Diffuse noxious inhibitory control

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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.

Contents

Mechanism

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

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

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

Related Research Articles

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<span class="mw-page-title-main">Pain</span> Type of distressing and unpleasant feeling

Pain is a distressing feeling often caused by intense or damaging stimuli. The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage." In medical diagnosis, pain is regarded as a symptom of an underlying condition.

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<span class="mw-page-title-main">Grey column</span>

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<span class="mw-page-title-main">Nociceptor</span> Sensory neuron that detects pain

A nociceptor is a sensory neuron that responds to damaging or potentially damaging stimuli by sending "possible threat" signals to the spinal cord and the brain. The brain creates the sensation of pain to direct attention to the body part, so the threat can be mitigated; this process is called nociception.

<span class="mw-page-title-main">Sensory neuron</span> Nerve cell that converts environmental stimuli into corresponding internal stimuli

Sensory neurons, also known as afferent neurons, are neurons in the nervous system, that convert a specific type of stimulus, via their receptors, into action potentials or graded potentials. This process is called sensory transduction. The cell bodies of the sensory neurons are located in the dorsal ganglia of the spinal cord.

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<span class="mw-page-title-main">Referred pain</span> Pain perceived at a location other than the site of the painful stimulus

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<span class="mw-page-title-main">Spinal interneuron</span>

A spinal interneuron, found in the spinal cord, relays signals between (afferent) sensory neurons, and (efferent) motor neurons. Different classes of spinal interneurons are involved in the process of sensory-motor integration. Most interneurons are found in the grey column, a region of grey matter in the spinal cord.

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

<span class="mw-page-title-main">Presynaptic inhibition</span>

Presynaptic inhibition is a phenomenon in which an inhibitory neuron provides synaptic input to the axon of another neuron to make it less likely to fire an action potential. Presynaptic inhibition occurs when an inhibitory neurotransmitter, like GABA, acts on GABA receptors on the axon terminal. Presynaptic inhibition is ubiquitous among sensory neurons.

Sandra M. Garraway is a Canadian-American neuroscientist and assistant professor of physiology in the Department of Physiology at Emory University School of Medicine in Atlanta, Georgia. Garraway is the director of the Emory Multiplex Immunoassay Core (EMIC) where she assists researchers from both academia and industry to perform, analyze, and interpret their multiplexed immunoassays. Garraway studies the neural mechanisms of spinal nociceptive pain after spinal cord injury and as a postdoctoral researcher she discovered roles for both BDNF and ERK2 in pain sensitization and developed novel siRNA technology to inhibit ERK2 as a treatment for pain.

References

  1. 1 2 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.
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