Peripheral Neurostimulation and Specific Motor Training of Deep Abdominal Muscles Improve Posturomotor Control in Chronic Low Back Pain Hugo Masse´-Alarie, PT, MSc,* Ve´ronique H. Flamand, OT, MSc,*w He´le`ne Moffet, PT, PhD,w and Cyril Schneider, PhD*z Objectives: Chronic low back pain (CLBP) is associated with an impaired control of transversus abdominis/internal oblique muscle (TrA/IO), volitionally and during anticipatory postural adjustment (delay) along with maladaptive reorganization of primary motor cortex (M1). Specific training of deep trunk muscles and repetitive peripheral magnetic stimulation (RPMS) improve motor control. We thus tested whether RPMS over TrA/IO combined with training could promote TrA/IO motor control and decrease pain beyond the gains already reached in CLBP. Methods: Thirteen CLBP patients, randomly allocated to RPMS and sham groups and compared with 9 pain-free controls, were tested in 1 session before/after (stimulation alone) and after (stimulation + TrA/IO training) combination. TrA/IO motor pat- terns were recorded during ballistic shoulder flexion using surface electromyography. Transcranial magnetic stimulation tested M1 excitability and short-interval intracortical inhibition. A blinded physical therapist assessed pain, disability, and kinesiophobia. Results: The missing short-interval intracortical inhibition in CLBP was restored by RPMS alone then reduced after combination of RPMS with training. This combination also normalized the (at-first delayed) anticipatory activation of iTrA/IO (ipsilateral to arm raised) and the (at-first shortened) TrA/IO coactivation duration. Sham did not influence. Pain was reduced in both groups but kinesiophobia was decreased only in RPMS 2 weeks later. Conclusions: This study supports that peripheral neurostimulation (adjuvant to training) could improve TrA/IO motor learning and pain in CLBP associated with motor impairment. Testing of enlarged samples over several sessions should question the long- term influence of this new approach in CLBP. Key Words: chronic low back pain, corticomotor excitability, anticipatory motor activation, motor training, repetitive peripheral magnetic stimulation, transversus abdominis, transcranial mag- netic stimulation (Clin J Pain 2013;29:814–823) P ersistence of low back pain (LBP) is associated with lumbar microtraumatisms 1 because of impairment of motor control of deep trunk muscles 2,3 involved in the inter- vertebral control of spine. 4 The conventional therapy utilizes vertebral mobilizations and manipulations in addition to exercises therapy that are usually successful to improve acti- vation, strength and/or endurance of core muscles, and trunk mobility to some extent. 5–8 However, these benefits are cir- cumscribed to the functional sphere and lumbar pain persists with only slight improvements according to a recent meta- analysis on the topic. 9 In chronic low back pain (CLBP), the transversus abdominis (TrA) presents a faulty volitional con- trol, 10 and, during tasks requiring anticipatory postural adjustments (APA), its activation is delayed 2,11 and asyn- chronous. 12 TrA delay in postural tasks was associated with maladaptive reorganization of the primary motor cortex (M1) 13 and the loss of intracortical inhibitory processes. 12 Such reorganization may result from changes in somato- sensory cortex (S1) 14 and thalamus 15 because of the influence of sensory inputs on the efficacy of M1 horizontal con- nections. 16 These cerebral changes may underlie the alteration of proprioception and tactile discrimination in CLBP 17 and the impairment of sensorimotor control. 10 Also, the loss of short- interval intracortical inhibition (SICI) of M1 circuits in many chronic pain conditions 18–20 suggests the alteration of motor programming that relies on M1 corticocortical afferents. 21,22 Repetitive transcranial magnetic stimulation that influences M1 excitability can decrease pain by reactivating SICI mechanisms 19,23 ; however, the effects were transient, weak, and variable. 24 Such limitations could be circum- vented by the application of repetitive peripheral magnetic stimulation (RPMS) directly over the nerve/muscle with impaired control. Indeed, RPMS recruits motor fibers rather than sensory at the periphery, 25 and bypasses noci- ceptors that could worsen motor impairment. 26 RPMS thus activates the muscle and generates a massive contraction- related flow of proprioceptive information to sensorimotor cortical networks. 27 This influence on M1 excitability is meaningful for the control of movement because RPMS may improve the ability to activate volitionally a given muscle. 27 In fact, neurostimulation (repetitive stimulation at a specific frequency) and motor training (repetition of movement, practice) share some mechanisms of neural plasticity, 28 such as enhanced synaptic efficacy (increase of glutamate and g-aminobutyric acid neurotransmitters release and multiplication of postsynaptic receptors) that influences networks function and cortical maps. Specifically Received for publication February 26, 2012; revised September 6, 2012; accepted September 27, 2012. From the *Clinical Neuroscience and Neurostimulation Laboratory, Axe Neurosciences du Centre de Recherche du CHU de Que´bec; zDepartment of Rehabilitation, Universite´ Laval; and wCentre Interdisciplinaire de Recherche en Re´adaptation et Inte´gration Sociale, Que´bec, QC, Canada. Author contributions: H.M-A. and C.S. conceived the experimental pro- tocol and conducted the experiments with V.H.F. H.M. contributed to the experimental design. H.M-A. ensured data analysis and inter- pretation of the results with C.S. H.M-A. and C.S. wrote the first draft of the manuscript and C.S. revised it with H.M-A. and V.H.F. All authors discussed the results and commented on the manuscript. The authors declare no conflict of interest. Reprints: Cyril Schneider, PhD, Clinical Neuroscience and Neuro- stimulation Laboratory, Axe Neurosciences du Centre de Recher- che du CHU de Que´bec, RC-9800, 2705 boul. Laurier, Que´bec, QC, Canada G1V 4G2 (e-mail: cyril.schneider@rea.ulaval.ca). Copyright r 2013 by Lippincott Williams & Wilkins ORIGINAL ARTICLE 814 | www.clinicalpain.com Clin J Pain  Volume 29, Number 9, September 2013