Diffuse noxious inhibitory control

Edit links
From Wikipedia, the free encyclopedia

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.

Mechanism[edit]

Noxious stimuli activate the endings of nociceptive C and A delta nerve fibers, which carry the signal to neurons in the dorsal horn of spinal cord. DNIC refers to the mechanism by which dorsal horn wide dynamic range neurons responsive to stimulation from one location of the body may be inhibited by noxious stimuli (such as heat, high pressure or electric stimulation) applied to another, remote location in the body.[1] The inhibition is thought to originate in the brain, and is thought to affect both wide dynamic range and nociception-specific neurons in the dorsal horn.[2]

Studies investigating gender differences in DNIC have shown mixed results with the effect dependent upon experimental methodology and measurement method.[3]

Measurement method[edit]

Pressure pain threshold (PPT) and pain tolerance (PTol) parameters are widely used as a measure of DNIC. Equipment such as metal pressure algometer with a rubber top is used to apply pressure to a person's finger or toe. The pressure at which the first sensation of pain is felt is recorded as PPT. The pressure is increased further and noted when the person says the pain is intolerable. This higher value is recorded as PTol. A second noxious stimulus (such as ice water) is then applied to a different part of the body and PPT/PTol measured. DNIC response is defined as an increase in the value of PPT during the second noxious stimulation.

Clinical use[edit]

The DNIC model is used frequently to quantify the central pain sensitization in chronic pain patients. DNIC inefficiency (or lower DNIC) has been implicated as a risk factor for development of chronic pain and pain syndromes.[4] Chronic pain disorders such as temporomandibular disorder[5] and fibromyalgia[6] have been associated with DNIC inefficiency. On the other hand, greater DNIC response is related to less pain, better physical functioning, and better self-rated health.[7] Diabetic neuropathy patients with low DNIC are more likely to benefit from treatment with duloxetine and tapentadol,[8][9] which are considered to restore altered descending modulation.[10]

DNIC forms the basis for the use of counterirritant to reduce pain.

See also[edit]

References[edit]

  1. ^ a b Le Bars D, Dickenson AH, Besson JM (June 1979). "Diffuse noxious inhibitory controls (DNIC). I. Effects on dorsal horn convergent neurones in the rat". Pain. 6 (3): 283–304. doi:10.1016/0304-3959(79)90049-6. PMID 460935. S2CID 36191807.
  2. ^ Le Bars D (October 2002). "The whole body receptive field of dorsal horn multireceptive neurones". Brain Research. Brain Research Reviews. 40 (1–3): 29–44. doi:10.1016/S0165-0173(02)00186-8. PMID 12589904. S2CID 53186033.
  3. ^ Popescu A, LeResche L, Truelove EL, Drangsholt MT (August 2010). "Gender differences in pain modulation by diffuse noxious inhibitory controls: a systematic review". Pain. 150 (2): 309–18. doi:10.1016/j.pain.2010.05.013. PMID 20557999. S2CID 27476459.
  4. ^ Yarnitsky D, Crispel Y, Eisenberg E, Granovsky Y, Ben-Nun A, Sprecher E, Best LA, Granot M (August 2008). "Prediction of chronic post-operative pain: pre-operative DNIC testing identifies patients at risk". Pain. 138 (1): 22–8. doi:10.1016/j.pain.2007.10.033. PMID 18079062. S2CID 26513812.
  5. ^ Kashima K, Rahman OI, Sakoda S, Shiba R (October 1999). "Increased pain sensitivity of the upper extremities of TMD patients with myalgia to experimentally-evoked noxious stimulation: possibility of worsened endogenous opioid systems". Cranio: The Journal of Craniomandibular Practice. 17 (4): 241–6. doi:10.1080/08869634.1999.11746100. PMID 10650395.
  6. ^ Lautenbacher S, Rollman GB (September 1997). "Possible deficiencies of pain modulation in fibromyalgia". The Clinical Journal of Pain. 13 (3): 189–96. doi:10.1097/00002508-199709000-00003. PMID 9303250.
  7. ^ Edwards RR, Ness TJ, Weigent DA, Fillingim RB (December 2003). "Individual differences in diffuse noxious inhibitory controls (DNIC): association with clinical variables". Pain. 106 (3): 427–37. doi:10.1016/j.pain.2003.09.005. PMID 14659526. S2CID 1053485.
  8. ^ Niesters M, Proto PL, Aarts L, Sarton EY, Drewes AM, Dahan A (July 2014). "Tapentadol potentiates descending pain inhibition in chronic pain patients with diabetic polyneuropathy". British Journal of Anaesthesia. 113 (1): 148–56. doi:10.1093/bja/aeu056. PMID 24713310.
  9. ^ Yarnitsky D, Granot M, Nahman-Averbuch H, Khamaisi M, Granovsky Y (June 2012). "Conditioned pain modulation predicts duloxetine efficacy in painful diabetic neuropathy". Pain. 153 (6): 1193–8. doi:10.1016/j.pain.2012.02.021. PMID 22480803. S2CID 35752776.
  10. ^ Bannister K, Patel R, Goncalves L, Townson L, Dickenson AH (September 2015). "Diffuse noxious inhibitory controls and nerve injury: restoring an imbalance between descending monoamine inhibitions and facilitations". Pain. 156 (9): 1803–11. doi:10.1097/j.pain.0000000000000240. PMID 26010460. S2CID 25554640.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Diffuse_noxious_inhibitory_control&oldid=1123101695"