Depending on whom you ask or what scientific paper you read last, spinal manipulation is either a mercifully quick, effective treatment for low-back pain or a complete waste of time.
It turns out everyone’s right.
Researchers at the University of Alberta have found that spinal manipulation—applying force to move joints to treat pain, a technique most often used by chiropractors and physical therapists—does indeed have immediate benefits for some patients with low-back pain but does not work for others with low-back pain. And though on the surface this latest conflict might appear to muddy the waters further, the results point to the complexity of low-back pain and the need to treat patients differently, says lead author Greg Kawchuk.
“Back pain, just like cancer, is a collection of different kinds of problems. We haven’t been very good at distinguishing who has which problem, so we throw a treatment at people and naively expect that treatment to fix everyone’s back pain,” says Kawchuk, an expert in spine function and professor in the Faculty of Rehabilitation Medicine who co-wrote the study with U of A colleagues Arnold Wong (now at Hong Kong Polytechnic University), Eric Parent, Sukhvinder Dhillon and Narasimha Prasad.
“This study shows that, just like some people respond differently to a specific medication, there are different groups of people who respond differently to spinal manipulation.”
In a non-randomized control study, individuals with low-back pain received spinal manipulation during two treatment sessions that spanned a week. Participants reported their pain levels and disability levels after spinal manipulation, and researchers used ultrasound, MRI and other diagnostics to measure changes in each participant’s back, including muscle activity, properties within the intervertebral discs, and spinal stiffness.
A control group of participants with low-back pain underwent similar clinical examinations but did not receive spinal manipulation. A third group — those who did not have low-back pain symptoms — were also evaluated.
The people who responded to spinal manipulation reported less pain right away and showed improvement in back muscle thickness, disc diffusion and spinal stiffness. Those changes were great enough to exceed or equal the measures in the control groups and stayed that way for the week of treatment, the research team found.
A patient receives spinal manipulation treatment.
Researchers measure back stiffness after a study participant received spinal manipulation.
Conversely, researchers also found that people with back pain who reported no improvement showed no physical changes either—there simply was no effect.
Kawchuk, who practised as a chiropractor before going on to obtain his PhD in biomechanics and bioengineering, said the results do not advocate one way or another for spinal manipulation but help explain why there has been so much conflicting data about its merits.
“Clearly there are some people with a specific type of back pain who are responding to this treatment and there are some people with another type of back pain who do not. But if you don’t know that and you mix those two groups together, you get an artificial average that doesn’t mean anything,” Kawchuk explained.
The research team is still fine-tuning how to distinguish who is a responder or non-responder before spinal manipulation is given; however, this study shows it can be used to identify an effective treatment course.
“Spinal manipulation acts so rapidly in responders that it could be used as a screening tool to help get the right treatment to the right patient at the right time.”
The study did not investigate the long-term effects of spinal manipulation, but this is next on the list for the researchers.
STUDY DESIGN: Nonrandomized controlled study.
OBJECTIVE: To determine whether patients with low back pain (LBP) who respond to spinal manipulative therapy (SMT) differ biomechanically from nonresponders, untreated controls or asymptomatic controls.
SUMMARY OF BACKGROUND DATA: Some but not all patients with LBP report improvement in function after SMT. When compared with nonresponders, studies suggest that SMT responders demonstrate significant changes in spinal stiffness, muscle contraction, and disc diffusion. Unfortunately, the significance of these observations remains uncertain given methodological differences between studies including a lack of controls.
METHODS: Participants with LBP and asymptomatic controls attended 3 sessions for 7 days. On sessions 1 and 2, participants with LBP received SMT (+LBP/+SMT, n = 32) whereas asymptomatic controls did not (-LBP/-SMT, n = 57). In these sessions, spinal stiffness and multifidus thickness ratios were obtained before and after SMT and on day 7. Apparent diffusion coefficients from lumbar discs were obtained from +LBP/+SMT participants before and after SMT on session 1 and from an LBP control group that did not receive SMT (+LBP/-SMT, n = 16). +LBP/+SMT participants were dichotomized as responders/nonresponders on the basis of self-reported disability on day 7. A repeated measures analysis of covariance was used to compare apparent diffusion coefficients among responders, nonresponders, and +LBP/-SMT subjects, as well as spinal stiffness or multifidus thickness ratio among responders, nonresponders, and -LBP/-SMT subjects.
RESULTS: After the first SMT, SMT responders displayed statistically significant decreases in spinal stiffness and increases in multifidus thickness ratio sustained for more than 7 days; these findings were not observed in other groups. Similarly, only SMT responders displayed significant post-SMT improvement in apparent diffusion coefficients.
CONCLUSION: Those reporting post-SMT improvement in disability demonstrated simultaneous changes between self-reported and objective measures of spinal function. This coherence did not exist for asymptomatic controls or no-treatment controls. These data imply that SMT impacts biomechanical characteristics within SMT responders not present in all patients with LBP. This work provides a foundation to investigate the heterogeneous nature of LBP, mechanisms underlying differential therapeutic response, and the biomechanical and imaging characteristics defining responders at baseline.
From the FULL TEXT Article:
Spinal manipulative therapy (SMT) is a common intervention for low back pain (LBP). Historically, the results of clinical trials designed to evaluate SMT have been mixed [1–5] with some (but not all) participants reporting a benefit. In recent years, growing evidence suggests that these mixed results are due partially to a differential treatment response in patients. [1, 2, 6]
Although some have suggested that a differential response of participants with LBP to SMT could be caused by psychosocial factors (e.g., expectation), [7, 8] others have developed and validated a clinical prediction rule (CPR) to identify likely responders to SMT on the basis of clinical characteristics. [1, 6] This work was based on the observation that patients with LBP who self-reported clinically significant improvement in the modified Oswestry Disability Index (mODI) displayed at least 4 of 5 specific clinical characteristics (see Supplemental Digital ContentAppendix I). After this work, Fritz and coworkers  demonstrated that CPR status might be related to LBP disability through its relation to lumbar multifidus (LM) contraction thickness. They also found that post-SMT improvement of the mODI score for more than 1 week was associated with
(1) immediate decrease in the spinal stiffness at L3 and
(2) immediate increase in the LM contraction thickness at L4–L5 during contralateral arm lifting. [9, 10]
Intervertebral disc (IVD) properties have also demonstrated a similar association with those who respond positively to SMT. Beattie and coworkers  found that patients with LBP who experienced clinically significant post-SMT reduction in pain showed statistically significant increases in water diffusion within the L1–L2, L2–L3, and L5–S1 discs, whereas patients without reduction in post-SMT LBP did not.
Individually, these prior studies suggest that several specific biomechanical measures change in SMT responders and are consistent with the assumption that SMT exerts its therapeutic effect through biomechanical and/or neurophysiological mechanisms. [12–14] Unfortunately, our understanding of the mechanisms underlying differential post-SMT responses in patients with LBP remains limited for several reasons. First, these studies employed different methodologies in different samples. It remains unknown whether these same post-SMT changes would exist within the same sample. Second, no prior study has included specific control groups to establish whether post-SMT biomechanical changes significantly differ from the variance in these same measures. Third, prior studies used the minimal clinically important difference to assess clinical significance. Although the minimal clinically important difference is a useful tool, it is an approximation.  Methodologically, if asymptomatic controls are used instead, then the absolute magnitudes of outcome measures in post-treatment participants can be compared with outcome magnitudes in asymptomatic controls for a more robust estimation of clinical relevance. Finally, it is unknown whether as a group, post-SMT changes in spinal stiffness, muscle contraction, and disc diffusion are related to LBP disability after 7 days. [9, 10] Assessment of disability at 1 week is ideal as it predicts clinical outcomes at 1 and 3 months. 
As discussed previously, the objective of this study was to determine whether patients with LBP who respond to SMT differ biomechanically from nonresponders, untreated controls, or asymptomatic controls.
MATERIALS AND METHODS
Participants aged 18 to 60 years with or without LBP were recruited from advertisements in local health care facilities and universities. Inclusion criteria for participants with LBP were LBP with or without leg symptoms, LBP intensity of at least 2 on the 11-point numeric pain rating scale,  and mODI score of at least 20%.  Exclusion criteria were “red flag” conditions, signs of nerve root compression, scoliosis, osteoporosis, joint hypermobility syndrome, previous lumbosacral surgery, and SMT/stabilization exercise treatment in the last 4 weeks. Individuals with LBP were enrolled into either the treatment (+LBP/+SMT) or untreated LBP control (+LBP/-SMT) group if they possessed either
(a) 4 or more of 5 CPR characteristics (predicted responders)
(see Supplemental Digital ContentAppendix I) or
(b) 2 or less CPR characteristics (predicted nonresponders). 
Individuals with exactly 3 characteristics were excluded. [9, 10] Approximately equal proportions of CPR-predicted responders (43.8%) and nonresponders (56.2%) were enrolled into the +LBP/+SMT or +LBP/–SMT group (see later). Importantly, the same screening strategy for recruiting potential responders and nonresponders has been used in prior SMT studies. [9, 10] Using the same recruitment methods, asymptomatic controls were enrolled with inclusion criteria of no current LBP and no history of LBP that required sick leave in the last 12 months. Participants provided informed consent via processes approved by the Human Research Ethics Board at the University of Alberta.
Participants With LBP Receiving SMT (+LBP/+SMT)
Thirty-two participants with LBP attended 3 sessions for more than 7 days (Figure 1). On session 1 (between 8:00 AM and 12:00 PM), participants with LBP reported baseline demographics, underwent a clinical examination, and completed the mODI. In addition, 3 biomechanical outcome measures were collected before, and after, the provision of SMT:
spinal stiffness through mechanized indentation,
LM contraction thickness from ultrasonography, and
apparent diffusion coefficient (ADC) of each lumbar disc via diffusion-weighted imaging (DWI).
On session 2 (3–4 d later, from 0800 to 1200), the same variables were repeated with the exception of ADC. During session 3 (day 7), only spinal stiffness and LM contraction were collected together with the mODI. The data collection was arranged in the morning to minimize the potential diurnal fluctuation in disc diffusion though prior research revealed no significant diurnal change in ADC values in the center of the nucleus pulposus of lumbar discs. 
Participants With LBP Not Receiving SMT (+LBP/–SMT)
A group of 16 LBP controls were taken through the same procedures outlined for session 1 but did not receive SMT or any further sessions (Figure 1).
Measurements included self-reported questionnaires, baseline and follow-up clinical examination, spinal stiffness assessment, and lumbar multifidus measurements using ultrasonography. Eligibility involved screening for inclusion and exclusion criteria.
LBP incicates low back pain MRI = magnetic resonance imaging
Asymptomatic Participants Not Receiving SMT (–LBP/–SMT)
Fifty-nine asymptomatic participants completed sessions 1, 2, and 3 without SMT and without DWI
Based on assessment at session 3, +LBP/+SMT participants were classified as SMT responders (a cutoff of ≥30% reduction in baseline mODI scores) or nonresponders (<30% reduction in baseline mODI scores). This cutoff represents an estimation of the minimal clinically important change in LBP-related disability. 
The ADC values in the first and second scans of +LBP/–SMT participants were compared with those of SMT responders/nonresponders. The spinal stiffness and LM thickness of SMT responders/nonresponders at various measurement time points were compared with those of –LBP/–SMT participants.
LBP-related disability was measured by mODI given its high reliability, validity, and responsiveness. 
Spinal stiffness was measured by a mechanical indentation device whose operation and reliability have been published previously (Figure 2).  Briefly, the device consists of a motorized indenter controlled by customized software (National Instruments, Austin, TX) used to control the loading velocity (2 mm/s) and collect force and displacement signals.  The L3 spinous process was identified in the participant in the prone position by ultrasonography. Spinal stiffness at the L3 level was measured during held exhalation. [9, 21] Stiffness was calculated as the slope of the force-displacement curve from a 5N preload to a maximal load of 60N. [9, 21] Three indentations were performed before, and after, SMT applications, with the mean of each set of 3 trials used for statistical analysis.
Mechanical Spinal Stiffness Test
Wach a video of this measuring device in action
The LM thickness ratio was quantified at L3–L4 and L4–L5 by ultrasonography — a valid proxy for LM activity having high reliability. [22–24] Ultrasonography was performed by a single examiner using video from a SonixTouch Q+ (Ultrasonix, Peabody, MA) and a 5-MHz curvilinear transducer. For participants with LBP, ultrasonography was performed on the more symptomatic side and on a random side for asymptomatic participants. Each participant in the prone position raised a weight (1.5–3.0 lb) 3 times in the contralateral hand to touch a bar fixed at a 5-cm height  toward creating a 30% maximal voluntary contraction.  From the recorded video, a blinded examiner selected the frame from the video, showing the LM at rest and then again at maximal contraction thickness. The mean of 3 LM thickness ratios was used for each measurement point in the protocol where thickness ratio was calculated as
using the distance between the posterior-most tip of the target facet joint and the thoracolumbar fascia (Figure 3, Image J software, National Institutes of Health, Bethesda, MD). [22, 25] For all imaging, the ultrasound transducer was fixed in the same position via a mechanized arm.
LM indicated lumbar multifidus.
All participants with LBP underwent DWI with a 1.5 Tesla imager (MAGNETOM Symphony, Siemens Medical Solutions, Malvern, PA) at the beginning and the end of their first/single visit. Scan parameters are listed in Table 1. Sagittal diffusion-weighted images were acquired using a single shot, dual spin echo, echo-planar imaging acquisition with multielement spine coils and abdominal coils. A total of 15 sagittal slices were obtained per participant.
Diffusion-weighted Imaging Parameter.
For each slice, DWI was obtained by applying diffusion gradients in 3 orthogonal directions.  The mean ADC was constructed on the basis of averages of signal intensity from 3 directional diffusion-weighted images.  To quantify lumbar IVD diffusion, the ADCs of all lumbar IVDs were measured from the midsagittal ADC maps. A blinded examiner then used a customized program (MathWorks, Natick, MA) to place a 40-mm2 circular region of interest (ROI) in the central, nuclear portion of each lumbar IVD to minimize the inclusion of vertebral bodies and/or endplates (Figure 4). The program calculated ADC from signal intensity within the ROI. If the ROI diameter larger than the IVD height, the segment was excluded. [26, 27] It is thought that ADC is a proxy for IVD diffusion; a high ADC value indicated high IVD diffusion. 
An apparent diffusion coefficient (ADC) map of a 32-year old male with low back pain.
The circles represent the regions of interest for measuring the mean ADC values of various lumbar intervertebral discs.
To establish the intrarater reliability of ADC measurements, 3 weeks after the initial ADC measurements, the examiner who was blinded to previous measurement results repeated the ADC measurements on the scans of 16 randomly selected participants.
Spinal Manipulative Therapy
A standardized application of SMT as described by the CPR derivation study was provided to relevant participants (see Supplemental Digital ContentAppendix 2). [1, 6] This technique applies a posteroinferior thrust to the patient's pelvis. A maximum of 2 thrusts were delivered to each side of the subject during each session.
Descriptive statistics were calculated for demographic data and outcome values for each group at each assessment. Continuous and categorical demographic data of various groups were compared by 1-way analysis of variance and χ2 test, respectively. Baseline physical characteristics of LBP and asymptomatic participants were compared by independent t tests. The significance level was set at 0.05.
The intraobserver reliability of ADC measurements at each vertebral level was analyzed by intraclass correlation coefficients (ICC3,1).
The serial changes in spinal stiffness and LM thickness ratios among groups were analyzed by separate repeated measures analyses of covariance, with time as a repeated measure, and group (LBP status and responder/nonresponder as defined by mODI) as the between-subject factor. The assumptions of analyses of covariance were evaluated. If the assumption of sphericity was violated, the Greehouse-Geisser correction was chosen to interpret the results.  The post hoc tests included simple effect tests and tetrad analyses,  with Bonferroni adjustment. Separate analyses of covariance were used to analyze the baseline and changes in diffusion at various IVD levels among LBP controls, responders, and nonresponders after the first SMT. The covariates for all tests were age, sex, and body mass index because prior research has suggested that these covariates may affect the measured physical variables. [9-11, 28, 31, 32]
Pearson correlation was calculated to analyze the associations among the percent change in spinal stiffness, LM thickness ratios, and ADC values after the first SMT in +LBP/+SMT participants using pooled data. The effect sizes of correlation were considered to be small, medium, and large if coefficients were 0.10, 0.30, and 0.50, respectively. 
Although no participant dropped out from the +LBP/+SMT or +LBP/–SMT group, 2 asymptomatic participants dropped out after session 1 because of time conflicts, leaving 57 asymptomatic controls in this study. The LM muscle boundaries of 1 LBP participant and 2 asymptomatic participants were unidentifiable, leaving complete data of ultrasonography on 86 participants. After assessment of mODI results, 15 participants with LBP were classified as SMT responders and 17 as nonresponders.
Reliability of ADC Measurements
Of the 80 IVDs from 16 participants evaluated in this study, 4 IVDs were excluded from the ADC measurements because the disc space was smaller than the ROI. The intraclass correlation coefficient estimates ranged from 0.97 to 0.98.
Baseline Characteristics Between Groups
Baseline characteristics of participants are depicted in Table 2. Compared with participants with LBP, asymptomatic controls had significantly less prior LBP episodes and lower mODI scores. At baseline, there was no significant difference in spinal stiffness or LM thickness ratio among the –LBP/–SMT, responder, and nonresponder groups (Table 2). There was no significant difference in baseline lumbar IVD diffusion among +LBP/–SMT controls, responders, and nonresponders.
Descriptive Analysis of Demographic and Baseline Data in Different Groups
(Mean ± Standard Deviation or Standard Error)
Post-SMT Change in Spinal Stiffness
The spinal stiffness of SMT responders was significantly reduced after each SMT (interaction for group-by-time:
F5,332 = 10.50, P < 0.01,
post hoc after each SMT, P < 0.05) (Figure 5), whereas the SMT nonresponders and –LBP/–SMT group showed no such change. These changes were sustained at day 7. Post hoc tests demonstrated that the responders' mean spinal stiffness at session 3 was significantly lower than their baseline values (average difference: –0.255 N/mm, 95% confidence interval [CI]: –0.079 to –0.431 N/mm).
Mean L3 spinal stiffness in asymptomatic controls and responser/nonresponder groups.
Error bars are standard error of the mean. Both the asymptomatic controls and nonresponders did not show statistically significant temporal changes in spinal stiffness.
* Statistically significant decrease or increase in mean spinal stiffness of the responders as compared with the previous measurement (P = <0.01)
† Statistically significant decrease in mean spinal stiffness of the responders with reference to the corresponding baseline values (P = <0.01).
Post-SMT Change in LM Thickness Ratios
SMT responders demonstrated significant increases in LM thickness ratios after the first SMT (interaction for group-by-time for L3–L4: F8,320 = 22.33, P < 0.01; L4–L5: F8,320 = 18.21, P < 0.01, post hoc test, P < 0.01) (Figure 6A, B). These improved post-SMT LM thickness ratios were sustained for more than 1 week (average difference of thickness ratio at L3–L4 LM: 3.83%, CI: 2.62%–5.04%; mean difference of L3–L4 LM: 4.38%, CI: 2.77%–5.98%). No similar change was noted in the nonresponders and the –LBP/–SMT group.
Figure 6. A and B, Mean L3–L4 and L4–L5 lumbar multifidus (LM) thickness ratio during a contralateral arm-lifting task in asymptomatic controls, responders, and nonresponders.
Error bars are standard error of the mean. Both the asymptomatic controls and nonresponders did not show statistically significant temporal changes in the L3–L4 or L4–L5 LM thickness ratio during a contralateral arm-lifting task.
* Statistically significant increase in the mean L3–L4 or L4–L5 LM thickness ratio of the responders as compared with the previous measurement (P < 0.01).
† Statistically significant decrease in the mean L3–L4 or L4–L5 LM thickness ratio of the responders with reference to the corresponding baseline values (P < 0.01). SMT indicates spinal manipulative therapy.
Post-SMT Change in IVD Diffusion
The inferior 3 lumbar IVDs showed significant between-group changes in ADC values (L3–L4: F2,42 = 8.66, P < 0.01; L4–L5: F2,41 = 19.93, P < 0.01; L5–S1: F2,41 = 6.45, P < 0.01) (Figure 7). Post hoc tests showed that only SMT responders had significant increases in diffusion within the L3–L4, L4–L5, and L5–S1 discs (P < 0.01) whereas no significant change was noted in the nonresponders, nor in the –LBP/–SMT group (average differences in percent changes of ADC values between responders and +LBP/–SMT group at
L3–L4 disc: 4.91%, CI: 1.94%–7.87%;
at L4–L5 disc: 6.50%, CI: 3.88%–9.13%; and
at L5–S1 disc: 8.15%, CI: 4.14%–12.15%).
The percent changes in mean ADC values of lumbar discs in untreated low back pain controls and the responders and nonresponders after the first spinal manipulative therapy.
Error bars are the standard error of the mean.
* Responders demonstrated significantly larger increases in disc diffusion than the untreated low back pain controls and nonresponders after the first spinal manipulative therapy, but significant difference was noted among the untreated low back pain controls and nonresponders across all disc levels. ADC indicates apparent diffusion coefficient.
Post-SMT Associations Between Outcome Change Scores
After SMT application on session 1, decreases in spinal stiffness of participants with LBP were significantly associated with an increased LM thickness ratio at all measured levels (r = ?0.59, P < 0.01) as well as with ADC values in the discs of L3–L4 and L4–L5 (r = ?0.42 and ?0.50, respectively, P < 0.01). Similarly, the percent increase in LM thickness ratio after the first SMT application was related to the corresponding increase in L3–L4 and L4–L5 disc diffusion (r = 0.35–0.47) (Table 3).
Zero-Order Correlations Among Percent Change in the
Mean L3 Global Stiffness,
Mean L3–L4 Thickness Ratio,
Mean L4–L5 Thickness Ratio,
Mean L3–L4 Apparent Diffusion Coefficient (ADC) Value, and
Mean L4–L5 ADC Value After the First Spinal Manipulative Therapy
The current study is the first to determine that multiple biomechanical outcomes (physical and imaging) respond differently in those reporting improvement after SMT compared with those who do not report improvement. Importantly, key comparison and control groups were included in our methodology to minimize the possibility that our observations were due to measurement variability (+LBP/?SMT). Our results consist of several important findings. First, after 1 SMT application, SMT responders show immediate and sustained alterations in spinal biomechanics. These post-SMT changes are statistically significant compared with nonresponders and overlap with measures observed in asymptomatic controls. The differential responses of patients with LBP imply that certain unidentified biomechanical characteristics of nonresponders (e.g., spinal degeneration) may impede the effect of SMT. Alternatively, the large between-subject variations (standard deviations) in spinal stiffness and LM thickness ratios at baseline (Table 2), the small to medium effect sizes of these comparisons, or low statistical power might have prevented the identification of significant between-group difference in these characteristics at baseline. Our results justify continued investigations into characteristics defining SMT responders at baseline.
Several studies have demonstrated that various biomechanics of SMT responders change compared with nonresponders. [9-11]
Comparatively, our results are a significant development in that they
(1) demonstrate that the various outcome measures that were responsive in prior individual investigations are also responsive when studied with a unified methodology in the same subjects and that
(2) these same measures are moderately to strongly associated with each other.
Furthermore, our addition of untreated controls allows for more robust conclusions regarding a selective treatment response between SMT responders and nonresponders. Specifically, the inclusion of nontreatment controls (+LBP/?SMT) showed that variation due to measurement or due to the LBP itself is insufficient to confound post-SMT changes in the responder group. Given that SMT responders showed significantly greater changes in biomechanical outcomes than nonresponders, we can say with increased confidence that changes in the SMT responders are more likely the result of SMT and less likely from treatment variability, measurement variability, or variability in the target condition. In other words, the biomechanical changes in SMT responders were clinically relevant. Importantly, the observation that self-reported measures of function are coherent with objective, physical measures in both the SMT responders and nonresponders implies that self-reports of spinal function and spinal biomechanics are related.
The observation that a specific group of participants responds to SMT is consistent with prior studies that show a change in stiffness and/or LM thickness ratio after SMT and, in particular, those studies that show a varied therapeutic benefit in subjects with nonspecific LBP. [9, 10, 34] This suggests that SMT is not a broad-spectrum therapy but one that impacts factors within SMT responders that are not present in all persons with LBP. Given the observed correlations between our biomechanical outcome measures (spinal stiffness, LM thickness ratio, ADC), we would suggest that the differential response of participants with LBP to SMT is based on a biomechanical mechanism. Although the mechanism remains unknown, it is biologically plausible that decreases in spinal stiffness may permit increased disc diffusion and increased segmental motion enabling increased LM thickness ratios. The increased disc diffusion may also improve IVD health and yields favorable clinical outcomes.  Although our data do not prove the existence of LBP subgroups, they do reinforce that LBP is a heterogeneous condition and that in the short term, SMT does not equally affect those who experience LBP.
As with all studies, this investigation has limitations that restrict its interpretation. First, ADC measures were taken only in participants with LBP. We assumed that the diffusion within the discs of asymptomatic participants would not change significantly given prior research.  Importantly, we did obtain ADC values from +LBP/?SMT to control for the magnitude of ADC measurement variability over the time it would have taken to provide SMT in the +LBP/+SMT group. The measured ADC values were also comparable with prior studies. [27, 36] Second, SMT was not given to asymptomatic participants, which may have allowed us to further determine the differential impact of SMT (i.e., Do asymptomatic individuals show post-SMT decreased stiffness or are asymptomatic stiffness values already minimal?). Third, as the pain intensity and disability level of the +LBP/+SMT and +LBP/?SMT groups were relatively low, our results may not be generalized to individuals with severe LBP.
Our results demonstrate that those reporting post-SMT improvement in disability have coherent changes in multiple, objective measures of spinal biomechanics. This same coherence does not exist for asymptomatic controls or no-treatment symptomatic controls. Our data further support a differential effect of SMT on a specific constellation of biomechanical outcomes that are not responsive in all patients with LBP. This work provides a foundation from which to investigate the heterogeneous nature of LBP, the mechanisms underlying differential therapeutic response, and the biomechanical characteristics defining the responders at baseline.
Responders to spinal manipulative therapy for low back pain are characterized by an immediate and sustainable decrease in spinal stiffness and an increase in lumbar multifidus muscle thickness ratio.
In comparison, spinal manipulative therapy nonresponders and asymptomatic controls showed no change in spinal stiffness or lumbar multifidus contraction ratio.
Immediate enhancement of lumbar disc diffusion was observed after the first spinal manipulative therapy in participants who reported improved back pain–related disability at 1 week.
The authors express their gratitude to Magnetic Imaging Consultants for providing advice and scan services. The authors are very grateful to the River Valley Health Clinic for providing professional SMT and clinical space. They also thank Mr. Karl Brandt and Ms. Carolyn Berendt for assisting the coding and decoding of various spinal stiffness, ultrasound imaging, and magnetic resonance imaging files.
Supplemental digital content is available for this article. Direct URL citations appearing in the printed text are provided in the HTML and PDF version of this article on the journal's Web site (http://www.spinejournal.com)
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