PLASMA ACTH AND § ENDORPHIN LEVELS IN RESPONSE TO LOW LEVEL LASER THERAPY FOR MYOFASCIAL TRIGGER POINTS

Laakso et al

Royal Brisbane hospital, Australia

Published Laser Therapy 1994 6: 133-142

ABSTRACT

The mechanism by which laser phototherapy (Low Level Laser Therapy - LLLT) induces analgesia in the treatment of chronic pain is not understood. To investigate a possible role for opioids in this treatment,, a double-blind, placebo-controlled study was designed to compare the effect of two dosages (1 J/cm2 and 5 J/cm2) of an infrared (JR) laser (820 nm), a visible red laser (670 nm) and a near-monochromatic light emitting device (660 nm, 30 nm bandwidth) on trigger points. Fifty-six consenting subjects with chronic pain conditions exhibiting myofascial trigger points in the neck and upper trunk region underwent six experimental sessions over a two week period. Blood samples were withdrawn before and after treatment on three of six appointments. Plasma was assayed for § -ENDORPHIN (radioimmunoassay, RIA) and adrenocoracotropic hormone (ACTH - two-site immunoradiometric assay, IRMA) to assess opioid response. ACTH was shown to have a cumulative response to treatment with 1 J/cm2 infrared laser (p < 0.001) and 5 J/cm2 red laser (p < 0.05) responding significantly.. § -endorphin was noted to be significantly elevated between days one and four (p < 0.05) in subjects who received IR (5 J/cm2) laser. Results indicated that the analgesic response to phototherapy may be mediated through hormona/opioid mechanisms, and that responses to LLLT are dose and wavelength dependent. A mechanism by which peripheral stimulation using LLLT may elicit activity in the central pathways is proposed.

EFFECT OF POWER OUTPUT AND ENERGY DENSITY

To understand the results of this study further, one must understand that LLLT conforms to the Arndt-Schultz principle which implies that very low doses of laser have no effect on cells, low doses stimulate cell processes, high doses inhibit cell processes, and that even higher doses result in photodynamic damage of cells. The results of this study appear to confirm this notion. That is, there may not have been sufficient photonic energy to stimulate responses using 660 nm near-monochromatic red light or low dose 670 nm (red) laser. This may explain why the Pearson correlation co-efficient between ACTH and ,B-endorphin levels for near-monochromatic red light was less than half that observed for the remaining treatment groups (Table 3). Power output may have been the critical factor in this study and future studies should control for this.

CONCLUSIONS

This study has confirmed that responses to LLLT are dose, power output and wavelength-dependent. The fact that low dose (1 J/cm2) IR laser (820 nm) and high dose (5 J/cm2) red laser (670 nm) resulted in a cumulative pre-treatment increase in ACTH and high dose (5 J/cm2) IR laser resulted in increases in plasma § -endorphin levels over the duration of the study suggests that localised, peripheral phototherapy of trigger points can induce cumulative activation of central hormonal/opioid pathways capable of regulating immune function. This was likely to have occurred through a link between mast cell degranulation, or stimulation of cytokine-mediated CRH release by altering macrophage responsiveness. As high dose (5 J/cm2) LLLT resulted in potentiation of overall levels of § -endorphin and ACTH, it is suggested that the therapeutic window of doses for LLLT treatment of trigger points could be extended to include 5 J/cm2. This would need to be validated by conducting adjunctive studies on subjective pain responses. It is acknowledged that power density may have resulted in the fact that neither low dose nor high dose near-monochromatic red light (660 nm) was found to be capable of eliciting significant changes in blood biochemistry. The suggestion that the laser is a necessary requirement for phototherapy of trigger points remains to be confirmed