the myofascial via relaxing/inhibiting/releasing of the strain located in the smooth muscle that is embedded in the soft