Mapping the Cortical Representation of Paraspinal Muscles Using Transcranial Magnetic Stimulation Optimized in People...

Chronic low back pain (CLBP) is a global burden with an unknown etiology. Reorganization of the cortical representation of paraspinal muscles in the primary motor cortex (M1) may be related to the pathology. Single-pulse transcranial magnetic stimulation (TMS), commonly used to map the functional organization of M1, is not potent enough to stimulate the cortical maps of paraspinal muscles in M1 in CLBP patients with reduced corticospinal excitability (CSE) with intensities even as high as maximum stimulator output (100% MSO). This makes TMS mapping impractical for these patients. The aim of this study was to increase the practicality of TMS mapping for people with CLBP.

This study included eight men and ten women who had CLBP for over three months. A biphasic paired-pulse TMS paradigm, conjunct anticipatory postural adjustment (APA), and maximal voluntary activation of paraspinal muscles (MVC) were used to facilitate TMS mapping.

TMS mapping was possible in all CLBP participants, with TMS intensities <50% of the MSO. Reorganization in terms of an anterior and lateral shift of the center of gravity (COG) of the cortical maps of paraspinal muscles was observed in all participants with CLBP, and a reduced number of discrete peaks was found in 33%.

The facilitation of the CSE to paraspinal muscles makes TMS mapping more practical and tolerable in people with CLBP, lowering the risk of seizure and discomfort associated with high-intensity TMS pulses.

Conventional transcranial magnetic stimulation (TMS) brain mapping is not optimal for patients with Chronic low back pain (CLBP).Paired-pulse TMS dramatically lessens the energy needed for brain mapping.Maximal voluntary contraction of back muscles facilitates TMS mapping.Anticipatory postural activity of back muscles enhances the efficacy of TMS mapping.

Chronic low back pain (CLBP) is a social, emotional, and economic burden and the leading cause of disability worldwide. Yet the etiology of the CLBP is unknown. The persistence of aberrant or antalgic movement patterns observed in people with CLBP has been suggested as a possible cause of pain chronification by inducing continuous damage to sensitive structures of the lumbar spine. It is well known that the brain is in charge of the production and planning of movements, so it is likely that abnormal movement patterns also stem from the abnormalities in the brain. However, until recently, human knowledge about the structure and function of the brain has been very limited. The invention of noninvasive and painless brain imaging and stimulating techniques such as transcranial magnetic stimulation (TMS) during the last decades has augmented our knowledge about the structure and function of the brain. Modification in terms of shift, shrinkage, or expansion of areas of the brain devoted to movement control or sensation of the back muscles has been documented in CLBP via these techniques, which are argued to relate to pain chronification but need further clarification. Yet monitoring the course of CLBP via TMS, despite its many potentials, is challenging. This could be due to the reduced cortical drive to back muscles in CLBP patients and the small area devoted to control of back muscles in the brain in general that increases the brain threshold to TMS in people with CLBP. The aim of this study was to tailor an approach to make TMS more applicable for CLBP patients by reducing the threshold to TMS. This could be achieved by engaging back muscles in anticipatory postural activity in combination with maximal voluntary activation of these muscles, along with TMS paradigms that induce intracortical facilitation.