The gate control theory of pain asserts that non-painful input closes the "gates" to painful input, which prevents pain sensation from traveling to the central nervous system. Therefore, stimulation by non-noxious input is able to suppress pain. Although there are some important observations which the gate control theory cannot explain adequately
It was proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibres carry information from the site of injury to two destinations in the dorsal horn of the spinal cord: transmission cells that carry the pain signal up to the brain, and inhibitory interneurons that impede transmission cell activity. Activity in both thin and large diameter fibres excites transmission cells. Thin fibre activity impedes the inhibitory cells (tending to allow the transmission cell to fire) and large diameter fibre activity excites the inhibitory cells (tending to inhibit transmission cell activity). So, the more large fibre (touch, pressure, vibration) activity relative to thin fibre activity at the inhibitory cell, the less pain is felt.
Gate control theory asserts that activation of nerves which do not transmit pain signals, called non-nociceptive fibres, can interfere with signals from pain fibres, thereby inhibiting pain. Afferent
pain-receptive nerves, those that bring signals to the brain, comprise at least two kinds of fibres - a fast, relatively thick, myelinated "Aδ" fibre
that carries messages quickly with intense pain, and a small, unmyelinated, slow "C" fibre
that carries the longer-term throbbing and chronic pain
. Large-diameter Aβ fibres are non-nociceptive (do not transmit pain stimuli) and inhibit the effects of firing by Aδ and C fibres.
The peripheral nervous system has centres at which pain stimuli can be regulated. Some areas in the dorsal horn of the spinal cord that are involved in receiving pain stimuli from Aδ and C fibres, called laminae, also receive input from Aβ fibres. The non-nociceptive fibres indirectly inhibit the effects of the pain fibres, 'closing a gate' to the transmission of their stimuli. In other parts of the laminae, pain fibres also inhibit the effects of non-nociceptive fibers, 'opening the gate'. This presynaptic inhibition of the dorsal nerve endings can occur through specific types of GABAA receptors regulate nociception and paintransmission.
An inhibitory connection may exist with Aβ and C fibres, which may form a synapse
on the same projection neuron
. The same neurons may also form synapses with an inhibitory interneuron
that also synapses on the projection neuron, reducing the chance that the latter will fire and transmit pain stimuli to the brain
(image on the right). The inhibitory interneuron fires spontaneously.The C fibers synapse would inhibit the inhibitory interneuron, indirectly increasing the projection neuron's chance of firing. The Aβ fibre, on the other hand, forms an excitatory
connection with the inhibitory interneuron, thus decreasing
the projection neuron's chance of firing (like the C fibre, the Aβ fibrer also has an excitatory connection on the projection neuron itself). Thus, depending on the relative rates of firing of C and Aβ fibres, the firing of the non-nociceptive fibre may inhibit the firing of the projection neuron and the transmission of pain stimuli.
Gate control theory thus explains how stimulus that activates only nonnociceptive nerves can inhibit pain. The pain seems to be lessened when the area is rubbed because activation of non-nociceptive fibres inhibits the firing of nociceptive ones in the laminae. In trans-cutaneous electrical nerve stimulation (TENS), non-nociceptive fibres are selectively stimulated with electrodes in order to produce this effect and thereby lessen pain.
One area of the brain involved in reduction of pain sensation is the periaqueductal gray matter
that surrounds the third ventricle
and the cerebral aqueduct
of the ventricular system
. Stimulation of this area produces analgesia
(but not total numbing) by activating descending pathways that directly and indirectly inhibit nociceptors in the laminae of the spinal cord.Descending pathways also activate opioid
receptor-containing parts of the spinal cord.
Afferent pathways interfere with each other constructively, so that the brain can control the degree of pain that is perceived, based on which pain stimuli are to be ignored to pursue potential gains. The brain determines which stimuli are profitable to ignore over time. Thus, the brain controls the perception of pain quite directly, and can be "trained" to turn off forms of pain that are not "useful". (Thanks to wikipedia)
Would this approach work in MS?
It is difficult to say it would need to be tried and tested, but it may work for some and not others as some of you know nerve pain is difficult to manage
Does TENS work for you? If so maybe there may be merit in this system. Time will tell