Laser Therapy
Infrared Photo Energy May Reduce Neuropathic Pain
Near infrared light therapy, together with physical therapy, may be able to reduce pain in
neuropathy patients and possibly reduce medication dosage levels of those undergoing
drug therapy.
Diabetic neuropathy is a common health problem today which often poses a variety of clinical challenges. In this article, Dr. Thomas J. Burke reports on the results of a study utilizing phototherapy (non-coherent light therapy) on patients with neu-ropathies. This is an exciting paper and demonstrates the potential value of light therapy in these clinical conditions. There is arapidly increasing body of evidence that is demonstrating the clinical value of using non laser light therapy for a wide variety ofpainful conditions. —William J. Kneebone, DC, CNC, DIHom, FIAMA, DIACT Inarecent issue of Practical Pain Man- Materials and Methods
agement, two papers discussed treat- The medical history and clinical notes related to pain were in- cluded as part of insurance claims made by a durable medical cleared alternative modalities referred to equipment (DME) supplier offering the Anodyne® Therapy Sys- generically as light therapy.1,2 This paper tem (ATS; Anodyne Therapy LLC, Tampa, FL) that delivers describes the effects of light therapy on MIRE at 890 nanometers from gallium aluminum arsenide diodes. The ATS has FDA 510k clearance for temporarily in- is a common complaint of patients with peripheral neuropathy creasing circulation and reducing pain, stiffness, and muscle (PN) due to either diabetes or other causes and it often inter- feres with quality of life, irrespective of pharmaceutical inter- The medical records and clinic notes provided by the health- vention.3 For example, painful PN may be a complication from 1) chemotherapy drugs, 2) metabolic diseases such as hypothy- • a physician diagnosis of peripheral neuropathy associated roidism, 3) abuse of alcohol, 4) environmental toxins or drugs, with diabetes (diabetic peripheral neuropathy; DPN) or 5) certain viral infections, 7) scar tissue formation following sur- other etiologies (peripheral neuropathy-other; PNO), gery, or 6) it may be idiopathic.4 There are only a few FDA ap- • the level of pre-treatment neuropathic pain measured on proved drugs for the pain of PN. These drugs do not modify an 11 point numeric pain rating scale (NPRS; 10 equating blood flow and, therefore, they do not correct microcirculatory to maximum pain and zero (0) equating to no pain), and defects that can, in some cases, contribute to ischemic, neuro- • pain levels measured after MIRE treatment. pathic pain. Some of the approved drugs have significant side 456 separate physicians attested to the accuracy of the med- effects that compromise quality of life.5 Beyond pharmacology, ical data that they supplied to justify these insurance claims.
there has been some success—in carefully selected patients—in MIRE was administered as part of a comprehensive care plan effecting significant neuropathic pain relief with surgical inter- that also included individualized physical therapy for various gait and balance problems that occur quite frequently in patients with An alternative to drugs or surgery— monochromatic infrared PN.12 Shurman and colleagues recommend physical therapy, ex- energy (MIRE™) along with concurrent physical therapy—has ercise and integrated techniques in their powerful tool, the Share been reported to provide significant pain relief to patients pre- The Risk Model, for managing patients with pain.13 However, it senting with neuropathic pain due to either diabetes or other is often difficult for patients to begin or complete a therapy pro- etiologies.7-10 This report documents the reduction in neuropath- gram if they are in constant, unremitting pain. ic pain achieved with use of MIRE in 493 consecutive, mostly Patients were told to anticipate being treated with MIRE ap- elderly, patients treated in health care facilities from the begin- proximately 12 times, 30 min. each time, 3 times per week, for ning of May 2006 to the end of June 2006. These patients also their pain. After completing outpatient therapy, 493 out of 550 detailed their use (or lack thereof) of various drugs for neuro- patients agreed to provide answers to a health questionnaire.
pathic pain relief prior to and during MIRE treatment.
This was done under HIPPA protection assurances by the DME.
Practical PAIN MANAGEMENT, July/August 2007 2007 PPM Communications, Inc. Reprinted with permission.
Table 1. Patient Demographics
and PNO groups (see Table 2). Post-treat-ment pain averaged 2.5 ± 2.3, a 64% re-duction; there was no significant differ- DPN and PNO groups (see Table 2). Theaverage number of PT visits during which MIRE was also given was 15±8. At the ini-tiation of MIRE therapy, 129 patients (26%) were not taking medications fortheir neuropathic pain, whereas 364 pa- medications. As one would expect, basedon the medical literature for neuropathic pain, drugs included anticonvulsants, an-tidepressants, and opiates. In 263 out of PNO = peripheral neuropathy from other causes 364 patients (72%), more than one drugwas being consumed. The most frequent-ly used medication was the anticonvulsantgabapentin, with 197 patients (54%) using Table 2. Changes in pain in response to MIRE treatment
in DPN and PNO Patients
medications for their neuropathic pain at initiation of MIRE therapy, 187 (51%) re- ported that they had reduced the use ofmedications during MIRE therapy, 151 (41%) reported that their use of medica-tions was unchanged throughout therapy, and 26 (7%) reported either a change inmedication, an increase in the dosage of one or more of the initial medications, or PNO = peripheral neuropathy from other causes Group 4: Patients utilizing one or more
the physician and therapist’s office. Pa- tient identifiers were removed prior to the analysis of the data. Patients answered the following questions: 1) the duration of the neuropathic pain, 2) which medications (if on average, for at least 3.5 – 4.5 years Statistics
ANOVA to test the null hypothesis that de- input as 99 months even if it was longer.
late spring of 2006. Neuropathic pain in- the course of MIRE treatments. All values tensity—before and after MIRE—was de- termined separately for patients collected viation (SD). Significance was accepted if Group 1: 20 of 129 patients (16%)
Group 2: 40 of 187 patients (21%)
Group 1: Patients not utilizing medica-
Group 3: 44 of 151 patients (29%)
Group 4: 9 of 26 patients (35%)
Group 2: Patients utilizing drug thera-
279 female) was 72 years (see Table 1). 248 Discussion
in an outpatient setting is associated with sociated with other etiologies (PNO).
Group 3: Patients utilizing drug thera-
both diabetic and non-diabetic patients.
Practical PAIN MANAGEMENT, July/August 2007 2007 PPM Communications, Inc. Reprinted with permission.
Table 3. Pain Response to MIRE is independent of medication usage.
No Meds during
No Change in
Decreased Meds
Changed Meds
a = mean ± SD. b = P<0.0001 vs. initial pain. Meds = medications. (n) = number of patients. Changed meds indicateseither a different dose or a different medication, or both.
These outcomes are consistent with a growing body of clinical be associated with any systemic side effects. There have been a evidence showing MIRE is able to significantly decrease pain in few reports of superficial burns when treatment guidelines were diabetic and non-diabetic neuropathy patients.7-10 Perhaps more important, the decrease in pain intensity in re- sponse to MIRE combined with therapy was independent of con- Mechanism of Action
comitant use of medications that are typically used for neuro- While the mechanism of action underlying neuropathic pain re- pathic pain. Patients who were not taking drugs for their pain lief associated with MIRE is not well understood, it may be due, responded exactly like those patients who were taking medica- in part, to a combination of topical heat and an increased local tions at the initiation of the therapy. For those who were already release of nitric oxide that has been reported using this wave- taking drugs, the reduction in symptomatic pain was not relat- length (890nm) of near infrared photo energy.18,19 The source of ed to either a continuation of current drug usage, to a reduc- released nitric oxide may be endothelial cells or red blood cells, tion in drug use or to changes in either the dosage or class of or both.20,21 Nitric oxide production is compromised in both type medications consumed throughout the period of treatment. In- 1 and type 2 diabetic patients.22-24 If near infrared light is able deed, 51% of patients achieved significant neuropathic pain re- to favorably alter local nitric oxide availability in the diabetic duction and were concomitantly able to decrease the dosage of patient, this may improve microcirculation via an alteration of medication(s) they had been taking at the initiation of MIRE cGMP-mediated vasodilation at the site of treatment.25 Better therapy. The similar degree of pain mitigation was not due a blood flow may, in part, explain the symptomatic decrease in difference in the number of treatments, age or gender, or the length of time the patients had been aware of neuropathic pain Nitric oxide also appears to be able to mitigate pain via a severe enough to cause them to seek medical attention. mechanism similar to morphine,26 namely via nitric oxide me- Clearly, pharmacologic agents have been found to be effec- diated production of cGMP and phosphorylation of ATP-de- tive in reducing pain in both diabetic and non-diabetic pa- pendent potassium channel activity.27 There may be a significant tients.14-17 However, as is the case with virtually all drugs, side ef- analgesic effect of MIRE if local concentrations of nitric oxide fects may limit the patient tolerance. Side effects also become are increased. Nitric oxide was not measured in any patient dur- more evident with the use of higher drug doses that are often necessary when low doses are no longer effective or when pa-tients report a waning effect. High drug doses often relieve pain Study Limitations
but the quality of life may be adversely affected. The answers to There are, of course, limitations to our conclusions. First, infor- the questionnaire revealed that a few patients were using some mation about the use and types of medications is based solely of the newer medications that had been approved recently by upon patient response to a health questionnaire administered the FDA for the reduction of neuropathic pain. However the vast just after the conclusion of outpatient MIRE therapy. However, majority of patients were continuing to take gabapentin and/or since patients self-administer medications for neuropathic pain antidepressants, which have been clinical mainstays for many based on perceived pain levels or physician prescription, we be- years for the treatment of neuropathic pain. Therefore, the re- lieve they were competent to accurately comment on the use of sults of this post-marketing survey may not apply to patients who medications during the fairly brief period of MIRE therapy (6- have begun to use newer drugs. MIRE has not been reported to 7 weeks). Additionally, the health questionnaire was very specif- Practical PAIN MANAGEMENT, July/August 2007 2007 PPM Communications, Inc. Reprinted with permission.
ic. Patients were required to name the ac- tered as part of a care plan prescribed by ness of monochromatic infrared photo energy andphysical therapy for peripheral neuropathy: changes in tual medications they were taking for neu- physicians—is associated with a substan- sensation, pain and balance – A preliminary, multi-cen- ropathic pain; this increased the likeli- tial reduction in neuropathic pain. Use of ter study. Phys Occup Therap Geriatr. 2006. 24:1-17.
MIRE may be an alternative for physicians 11. Burke TJ. 5 questions and answers about MIRE to consider for patients with neuropathy, treatment. Adv Skin Wound Care. 2003. 16:369-371.
especially those who have obtained an un- 12. Richardson JK, Hurvitz EA. Peripheral neuropa-thy: a true risk factor for falls. J Gerontol A Biol Sci pain intensity in this group of patients was satisfactory level of neuropathic pain re- not due to a “placebo effect” since there lief while using various oral medications.
13. Shurman J, Sack J, Shurman G, Schnierow B, and Gabriel C. Share the risk. Prac PainManagement. 2006. 6:10-20.
line treatment in some patients with sig- 14. Wiffen PJ, McQuay HJ, and Moore RA. Carba- er, these patients experienced a mean re- mazepine for acute and chronic pain. Cochrane Data- duction of 64% in their pain intensity dur- base Syst Rev. 2005. (3):CD005451. 15. Zareba G. Pregabalin: a new agent for the treat-ment of neuropathic pain. Drugs Today (Barc) 2005.
greater than either any placebo effect in Acknowledgements
response to infrared therapy (less than a Appreciation is extended to the 456 physi- 16. Raskin J, Pritchett YL, Wang F, et al. A double- blind, randomized multicenter trial comparing duloxe-tine with placebo in the management of diabetic pe- ed PN in their patients, noted the neuro- ripheral neuropathic pain. Pain Med. 2005. 6:346-356.
ed with placebo treatment during clinical 17. Dogra S, Beydoun S, Mazzola J, et al. Oxcar- bazepine in painful diabetic neuropathy: a random- balta®) and pregabalin (Lyrica®), which support their observations. Also, appreci- ized, placebo-controlled study. Eur J Pain. 2005.
9:543-554. Epub. Dec 18, 2004.
18. Maegawa Y, Itoh T, Hosokawa T, et al. Effects of management of neuropathic pain.29,30 Fur- near-infrared low-level laser irradiation on microcircu- furnished a significant portion of the data lation. Lasers Surg Med. 2000. 27:427-37.
19. Karu TI, Pyatibrat LV, and Afanasyeva NI. Cellulareffects of low power laser therapy can be mediated is consistent with other published reports by nitric oxide. Lasers Surg Med. 2005. 36:307-314.
20. Furchgott RF and Jothianandan D. Endothelium- dependent and -independent vasodilation involvingcyclic GMP: Relaxation induced by nitric oxide, carbon Thomas J. Burke, PhD, is Director of Research monoxide and light. Blood Vessels. 1991. 28:52-61.
clude that the decrease in pain was not de- and Clinical Affairs, Anodyne Therapy LLC, 21. Jia L, Bonaventura C, Bonaventura J, et al. S-ni- trosohaemoglobin: a dynamic activity of blood in- ications (i.e., Group 1), we cannot exclude volved in vascular control. Nature. 1996. 380:221-226.
22. Rabini RA, Staffolani R, Fumelli P, et al. De- References
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IDDM and NIDDM patients. Diabetologia. 1998.
ceived MIRE adjunctively as part of a plan 2. Hsin J and Weston J. Treating sports-related injury of care that also included skilled thera- and pain with light therapy. Prac Pain Management.
23. Milsom AB, Jones CJ, Goodfellow J, et al. Abnor- mal metabolic fate of nitric oxide in Type I diabetes pies, if necessary, to improve balance and 3. Armstrong DG, Todd WF, Lavery LA, Harkless LB, mellitus. Diabetologia. 2002. 45:1515-1522.
gait that are often complications of neu- and Bushman TR. The natural history of acute Char- 24. Brodsky SV, Morrishow AM, Dharia N, et al. Glu- cot's arthropathy in a diabetic foot specialty clinic. J cose scavenging of nitric oxide. Am J Physiol Renal Am Podiatr Med Assoc. 1997. 87:272-278. 4. Prendergast JJ, Miranda G, and Sanchez M. Im- 25. Ignarro LJ, Cirino G, Casini A, et al. Nitric oxide balance and gait related physical therapy provement of sensory impairment in patients with pe- as a signaling molecule in the vascular system: an ripheral neuropathy. Endocr Pract. 2004. 10:24-30. overview. J Cardiovasc Pharmacol. 1999. 34:879-886. effective for the reduction of neuropathic 5. Greenman RL, Panasyuk S, Wang X, et al. Early 26. Ferreira SH, Duarte ID, Lorenzetti BB. The molec- changes in the skin microcirculation and muscle me- ular mechanism of action of peripheral morphine tabolism of the diabetic foot. Lancet. 2005.
analgesia: stimulation of the cGMP system via nitric records, the 456 attending physicians cer- oxide release. Eur J Pharmacol 1991. 201:121-122.
tified that, in their medical judgment, the 6. Dellon AL. Diabetic neuropathy: review of a surgi- 27. Rodrigues AR, Duarte ID. The peripheral antinoci-ceptive effect induced by morphine is associated with reductions in neuropathic pain were in di- cal approach to restore sensation, relieve pain, andprevent ulceration and amputation. Foot Ankle Int.
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rect response to the MIRE treatments. Fi- nally, many patients—either those using 7. Leonard DR, Farooqi MH, and Myers S. Restora- 28. Zinman LH, Ngo M, Ng ET, et al. Low-intensity tion of sensation, reduced pain, and improved bal- laser therapy for painful symptoms of diabetic senso- ance in subjects with diabetic peripheral neuropathy: rimotor polyneuropathy. A controlled trial. Diabetes a double-blind, randomized, placebo-controlled study with monochromatic near-infrared treatment. Diabetes 29. Goldstein DJ, Lu Y, Detke MJ, et al. Duloxetine vs.
placebo in patients with painful diabetic neuropathy.
8. Powell MW, Carnegie DH, and Burke TJ. Reversal of diabetic peripheral neuropathy with phototherapy 30. Freynhagen R, Strojek K, Griesing T, et al. Effica- (MIRE) decreases falls and the fear of falling and im- cy of pregabalin in neuropathic pain evaluated in a proves activities of daily living in seniors. Age Ageing.
12-week, randomised, double-blind, multicentre, placebo-controlled trial of flexible- and fixed-dose factor in the effect of MIRE plus physical 9. Harkless LR, Carnegie DH, and Burke TJ. Im- regimens. Pain. 2005. 115:254-263. Epub. Apr 18, proved foot sensitivity and pain reduction in patients with peripheral neuropathy after treatment with mono- 31. Maurer MS, Burcham J, and Cheng H. Diabetes Conclusion
chromatic infrared photo energy-MIRE. J Diabetes mellitus is associated with an increased risk of falls in Complications. 2006. 20:81-87.
elderly residents of a long-term care facility. Gerontol 10. Volkert W, Hassan A, Hassan M, et al. Effective- A Biol Sci Med Sci. 2005. 60:1157-1162. Practical PAIN MANAGEMENT, July/August 2007 2007 PPM Communications, Inc. Reprinted with permission.

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