FCS Developer Expands Physiological Rationale for Indirect Tissue Manipulation
The following is an excerpt from “Impaired Lymphatic Drainage and Interstitial Inflammatory Stasis in Chronic Musculoskeletal and Idiopathic Pain Syndromes: Exploring a Novel Mechanism” by Fascial Counterstrain-developer Brian Tuckey, PT, OCS, JSCCI, along with John Srbely, Grant Rigney, Meena Vythilingam, and Jay Shah.
Abstract
A normal functioning lymphatic pump mechanism and unimpaired venous drainage are required for the body to remove inflammatory mediators from the extracellular compartment. Impaired vascular perfusion and/or lymphatic drainage may result in the accumulation of inflammatory substances in the interstitium, creating continuous nociceptor activation and related pathophysiological states including central sensitization and neuroinflammation. We hypothesize that following trauma and/or immune responses, inflammatory mediators may become entrapped in the recently discovered interstitial, pre-lymphatic pathways and/or initial lymphatic vessels. The ensuing interstitial inflammatory stasis is a pathophysiological state, created by specific pro-inflammatory cytokine secretion including tumor necrosis factor alpha, interleukin 6, and interleukin 1b. These cytokines can disable the local lymphatic pump mechanism, impair vascular perfusion via sympathetic activation and, following transforming growth factor beta 1 expression, may lead to additional stasis through direct fascial compression of pre-lymphatic pathways. These mechanisms, when combined with other known pathophysiological processes, enable us to describe a persistent feed-forward loop capable of creating and maintaining chronic pain syndromes. The potential for concomitant visceral and/or vascular dysfunction, initiated and maintained by the same feed-forward inflammatory mechanism, is also described.
Introduction
Chronic pain is the leading cause of disability with up to 49% of the population experiencing pain <3 months duration. The estimated cost of chronic pain and associated opioid use disorder in the USA is currently between $560 and 635 billion annually. Chronic pain is positively correlated with age and, given the rapidly aging demographic, the burden of chronic pain will continue to impose significant challenges to our healthcare system.
Myofascial pain syndrome (MPS) is among the most common, yet least understood forms of chronic musculoskeletal pain, and is a frequent cause of primary care physician and pain clinic visitation. Few people live without experiencing muscle pain following injury, overuse, strain, or trauma. Although pain associated with MPS frequently resolves in a few weeks, in some cases it can persist long after the inciting event and/or spread to distant, uninjured tissues. Although MPS is typically characterized by the expression of pain localized to myofascial tissues, it is also associated with a broad and growing profile of non-musculoskeletal symptoms including fatigue, sleep disturbance, and visceral pain syndromes. These associations suggest a shared pathophysiology between MPS and several common idiopathic conditions (e.g., visceral pain syndromes). The pathophysiological mechanisms underlying this association, however, are not fully understood and remain largely undescribed.
It is well-established that persistent, peripheral nociceptive sources can initiate, maintain, and perpetuate chronic pain states. This occurs, in part, through central mechanisms including retrograde inflammation produced by dorsal root reflexes, and/or areas of secondary hyperalgesia produced by glial cell neuroinflammation. However, in idiopathic peripherally generated chronic pain, our understanding of the pathological processes that generate and maintain ongoing nociceptive input is limited. Examples include whiplash associated disorders which present with pain, proprioceptive and autonomic-linked symptoms despite a lack of correlative pathological evidence on computer tomography and/or magnetic resonance imaging. Additionally, existing pain hypotheses are limited in their ability to address many of the pathophysiological findings common to both chronic pain and idiopathic visceral/vascular syndromes. This includes elevated levels of plasma and interstitial pro-inflammatory cytokines in myofascial and visceral pain syndromes, and evidence of sympathetic nerve activation (SNA) in MPS, visceral disease, and vascular disorders. Microvascular disturbances and impaired lymphatic function have also been identified in both MPS and visceral disease, supporting the concept of a shared pathophysiology.
Considering the limitations in current understanding, we hypothesize that elevated pro-inflammatory cytokine levels, through specific pathophysiological mechanisms, adversely impact vascular hemodynamics and lymphatic function in the extracellular compartment. Impaired venous and lymphatic drainage can create a state of inflammatory interstitial stasis (IIS), which results in ongoing nociceptive bombardment of the dorsal horn (central sensitization). Recent anatomical discovery and advances in pre-clinical and clinical research, enable us to further elucidate the potential pathophysiological factors involved in this process. This includes contraction of fascial myofibroblasts following local TGF-b1 expression which we hypothesize can cause pre-lymphatic/lymphatic vessel contraction and/or fibrosis. And the effect of specific pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-a), interleukin-6 (IL-6) and interleukin (IL-1b) in cessation of the normal lymphatic pump mechanism, the development of chronic pain states and the creation of long-term microvascular disturbance following stimulation of segmentally linked somato/visceral-sympathetic reflexes.
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