Therapeutic modulation of somatosensory evoked response in pain-related cortex on chronic lumbago.
CHUZO TANAKA1,2, TOMOKAZU MURASE3, MASAKI FUKUNAGA4, MASAHIRO UMEDA5, YASUHIRO WATANABE5, YUKO KAWAI5, SETSUO HAKATA6, SHOJI NARUSE7, and TOSHIHIRO HIGUCHI8

1NEUROSURGERY, RAKUWA VILLA-ILIOS, Kyoto, Japan, 2Meiji University of Integrative Medicine, kyoto, Japan, 3Meiji University of Integrative Medicine, Kyoto, Japan, 4Cerebral Integration, National Institute for Physiological Sciences, Okazaki, Japan, 5Medical Informatics, Meiji University of Integrative Medicine, Kyoto, Japan, 6Japanese Medical Society of Arthrokinematic Approach, Osaka, Japan, 72nd Okamoto General Hospital, Kyoto, Japan, 8Neurosurgery, Meiji University of Integrative Medicine, Kyoto, Japan

Synopsis

To clarify therapeutic modulatory effects on brain activation in pain-related cortex of chronic lumbago using somatosensory stimulation with treatment for pain relief, twenty participants were divided into two groups, S1 activated (S1(+)) and S1 non-activated (S1(-)) group. There were no activated areas in pain-related cortex in S1 (-) group immediately after treatment for pain relief. Immediately after treatment, rs-fMRI of S1(-) group showed a significant signal decrease in contralateral S2 of pain-related network. It was suggested to diminish pain-related network activation by somatosensory stimulation on chronic lumbago immediately after treatment for pain relief.

Introduction

It is still unknown that modulatory effect of pain to the somatosensory evoked response in primary somatosensory cortex (S1). Roughly only half of fMRI studies reported pain evoked response in S1. In addition, S1 activation appears related to the total amount of surface area that was applied stimulation, and probably related to rate of stimulation and subjects’ attention[1]. From this aspect, we investigate the modulatory effect of pain-relief manipulation therapy to the somatosensry evoked response in S1 on chronic lumbago patients. AKA-Hakata method[2], one of arthrokinematic approach (AKA)[3] in Japan is used as treatment for pain relief.

Materials and Methods

Twenty subjects (average age 23.6±4.3 years) who have chronic lumbago, participated in this study. All subjects were right handed and all gave informed consent to procedures approved by Meiji University of Integrative Medicine IRB committee. After anatomical and rs-fMRI measurements, all participants periodically received passive intra-articular movement in the right talono-vicular joint for a fMRI of the block paradigm. And then, all participants were treated by AKA-Hakata method, which were both sliding and flexor-distraction techniques in intra-articular movement of the bilateral sacroiliac joints, on a table of MR scanner. After treatment, again, the anatomical, rs-fMRI, and block paradigm fMRI measurements were performed. The block design consisted of 40s rest following 4 times [40s stimulation (on) - 40s rest scans (off)] and the rs-fMRI measurements were 6min. All experiments were performed on a Siemens 3 T Trio MRI scanner with a 32 channel head coil. Subjects underwent GE-EPI scans with 37 axial slices (3 mm thickness; matrix 64x64, FOV 23x23 cm2; TR/TE: 2000/30 ms). Statistical analysis was performed using SPM 12 and FSL (FMRIB Software Library) (p< 0.05). All participants were demanded ODI score (Oswestry disability index 2.0: score for chronic lumbago correlated closely to ADL (activities of daily living)) before MRI measurements, and VAS (visual analog scale) after measurements.

Results

1) All participants were divided into two group, S1 activation (+) group (n=11 (S1(+) group)) and S1 activation (-) group (n=9 (S1(-) group)) using pre-treatment block paradigm study. 2) ODI score were significantly higher in S1(-) group (S1(+) group=14.1±4.2% and S1(-) group=20.2±6.6% (p<0.05)) (Table 1). 3) VAS showed 35.1±19.0 in S1(+) group and 49.8±16.9 in S1(-) group before treatment, and significantly decreased at 22.3±19.2 and 24.5±16.0 (p<0.01) after treatment in both group (Table 1). In addition, VAS before treatment in S1(+) group showed smaller than S1(-) group (p < 0.5) (Table 1). 4) Before treatment, S1(+) group showed activated areas in bilateral S1, S2, and frontal base and also in left insula and posterior temporal cortex (Fig. 1 upper). S1(-) group showed activated areas in bilateral S2, insula, posterior temporal cortex, cerebellum, and frontal base and also in right medial parietal cortex before treatment (Fig. 2 upper). After lumbago treatment, in S1(+) group, there was no substantial difference among before and after treatment (Fig.1 lower). In S1(-) group, there was no significant activated areas except a part of posterior temporal cortex and cerebellum (Fig. 2 lower) and significant deactivated areas, such as ACC. 6) Before treatment, rs-fMRI of S1(-) group showed a significant signal increased areas in left S2 of pain-related network compared with that of after treatment (Fig.3).

Discussion and Conclusion

1) S1(+) group, which is considered as no remarkable effect to ADL by chronic lumbago, showed no significant brain activity changes in before and after treatment. 2) S1(-) group, which is considered as disturbed effect to ADL with chronic lumbago, showed no activated areas in pain-related cortex immediately after lumbago treatment using hand therapy. Although VAS in both group were significantly decrease after lumbago treatment, S1(+) group remained S1 and S2 activation, on the other hand S(-) group did not present any activation in S1 and S2. According to VAS reduction in S1(-) group, relatively strong pain relief effect might be modified somatosensory evoked response in S2 and insular cortex. It might be sustained attentional change or shift due to diminish painful sensation of lumbago after treatment, which is not synchronized passive intra-articular movement task, was caused disappearance of S1 and S2 activation. This hypothesis might be supported by ACC of S1(-) group deactivation after treatment. With rs-fMRI, activation in contralateral S2 cortex in pain-related network showed more signal decrease after treatment. This is a first report to diminish a pain-related network activation by somatosensory stimulation with chronic lumbago immediately after treatment for pain relief.

Acknowledgements

This work was supported by JSPS KAKENHI Grant Number 25462280.

References

[1] Peyron R, Laurent B, et al Neurophysiol Clin: 30: 263-288, 2000. [2] Hakata S, Sumita, K, et al. Manuelle Medizin, 2005; 43:19-24. [3] Kaltenborn, FM : Manual therapy for the extremity joints, 1976.

Figures

Fig.1 fMRI of S1 activation (+) group (n=11) upper: Before lumbago treatment; Activated areas in contra-lateral S1, S2, and insula (arrow)

Fig.2 fMRI of S1 activation (-) group (n=9) upper: Before lumbago treatment; Activated areas in bilateral S2 (Lt>Rt) and insula (arrow) lower: After lumbago treatment; No activated areas in both S2 and insular cortex


Fig.3 rs-fMRI of S1 activation (-) group (n=9) Activation change of contra-lateral S2 cortex in pain-related network: S2 showed decreased activation immediately after lunbago treatment compared with that of before treatment (arrow).


Table 1 Changes of ODI score and VAS of chronic lumbago



Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)
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