Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain

Department of Neurology, Given Building, University of Vermont, Burlington, VT 05405, USA.
BMC Musculoskeletal Disorders (Impact Factor: 1.72). 12/2009; 10(1):151. DOI: 10.1186/1471-2474-10-151
Source: PubMed


Although the connective tissues forming the fascial planes of the back have been hypothesized to play a role in the pathogenesis of chronic low back pain (LBP), there have been no previous studies quantitatively evaluating connective tissue structure in this condition. The goal of this study was to perform an ultrasound-based comparison of perimuscular connective tissue structure in the lumbar region in a group of human subjects with chronic or recurrent LBP for more than 12 months, compared with a group of subjects without LBP.
In each of 107 human subjects (60 with LBP and 47 without LBP), parasagittal ultrasound images were acquired bilaterally centered on a point 2 cm lateral to the midpoint of the L2-3 interspinous ligament. The outcome measures based on these images were subcutaneous and perimuscular connective tissue thickness and echogenicity measured by ultrasound.
There were no significant differences in age, sex, body mass index (BMI) or activity levels between LBP and No-LBP groups. Perimuscular thickness and echogenicity were not correlated with age but were positively correlated with BMI. The LBP group had approximately 25% greater perimuscular thickness and echogenicity compared with the No-LBP group (ANCOVA adjusted for BMI, p<0.01 and p<0.001 respectively).
This is the first report of abnormal connective tissue structure in the lumbar region in a group of subjects with chronic or recurrent LBP. This finding was not attributable to differences in age, sex, BMI or activity level between groups. Possible causes include genetic factors, abnormal movement patterns and chronic inflammation.

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    • "The pain radiation after fascia injection was in the typical locations of ''lumbago'' in LBP patients. The notion that the thoracolumbar fascia may play a major role in LBP is supported by its increased thickness [39] and reduced shear strain in subjects with chronic LBP [38]. But pain radiation after fascia injection was also similar to that seen in pseudoradicular LBP patients [18], and even consistent with that given by patients with lumbar facet joint syndrome [51]. "
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    ABSTRACT: Injection of hypertonic saline into deep tissues of the back (subcutis, muscle or the surrounding fascia) can induce acute low back pain (LBP). So far, no study has analyzed differences in temporal, qualitative and spatial pain characteristics originating from these tissues. The current study aimed to investigate the role of the thoracolumbar fascia as a potential source of LBP. In separate sessions, twelve healthy subjects received ultrasound-guided bolus injections of isotonic saline (0.9%) or hypertonic saline (5.8%) into the erector spinae muscle, the thoracolumbar fascia (posterior layer) and the overlying subcutis. Subjects were asked to rate pain intensity, duration, quality and spatial extent. Pressure pain thresholds were determined pre- and post-injection. Injections of hypertonic saline into the fascia resulted in significantly larger area under the curve of pain intensity over time than injections into subcutis (p<0.01) or muscle (p<0.001), primarily based on longer pain durations and to a lesser extent on higher peak pain ratings. Pressure hyperalgesia was only induced by injection of hypertonic saline into muscle, but not fascia or subcutis. Pain radiation and pain affect evoked by fascia injection exceeded those of the muscle (P<0.01) and the subcutis significantly (P<0.05). Pain descriptors after fascia injection (burning, throbbing and stinging) suggested innervation by both A- and C-fiber nociceptors. These findings show that the thoracolumbar fascia is the deep tissue of the back that is most sensitive to chemical stimulation, making it a prime candidate to contribute to non-specific LBP but not to localized pressure hyperalgesia.
    Full-text · Article · Sep 2014 · Pain
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    • "Recent studies have demonstrated involvement of connective tissue structures in the aetiology of low back pain (Langevin et al., 2009), yet there is little research regarding the possible role of muscular fascia in idiopathic scoliosis or postural hyperkyphosis. One case-study (LeBauer et al., 2008) has examined the effects of a manual therapy technique (myofascial release) on an adult with idiopathic scoliosis but similar studies on pubescent or adolescent subjects are lacking. "
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    ABSTRACT: Background: Treatment of pubescent postural hyperkyphosis commonly includes postural exercises and auto-elongation. Myofascial imbalances can be involved in functional, sagittal plane deviations of spinal curves. This pilot-study assesses the effects of one manual therapy approach that addresses fascial dysfunctions (Fascial Manipulation(®)) in pubescent subjects with postural hyperkyphosis. Methods: 17 subjects (mean age 11.8 DS 0.8; 9 males, 8 females) were evaluated for familiarity; psychological aspects; sport; pain; anteposition of shoulders, head, and pelvis; distance C7 and L3 from plumb-line; distance fingers to floor on forward bend. Each subject received 2-4 weekly sessions of Fascial Manipulation(®). Parameters were evaluated before and after manual treatment, with a follow-up at 7 months. Results: A statistically significant difference (p < 0.05) was present in all the parameters analysed before and after treatment and at a 7 month follow-up. Conclusions: Results suggest that Fascial Manipulation(®) could represent an approach to integrate into treatment of postural hyperkyphosis in pubescent subjects.
    Full-text · Article · Dec 2013 · Journal of Bodywork and Movement Therapies
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    • "It has long been known that scar tissue is a common cause of chronic musculoskeletal pain. Evidences have been produced suggesting that connective tissue may become thicker and less compliant in patients with chronic pain, possible as a result of chronic inflammation and fibrosis [2-4]. Therefore, the normal response to mechanical stretch may be dampened by disturbance of the viscoelastic properties of the subcutaneous connective tissue as a consequence of fibroblast remodeling promoted by inflammatory mediators, like neurotrophins, cytokines, peptides, protons, free radicals, histamine, bradykinin, serotonin, and prostanoids [5]. "
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    ABSTRACT: Chronic musculoskeletal pain involves connective tissue remodeling triggered by inflammatory mediators, such as bradykinin. Fibroblast cells signaling involve changes in intracellular Ca2+ ([Ca2+]i). ATP has been related to connective tissue mechanotransduction, remodeling and chronic inflammatory pain, via P2 purinoceptors activation. Here, we investigated the involvement of ATP in bradykinin-induced Ca2+ signals in human subcutaneous fibroblasts. Bradykinin, via B2 receptors, caused an abrupt rise in [Ca2+]i to a peak that declined to a plateau, which concentration remained constant until washout. The plateau phase was absent in Ca2+-free medium; [Ca2+]i signal was substantially reduced after depleting intracellular Ca2+ stores with thapsigargin. Extracellular ATP inactivation with apyrase decreased the [Ca2+]i plateau. Human subcutaneous fibroblasts respond to bradykinin by releasing ATP via connexin and pannexin hemichannels, since blockade of connexins, with 2-octanol or carbenoxolone, and pannexin-1, with 10Panx, attenuated bradykinin-induced [Ca2+]i plateau, whereas inhibitors of vesicular exocytosis, such as brefeldin A and bafilomycin A1, were inactive. The kinetics of extracellular ATP catabolism favors ADP accumulation in human fibroblast cultures. Inhibition of ectonucleotidase activity and, thus, ADP formation from released ATP with POM-1 or by Mg2+ removal from media reduced bradykinin-induced [Ca2+]i plateau. Selective blockade of the ADP-sensitive P2Y12 receptor with AR-C66096 attenuated bradykinin [Ca2+]i plateau, whereas the P2Y1 and P2Y13 receptor antagonists, respectively MRS 2179 and MRS 2211, were inactive. Human fibroblasts exhibited immunoreactivity against connexin-43, pannexin-1 and P2Y12 receptor. Bradykinin induces ATP release from human subcutaneous fibroblasts via connexin and pannexin-1-containing hemichannels leading to [Ca2+]i mobilization through the cooperation of B2 and P2Y12 receptors.
    Full-text · Article · Sep 2013 · Cell Communication and Signaling
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