Tactile induced analgesia

From Wikipedia, the free encyclopedia

Tactile induced analgesia is the phenomenon where concurrent touch and pain on the skin reduces the intensity of pain that is felt.

Somatosensory afferent fibres[edit]

There are four main types of sensory fibres responsible for somatosensation: Aα, Aβ, Aδ and C fibres (more details can be found at the axon page). The Aβ fibres are from cutaneous mechanoreceptors and respond to touch stimuli; the Aδ and C fibres are nociceptor afferents which respond to painful stimuli. The touch fibres have a larger diameter than the pain fibres, which means that they transmit their action potentials much faster than the smaller diameter fibres.

Gate Control Theory[edit]

Melzack and Wall[edit]

The Gate Control Theory of Pain, first proposed in the 1960s by Melzack and Wall, states that the concurrent activation of tactile afferent nerve fibers inhibits activation of nociceptive afferent fibres.[1] Melzack and Wall suggested that a gating mechanism is present in the dorsal horn of the spinal cord. They suggested that both touch and pain afferent fibres synapse on to 'projection cells' and inhibitory interneurons in the dorsal horn. It is the projection cells which then travel up the spinothalamic tract to the brain. Interactions between these connections is thought to mediate the perception of painful stimuli:

  1. With no input, the inhibitory interneuron stops signals being sent to the brain from the projection neuron, i.e. the gate is closed.
  2. Stimulation of large tactile afferents leads to somatosensory input. The inhibitory interneuron and projection neuron are both activated, but the inhibitory interneuron stops signals travelling to the brain via the projection neuron, i.e. the gate is closed.
  3. Nociception occurs if there is greater stimulation of the smaller pain afferents. The interneuron becomes inactivated, so that the projection neuron can send signals to the brain leading to pain perception, i.e. the gate is open.

The theory shows that rubbing a painful site leads to stimulation of somatosensory input to projector neurons, which reduces the intensity of pain perceived.

Development of the Gate Control Theory[edit]

More recently neurophysiological studies in animals have indicated that the wide range dynamic neurons (WDR neurons) in the dorsal horn are the homologue of Wall and Melzack's proposed projector neurons and inhibitory interneurons.[2] The neurons are multimodal (respond to both touch and pain input), with an inhibitory surround receptive field. Experiments looking at the WDR neurons in animals have shown that a strong tactile stimulus in the peripheral inhibitory field could reduce the response to a painful stimulus to the same extent as a weak tactile stimulus closer to the centre of the receptive field.[3][4] These data show the Gate Control Theory of Pain was correct in the prediction that activation of large tactile afferent fibres inhibit the nociceptive afferent signal being transmitted to the brain.

Interactions between touch and pain[edit]

The interactions between touch and pain are mostly inhibitory (as is predicted by the Gate Control Theory). Research shows that there both acute and chronic pain perception is influenced by touch, with both psychophysical changes and differences in brain activation.

Touch and acute pain[edit]

The intensity of pain reported is consistently reduced in response to touch.[5][6][7] This occurs whether the touch is at the same time as the pain, or even if the touch occurs before the pain.[8] Touch also reduces the activation of cortical areas that respond to painful stimuli.[9]

Touch and chronic pain[edit]

Individuals suffering from chronic pain tend to show reduced tactile sensitivity in the affected area.[10] This means that they find it more difficult to distinguish whether there is one or two tactile points on the skin surface when the points are very close together. If patients are trained on the task of discriminating between two tactile points, it is shown that participants report reduced intensity of chronic pain.[11]

References[edit]

  1. ^ R., Melzack; P.D., Wall (1965). "Pain Mechanisms: A New Theory". Survey of Anesthesiology. 11 (3699): 89–90. Bibcode:1965Sci...150..971M. doi:10.1126/science.150.3699.971. PMID 5320816.
  2. ^ Le Bars D (October 2002). "The whole body receptive field of dorsal horn multireceptive neurones". Brain Res. Brain Res. Rev. 40 (1–3): 29–44. doi:10.1016/s0165-0173(02)00186-8. PMID 12589904. S2CID 53186033.
  3. ^ Salter MW, Henry JL (1990). "Differential responses of nociceptive vs. non-nociceptive spinall dorsal horn neurons to cutaneously applied vibration in the cat". Pain. 40 (3): 311–322. doi:10.1016/0304-3959(90)91128-6. PMID 2326096. S2CID 40710000.
  4. ^ Salter MW, Henry JL (1990). "Physiologicl characteristics of responses of wide dynamic range spinal neurones to cutaneously applied vibration in the cat". Brain Research. 507 (1): 69–84. doi:10.1016/0006-8993(90)90524-f. PMID 2302582. S2CID 12841536.
  5. ^ Wall PD, Sweet WH (January 1967). "Temporary abolition of pain in man". Science. 155 (3758): 108–9. Bibcode:1967Sci...155..108W. doi:10.1126/science.155.3758.108. PMID 6015561. S2CID 33458415.
  6. ^ Higgens JD, Tursky B, Schwartz GE (May 1971). "Shock-elicited pain and its reduction by concurrent tactile stimulation". Science. 172 (3985): 866–7. Bibcode:1971Sci...172..866H. doi:10.1126/science.172.3985.866. PMID 5572910. S2CID 44780022.
  7. ^ P.D., Wall (1996). "Comments after 30 years of the Gate Control Theory". Pain Forum. 5: 12–22. doi:10.1016/s1082-3174(96)80063-8.
  8. ^ Mancini F, Nash T, Iannetti GD, Haggard P (March 2014). "Pain relief by touch: a quantitative approach". Pain. 155 (3): 635–42. doi:10.1016/j.pain.2013.12.024. PMC 3988987. PMID 24361816.
  9. ^ Inui K, Tsuji T, Kakigi R (March 2006). "Temporal analysis of cortical mechanisms for pain relief by tactile stimuli in humans". Cereb. Cortex. 16 (3): 355–65. doi:10.1093/cercor/bhi114. PMID 15901650.
  10. ^ Moriwaki K, Yuge O (May 1999). "Topographical features of cutaneous tactile hypoesthetic and hyperesthetic abnormalities in chronic pain". Pain. 81 (1–2): 1–6. doi:10.1016/s0304-3959(98)00257-7. PMID 10353487. S2CID 24339479.
  11. ^ Moseley GL, Zalucki NM, Wiech K (July 2008). "Tactile discrimination, but not tactile stimulation alone, reduces chronic limb pain". Pain. 137 (3): 600–8. doi:10.1016/j.pain.2007.10.021. PMID 18054437. S2CID 2757963.