The Science Behind Topical Menthol and Camphor for Pain Relief

The Science Behind Topical Menthol and Camphor for Pain Relief

Menthol and camphor are terpene compounds with a long history of therapeutic use including topically for pain.1,2,3 Their molecular mechanisms of action, however, have only begun to be understood within the last couple of decades. They each belong to a class of analgesics known as counterirritants. Counterirritants have their effects by first activating and then desensitizing nociceptors in the skin.4

Menthol and camphor are able to penetrate the outer layer of the epidermis (stratum corneum) and interact with peripheral sensory neurons in the dermal-epidermal junction that extend close to the skin surface.5

Mechanism of Action

Counterirritants work by activating a subgroup of receptors within the superfamily of sensory neurons known as the transient receptor potential (TRP) ion channels. TRP receptors are found throughout the body in both sensory neurons and non-neuronal tissue. Menthol and camphor interact with a subgroup within this superfamily known as TRPV receptors. The TRPV subgroup consists of thermosensitive ion channels that detect a wide range of stimuli including temperature, chemicals, and pressure, as well as changes in extracellular osmolarity. Camphor may directly interact with TRPV1 (transient receptor potential vanilloid 1) and TRPA1 (transient receptor potential ankyrin 1) receptors, both of which are involved in nociception.6 Menthol is a selective activator of transient receptor potential melastatin-8 (TRPM8).7 Because of its association with menthol, TRPM8 is also known as the Cold and Menthol receptor.8

Menthol produces a cooling sensation on the skin, while camphor can elicit warming and cooling sensations. In reality, skin temperature does not change, but the perception of cooling and warming occurs as a consequence of menthol or camphor interacting with TRP receptors. In effect, topical application of a counterirritant acts as an ongoing agonist at TRP receptor sites. Applied topically, menthol and camphor initially induce their TRP receptors to release inflammatory mediators that include calcitonin gene-related peptide (CGRP), which is associated with migraine pain; and substance P, which is a neuropeptide that modulates the transmission of pain signals to the CNS. The repeated stimulation sensitizes and then ultimately desensitizes the specific TRP channels, leading first to a diminished response and then to functional desensitization of nociceptive sensory neurons. The net effect is that ion channel signaling to the same segmental CNS level that elicited a pain response in the first place is now blocked, thereby providing relief from the experience of both acute and inflammatory pain.6,9,10

The effect of these pharmacodynamics is largely explained by a model of nociception known as Gate Theory. According to Gate Theory, competition from certain non-painful stimuli will cause nerve “gates” in the spinal dorsal horn to shut in the presence of painful stimuli, with the result that pain signals are prevented from reaching the CNS.11,12

Menthol

Menthol has analgesic effects on acute and inflammatory pain primarily by activating cold-sensitive TRPM8 receptors in the skin. It may also have additional analgesic effects by binding to kappa-opioid receptors.13 Menthol has anesthetic properties as well, which may be mediated by interaction with GABA receptors.14 In addition to these mechanisms, menthol is vasoactive. It dilates local blood vessels in the skin at the site of application, thereby improving blood flow to any areas of injury or inflammation.15

In a double-blind, randomized placebo-controlled crossover study, cutaneous application of menthol oil was shown to provide sustained pain relief and to alleviate symptoms of nausea, vomiting, photophobia, and phonophobia in migraine patients.16 In a triple-blind, randomized placebo-controlled study of carpal tunnel syndrome, topical menthol reduced pain intensity to an extent that study authors recommended it should be considered as an alternative to analgesic drugs for the management of chronic and neuropathic pain in the workplace.17

The results of a proof-of-concept study also suggest that topical menthol may be effective for neuropathic pain.18

In a double-blind, placebo-controlled study, the addition of menthol to a transdermal patch was shown to enhance lidocaine delivery to the site of pain in patients with back pain and arthritis.19

Camphor

Like menthol, camphor has vasoactive properties and has been shown to improve blood circulation to the skin and muscles.20 Camphor has also been shown to inhibit pain and improve inflammatory signs in several animal models of joint inflammation.21In a human study using a multimodal approach for the treatment of low back pain, camphor was found to help relieve neuropathic pain.22

Camphor has also been shown to have anti-inflammatory effects in an animal model of arthritis.23

A clinical pilot study that looked at a spray containing camphor and menthol in combination with other natural oils, found they were effective at relieving mild to moderate pain and inflammation in the knee and wrist joints, neck, shoulders, forearms, and low back when applied topically for a period of 14 days.24

In experimental studies, camphor was found to better alleviate signs of allergic skin inflammation than hydrocortisone cream by potentially acting through a number of anti-inflammatory mechanisms.25 An ointment containing camphor was compared with Vaseline for the treatment of second-degree burns in an animal model. After 28 days, wounds treated with camphor ointment had healed more and had less scar tissue.26 Camphor also stimulated collagen growth and reduced skin damage following exposure to UV light.27

CBD CLINIC™ products are manufactured in a good manufacturing practices (GMP) compliant facility to ensure the highest quality control standards.

References

  1. https://www.sciencedirect.com/science/article/abs/pii/S0190962207007554
  2. https://pubmed.ncbi.nlm.nih.gov/26196538/
  3. http://www.ijcasereportsandimages.com/archive/2013/002-2013-ijcri/001-02-2013-hamidpour/ijcri-00102201311-hamidpour-full-text.php#ref9
  4. https://pubmed.ncbi.nlm.nih.gov/24547599/
  5. https://pubmed.ncbi.nlm.nih.gov/19557201/
  6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6725586/
  7. https://pubmed.ncbi.nlm.nih.gov/23820004/
  8. https://www.ncbi.nlm.nih.gov/books/NBK5238/
  9. https://pubmed.ncbi.nlm.nih.gov/29524352/
  10. https://go.drugbank.com/articles/A33089
  11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4009371/
  12. https://pubmed.ncbi.nlm.nih.gov/22172548/
  13. https://pubmed.ncbi.nlm.nih.gov/11897159/
  14. https://pubmed.ncbi.nlm.nih.gov/18593637/
  15. https://pubmed.ncbi.nlm.nih.gov/27131832/
  16. https://pubmed.ncbi.nlm.nih.gov/20456191/
  17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4178917/
  18. https://link.springer.com/article/10.1007/s00520-015-2642-8
  19. https://pubmed.ncbi.nlm.nih.gov/28805147/
  20. https://pubmed.ncbi.nlm.nih.gov/25451841/
  21. https://pubmed.ncbi.nlm.nih.gov/33316364/
  22. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968782/
  23. https://pubmed.ncbi.nlm.nih.gov/20353012/
  24. https://pubmed.ncbi.nlm.nih.gov/25553684/
  25. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6629446/
  26. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5890368/
  27. https://pubmed.ncbi.nlm.nih.gov/26458283/

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