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Diffuse noxious inhibitory controls (DNIC) or conditioned pain modulation (CPM) refers to an endogenous pain modulatory pathway which has often been described as "pain inhibits pain". [1] It occurs when response from a painful stimulus is inhibited by another, often spatially distant, noxious stimulus.
The gate control theory of pain asserts that non-painful input closes the nerve "gates" to painful input, which prevents pain sensation from traveling to the central nervous system. In the top panel, the nonnociceptive, large-diameter sensory fiber (orange) is more active than the nociceptive small-diameter fiber (blue), therefore the net input ...
Then, there are also the descending pathways for the modulation of pain sensation. One of the brainstem regions responsible for this is the periaqueductal gray of the midbrain, which both relieves pain by behavior as well as inhibits the activity of the nociceptive neurons in the dorsal horn of the spinal cord.
Neuromodulation is the physiological process by which a given neuron uses one or more chemicals to regulate diverse populations of neurons. Neuromodulators typically bind to metabotropic, G-protein coupled receptors (GPCRs) to initiate a second messenger signaling cascade that induces a broad, long-lasting signal.
Most pain resolves once the noxious stimulus is removed and the body has healed, but it may persist despite removal of the stimulus and apparent healing of the body. Sometimes pain arises in the absence of any detectable stimulus, damage or disease. [3] Pain is the most common reason for physician consultation in most developed countries.
Existing and emerging neuromodulation treatments also include application in medication-resistant epilepsy, [5] chronic head pain conditions, and functional therapy ranging from bladder and bowel or respiratory control to improvement of sensory deficits, such as hearing (cochlear implants and auditory brainstem implants) and vision (retinal ...
Nociceptive pain consists of an adaptive alarm system. [6] Nociceptors have a certain threshold; that is, they require a minimum intensity of stimulation before they trigger a signal. Once this threshold is reached, a signal is passed along the axon of the neuron into the spinal cord.
The organism's sensitivity to the stimulus increases, meaning the pain or itch elicited will be greater at those temperatures than they would be at room temperature. [15] Though these pathways display many similarities, there are other mechanisms by which itch sensations can be controlled, such as those through nerve growth factor and substance ...