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FT09 Fascia as the origin of chronic pain

rapm · 2025-09-10 · canonical JSON source

13 visible annotations · policy: published · automated confidence ≥ 75.00%

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Fascia is a continuous connective tissue network surrounding muscles, bones, nerves, and organs. Historically dismissed as packing material, fascia indeed acts as a dynamic structure playing an active role in coordinating movement and transmitting force. 1 To overcome difficulties in terminology, we will focus on the concept of the fascial system which includes superficial, deep (muscular), visceral and neural fascia.2 3 The superficial fascia, in the subcutaneous tissue, consists of two fibro-adipose layers: superficial and deep adipose tissue connected to the skin and deep fascia by cutaneous ligaments. Rich in fat, vessels, nerve endings and corpuscles, superficial fascia interacts with the external environment, and plays a role in lymphatic drainage, skin trophism, thermoregulation and allows sliding between the skin and muscular planes.4 Deep fascia surrounds muscles and comprises epimysial and aponeurotic fascia. It works together with muscles to perform movements, to manage posture and proprioception. A sliding plane between superficial and deep fascia maintains functional autonomy between external stimuli and internal perception. For these planes to operate properly, their autonomy must be maintained. The visceral fascia creates the vital space that houses the organs and permits their physiological movement. Finally, there is the neural fascia, which comprises the connective tissue surrounding peripheral nerves as well as the meninges. All these structures work together to create a sophisticated network that is the fascial system. The properties of the fascial system can be conceptually split into a microlevel (molecular and cellular responses) and a macrolevel (mechanical properties). At the microscopic level, fascia is composed of collagen-rich tissue and contains various cell types embedded in extracellular matrix (ECM). Fibroblasts, the main resident fascial cells, are responsive to mechanical stimuli, and can become contractile (myofibroblasts) or synthetic, increasing tension and ECM output. Following trauma, fibroblasts contribute to fibrosis through N-cadherin-mediated collective migration, especially in deep fascia.5 Changes in fibroblast and macrophage subtypes have been observed during conditions like acute compartment syndrome and necrotizing fasciitis, highlighting their roles in inflammation.6 7 The ECM - composed of water, collagens, proteoglycans/glycosaminoglycans, elastin, laminins, and other glycoproteins - is a reservoir of extracellular and signaling molecules secreted locally. It provides structural support, elasticity, and adaptability. Collagen types I and III offer tensile strength and flexibility, while elastin allows tissue recoil. Hydrophilic glycosaminoglycans (in particular hyaluronic acid [HA]) maintain lubrication and regulate osmotic pressure. Healthy fascia requires specific levels of matrix components. For example, HA content varies regionally, with higher concentrations in the fascia lata or rectus sheath (43 μg/g) compared to the epimysium of the deltoid and trapezius muscles (6 μg/g). These variations correspond with different gliding functions of the fascia, depending on the anatomical site. The aponeurotic fascia, like the thigh’s fascia lata or the abdomen rectus sheath, should glide over the muscles.8 Alterations in HA viscosity (affected by pH, temperature, pressure) contribute to fascial stiffness. Structural and biochemical properties of fascia are intimately linked to its innervation which is essential to its functions. Superficial fascia is densely innervated, with Pacinian and Ruffini corpuscles (exteroception), enabling it to perceive mechanical stimuli linking with skin mechanoreceptors and thermoreceptors. Superficial fascia of the human hip was found to be the second most highly innervated tissue after the skin, with a density of 33 ± 2.5/cm2 and a mean nerve size of 19.1 ± 7.2 µm. Superficial fascia is highly sensitive, providing fine tactile discrimination and autonomic innervation is well represented, with sympathetic fibers that account for 30% of superficial fascia innervation, often associated with small arteries.9 The deep aponeurotic fascia contains free nerve endings while epimysial is rich in encapsulated receptors (Golgi corpuscles and muscle spindles) interconnected in a network (perimysium septa) for detecting multidirectional tension and it plays a role in dynamic proprioception and pain.10 Muscle spindles’ capsule is structurally continuous with the perimysium and forms multiple connections in different orientations. Spindles are very sensitive to the tension of the epimysial fascia. Changes in muscle length and alterations in the (epimysial) fascia tension (for example with fibrosis and aging) influence muscle spindles and accordingly proprioception and posture.11 Electrical stimulation of deep fascia evokes dull and unpleasant pain, whereas stimulation of the hypodermis and superficial fascia produces a sharp, well-localized pain, confirming that the two fasciae have different roles. In healthy volunteers, stimulation of the thoracolumbar fascia with hypertonic saline generates pain, and this pain is more intense referring to a larger area compared to injection within the erector spinae muscles.12 The presence of substance P (presumably nociceptive) fibers in chronically inflamed thoracolumbar fascia suggests that fascia can undergo pathological changes leading to chronic pain.13 Chronic irritation of the deep fascia can also induce central sensitization. In rats with chronic thoracolumbar fascia inflammation, Hoheisel et al. showed that the spinal segments involved in nociceptive afference expanded14 while Taguchi et al. demonstrated that repeated mechanical (pinching) stimuli could induce c-Fos protein expression in the spinal segments receiving sensory input.15 Normal fascia is elastic and adaptable, supports muscles and regulates muscular function. Many factors can disrupt fascial architecture leading to fibrosis, HA densification, reduced gliding, with different impacts on stiffness.16 Fibrotic fascia limits muscle mobility and induces dysfunction and pain also in distant regions. Some estimates suggest that bone receives 70% of the muscular force to perform movement, while peri-muscular fascia receives 30%. Subsequently, when the muscles contract, they create tension in the fascia. The myofascial connections may affect how the body works and explain pain and dysfunction in distant areas.17 Thoracolumbar fascia shear strain is about 20% lower in human subjects with chronic low back pain.18 In a recent systematic review and meta-analysis, including over 4000 patients, thoracolumbar fascia injury (TLFI) has 28% incidence rate after percutaneous vertebral augmentation. Additionally, uni- and multivariate analyses show that TLFI significantly increases the risk of residual chronic back pain.19 Prolonged static posture or repetitive activities can cause degeneration and fibrosis, reducing elasticity and impairing fascial gliding.20 Nordez et al. also hypothesized that fascial stiffness could limit the maximal range of motion of a joint.21 Hip osteoarthritis is associated with a dysfunctional, stiffened fascia lata, with impaired sliding. Changes in composition of the collagen and significant decrease in the content of HA suggest that osteoarthritis may be considered as an extra-articular disease affecting the normal physiology of the fascia.22 Interestingly, fascia also exhibits active mechanical behavior. Schleip et al. showed that active contraction of fascia could influence the coordination of motor neurons in the lumbar region, affecting the biomechanical behavior of the entire musculoskeletal system. Fascia contains myofibroblasts, which can actively regulate the tension of the fascia through a contraction mechanism similar to smooth muscle. When the fascia is biochemically stimulated (such as with transforming growth factor β1 or thromboxane A2), it can respond in ways that affect its biomechanical properties.23 24 Mechanical stress can degrade hyaluronan, triggering inflammatory cascades that impair fascia function and regeneration.25 The biomechanical properties of the fascia change with muscle exercise, overuse, disuse or pathological loading, often leading to HA fascial densification, which results in greater resistance to fascial layers sliding and increased stiffness.26 27 Zhao et al. evaluated hyaluronan and collagen concentration in the gastrocnemius muscle and thoracolumbar fascia in unilateral lower limb peripheral nerve-injured rats to explore systemic ECM alterations following peripheral nerve injury and impacts on functional recovery. They highlighted systemic ECM alterations following sciatic nerve injury, focusing on HA and collagen changes in lower limb muscles and the thoracolumbar fascia.28 Fascia may contribute to complex regional pain syndrome through neuro-inflammation, fibrosis and autonomic dysregulation. Fascia’s rich innervation facilitates peripheral and central sensitization, while inflammatory mediators drive fibrosis, and reduce elasticity. Autonomic dysfunction worsens hypoxia and oxidative stress, fueling chronic dysfunction.29 Ultrasound (US) and sonoelastography are increasingly used to assess fascial alterations.30 In a 68-year-old man with chronic pain caused by thoracic zoster, Fusco et al. studied the affected regions through elastography. They highlighted high muscular rigidity and fascial densification. After erector spinae plane (ESP) block, sonoelastography showed reduction in densification of the deep fascia and less muscular stiffness. The mechanism of the ESP block is still debated and potentially related to the injectate spread toward thoracic intercostal nerve, paravertebral space and dorsal root ganglion. Nevertheless, considering the rich innervation of fascia, the authors postulated that the fascial block worked on the fascial nerve endings, and by reducing densification and muscular stiffness, as elastography demonstrated, revealing a possible clinical relationship between the fascial administration of local anesthetic and the reduction of stiffness and pain generation. Further, the duration of the pain relief after the block was much longer than the effect of the local anesthetic itself.31 This may suggest that fascia may become a target itself for fascial blocks in pain management,32 by administering not only local anesthetic, but also electric or mechanical stimulation, as dry needling.33 Another confirmation of the potential role of the fascial system as pain generator was shown when Fusco and colleagues found that injecting hot saline (40°C) into the ESP caused immediate pain relief in chronic myofascial pain. Hot saline does not block the pain transmission as the local anesthetic does, but the fascial hydro-dissection with warm solution potentially stimulates the nerve endings and reduces HA aggregation (macromolecules and densification) with improvement in fascial gliding, muscle stiffness and pain.34 In chronic pain, alterations in fascia can cause fibrosis (adhesions and connective septa) that may compromise sliding with an alteration of the synergistic contraction of the interconnected muscles. The injection of local anesthetic (fascial hydro-dissection or hydro-release) in the fascial planes may break the connective septa and optimizes the fascial sliding.35 36 An interesting report by Fusco et al. further advanced this approach.37 Both ultrasound and micro-endoscopic guidance were used to perform a targeted ESP block in a patient who had refractory chronic post-surgical thoracic pain. This technique made it possible to dynamically hydro-dissect the planes and directly visualize adhesions. (Figure 1) After the block, significant tissue (fascial and muscular) elasticity improvement was confirmed by elastography, closely mirroring the patient‘s recovery. The authors argued how this imaging-guided intervention could disrupt fibrous septa, restore fascial gliding, and facilitate recovery. In conclusion, nowadays, fascia is seen as a functional, innervated network essential to movement, force transmission, and pain modulation rather than as inert connective tissue. Novel approaches to diagnosing and treating chronic pain originating from fascial dysfunction are made possible by developments in imaging and interventional techniques, such as elastography and ultrasound-guided fascial plane blocks.38 Gaining a better understanding of the biomechanical and neurophysiological functions of fascia offers encouraging prospects for functional rehabilitation and individualized pain management.Abstract FT09 Figure 1Endoscopic view of fascia with fascial fibrosis (yellow stars). High-resolution native images (Courtesy of Dr Fusco)References Wilke J, Schleip R, Yucesoy CA, Banzer W. Not merely a protective packing organ? A review of fascia and its force transmission capacity. J Appl Physiol. 2018;124:234–44.Adstrum S, Hedley G, Schleip R, Stecco C, Yucesoy CA. Defining the fascial system. J Bodyw Mov Ther. 2017;21:173–7.Stecco C, Pratt R, Nemetz LD, Schleip R, Stecco A, Theise ND. Towards a comprehensive definition of the human fascial system. 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