Does peripheral neuroinflammation predict chronicity following whiplash injury? Protocol for a prospective cohort study.

INTRODUCTION: Whiplash-associated disorder grade 2 (WAD2) is characterised by musculoskeletal pain/tenderness but no apparent nerve injury. However, studies have found clinical features indicative of neuropathy and neuropathic pain. These studies may indicate peripheral nerve inflammation, since preclinical neuritis models found mechanical sensitivity in inflamed, intact nociceptors. The primary aim of this study is to establish the contribution of peripheral neuroinflammation to WAD2 and its role in prognosis. Participants will be invited to participate in a sub-study investigating the contribution of cutaneous small fibre pathology to WAD2. METHODS AND ANALYSIS: 115 participants within 1 month following whiplash injury and 34 healthy control participants will be recruited and complete validated questionnaires for pain, function and psychological factors. Data collection will take place at the Universities of Sussex and Oxford, UK. Clinical examination, quantitative sensory testing and blood samples will be undertaken. MRI scans using T2-weighted and diffusion tensor images of the brachial plexus and wrist will determine nerve inflammation and nerve structural changes. Skin biopsies from a substudy will determine structural integrity of dermal and intraepidermal nerve fibres. At 6 months, we will evaluate recovery using Neck Disability Index and a self-rated global recovery question and repeat the outcome measures. Regression analysis will identify differences in MRI parameters, clinical tests and skin biopsies between participants with WAD2 and age/gender-matched controls. Linear and logistic regression analyses will assess if nerve inflammation (MRI parameters) predicts poor outcome. Mixed effects modelling will compare MRI and clinical measures between recovered and non-recovered participants over time. ETHICS AND DISSEMINATION: Ethical approval was received from London-Brighton and Sussex Research Ethics Committee (20/PR/0625) and South Central-Oxford C Ethics Committee (18/SC/0263). Written informed consent will be obtained from participants prior to participation in the study. Results will be disseminated through publications in peer-reviewed journals, presentations at national/international conferences and social media. TRIAL REGISTRATION NUMBER: NCT04940923.

Nerve pathology and neuropathic pain after whiplash injury: a systematic review and meta-analysis.

ABSTRACT: There is no clear understanding of the mechanisms causing persistent pain in patients with whiplash-associated disorder (WAD). The aim of this systematic review was to assess the evidence for nerve pathology and neuropathic pain in patients with WAD. EMBASE, PubMed, CINAHL (EBSCO), and MEDLINE were searched from inception to September 1, 2020. Study quality and risk of bias were assessed using the Newcastle-Ottawa Quality Assessment Scales. Fifty-four studies reporting on 390,644 patients and 918 controls were included. Clinical questionnaires suggested symptoms of predominant neuropathic characteristic in 34% of patients (range 25%-75%). The mean prevalence of nerve pathology detected with neurological examination was 13% (0%-100%) and 32% (10%-100%) with electrodiagnostic testing. Patients independent of WAD severity (Quebec Task Force grades I-IV) demonstrated significantly impaired sensory detection thresholds of the index finger compared with controls, including mechanical (SMD 0.65 [0.30; 1.00] P < 0.005), current (SMD 0.82 [0.25; 1.39] P = 0.0165), cold (SMD -0.43 [-0.73; -0.13] P = 0.0204), and warm detection (SMD 0.84 [0.25; 1.42] P = 0.0200). Patients with WAD had significantly heightened nerve mechanosensitivity compared with controls on median nerve pressure pain thresholds (SMD -1.10 [-1.50; -0.70], P < 0.0001) and neurodynamic tests (SMD 1.68 [0.92; 2.44], P = 0.0004). Similar sensory dysfunction and nerve mechanosensitivity was seen in WAD grade II, which contradicts its traditional definition of absent nerve involvement. Our findings strongly suggest a subset of patients with WAD demonstrate signs of peripheral nerve pathology and neuropathic pain. Although there was heterogeneity among some studies, typical WAD classifications may need to be reconsidered and include detailed clinical assessments for nerve integrity.

Aberrant Neuronal Activity in a Model of Work-Related Upper Limb Pain and Dysfunction.

Work-related musculoskeletal disorders associated with intense repetitive tasks are highly prevalent. Painful symptoms associated with such disorders can be attributed to neuropathy. In this study, we characterized the neuronal discharge from the median nerve in rats trained to perform an operant repetitive task. After 3-weeks of the task, rats developed pain behaviors and a decline in grip strength. Ongoing activity developed in 17.7% of slowly conducting neurons at 3-weeks, similar to neuritis. At 12-weeks, an irregular high frequency neuronal discharge was prevalent in >88.4% of slow and fast conducting neurons. At this time point, 8.3% of slow and 21.2% of fast conducting neurons developed a bursting discharge, which, combined with a reduction in fast-conducting neurons with receptive fields (38.4%), is consistent with marked neuropathology. Taken together, we have shown that an operant repetitive task leads to an active and progressive neuropathy that is characterized by marked neuropathology following 12-weeks task that mainly affects fast conducting neurons. Such aberrant neuronal activity may underlie painful symptoms in patients with work-related musculoskeletal disorders. PERSPECTIVE: Aberrant neuronal activity, similar to that reported in this study, may contribute to upper limb pain and dysfunction in patients with work-related musculoskeletal disorders. In addition, profiles of instantaneous frequencies may provide an effective way of stratifying patients with painful neuropathies.

Excursion of the median nerve during a contra-lateral cervical lateral glide movement in people with and without cervical radiculopathy.

BACKGROUND: A segmental, contra-lateral cervical lateral glide (CCLG) mobilization technique is effective for patients with cervical radiculopathy (CR). The CCLG technique induces median nerve sliding in healthy individuals, but this has not been assessed in patients with CR. OBJECTIVE: This study aimed to 1) assess longitudinal excursion of the median nerve in patients with CR and asymptomatic participants during a CCLG movement, 2) reassess nerve excursions following an intervention at a 3-month follow-up in patients with CR and 3) correlate changes in nerve excursions with changes in clinical signs and symptoms. DESIGN: Case-control study. METHODS: During a computer-controlled mechanically induced CCLG, executed by the Occiflex™, longitudinal median nerve excursion was assessed at the wrist and elbow with ultrasound imaging (T0) in 20 patients with CR and 20 matched controls. Patients were re-assessed at a 3-month follow-up (T1), following conservative treatment including neurodynamic mobilization. RESULTS: There was a significant difference between patients and controls in the excursion of the median nerve at both the wrist (Mdn = 0.50 mm; IQR = 0.13-1.30; 2.10 mm (IQR = 1.42-2.80, p < 0.05)) and elbow (Mdn = 1.21 mm (IQR = 0.85-1.94); 3.49 mm (IQR = 2.45-4.24, p < 0.05)) respectively at T0. There was also a significant increase in median nerve excursion at both sites between T0 and T1 in those with CR (Mdn = 1.96, 2.63 respectively). Wilcoxon Signed-Ranks Test indicated median pre-test ranks (Mdn = 0.5, 1.21; Z = - 3.82, p < 0.01; Z = -3.78, p < 0.01 respectively) and median post-test ranks. There was a strong correlation between improvement in median nerve excursion at the elbow at T1 and improvement in pain intensity (r = 0.7, p < 0.001) and functional limitations (r = 0.6, p < 0.01). CONCLUSION: Longitudinal median nerve excursion differs significantly between patients with CR and asymptomatic volunteers at baseline, but this difference is no longer present after 3 months of conservative physiotherapy management. Improvement in nerve excursion correlates with improvement in clinical signs and symptoms.

Ankle Motion Is Associated With Soft Tissue Displacement in the Dorsal Thigh: An in vivo Investigation Suggesting Myofascial Force Transmission Across the Knee Joint.

Experiments in cadavers have demonstrated significant mechanical interactions between constituents of myofascial chains. However, evidence for such force transmission effects is scarce under in vivo conditions. The purpose of this trial was to examine the impact of ankle motion on soft tissue displacement of the dorsal thigh. Eleven healthy active individuals (26.8 ± 4.3 years, six males), in prone position and with the knee extended, underwent passive calf stretches (ankle dorsal extension) imposed by an isokinetic dynamometer. High-resolution ultrasound was used to simultaneously capture the displacement of the semimembranosus muscle, which was quantified by means of cross-correlation analysis. Inactivity of the leg muscles was controlled using surface electromyography (EMG). One participant had to be excluded due to major EMG activity during the experiment. According to a one-sample t test testing the difference to the neutral zero position, ankle dorsal extension induced substantial caudal muscle displacements (5.76 ± 2.67 mm, p < 0.0001). Correlation analysis (Spearman), furthermore, revealed a strong association between maximal dorsal extension and semimembranosus motion (rho = 0.76, p = 0.02). In conclusion, the present trial provides initial in vivo evidence for a mechanical force transmission between serially connected skeletal muscles. This means that local alterations of the mechanical tissue properties may modify flexibility in neighboring (superior or inferior) joints.

Characterizing the Mechanical Properties of Ectopic Axonal Receptive Fields in Inflamed Nerves and Following Axonal Transport Disruption.

Radiating pain is a significant feature of chronic musculoskeletal pain conditions such as radiculopathies, repetitive motion disorders and whiplash associated disorders. It is reported to be caused by the development of mechanically-sensitive ectopic receptive fields along intact nociceptor axons at sites of peripheral neuroinflammation (neuritis). Since inflammation disrupts axonal transport, we have hypothesised that anterogradely-transported mechanically sensitive ion channels accumulate at the site of disruption, which leads to axonal mechanical sensitivity (AMS). In this study, we have characterised the mechanical properties of the ectopic axonal receptive fields in the rat and have examined the contribution of mechanically sensitive ion channels to the development of AMS following neuritis and vinblastine-induced axonal transport disruption. In both models, there was a positive force-discharge relationship and mechanical thresholds were low (∼9 mN/mm2). All responses were attenuated by Ruthenium Red and FM1-43, which block mechanically sensitive ion channels. In both models, the transport of TRPV1 and TRPA1 was disrupted, and intraneural injection of agonists of these channels caused responses in neurons with AMS following neuritis but not vinblastine treatment. In summary, these data support a role for mechanically sensitive ion channels in the development of AMS.

Neuritis and vinblastine-induced axonal transport disruption lead to signs of altered dorsal horn excitability.

BACKGROUND: Many patients with neuropathic pain present without signs of nerve injury on routine clinical examination. Some of these patients may have inflamed peripheral nerves (neuritis). In this study, we have examined whether neuritis causes changes within the dorsal horn that may contribute to a central pain mechanism. Comparisons have been made to a model of axonal transport disruption induced using vinblastine, since neuritis disrupts such processes. RESULTS: At the peak of cutaneous hypersensitivities, recordings from wide dynamic range neurons revealed increases in wind-up following neuritis but not vinblastine treatment. Ongoing activity from these neurons was unchanged. Vinblastine treatment caused a reduction in the responses of wide dynamic range neurons to noxious mechanical stimulation of the receptive field. The response of neurons to innocuous mechanical stimulation was also reduced in wide dynamic range neurons that were at a depth ≥550 µm following vinblastine treatment. An examination of the superficial dorsal horn revealed an increase in c-Fos-positive neurons in both groups following electrical stimulation of the sciatic nerve. The area of dorsal horn expressing substance P was also decreased following vinblastine treatment. CONCLUSION: These findings indicate that a minor nerve insult, such as neuritis, can lead to changes within the dorsal horn that are consistent with a central neuropathic pain mechanism.

Evidence for Increased Magnetic Resonance Imaging Signal Intensity and Morphological Changes in the Brachial Plexus and Median Nerves of Patients With Chronic Arm and Neck Pain Following Whiplash Injury.

Background Whiplash following a motor vehicle accident can result in chronic neck and arm pain. Patients frequently present with cutaneous hypersensitivities and hypoesthesia, but without obvious clinical signs of nerve injury. T2-weighted magnetic resonance imaging (MRI) has previously been used to identify nerve pathology. Objectives To determine whether there are signs of peripheral nerve pathology on MRI in patients with chronic arm and neck pain following whiplash injury. Methods This cross-sectional study used T2-weighted MRI to examine the brachial plexus and median nerve in patients and age-matched, healthy control subjects. Clinical examination included tests of plexus and nerve trunk mechanical sensitivity. Results The T2 signal intensity was greater in the brachial plexus and median nerve at the wrist in the patient group (mean intensity ratio = 0.52 ± 0.13 and 2.09 ± 0.33, respectively) compared to the control group (mean intensity ratio = 0.45 ± 0.07 and 1.38 ± 0.31, respectively; P<.05). Changes in median nerve morphology were also observed, which included an enlargement (mean area: patient group, 8.05 ± 1.29 mm2; control group, 6.52 ± 1.08 mm2; P<.05) and flattening (mean aspect ratio: patient group, 2.46 ± 0.53; control group, 1.62 ± 0.30; P<.05) at the proximal carpal row. All patients demonstrated signs of nerve trunk mechanical sensitivity. Conclusion These findings suggest that patients with chronic whiplash may have inflammatory changes and/or mild neuropathy, which may contribute to symptoms. J Orthop Sports Phys Ther 2018;48(7):523-532. Epub 24 Apr 2018. doi:10.2519/jospt.2018.7875.

Time course of ongoing activity during neuritis and following axonal transport disruption.

Local nerve inflammation (neuritis) leads to ongoing activity and axonal mechanical sensitivity (AMS) along intact nociceptor axons and disrupts axonal transport. This phenomenon forms the most feasible cause of radiating pain, such as sciatica. We have previously shown that axonal transport disruption without inflammation or degeneration also leads to AMS but does not cause ongoing activity at the time point when AMS occurs, despite causing cutaneous hypersensitivity. However, there have been no systematic studies of ongoing activity during neuritis or noninflammatory axonal transport disruption. In this study, we present the time course of ongoing activity from primary sensory neurons following neuritis and vinblastine-induced axonal transport disruption. Whereas 24% of C/slow Aδ-fiber neurons had ongoing activity during neuritis, few (<10%) A- and C-fiber neurons showed ongoing activity 1-15 days following vinblastine treatment. In contrast, AMS increased transiently at the vinblastine treatment site, peaking on days 4-5 (28% of C/slow Aδ-fiber neurons) and resolved by day 15. Conduction velocities were slowed in all groups. In summary, the disruption of axonal transport without inflammation does not lead to ongoing activity in sensory neurons, including nociceptors, but does cause a rapid and transient development of AMS. Because it is proposed that AMS underlies mechanically induced radiating pain, and a transient disruption of axonal transport (as previously reported) leads to transient AMS, it follows that processes that disrupt axonal transport, such as neuritis, must persist to maintain AMS and the associated symptoms. NEW & NOTEWORTHY Many patients with radiating pain lack signs of nerve injury on clinical examination but may have neuritis, which disrupts axonal transport. We have shown that axonal transport disruption does not induce ongoing activity in primary sensory neurons but does cause transient axonal mechanical sensitivity. The present data complete a profile of key axonal sensitivities following axonal transport disruption. Collectively, this profile supports that an active peripheral process is necessary for maintained axonal sensitivities.

Posture-induced changes in peripheral nerve stiffness measured by ultrasound shear-wave elastography.

INTRODUCTION: Peripheral nerves slide and stretch during limb movements. Changes in nerve stiffness associated with such movements have not been examined in detail but may be important in understanding movement-evoked pain in patients with a variety of different musculoskeletal conditions. METHODS: Shear-wave elastography was used to examine stiffness in the median and tibial nerves of healthy individuals during postures used clinically to stretch these nerves. RESULTS: Shear-wave velocity increased when limbs were moved into postures that are thought to increase nerve stiffness (mean increase: median nerve = 208% in arm, 236% in forearm; tibial nerve = 136%). There was a trend toward a negative correlation between age and shear-wave velocity (r = 0.58 for tibial nerve). CONCLUSIONS: Shear-wave elastography provides a tool for examining nerve biomechanics in healthy individuals and patients. However, limb position, age, and effects of nerve tension on neural architecture should be taken into consideration. Muscle Nerve 55: 213-222, 2017.

Altered tibial nerve biomechanics in patients with diabetes mellitus.

INTRODUCTION: Hyperglycemia associated with diabetes mellitus (DM) has adverse impacts on peripheral nerve connective tissue structure, and there is preliminary evidence that nerve biomechanics may be altered. METHODS: Ultrasound imaging was utilized to quantify the magnitude and timing of tibial nerve excursion during ankle dorsiflexion in patients with DM and matched healthy controls. RESULTS: Tibial nerve longitudinal excursion at the ankle and knee was reduced, and timing was delayed at the ankle in the DM group. Severity of neuropathy was correlated with larger reductions in longitudinal excursion. Nerve cross-sectional area was increased at the ankle in the DM group. CONCLUSIONS: Larger tibial nerve size within the tarsal tunnel in patients with DM may restrict longitudinal excursion, which was most evident with more severe neuropathy. It is hypothesized that these alterations may be related to painful symptoms during functional activities that utilize similar physiological motions through various biomechanical and physiological mechanisms.

Disruption of fast axonal transport in the rat induces behavioral changes consistent with neuropathic pain.

UNLABELLED: Studies of peripheral nerve inflammation (neuritis) suggest that some symptoms of neuropathic pain can be generated from inflamed but otherwise uninjured axons. We have previously inferred a role for inflammation-induced axonal transport disruption in the underlying mechanisms. In the present study, we have investigated the development of sensory hypersensitivities following vinblastine-induced axonal transport disruption. Similar to neuritis, locally applied .1 mM vinblastine caused the rapid development of mechanical hypersensitivity within the first week postsurgery. The same animals did not develop heat hypersensitivity. Because aberrant firing from primary sensory neurons is considered necessary to drive spinal mechanisms that lead to hypersensitivities, the levels of ongoing activity and axonal mechanical sensitivity were examined. Recordings from A- and C-fiber neurons did not reveal differences in the levels of ongoing activity between vinblastine-treated (<5.8%) and saline-treated control animals (<4.6%). However, 28% of C-fiber axons were mechanically sensitive at the vinblastine treatment site. Using kinesin immunohistochemistry, we confirmed a reduction of anterograde axonal transport in vinblastine-treated and neuritis animals. In summary, this study has revealed an alternative pain model, which may be relevant to conditions that are not accompanied by frank nerve injury. PERSPECTIVE: In this study, we expand our previous reports and demonstrate that focal reduced axonal transport causes distal mechanical hypersensitivity considered consistent with neuropathic pain but in the absence of nerve injury. These findings may inform pain conditions that have a neural inflammatory component.

ARA290 in a rat model of inflammatory pain.

Chronic pain affects as many as one in five people. A proportion of patients with symptoms of neuropathic -pain do not have clinical signs of any obvious tissue or nerve injury. Such patients include those with diffuse limb pain, back pain, and complex regional pain syndrome type 1. These patients remain a clinical enigma. However, through the development of the neuritis model, it has become apparent that local nerve inflammation in the absence of gross pathology (i.e., axonal degeneration and demyelination) may underlie part of the mechanisms of pain. In this chapter, we describe a method to induce the neuritis model. We also describe in detail a reliable method to test for mechanical allodynia and heat hyperalgesia. Data that demonstrates the potential benefits of the neuroprotective agent ARA290 in reducing pain behavior in the neuritis model are presented.

The pattern of tibial nerve excursion with active ankle dorsiflexion is different in older people with diabetes mellitus.

BACKGROUND: The peripheral nervous system has an inherent capability to tolerate the gliding (excursion), stretching (increased strain), and compression associated with limb motions necessary for functional activities. The biomechanical properties during joint movements are well studied but the influence of other factors such as limb pre-positioning, age and the effects of diabetes mellitus are not well established for the lower extremity. The purposes of this pilot study were to compare the impact of two different hip positions on lower extremity nerve biomechanics during an active ankle dorsiflexion motion in healthy individuals and to determine whether nerve biomechanics are altered in older individuals with diabetes mellitus. METHODS: Ultrasound imaging was used to quantify longitudinal motion of the tibial nerve and transverse plane motion of the tibial and common fibular nerves in the popliteal fossa during active ankle movements. FINDINGS: In healthy individuals, ankle dorsiflexion created mean tibial nerve movement of 2.18 mm distally, 1.36 mm medially and 3.98 mm superficially. When the hip was in a flexed position there was a mean three-fold reduction in distal movement. In people with diabetes mellitus there was significantly less distal movement of the tibial nerve in the neutral hip position and less superficial movement of the nerve in both hip positions compared to healthy individuals. INTERPRETATION: We have documented reductions in tibial nerve excursion due to limb pre-positioning thought to pre-load the nervous system using a non-invasive methodology. Thus, lower limb pre-positioning impacts nerve biomechanics during ankle motions common in functional activities. Additionally, our findings indicate that nerve biomechanics have the potential to be altered in older individuals with diabetes mellitus compared to younger healthy individuals.

Magnetic resonance imaging signal hyperintensity of neural tissues in diffuse chronic pain syndromes: a pilot study.

In this pilot study we use T2-weighted magnetic resonance imaging (MRI) to identify possible peripheral nerve inflammation in 4 patients with diffuse chronic pain. In all 4 patients, there was an increase in median and ulnar nerve T2 signal intensity at the wrist (P < 0.05 vs. controls). Positive clinical signs of peripheral nerve mechanosensitivity combined with MRI findings suggest that these patients may have an underlying peripheral nerve pathology.

CCL2 has similar excitatory effects to TNF-α in a subgroup of inflamed C-fiber axons.

Peripheral nerve inflammation can cause neuronal excitability changes that have been implicated in the pathogenesis of chronic pain. Although the neuroimmune interactions that lead to such physiological changes are unclear, in vitro studies suggest that the chemokine CCL2 may be involved. This in vivo study examines the effects of CCL2 on untreated and inflamed neurons and compares its effects with those of TNF-α. Extracellular recordings were performed in the anesthetized rat on isolated neurons with C-fiber axons. On untreated neurons, CCL2, as well as TNF-α, had negligible effects. Following neuritis, both cytokines transiently caused the firing of action potentials in 27-30% of neurons, which were either silent or had background (ongoing) activity. The neurons with ongoing activity, which responded to either cytokine, had significantly slower baseline firing rates {median = 3.0 spikes/min [interquartile range (IQR) 3.0]} compared with the nonresponders [median = 24.4 spikes/min (IQR 24.6); P < 0.001]. In an additional group, 26-27% of neurons, which were sensitized due to repeated noxious mechanical stimulation of the periphery, also responded to the effects of both cytokines. Neither cytokine caused axons to become mechanically sensitive. Immunohistochemistry confirmed that the cognate CCL2 receptor, CCR2, is mainly expressed on glia and is therefore not likely to be an axonal target for CCL2 following inflammation. In contrast, the cognate TNF-α receptor (TNFR), TNFR1, was present on untreated and inflamed neurons. In summary, CCL2 can excite inflamed C-fiber neurons with similar effects to TNF-α, although the underlying mechanisms may be different. The modulatory effects of both cytokines are limited to a subgroup of neurons, which may be subtly inflamed.

The conundrum of sensitization when recording from nociceptors.

Nociceptors are sensory neurons that detect harmful, or potentially harmful, stimuli, and can become sensitized following injury or repetitive stimulation. When sensitized, nociceptors often exhibit activity in the absence of apparent or additional stimulation, called ongoing (or spontaneous) activity (OA). In this report, we provide evidence that OA in nociceptors can be caused by the stimuli typically used to identify and characterize the neuron, which must by definition be noxious and therefore potentially sensitizing. Such OA caused by the experimental methodology can confound interpretation. In our nerve inflammation model, OA can potentially arise from multiple sites, including the lesion site and the receptive field. We provide evidence that the OA rate recorded during these experiments may be related to the site and cause of OA generation. We suggest that there are two types of OA, characterized by their rates. Very slow rates of ongoing activity (<0.2 Hz) are likely to arise from the receptive field and may indicate sensitization during the experiment. Faster rates are likely to arise from the nerve trunk, i.e. the neuritis, or the neuronal cell body. Without appropriate methodological consideration, interpretations of results from such studies of nociceptor function may be methodologically confounded.

Sonographic measurements of longitudinal median nerve sliding in patients following nerve repair.

Nerve sliding may be restricted following nerve repair. This could result in increased tension across the repair site and lead to poor functional recovery of the nerve. Ultrasound was used to examine longitudinal median nerve sliding in 10 patients who had previously undergone nerve repair surgery following complete division of the median nerve. The median longitudinal movement in the forearm in response to metacarpophalangeal (MCP) joint movements was 2.15 mm on the injured side, compared with 2.54 mm on the uninjured side, a difference that was significant. There was a significant reduction in nerve sliding following repair (median = 8%, range -8% to 54%; P = 0.02), which correlated with time from injury to surgery (rho = 0.87; P = 0.001). These results indicate that ultrasound can be used as an adjunct assessment tool to monitor both morphology and sliding of the nerve through the repair site. It may have future application in the investigation of patients with persisting functional impairment following primary nerve repair.

Effects of posture on the thickness of transversus abdominis in pain-free subjects.

The role of transversus abdominis (TrA) on spinal stability may be important in low back pain (LBP). To date, there have not been any investigations into the influence of lumbo-pelvic neutral posture on TrA activity. The present study therefore examines whether posture influences TrA thickness. A normative within-subjects single-group study was carried out. Twenty healthy adults were recruited and taught five postures: (1) supine lying; (2) erect sitting (lumbo-pelvic neutral); (3) slouched sitting; (4) erect standing (lumbo-pelvic neutral); (5) sway-back standing. In each position, TrA thickness was measured (as an indirect measure of muscle activity) using ultrasound. In erect standing, TrA (mean TrA thickness: 4.63+/-1.35 mm) was significantly thicker than in sway-back standing (mean TrA thickness: 3.32+/-0.95 mm) (p=00001). Similarly, in erect sitting TrA (mean thickness=4.30 mm+/-1.58 mm) was found to be significantly thicker than in slouched sitting (mean thickness=3.46 mm+/-1.13 mm) (p=0002). In conclusion, lumbo-pelvic neutral postures may have a positive influence on spinal stability compared to equivalent poor postures (slouched sitting and sway-back standing) through the recruitment of TrA. Therefore, posture may be important for rehabilitation in patients with LBP.