. Low back pain (LBP) is a major health problem in the United States costing annually over $50 billion in treatment-related costs and $100 billion in indirect costs (i.e. lost productivity). This national health crisis is further compounded by a recent over-reliance on prescription opioids for therapeutic pain management. High velocity low amplitude spinal manipulation (HVLA-SM) is a non-pharmacological LBP approach recommended by a majority of clinical practice guidelines. However, a lack of knowledge concerning underlying neurophysiological mechanisms hinders wider clinical acceptance, usage, and optimization of this therapeutic approach. Proposed mechanisms of HVLA-SM efficacy include changes in muscle spindle sensitivity related to rapid stretch-induced stimulation of mechanoreceptors in muscle and/or other trunk tissues. Previous work in our lab has shed light on the relationship between the mechanical characteristics of HVLA-SM (thrust duration, thrust amplitude, thrust rate, preload magnitude & duration, and thrust contact site) and trunk muscle spindle afferent responsiveness in non-chemosensitized environments. Recently pilot studies using commercially available HVLA-SM devices with extremely short thrust durations of 2-3ms revealed a dichotomy among post-HVLA-SM return to baseline muscle spindle discharge. Distinct subpopulations of spindle afferents returned to baseline discharge post-HVLA-SM relatively rapidly (<2s), while others required substantially longer periods (>10s), which far outlasted the mechanical stimulus of HVLA-SM. The biological and/or biomechanical factors responsible for this post-HVLA-SM response dichotomy, as well as whether or not clinically relevant tissue chemosensitization acts to maximize these dichotomous post-HVLA-SM responses is currently unknown. A recently developed preclinical LBP model has been established using a translationally relevant pain molecule, nerve growth factor (NGF). NGF is a neurotrophin associated with pain which is naturally upregulated after muscle damage, inflammation, and/or peripheral nerve injury. Injection of NGF into deep trunk musculature creates persistent (days/weeks), localized trunk hyperalgesia by sensitizing skeletal muscle nociceptors and producing marked spinal dorsal horn neuron hyperexcitability; both of which are thought to be key components of LBP chronicity. This proposal will characterize post-HVLA-SM muscle spindle response based on intrafusal fiber classification, HVLA-SM thrust duration (2-3ms vs 100ms), and HVLA-SM peak biomechanical forces reaching deep spinal tissues (multifidus muscle) in control and trunk chemosensitized (NGF-induced LBP) environments in order to reveal neurophysiological mechanisms underlying spinal manipulation and to establish another preclinical NGF-induced LBP model so as to better inform and/or optimize this non-pharmacological approach to LBP.
Low back pain (LBP) is associated with more global disability than any other health condition and it exerts a major economic impact in the United States with total costs exceeding 100 billion per year. Spinal manipulation (SM) is recommended by clinical guidelines to treat LBP, however efficacy, utilization and therapeutic optimization is hindered by gaps in knowledge regarding underlying physiological mechanisms. This proposal seeks to characterize changes in post-SM muscle spindle afferent response using extremely short (2-3ms) and longer (100ms) manipulative thrusts in control and chemosensitized LBP environments using a preclinical model.
