September 5, 2012
The primary role of the veterinarian is to control pain and suffering and the range of tools and methods to accomplish this is ever-increasing. Therapeutic photobiomodulation, such as provided by therapy lasers, has become an important element in a multimodal approach to pain management.
The analgesic effects achieved with the administration of therapeutic photobiomodulation are well documented in the literature. The first of the peer-reviewed papers appeared in 1991 with the bulk of the documentation detailing the mechanisms and the effectiveness of this modality being presented from 2009 to 2012.1-5
Practicing scientific, evidence-based medicine does not allow us to merely believe: “photons enter, a miracle happens, and then the pain is gone!” The mechanisms resulting in this physiological achievement are clearly understood. Photons, within the infrared spectrum, act on the endogenous photoreceptors, or chromophores, of the individual cells resulting in a biochemical cascade of events. A combination of localized and systemic enzymatic, chemical, and physical events effectively produce a state of analgesia.6-9
Once the target cells receive a therapeutic dosage of photonic energy, there is a release of beta endorphins.10 “Endorphin” comes from the words endogenous + morphine. These endogenous peptides attach to the same cell receptors in the brain, spinal cord and other nerve endings that would accept morphine and act presynaptically to inhibit the release of the inhibitory neurotransmitter GABA (gamma-aminobutyric acid).11 The almost instantaneous clinical result is a reduction in pain perception coupled with a mild euphoria.
Nitric oxide, produced in the mitochondria, can inhibit respiration, by binding to cytochrome c oxidase, thus competitively displacing oxygen. This is especially true in stressed or hypoxic cells.11 Following therapeutic photobiomodulation there is a photodissociation of nitric oxide from cytochrome c oxidase thereby reversing the mitochondrial inhibition of the respiratory rate due to excessive nitric oxide binding.12
This increased level of nitric oxide has multiple pain relieving effects for the patient:
Bradykinins, released from plasma protein at the site of injured tissue, elicit pain by stimulating nociceptive afferents in the skin and viscera. Mitigation of these elevated levels through therapeutic photobiomodulation will therefore result in a reduction of pain. The photobiomodulated induced decrease in plasma kallikrein, increase in kininase II and the increases in Nitric oxide are considered the contributors to the decrease in bradykinin levels.18
Another extremely important analgesic event occurs when therapeutic photobiomodulation results in the blockage of the C fiber afferent nerves.22 These nonmyelinated fibers convey input signals from the periphery to the central nervous system and respond to various stimuli that can be thermal, mechanical, or chemical in nature.
Photoreceptors within the neuronal mitochondria absorb photonic energy which is then mediated and transducted into electrochemical changes.2,12 This results in a secondary cascade of intracellular events within the neuron that initiates a decrease in the following: mitochondrial membrane potential, available ATP required for nerve function and the maintenance of microtubules and molecular motors, dyneins and kinesins that are responsible for fast axonal flow.19 
Therefore, it is a photonic induced neural blockade that slows the conduction velocity and reduces the amplitudes of the compound action potentials.20,21 This photobiomodulatory reaction and consequential blockade is the mechanism that reduces nociceptive pain.27
There is an increase in the reaction time in the formation of acetylcholine following therapeutic photobiomodulation. The increased availability of this neuromodulator allows for a normalization of nerve signal transmissions within the peripheral and central nervous systems.23
Several studies have documented the ability of laser therapy to induce axonal sprouting and some nerve regeneration in damaged nerve tissues. Where pain sensation is being magnified due to nerve structure damage, cell regeneration and sprouting assists in alleviating this maladaptive, neuropathic pain.24,25,28
Therapeutic photobiomodulation is dependent upon the delivery of a therapeutic dosage of energy to the target nerve cells. Wavelength determines the depth of penetration and the power of the laser determines the delivery of the dosage. The current literature states that a physiological and biological response within the cells is achieved at a dosage of 2 to 12 Joules/cm2. 27-30
Incidental absorption of photons must be considered when trying to calculate the therapeutic dose. Body mass, color and thickness of the dermis and hair coat must be taken into consideration for successful, consistent results.
Prevention and treatment of superficial acute pain should be dosed at 2 to 6 Joules/cm2.
A post-op incision site of 2 inches by 3 inches would require:
5.08 cm X 7.62 cm = 38.7 cm2
38.7 cm2 X 2 Joules/cm2 = 77.4 Joules/treatment
Chronic pain that is deep within the tissues would require a dosage in the range of 7 – 12 Joules/cm2
Treatment of a 40 lb., dark skinned, long haired dog with chronic hip dysplasia would require:
8 cm X 8 cm = 64 cm2
64 cm2 X 8 Joules/cm2 = 512 Joules/treatment
Aggressive phase: each day for three to four treatments
Transitional phase: (less frequent) every other day or twice per week until condition is resolved.
Aggressive phase: each day or every other day for 3 to 4 treatments.
Transitional phase: every other day or twice per week until therapeutic goal has been achieved.
Maintenance phase: as often as needed to control pain and maintain a satisfactory quality of life.
These are generic case examples. Each patient is unique and pain management plans need to be tailored to correspond to the patient and the owner’s individual situation. The pharmacological portions of the treatment plan below are merely an example. Each practitioner will have his own standard of pharmacological care.
Canine Ovariohysterectomy; hospitalized for 24 hours.
Morphine: 0.5 – 1.0 mg/kg SQ 30 minutes before general anesthesia.
Acepromazine: .02 mg/kg SQ.
Atropine: .04mg/kg SQ.
Pre-emptive and postsurgical analgesia
Administration of photobiomodulation utilizing a non-contact sterile technique:
Dosage: 2 Joules/cm2
1. Stretched associated ligaments and to any manipulated visceral structures.
2. Incision before closure of peritoneum
3. Incision upon closure of dermis.
Good nursing care: Ice, lubricate eyes, soft recovery area and support during recovery
Morphine: .5 – 1.0 mg/kg at 3 to 4 hours post-op.
Analgesia for night
Buprenorphine: 0.01 mg/kg SQ.
Twenty-four hour analgesia
Administration of photobiostimulation in a non-contact technique over the incision site:
Dosage: 2 – 4 Joules/cm2
NSAID: carprofen or melozicam
Carprofen 4 mg/kg PO or tramadol 2 – 3 mg/kg PO.
DX: Bilateral degenerative joint disease of the coxofemoral joints; eight years duration.
Initial pharmacological plan
Amantadine: 2 – 5 mg/kg PO sid. Treatment for central neuronal hyperexcitability (windup).
Carprofen: 4 mg/kg PO sid. NSAID
Gabapentin: a form without xylitol. 5 – 10 mg/kg bid.
Adequan®: 2 mg/lb. twice weekly for four weeks.
Aggressive phase: every other day; at least three treatments; dosage 8 to 10Joules/cm2. Include treatments of the lumbar spine and acupuncture points: GB 29 to 30, BL 40 – 54, GB 34 and BL 11.
Transitional phase: twice/week on both hips and lumbar spine with constant re-evalutation at each therapy session.
Maintenance phase: therapy as needed (one treatment every 3 – 5 weeks) to maintain comfort.
Nutrition and neutriceuticals
Modifications to environment
Rugs on slippery floors
Limit access to stairs
Therapeutic photobiomodulation is a scientifically proven modality that is an extremely effective tool for the management of pain.31 It is one that is easily woven into pain management protocols that already exist in the practice. For many practices, it has become part of the standard of care, and not simply reserved for those cases that fail to respond to traditional methods.
Dr. Riegel is a director and one of the founders of the American Institute of Medical Laser Applications. He is the author of “Laser Therapy in the Companion Animal Practice” and co-author of “Laser Therapy for the Equine Athlete.”
This Education Series article was underwritten by Companion Therapy Laser of Newark, Del.
3. Yan W, Chow R, Armati PJ. Inhibitory effects of visible 650-nm and infrared 808-nm laser irradiation on somatosensory and compound muscle action potentials in rat sciatic nerve: implications for laser-induced analgesia. J Peripher Nerv Syst. 2011 Jun;16(2):130-5.
4. Chow R, Armati P, Laakso EL, Bjordal JM, Baxter GD. Inhibitory effects of laser irradiation on peripheral mammalian nerves and relevance to analgesic effects: a systematic review. Photomed Laser Surg. 2011 Jun;29(6):365-81.
5. Chow RT, Johnson MI, Lopes-Martins RA, Bjordal JM. Efficacy of low-level laser therapy in the management of neck pain: a systematic review and meta-analysis of randomized placebo or active-treatment controlled trials. Lancet. 2009 Dec 5;374(9705):1897-908. Epub 2009 Nov 13. Review. Erratum in: Lancet. 2010 Mar 13;375(9718):894.
15. Rochkind S. and Ouaknine GE.(1992) "Review: new trend in neuroscience: low-power laser effect on peripheral and central nervous system (basic science, preclinical and clinical studies)". Neurological Research 14:2-11.
20. Huang Y-Y, Chen AC-H, Wu Q, Sharma SK, Hamblin MR. Comparison of cellular responses induced by low level light in different cell types. In: Hamblin MR, Anders JJ, Waynant RW, Editors. Mechanisms for Low-Light Therapy V, Bellingham, WA, The International Society for Optical Engineering,. Proc SPIE 2010, Vol. 7552: 75520A-1
21. Chow RT, David MA, Armati PJ. 830 nm laser irradiation induces varicosity formation, reduces mitochondrial membrane potential and blocks fast axonal flow in small and medium diameter rat dorsal root ganglion neurons: implications for the analgesic effects of 830 nm laser. J Peripher Nerv Syst. 2007 Mar;12(1):28-39.
22. OHNO-SHOSAKU, T., SAWADA, S. & YAMAMOTO, C. (1995). Presynaptic modulation of glutamatergic and GABAergic transmissions in rat cultured hippocampal neurons. 4th IBRO World Congress of Neuroscience, Kyoto, Japan, Abstract P176.
23. Nicolau, R.A., Martinez, M.S., Rigau, J. and Tomás, J. Neurotransmitter release changes induced by low power 830 nm diode laser irradiation on the neuromuscular junctions of the mouse. Lasers Surg Med 2004: 35(3): 236-41.
24. Xingjia, W.U., Alberico, S., Erbele, I., Moges, H., Pryor, B., Anders, J. Differential Response of Neurons to Light Irradiation in an in vitro Diabetic Model. Dept. of Anatomy, Physiology and Genetics, USUHS, Bethesda, MD. ASLMS proceedings 2010.
25. Huang YY, Tedford CE, McCarthy T, Hamblin MR. Low level laser therapy reduces oxidative stress in cortical neurons in vitro. In : Hamblin MR, Anders JJ, Waynant RW, Editors. Mechanisms for Low-Light Therapy VII, Bellingham, WA, The International Society for Optical Engineering, Proc SPIE 2012
26. Naeser, M. A., Neurological rehabilitation: acupuncture and laser acupuncture to treat paralysis in stroke, other paralytic conditions, and pain in carpal tunnel syndrome. J Alt Compl Medicine. 1997;3:425-428
27. Chow, R., Armati, P., Laakso, E-Liisa, Bjordal, J.M., Baxter, D.G. Inhibitory Effects of Laser Irradiation on Peripheral Mammalian Nerves and Relevance to Analgesic Effects: A Systematic Review. Photomedicine and Laser Surgery. Volume X, Number X, 2011. Pp. 1–17
31. Chow, R.T., Johnson, M., Lopes-Martins, R., Bjordal, J.M.. Efficacy of low-level laser therapy in the management of neck pain: a systemic review and meta-analysis of randomized placebo or active-treatment controlled trials. Lancet 2009; 374: 1897-908.
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