Distinguishing chronic low back pain in young adults with mild to moderate pain and disability using trunk compliance.

Chronic low back pain (cLBP) rates among younger individuals are rising. Although pain and disability are often less severe, underlying changes in trunk behavior may be responsible for recurrence. We examine the biomarker capacity of a simple Trunk Compliance Index (TCI) to distinguish individuals with and without cLBP. A random subset (n = 49) of the RELIEF RCT were matched to healthy controls for sex, age, height and weight. We measured TCI (as displacement/ weight-normalized perturbation force) using anthropometrically-matched, suddenly-applied pulling perturbations to the trunk segment, randomized across three planes of motion (antero-posterior, medio-lateral, and rotational). Mean differences between cLBP, sex and perturbation direction were assessed with repeated-measures analysis of variance. Discriminatory accuracy of TCI was assessed using Receiver Operator Characteristic (ROC) analysis. Baseline characteristics between groups were equivalent (x̅ [range]): sex (57% female / group), age (23.0 [18-45], 22.8 [18-45]), height, cm (173.0 [156.5-205], 171.3 [121.2-197], weight, kg (71.8 [44.5-116.6], 71.7 [46.8-117.5]) with cLBP associated with significantly lower TCI for 5 of 6 directions (range mean difference, - 5.35: - 1.49, range 95% CI [- 6.46: - 2.18 to - 4.35: - 0.30]. Classification via ROC showed that composite TCI had high discriminatory potential (area under curve [95% CI], 0.90 [0.84-0.96]), driven by TCI from antero-posterior perturbations (area under curve [95% CI], 0.99 [0.97-1.00]). Consistent reductions in TCI suggests global changes in trunk mechanics that may go undetected in classic clinical examination. Evaluation of TCI in younger adults with mild pain and disability may serve as a biomarker for chronicity, leading to improved preventative measures in cLBP.Trial Registration and Funding RELIEF is registered with clinicaltrials.gov (NCT01854892) and funded by the NIH National Center for Complementary & Integrative Health (R01AT006978).

The power of the mind: the cortex as a critical determinant of muscle strength/weakness.

We tested the hypothesis that the nervous system, and the cortex in particular, is a critical determinant of muscle strength/weakness and that a high level of corticospinal inhibition is an important neurophysiological factor regulating force generation. A group of healthy individuals underwent 4 wk of wrist-hand immobilization to induce weakness. Another group also underwent 4 wk of immobilization, but they also performed mental imagery of strong muscle contractions 5 days/wk. Mental imagery has been shown to activate several cortical areas that are involved with actual motor behaviors, including premotor and M1 regions. A control group, who underwent no interventions, also participated in this study. Before, immediately after, and 1 wk following immobilization, we measured wrist flexor strength, voluntary activation (VA), and the cortical silent period (SP; a measure that reflect corticospinal inhibition quantified via transcranial magnetic stimulation). Immobilization decreased strength 45.1 ± 5.0%, impaired VA 23.2 ± 5.8%, and prolonged the SP 13.5 ± 2.6%. Mental imagery training, however, attenuated the loss of strength and VA by ∼50% (23.8 ± 5.6% and 12.9 ± 3.2% reductions, respectively) and eliminated prolongation of the SP (4.8 ± 2.8% reduction). Significant associations were observed between the changes in muscle strength and VA (r = 0.56) and SP (r = -0.39). These findings suggest neurological mechanisms, most likely at the cortical level, contribute significantly to disuse-induced weakness, and that regular activation of the cortical regions via imagery attenuates weakness and VA by maintaining normal levels of inhibition.

The biology of manual therapies.

Each year, more than 18 million adults in the United States receive manual therapies, at a total annual out-of-pocket cost of $3.9 billion. Although there is growing evidence supporting the efficacy of manual therapies, little is known about the mechanisms underlying these treatments. This lack of basic knowledge significantly limits the development of rational strategies for the use of these treatments and potentially hinders their acceptance by the wider scientific and health care communities. Many authors have hypothesized that manual therapies act by disrupting the pain-spasm-pain cycle, but relatively little experimental evidence has supported this hypothesis. The authors have tested this hypothesis and summarize their work on the biology of manual therapies.

Non-thrust manual therapy reduces erector spinae short-latency stretch reflex asymmetries in patients with chronic low back pain.

The purpose of this study was to determine if non-thrust manual therapy (MT) attenuated side-to-side differences (asymmetry) of the erector spinae (ES) stretch reflex amplitude in nine patients with chronic LBP. We used electromechanical tapping to elicit short-latency stretch reflexes (SR) from the ES muscles before and after non-thrust MT. A large asymmetry in the SR was observed at baseline, with the higher of the paraspinal sides exhibiting a 100.2±28.2% greater value than the lower side. Following the intervention, this SR asymmetry was reduced (100.2±28.2% to 36.6±23.1%; p=0.03). This change was largely due to reduced amplitude on the side that was higher at baseline (35% reduction following treatment; p=0.05), whereas no change over time was observed in the low side (p=0.23). Additionally, there was no difference between the respective sides following the intervention (p=0.38), indicating that the asymmetry was normalized following treatment. These findings provide insight into the mechanism(s) of action of non-thrust MT, and suggest that it acts to down regulate the gain of the muscle spindles and/or the various sites of the Ia reflex pathway. Ultimately, developing a better understanding of the physiologic effects of manual therapies will assist in optimizing treatment strategies for patients with LBP.

Muscle functional magnetic resonance imaging and acute low back pain: a pilot study to characterize lumbar muscle activity asymmetries and examine the effects of osteopathic manipulative treatment.

BACKGROUND: Muscle functional magnetic resonance imaging (mfMRI) measures transverse relaxation time (T2), and allows for determination of the spatial pattern of muscle activation. The purposes of this pilot study were to examine whether MRI-derived T2 or side-to-side differences in T2 (asymmetries) differ in low back muscles between subjects with acute low back pain (LBP) compared to asymptomatic controls, and to determine if a single osteopathic manipulative treatment (OMT) session alters these T2 properties immediately and 48-hours after treatment. METHODS: Subjects with non-specific acute LBP (mean score on 110 visual analog score = 3.02 +/- 2.81) and asymptomatic controls (n = 9/group) underwent an MRI, and subsequently the LBP subjects received OMT and then underwent another MRI. The LBP subjects reported back for an additional MRI 48-hours following their initial visit. T2 and T2 asymmetry were calculated from regions of interest for the psoas, quadratus lumborum (QL), multifidus, and iliocostalis lumborum/longissimus thoracis (IL/LT) muscles. RESULTS: No differences were observed between the groups when T2 was averaged for the left and right side muscles. However, the QL displayed a significantly greater T2 asymmetry in LBP subjects when compared to controls (29.1 +/- 4.3 vs. 15.9 +/- 4.1%; p = 0.05). The psoas muscle also displayed a relatively large, albeit non-significant, mean difference (22.7 +/- 6.9 vs. 9.5 +/- 2.8%; p = 0.11). In the subjects with LBP, psoas T2 asymmetry was significantly reduced immediately following OMT (25.3 +/- 6.9 to 6.1 +/- 1.8%, p = 0.05), and the change in LBP immediately following OMT was correlated with the change in psoas T2 asymmetry (r = 0.75, p = 0.02). CONCLUSION: Collectively, this pilot work demonstrates the feasibility of mfMRI for quantification and localization of muscle abnormalities in patients with acute low back pain. Additionally, this pilot work provides insight into the mechanistic actions of OMT during acute LBP, as it suggests that it may attenuate muscle activity asymmetries of some of the intrinsic low back muscles.

Adaptations in human neuromuscular function following prolonged unweighting: II. Neurological properties and motor imagery efficacy.

Strength loss following disuse may result from alterations in muscle and/or neurological properties. In this paper, we report our findings on human plantar flexor neurological properties following 4 wk of limb suspension [unilateral lower limb suspension (ULLS)], along with the effect of motor imagery (MI) training on these properties. In the companion paper (Part I), we report our findings on the changes in skeletal muscle properties. Additionally, in the present paper, we analyze our findings to determine the relative contribution of neural and muscular factors in strength loss. Measurements of central activation, the H-reflex, and nerve conduction were made before and after 4 wk of ULLS (n = 18; 19-28 yr). A subset of the subjects (n = 6) performed PF MI training 4 days/wk. Following ULLS, we observed a significant increase in the soleus H-reflex (45.4 +/- 4.0 to 51.9 +/- 3.7% expressed relative to the maximal muscle action potential). Additionally, there were longer intervals between the delivery of an electrical stimulus to the tibial nerve and the corresponding muscle action potential (M-wave latency; mean prolongation 0.49 ms) and H-reflex wave (H-wave latency; mean prolongation 0.46 ms). The efficacy of MI on strength was ambiguous, with no significant effect detected (although a modest effect size was observed; eta2 = 0.18). These findings suggest that unweighting induces plastic changes in neural function that appear to be spatially distributed throughout the nervous system. In terms of the relative contribution of neural and muscular factors regulating strength loss, we observed that neural factors (primarily deficits in central activation) explained 48% of the variability in strength loss, whereas muscular factors (primarily sarcolemma function) explained 39% of the variability.