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This thesis is presented for the Honours degree in Science (Chiropractic) at Murdoch
University
THE EFFECT OF LUMBAR SPINAL MANIPULATION UPON LOCAL AND REMOTE
DEEP AND SUPERFICIAL PAIN PERCEPTION
Student Researcher
Dr Sasha Louise Dorron
B.Sc (Chiro), B.Chiro, PostgradCertBusAdmin (MasterClass)
Primary Supervisor
Dr Barrett Losco
Chiropractic Discipline, School of Health Professions, Murdoch University
Co-Supervisors
Professor Peter Drummond
Psychology Discipline, School of Psychology and Exercise Science, Murdoch University
Associate Professor Bruce Walker
Head of Chiropractic Discipline, School of Health Professions, Murdoch University
Submitted
November 2015
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I declare this thesis is my own account of my research and contains as its main content, work which
has not been previously submitted for a degree at any tertiary educational institution.
Dr Sasha Louise Dorron
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Abstract
Introduction: The mechanism for pain relief associated with spinal manipulation (SM) is not well
understood. Cervical SM decreases pressure sensitivity in the cervical spine and upper limb for at
least 10 minutes. Lumbar spine studies to date have demonstrated no effect.
Objectives: To determine whether lumbar SM has an effect on pressure pain threshold (PPT) and
pinprick sensitivity (PPS) at local and remote locations, the duration of any change, and whether
changes are related to the side of SM.
Methods: 34 asymptomatic participants, mean age 22.56 years (SD 3.99), were randomised to
receive a lumbar SM on the right or left side. PPT and PPS were measured bilaterally at the calf,
lumbar spine, scapula, and forehead at baseline, immediately post-SM, and after 10, 20, and 30
minutes. Effects of SM on PPT and PPS were investigated in repeated-measures ANOVAs.
Results: Calf and lumbar spine PPT increased bilaterally at 10, 20 and 30 minutes (7.2 - 11.8%
changes). PPS decreased in all locations at various times (9.8 – 22.5% changes). For the calf and
lumbar spine, increases in PPT tended to be greater on the side of SM compared to contralaterally,
although this varied over the follow-up period. Throughout the experiment, the left lumbar spine and
calf were more sensitive to pressure than the right, whereas the right calf and forehead were more
sensitive to pinprick than the left.
Conclusion: Lumbar SM appears to reduce pressure sensitivity locally and in the lower limb for at
least 30 minutes. These findings contradict prior lumbar spine studies, but are consistent with
cervical spine studies. The observed changes in pressure sensitivity may reflect local spinal or
complex supraspinal analgesic mechanisms. Pinprick sensitivity was reduced globally, and likely
represents a non-specific effect. However, a lack of control/sham limits the strength of the
conclusions.
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Table of Contents
1. Introduction .............................................................................................................................. 1
1.1. Topic and Purpose ....................................................................................................................... 2
1.2. Background on Spinal Manipulation ........................................................................................... 3
1.2.1. Force Time Characteristics of Spinal Manipulation ............................................................ 3
1.2.2. Clinical Application of Spinal Manipulation ........................................................................ 4
1.2.3. The Cavitation Phenomenon .............................................................................................. 4
1.3. Spinal Manipulation and Hypoalgesia ......................................................................................... 5
1.3.1. Pressure Pain Threshold ...................................................................................................... 7
1.3.1.1. Local Effects ................................................................................................................ 7
1.3.1.2. Remote Effects .......................................................................................................... 10
1.3.1.3. Sham-Controlled Studies .......................................................................................... 13
1.3.1.4. Asymmetric Effects ................................................................................................... 19
1.3.1.5. Other Factors ............................................................................................................ 19
1.3.2. Pinprick Sensitivity ............................................................................................................ 21
1.3.3. Thermal, Chemical, and Electrical Stimuli ......................................................................... 21
1.3.4. Biomechanical Factors ...................................................................................................... 22
1.3.5. Neurophysiological Factors ............................................................................................... 24
1.3.6. Biochemical Factors .......................................................................................................... 25
1.3.6.1. β-endorphins ............................................................................................................. 25
1.3.6.2. Substance P ............................................................................................................... 25
1.3.6.3. Cortisol ...................................................................................................................... 26
1.3.6.4. Other Biochemicals ................................................................................................... 27
1.3.7. Theories for Post-Manipulation Hypoalgesia.................................................................... 28
1.3.7.1. Descending Inhibitory Pain Control Theory .............................................................. 28
1.3.7.2. Pain Gate Theory....................................................................................................... 31
1.3.7.3. Altered Spinal Cord Dorsal Horn Excitability ............................................................ 31
1.3.7.4. Placebo and Psychosocial Factors ............................................................................. 32
1.4. State of the Literature ............................................................................................................... 32
2. Methods ................................................................................................................................. 33
2.1. Power Calculation ..................................................................................................................... 34
2.2. Participant Recruitment ............................................................................................................ 34
2.3. Randomisation .......................................................................................................................... 35
2.4. Procedure .................................................................................................................................. 35
2.5. Pressure Pain Threshold ............................................................................................................ 37
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2.6. Pinprick Sensitivity ..................................................................................................................... 38
2.7. Spinal Manipulation ................................................................................................................... 38
2.8. Data Analysis .............................................................................................................................. 39
3. Results ................................................................................................................................... 40
3.1. Algometer Standardisation ........................................................................................................ 40
3.2. Pain Sensitivity Results............................................................................................................... 40
3.2.1. Calf Pressure Pain Threshold ............................................................................................. 43
3.2.2. Lumbar Spine Pressure Pain Threshold ............................................................................. 45
3.2.3. Scapula Pressure Pain Threshold ....................................................................................... 47
3.2.4. Forehead Pressure Pain Threshold .................................................................................... 49
3.2.5. Calf Pinprick Sensitivity ...................................................................................................... 52
3.2.6. Lumbar Spine Pinprick Sensitivity ...................................................................................... 53
3.2.7. Scapula Pinprick Sensitivity................................................................................................ 55
3.2.8. Forehead Pinprick Sensitivity ............................................................................................. 56
3.2.9. Ipsilateral vs. Contralateral Changes ................................................................................. 58
4. Discussion .............................................................................................................................. 64
4.1. Baseline Characteristics ............................................................................................................. 64
4.2. Pressure Pain Threshold ............................................................................................................ 65
4.3. Pinprick Sensitivity ..................................................................................................................... 68
4.4. Interpretation ............................................................................................................................ 68
4.5. Limitations ................................................................................................................................. 71
5. Conclusion .............................................................................................................................. 72
References ............................................................................................................................. 74
Appendix A – Participant Checklist and Medical History Questionnaire .................................... 83
Appendix B – Information Letter ............................................................................................. 84
Appendix C – Consent Form .................................................................................................... 86
Appendix D – Shapiro-Wilk tests for Normality Results ............................................................ 87
vi
Acknowledgements
Firstly, I would like to express my sincere gratitude to my primary supervisor Dr Barrett Losco. His
continuous support, guidance, and patience have been priceless. Even amongst his very busy
schedule, he always had time for my unsolicited visits and endless questions. I could not have
imagined having a better advisor and mentor to ease me into the daunting world of research.
I would also like to sincerely thank my co-supervisor Professor Peter Drummond, for his willingness
to venture into something of a new area of study and his excellent statistics knowledge. His patience
in helping me learn the ins and outs of the stats was invaluable, as were his comments and attention
to detail.
I cannot forget my final co-supervisor Associate Professor Bruce Walker. A huge thanks go to him for
guiding me through many of the broader research concepts, giving me a good foundation for future
research. At times I struggled to see the forest for the trees, and he helped a great deal in widening
my perspective.
My thanks also go to Dr Norman Stomski and Dr Jeffrey Hebert for their help and advice in the
complicated world of statistics, to Dr Amanda Meyer and my dear friend Amy for their support in the
recruitment drive, and to Dr Gareth Calvert for being an understanding boss over the last two years.
Last but not least, a huge thank you to my fiancée Sam, my family, and my friends. For your
continuing support through this journey and in my grand plans for the future. For keeping me
grounded, coaxing me away from the keyboard, and making me laugh through it all. This would not
have been possible without you.
vii
List of Abbreviations
Abbreviations used in the following text are:
HVLA = high-velocity, low-amplitude
LBP = lower back pain
L-SM = group 2, receiving left L5-S1 spinal manipulation
MDC = minimum detectable change
NRS = numerical rating scale
PAG = periaqueductal gray
PPT = pressure pain threshold
PPS = pinprick sensitivity
R-SM = group 1, receiving right L5-S1 spinal manipulation
SM = spinal manipulation
SD = standard deviation
TSS = temporal sensory summation
Vertebral segments are described using the following paradigm:
C1 = first cervical vertebra (of seven)
T1 = first thoracic vertebra (of twelve)
L1 = first lumbar vertebra (of five)
C0-C1 = joint between occiput and first cervical vertebra
C5-C6 = joint between fifth and sixth cervical vertebrae
L5-S1 = joint between fifth lumbar vertebra and sacrum
1
1. Introduction
Spinal manipulation (SM) is a manual therapy technique which is used within a number of health
care professions, particularly by chiropractors as well as osteopaths and physiotherapists
(Hurwitz 2012). It is primarily used in the treatment of musculoskeletal disorders including non-
specific lower back pain (LBP) and neck pain, among others. Current evidence supports the use
of SM in these scenarios, showing that it may be helpful in managing spinal pain and some types
of headache (Bronfort et al. 2012; Bryans et al. 2011; Giles and Muller 2003; Goertz et al. 2012;
Gross et al. 2010; Schneider et al. 2015). There is however a lack of evidence to explain the
physiological mechanism behind any positive clinical outcomes such as pain reduction. In
particular, this study is interested in further characterising hypoalgesia, or decreased pain
sensitivity, following SM. Gaining a better understanding of any hypoalgesia associated with SM
may improve its clinical application, allowing for practitioners to make better choices with
regard to when and where to apply SM.
Since SM is typically a regular component of the care delivered by a chiropractor (French et al.
2013), the topic of how SM exerts its clinical effects is a key area of research that could help
modernise the role of chiropractic in the health care arena. By facilitating greater understanding
of this technique the usefulness of SM may be better understood and applied with specificity
and improved clinical outcomes.
Improving our understanding of SM is an important area. LBP, for example, represents a
significant economic burden in Australia (Walker, Muller, and Grant 2003) and affects on
average 38% of people globally at some time (Hoy et al. 2012). Most cases of LBP are “non-
specific” or “mechanical” and thus conservative or non-invasive treatment options are most
appropriate (Cohen, Argoff, and Carragee 2009). Research into these conservative options,
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which includes SM, is of paramount importance in enabling health care providers to address
significant health concerns such as LBP from an evidence-based perspective.
1.1. Topic and Purpose
This study aims to investigate the effects of lumbar SM on local and remote pain sensitivity for
30 minutes following SM, as well as whether the effects are dependent on the side of SM.
The objective is to help fill significant gaps in our present knowledge surrounding the underlying
pain-relieving mechanisms of this modality. Specifically, the lumbar spine remains an area that
is understudied, with conflicting findings between the lumbar and cervical regions. The present
study will also investigate whether remote effects of SM on pain sensitivity are related to the
site of manipulation, or are global. The duration of changes to pain sensitivity following SM
beyond five to ten minutes is also a poorly studied topic, and thus this study will measure
changes up to 30 minutes following SM. The duration of changes to pain sensitivity is important
when considering the clinical value of SM.
In addition, it is unknown whether the effects of SM on pain sensitivity are dependent on which
side the SM is applied to. A greater understanding of this relationship may contribute to the
targeted use of SM in a clinical setting.
A novel measure of superficial pain sensitivity will be assessed alongside a more commonly
studied measure of deep pain sensitivity to enhance our understanding of the relationship
between SM and pain sensitivity.
3
1.2. Background on Spinal Manipulation
There is significant variety in the specific SM techniques used by practitioners (Bergmann 2005).
High-velocity low-amplitude (HVLA) SM techniques are the most commonly utilised by
chiropractors, and involve a “quick thrust carried through a short distance” to a specific spinal
joint, using the practitioner’s hands (Bergmann 2005). Other techniques may variably utilise low-
force or non-thrust methods, or are delivered using instruments or other devices to assist
(Bergmann 2005). The bulk of the literature surrounding SM uses HVLA techniques, as does the
present study. As such, all future references to SM will refer specifically to HVLA SM, unless
specified.
It is theorised that the neurophysiological and clinical effects of different techniques may vary
(Bergmann 2005), though our understanding is limited at present. HVLA SM has unique
characteristics in terms of the forces applied to the spine, and the time over which these forces
are delivered. These are known as the force-time characteristics, and are discussed in section
1.2.1. The cavitation phenomenon frequently associated with SM is also discussed in section
1.2.3.
1.2.1. Force-Time Characteristics of Spinal Manipulation
An HVLA SM procedure has a distinct force-
time profile. It consists of a preload phase
followed by a rapid thrust phase where the
applied forces increase to a peak, which then
fall again after the thrust is completed
(Herzog 2010) (see Figure 1.1). In a review of
the topic by Herzog (2010), it is concluded
that preload and peak forces vary significantly by region. Peak forces are on average 400
Figure 1.1. HVLA spinal manipulation force-time characteristics.
4
newtons in the lumbosacral region (Herzog 2010). There is also significant inter-practitioner
variation (Herzog 2010). Thrust times also vary, with lumbosacral HVLA SM thrusts being on
average 150 milliseconds (from the beginning of the thrust to the time of peak force) (Herzog
2010). Thus the mechanical stimulus applied to the spine during an HVLA SM varies depending
on the region and the practitioner.
1.2.2. Clinical Application of Spinal Manipulation
In a clinical setting, SM is typically performed on a suspected ‘dysfunctional’ spinal joint
(Bergmann and Peterson 2011). ‘Dysfunctional’ spinal joints are identified clinically using a
variety of patient history and physical examination factors (Walker and Buchbinder 1997). It is
anecdotally held that SM can restore the ‘dysfunctional’ segment to ‘normal’ (Bergmann and
Peterson 2011). It has however been shown that the identification of a ‘dysfunctional’ spinal
joint has quite poor inter-rater reliability (French, Green, and Forbes 2000).
In the following discussion, specific spinal vertebrae or joints will be described using the method
most commonly employed in chiropractic practice. “C1” would denote the first of seven cervical
vertebra, while “T1” and “L1” would denote the first (of twelve) thoracic and first (of five) lumbar
vertebrae respectively. “C5-C6” then describes specifically the joint between the fifth and sixth
cervical vertebrae. “C0” refers to the occiput (having a joint with the first cervical vertebra), and
“S1” refers to the sacrum.
1.2.3. The Cavitation Phenomenon
HVLA SM techniques are often associated with a ‘cracking’ or ‘popping’ noise heard by patients
and practitioners, called an audible release or cavitation (Bergmann 2005). This phenomenon is
believed to represent the sudden formation and collapse of a gas bubble within a facet joint
capsule following an SM procedure, as a result of altered intra-articular pressure (Bergmann
2005). This cavitation does not typically occur with non-HVLA techniques, but is sometimes
5
heard during mobilisation procedures (Bergmann and Peterson 2011). It is unclear if the
occurrence of a cavitation is necessary to elicit clinical or physiological changes, but clinically it
is often used as a marker of the ‘success’ or ‘non-success’ of a SM procedure (Bergmann and
Peterson 2011). Most studies to date have found no difference in a variety of clinical or
physiological outcomes, whether a cavitation did or did not occur during a SM procedure
(Bialosky et al. 2010; Cleland et al. 2007; Flynn, Childs, and Fritz 2006; Flynn et al. 2003; Herzog
et al. 1995; Sillevis and Cleland 2011; Teodorczyk-Injeyan et al. 2008). Some studies have
however noted that an HVLA SM procedure that elicited a cavitation showed unique mechanical
properties or effects compared to procedures that did not elicit a cavitation (Cramer et al. 2012;
Gál et al. 1995). This suggests that SM procedures that elicit a cavitation may differ in their
mechanical effect on facet joints, but appear not to influence outcomes.
Several studies have revealed that HVLA SM may not be particularly accurate when comparing
where force is delivered and where cavitations occur, with around 50% accuracy depending on
the region of the spine (Dunning et al. 2013; Ross, Bereznick, and McGill 2004). We can surmise
from this that HVLA SM affects multiple facet joints in the broad vicinity around the target
segment (Cramer et al. 2011; Dunning et al. 2013; Ross, Bereznick, and McGill 2004).
1.3. Spinal Manipulation and Hypoalgesia
The majority of the literature investigating SM and hypoalgesia uses pressure pain threshold
(PPT) as the primary outcome measure. PPT is a form of experimentally-induced pain, and
represents the force required for mechanical pressure to elicit a nociceptive sensation.
Nociceptive signals are generated in response to potentially harmful stimuli (Mendell 2014).
Pinprick sensitivity (PPS) is another form of experimentally-induced pain, where a sharp stimulus
is applied to the skin and the resulting sensation subjectively measured.
6
The nociceptive stimulus when measuring
PPT is generated by activating Aδ (small
diameter, thinly myelinated) and C (small
diameter, unmyelinated) sensory fibres
(Curatolo, Petersen-Felix, and Arendt-
Nielsen 2000; Julius and Basbaum 2001).
PPS is thought to be elicited through
stimulation of Aδ-fibres only (Curatolo,
Petersen-Felix, and Arendt-Nielsen 2000).
The afferent signals travel to lamina I and
V in the dorsal horn of the spinal cord and
ascend within the spinothalamic tract (Blumenfeld 2010) (see Figure 1.2). PPT (when measured
with a 1cm2 probe) appears to reflect sensitivity to deep mechanical stimulus, while PPS is a
measure of more superficial sensitivity (Takahashi et al. 2005).
There are a number of potentially confounding variables that affect pain sensitivity. It appears
that anxiety causes increased sensitivity to experimentally-induced pain, termed anxiety-
induced hyperalgesia (Martenson, Cetas, and Heinricher 2009; Rhudy and Meagher 2000). There
is a moderate to strong body of evidence to suggest that females have lower PPT compared to
males, while the effects of gender on PPS do not appear to have been studied (Fillingim et al.
2009; Racine et al. 2012). Many studies have also investigated the effects of the menstrual cycle
on experimental pain. The studies are conflicting, and at present no conclusion can be made
with regard to how PPT or PPS might be affected by the menstrual cycle (Fillingim et al. 2009;
Racine et al. 2012).
Figure 1.2. C-fibre and Aδ-fibre pathways.
7
1.3.1. Pressure Pain Threshold
A recent systematic review by Coronado et al. (2012) included a meta-analysis on the effects of
SM on PPT. It was found that SM appeared to significantly increase PPT at sites remote to the
site of SM (the remote sites under investigation varied with each study), with an overall
favourable effect on increasing PPT compared to other interventions. The data from ten studies
was included in this meta-analysis, and the authors highlighted the paucity of quality literature
in this area. As such it is still a valuable area for future research. Seven further studies
investigating SM and PPT were identified which have been published in the interim (de Oliveira
et al. 2013; Fernández-Carnero, Cleland, and Arbizu 2011; Gay et al. 2014; Molina-Ortega et al.
2014; Orakifar et al. 2012; Packer et al. 2014; Srbely et al. 2013), and another which was
excluded from the review by Coronado et al. (2012) based on methodological factors (Suter and
McMorland 2002). It should be kept in mind that an increase in PPT represents a decrease in
pain sensitivity; an increased PPT means the participant was able tolerate more pressure before
feeling pain.
1.3.1.1. Local Effects
This section focuses on the effects of SM on PPT at locations within close anatomical vicinity
(local) to the site receiving SM, with the studies under discussion summarised in Table 1.1.
An early study with participants with chronic mechanical neck pain found that cervical SM
increased PPT at cervical paraspinal tender points when compared to cervical mobilisation,
measured five minutes after intervention (Vernon et al. 1990). The small sample size (N=9) limits
this study. More recently, Fernández-de-las-Peñas et al. (2008) studied asymptomatic
participants and found that cervical facet PPT increased following C7-T1 SM at five minutes,
which occurred bilaterally and was independent of the participant’s dominant side. This was in
comparison to a sham manipulative procedure, though each group only contained ten
participants. They also noted that male participants experienced greater increases in PPT than
8
females. Molina-Ortega et al. (2014) demonstrated that C5-C6 SM in an asymptomatic
population lead to a significant immediate increase in PPT at the cervical musculature (and the
lateral elbow but not the calf), when compared with T4 SM and sham cervical SM. These changes
were not sustained at two hours, and again there were only ten participants per group. In a
study by Suter and McMorland (2002) in which all of the chronic neck pain participants received
C5-C6 or C6-C7 SM, PPT was noted to increase significantly in the cervical musculature
immediately post-SM. The study, however, lacks a comparator intervention or sham and thus
should be interpreted with caution. Maduro de Camargo et al. (2011) found that C5-C6 SM in
participants with mechanical neck pain resulted in increased PPT at the C5 spinous process and
the deltoid muscle, but not the upper trapezius muscle, compared to quiet rest. A study on
asymptomatic participants by Ruiz-Saez et al. (2007) found that upper trapezius muscle trigger
point PPT was increased five and ten minutes after a C3-C4 SM, when compared to sham SM.
Also in asymptomatic participants, Hamilton, Boswell, and Fryer (2007) found that bilateral C0-
C1 SM elicited a significant within-group increase in PPT at the midline suboccipital region at five
minutes but not at 30 minutes post-intervention. However, there were no significant differences
when compared to suboccipital muscle stretch and a sham manual technique. Fryer, Carub, and
Mclver (2004) compared upper thoracic SM to upper thoracic mobilisation and sham laser
acupuncture, in an asymptomatic population. The SM and mobilisation groups both showed an
immediate significant within-group increase in thoracic PPT. The mobilisation group, but not the
SM group, reached significance compared to the sham group. The study population was drawn
from osteopathic students thus a participant expectancy effect may have occurred, and a small
placebo effect was noted.
A study by Cote, Mior, and Vernon (1994) looked at PPT in a chronic LBP population following
lumbar SM compared to mobilisation. No significant changes in PPT were found in any location
(lumbar, sacroiliac or gluteal regions) immediately, 15 minutes or 30 minutes post-intervention,
compared to baseline and to mobilisation. Thomson, Haig, and Mansfield (2009) also
9
investigated the effects of lumbar SM compared to mobilisation and sham laser acupuncture in
an asymptomatic population. PPT at the ‘most tender’ lumbar spinous process showed no
significant changes pre- and immediately post-intervention within any group or between groups.
There are several potential limitations with this study; as PPT appears to represent a measure
of deep pressure sensitivity (as discussed in section 1.3), PPT measured at a spinous process (a
bony landmark) may not provide reliable results due to the relative absence of deep soft tissue.
Difficulty with the algometer slipping off the spinous process has also been reported (Frank,
McLaughlin, and Vaughan 2013). The study also recruited participants from an osteopathic
student and teacher group, thus it may be subject to participant expectancy effects. A novel
study by de Oliveira et al. (2013) compared lumbar SM to upper thoracic SM in a chronic LBP
population. PPT was measured at the lumbar paraspinal and tibialis anterior muscles, with
lumbar PPT increasing significantly in the thoracic SM group only. It was noted by the authors
that the absolute change in PPT was small and may represent chance or measurement error.
Subjective pain intensity, however, decreased significantly in both groups. In a population of
asymptomatic females, Orakifar et al. (2012) found no changes to PPT at the sacroiliac joint
immediately or up to 15 minutes after sacroiliac joint SM. There was no comparison or placebo
group, and combined with the all-female participants mean these results should be interpreted
cautiously. In an interesting study by Gay et al. (2014), asymptomatic participants completed an
exercise protocol designed to induce LBP, and were then randomised to receive lumbar SM,
mobilisation, or therapeutic touch. There were no significant changes to PPT in any group when
tested at the lumbar paraspinal muscles, or the upper and lower limb. There was a statistically
significant decrease in pain intensity in all groups, which might represent the natural history of
exercise-induced LBP.
The above studies provide reasonable evidence that cervical SM leads to increases in local PPT.
In addition to the systematic review by Coronado et al. (2012), two further studies (as discussed)
support this conclusion (Molina-Ortega et al. 2014; Suter and McMorland 2002). The thoracic
10
spine remains significantly under-studied, with only a single article finding that thoracic SM led
to increased local PPT. In the lumbar spine, the evidence from all identified studies indicates
that lumbar or lumbosacral SM does not lead to any changes in local PPT, though there are few
studies and they tend to be of poor quality. Given the differences in findings between the
cervical and lumbar regions, further studies are warranted to investigate if these apparent
differences are accurate, and why this might be so.
1.3.1.2. Remote Effects
This section focuses on the effects of SM on PPT at locations remote to or separate from the site
receiving SM. See Table 1.2 for a summary of these studies. The neurological relationship
between the site receiving SM and the site/s where PPT is measured are described in each case,
in order to note whether there is a direct neurological link between the two. For example, a
direct or ‘segmental’ link is considered present if spinal nerve roots at or close to the site of SM
innervate structures at the site where PPT is measured (e.g. skin or muscle). This is potentially
important when considering the mechanism behind post-SM hypoalgesia, and whether any
hypoalgesia is regional or global.
The study by Maduro de Camargo et al. (2011) found that C5-C6 SM in mechanical neck pain
participants led to an increase in PPT at the C5 spinous process and deltoid muscle bilaterally at
five minutes, compared to control, though no significant changes in PPT at the upper trapezius
muscle were found. Both the deltoid and upper trapezius muscles are segmentally linked the
C5-C6 region. Srbely et al. (2013) compared PPT findings following bilateral C5-C6 SM or sham
cervical SM at myofascial trigger points in the right infraspinatus muscles (segmentally linked via
the C5 and C6 nerve roots) and gluteus medius muscles (segmentally unrelated). Significant
increases in PPT were observed for at least 15 minutes at the infraspinatus muscle after SM
compared to sham, with no changes in gluteus medius PPT.
11
Two studies with similar protocols measured changes in PPT at the lateral epicondyle (within
the C6 dermatome) immediately before and after C5-C6 level SM, compared to sham/control.
One recruited asymptomatic participants (Fernández-de-las-Peñas et al. 2007), and the other
used participants with lateral epicondylalgia (lateral elbow pain) (Fernández-Carnero,
Fernández-de-las-Peñas, and Cleland 2008), each employing a cross-over design with 15 and 10
participants respectively. Both found significant bilateral increases in PPT at the lateral
epicondyle in the SM groups compared to sham/control. Another very similar study by
Fernández-Carnero, Cleland, and Arbizu (2011) compared the effects of C5-C6 SM to mid-
thoracic SM on PPT over the lateral epicondyle (segmentally linked to the cervical but not mid-
thoracic spine), in 18 participants with lateral epicondylalgia. Cervical SM was found to
significantly increase PPT bilaterally while thoracic SM did not. The study by Molina-Ortega et
al. (2014) noted that PPT in the cervical spine and lateral elbow (segmentally linked to C5 and
C6) increased, but there was no change at the tibialis anterior muscle (segmentally unrelated to
the cervical or thoracic spine). This was following C5-C6 SM in asymptomatic participants, when
compared to upper thoracic SM and sham.
Bishop, Beneciuk, and George (2011) studied changes to PPT in the web spaces of the first and
second fingers, and first and second toes, following upper thoracic SM in an asymptomatic
population. No significant differences in PPT were identified at either location in the SM group,
compared to a cervical exercise group and control. The lower limb testing site is segmentally
unrelated to the upper thoracic spine. The upper limb testing site is situated within the C6
dermatome, and is anatomically overlying the first dorsal interosseus and adductor pollicis
muscles (though this was not specifically identified), which are innervated by the C8 and T1
nerve roots. The thoracic manipulation technique used was a supine manoeuvre that was
theorised by Bishop, Beneciuk, and George (2011) to affect the upper thoracic and lower cervical
regions. It is possible, however, that the technique exerted its main effect below these levels.
12
The study by de Oliveira et al. (2013) found no change to PPT at the tibialis anterior muscle
following lumbar SM (segmentally linked via the L5 nerve root). Gay et al. (2014) demonstrated
no changes to PPT in the lumbar spine, or the web spaces of the first and second fingers
(segmentally unrelated), and first and second toes (segmentally related via L5 and S1 nerve
roots), after lumbar SM, mobilisation or therapeutic touch in participants with exercise-induced
LBP. Subjective pain intensity did improve in all groups.
Interestingly, a study by Oliveira-Campelo et al. (2010) found that C0-C1 SM in asymptomatic
individuals led to increases in PPT in the masseter muscles compared to both soft tissue therapy
and control. Significant increases in PPT at the temporalis muscles occurred in both the SM and
soft tissue therapy groups compared to control. This is further supported by the findings of
Mansilla-Ferragut et al. (2009), where increases in PPT over the sphenoid bone bilaterally were
observed five minutes following bilateral C0-C1 SM, in a female population with mechanical neck
pain. It was speculated that this effect is mediated by the trigemino-cervical nucleus caudalis,
which extends into the upper cervical spinal cord (Blumenfeld 2010). A study by Packer et al.
(2014) investigated PPT in the masseter and temporalis muscles and at the temporomandibular
joint, as well as subjective pain intensity, in female participants with temporomandibular
disorders. Participants received a single session of upper thoracic SM. No significant changes to
PPT or pain intensity were observed, which may be explained by the absence of a direct
segmental link between the upper thoracic spine and trigeminal nerve.
The studies investigating cervical SM support the conclusions of Coronado et al. (2012), including
three since the review (Fernández-Carnero, Cleland, and Arbizu 2011; Molina-Ortega et al. 2014;
Srbely et al. 2013). There appears to be moderate evidence of at least a short term increase in
PPT in locations with a segmental neurological link to the site of cervical SM (the upper limb and
jaw/head). The conclusions from two lumbar spine studies suggest that lumbar SM does not
lead to a segmental change in PPT (i.e. in the lower limb). Just as for local hypoalgesia, the topic
13
of remote hypoalgesia following lumbar SM is significantly understudied. Considering the
conflicting evidence with the cervical spine, further research to clarify this topic is important. No
studies were identified that suggest SM might have a non-segmental or global effect on PPT.
1.3.1.3. Sham-Controlled Studies
When considering just the sham-controlled studies, there is significant support for a mechanical
hypoalgesic effect in the cervical spine and upper limb following cervical SM over sham
(Fernández-Carnero, Fernández-de-las-Peñas, and Cleland 2008; Fernández-de-las-Peñas et al.
2008; Fernández-de-las-Peñas et al. 2007; Molina-Ortega et al. 2014; Ruiz-Saez et al. 2007;
Srbely et al. 2013). Only a single study found an increase in cervical spine PPT in all groups
including cervical SM and sham (Hamilton, Boswell, and Fryer 2007). Mansilla-Ferragut et al.
(2009) demonstrated an increase in PPT over the sphenoid bone after cervical SM but not sham,
and Packer et al. (2014) found no change in PPT at the jaw after thoracic SM compared to sham.
One study noted local mechanical hypoalgesia in the thoracic spine following thoracic SM but
not sham, though the effect appeared to be equivalent to or less than after thoracic mobilisation
(Fryer, Carub, and Mclver 2004). Two studies in the lumbar region indicate the absence of a local
or remote mechanical hypoalgesic effect following lumbar SM, mobilisation and sham (Gay et
al. 2014; Thomson, Haig, and Mansfield 2009).
Overall, it appears that a mechanical hypoalgesic effect occurs in the cervical spine and upper
limb, and possibly the head, following cervical SM, and may occur in the thoracic spine after
thoracic SM. The lumbar spine or lower limb does not appear to develop mechanical hypoalgesia
in response to lumbar SM.
14
Table 1.1. Summary of studies for local effects of spinal manipulation on PPT.
Reference Participants Intervention/s Outcome Measures Main Findings
(Vernon et al. 1990) N=9 (6 male) Chronic mechanical neck pain, mean age 38yrs
Participants randomised to either: 1) Cervical HVLA SM 2) Cervical mobilisation
PPT bilaterally at cervical paraspinal muscles. Measured baseline and 5min post-intervention.
Significant increase in PPT bilaterally in the SM group compared to mobilisation.
(Fernández-de-las-Peñas et al. 2008)
N=30 (13 male) Asymptomatic, right-hand dominant, mean age 26yrs
Participants randomised to one of: 1) Right C7-T1 HVLA SM 2) Left C7-T1 HVLA SM 3) Sham, simulated C7-T1 SM without tension or thrust
PPT bilaterally at C5-C6 joint. Measured baseline and 5min post-intervention.
Significant increase in PPT bilaterally in both SM groups compared to sham.
(Molina-Ortega et al. 2014)
N=30 (16 male) Asymptomatic, mean age 25.8-29.8yrs
Participants randomised to one of: 1) Right or left C5-C6 HVLA SM 2) T4 HVLA SM 3) Sham, simulated C5-C6 SM without tension or thrust
PPT bilaterally at the C5-C6 joint, lateral epicondyle, and tibialis anterior muscles. Serum substance P and nitric oxide concentrations. Measured baseline, and immediately and 2hrs post-intervention.
Significant increase in PPT bilaterally at C5-C6 and lateral epicondyle in cervical SM group immediately but not at 2hrs, compared to other groups. No change to tibialis anterior PPT. Significant increase in substance P in cervical SM group compared to other groups.
(Suter and McMorland 2002)
N=16 (2 male) Chronic neck pain, mean age 33.8yrs
All participants received: 1) Right or left C5-C6 or C6-C7 HVLA SM
PPT bilaterally at upper trapezius, sternocleidomastoid and mid-cervical muscles. Cervical range of motion, subjective pain intensity, and biceps muscle inhibition and force. Measured baseline and immediately post-intervention.
Significant increase in PPT at all sites. Significant increase in range of motion. Significant bilateral decrease in biceps muscle inhibition and increase in force.
(Maduro de Camargo et al. 2011)
N=37 (21 male) Mechanical neck pain, mean age 30yrs
Participants randomised to either: 1) Right-sided C5-C6 HVLA SM 2) Control, sitting, 2min of quiet rest
PPT bilaterally at upper trapezius and deltoid muscles, and C5 spinous process. Electromyographic data of deltoid muscles during different contractions. Measured baseline and 5min post-intervention.
Significant increase in PPT at deltoid and C5 spinous process in the SM group only. Significant increase in EMG amplitude and fatigue resistance in deltoid muscle during 30sec isometric contraction.
(Ruiz-Saez et al. 2007) N=72 (27 male) MTrPs in upper trapezius and C3-C4 facet joint dysfunction, mean age 31yrs
Participants randomised to either: 1) Right or left C3-C4 HVLA SM 2) Sham, simulated C3-C4 SM without tension or thrust
PPT at upper trapezius muscle MTrP on the side of SM. Measured baseline, and at 1min, 5min, and 10min post-intervention.
Trend toward increase in PPT in SM group only at all time points, not statistically significant. Significant decrease in PPT in sham group at 5min and 10min.
15
Reference Participants Intervention/s Outcome Measures Main Findings
(Hamilton, Boswell, and Fryer 2007)
N=90 (29 male) Asymptomatic, mean age 23yrs
Participants randomised to one of: 1) Bilateral C0-C1 HVLA SM 2) Bilateral muscle-energy technique suboccipital muscle stretch 3) Sham, ‘subtle positioning of the upper neck’, held for 30sec, no ‘barrier was engaged’
PPT at midline suboccipital region. Measured baseline, and at 5min and 30min post-intervention.
Significant increase in PPT across entire cohort, no significant between-group differences.
(Fryer, Carub, and Mclver 2004)
N=96 (39 male) Asymptomatic, osteopathic students, age 19-34yrs
Participants randomised to one of: 1) HVLA SM to ‘most tender’ thoracic joint 2) 30sec extension mobilisation to ‘most tender’ thoracic joint 3) Sham, simulated laser acupuncture to ‘most tender’ thoracic joint
PPT at ‘most tender’ thoracic spinous process. Measured baseline and immediately post-intervention.
Significant increase in PPT in both experimental groups pre- and post- intervention. Significant increase in PPT in the mobilisation group, but not the SM group, compared to sham.
(Cote, Mior, and Vernon 1994)
N=39 (6 male) Chronic mechanical LBP, mean age 31yrs
Participants randomised to either: 1) Lumbar SM 2) Supine lumbar mobilisation
PPT at the ipsilateral lumbar paraspinal muscles, gluteal muscle and sacroiliac joint. Measured baseline, and immediately, 15min, and 30min post-intervention.
No significant changes to PPT in either group.
(Thomson, Haig, and Mansfield 2009)
N=50 (29 male) Asymptomatic, osteopathic college students/staff, mean age 27yrs
Participants randomised to one of: 1) Right-sided HVLA SM to ‘most tender’ lumbar joint 2) 30sec right-sided mobilisation to ‘most tender’ lumbar joint 3) Sham, 30sec simulated laser acupuncture to ‘most tender’ lumbar joint
PPT at the ‘most tender’ lumbar spinous process. Measured baseline and immediately post-intervention.
No significant changes to PPT in any group.
(de Oliveira et al. 2013) N=148 (39 male) Chronic non-specific LBP, mean age 46yrs
Participants randomised to either: 1) Upper thoracic HVLA SM 2) Lumbar HVLA SM
PPT bilaterally at the L3 and L5 paraspinal muscles and tibialis anterior muscle. Subjective pain intensity. Measured baseline and immediately post-intervention.
Significant increase in PPT at all lumbar levels within the thoracic SM group only, but no significant between-group differences. Pain intensity decreased significantly in both groups.
(Orakifar et al. 2012) N=20 (0 male) Asymptomatic, age 18-30yrs
All participants received: 1) Right-sided sacroiliac joint HVLA SM
PPT at the posterior superior iliac spine. Hoffman reflex at the tibial nerve. Measured baseline, and at 1min, 5min, 10min and 15min post-intervention.
No significant change to PPT. Significant transient attenuation of Hoffman reflex.
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Reference Participants Intervention/s Outcome Measures Main Findings
(Gay et al. 2014) N=24 (17 male) Asymptomatic, mean age 21.6yrs
Participants completed exercise protocol to induce LBP, then randomised to receive one of: 1) Lumbar HVLA SM 2) Lumbar mobilisation 3) Therapeutic touch to the lumbosacral region
PPT bilaterally at the L1, L5, and S2 paraspinal muscles, and at the dorsal web space of 1st and 2nd fingers and 1st and 2nd toes. Brain functional connectivity using MRI. Subjective pain intensity. Measured baseline and immediately post-intervention.
No significant changes to PPT occurred in any group. Various significant changes in functional connectivity occurred. Significant decrease in subjective pain intensity in all groups.
Abbreviations: HVLA = high-velocity low-amplitude, LBP = lower back pain, PPT = pressure pain threshold, SM = spinal manipulation.
Table 1.2. Summary of studies for remote effects of spinal manipulation on PPT.
Reference Participants Intervention/s Outcome Measures Main Findings
(Maduro de Camargo et al. 2011)
N=37 (21 male) Mechanical neck pain, mean age 30yrs
Participants randomised to either: 1) Right-sided C5-C6 HVLA SM 2) Control, sitting, 2min of quiet rest
PPT bilaterally at upper trapezius and deltoid muscles, and C5 spinous process. Electromyographic data of deltoid muscles during different contractions. Measured baseline and 5min post-intervention.
Significant increase in PPT at deltoid and C5 spinous process in the SM group only. Significant increase in EMG amplitude and fatigue resistance in deltoid muscle during 30sec isometric contraction.
(Srbely et al. 2013) N=36 (19 male) MTrPs in right infra-spinatus and gluteus medius muscles, mean age 28yrs
Participants randomised to either: 1) Bilateral C5-C6 HVLA SM 2) Sham, simulated C5-C6 SM with similar pre-load forces but inert thrust
PPT at right infraspinatus and gluteus medius muscle MTrPs. Measured baseline, and at 1min, 5min, 10min, and 15min post-intervention.
Significant increase in PPT at the infraspinatus muscle in the SM group compared to the gluteus medius muscle and to sham.
(Fernández-de-las-Peñas et al. 2007)
N=15 (7 male) Asymptomatic, mean age 21yrs
Participants received each, on 3 separate days >48hrs apart: 1) Right or left C5-C6 HVLA SM 2) Placebo, simulated C5-C6 SM without tension or thrust 3) Control, active cervical lateral flexion and rotation (no therapist contact)
PPT bilaterally at the lateral epicondyle. Measured baseline and 5min post-intervention.
Significant increase in PPT at both elbows in the SM group compared to placebo and control groups.
17
Reference Participants Intervention/s Outcome Measures Main Findings
(Fernández-Carnero, Fernández-de-las-Peñas, and Cleland 2008)
N=10 (5 male) Right-sided lateral elbow pain, mean age 42yrs
Participants received each, on 2 separate days >48hrs apart: 1) Right-sided C5-C6 HVLA SM 2) Manual contact intervention, simulated C5-C6 SM without tension or thrust
PPT bilaterally at the lateral epicondyle. Hot and cold pain thresholds bilaterally at the lateral epicondyle. Pain-free grip force on the symptomatic side and maximum grip force on the unaffected side. Measured baseline and 5min post-intervention.
Significant increase in PPT bilaterally in the SM group compared to manual contact. No significant changes for hot or cold pain thresholds. Significant increase in pain-free grip force in the SM group compared to manual contact.
(Fernández-Carnero, Cleland, and Arbizu 2011)
N=18 (8 male) Right-sided lateral elbow pain, mean age 44.8yrs
Participants randomised to either: 1) Right-sided C5-C6 HVLA SM 2) HVLA SM to the T5-T8 region
PPT bilaterally at the lateral epicondyle. Pain-free grip strength on symptomatic side and maximum voluntary grip strength on the unaffected side. Measured baseline and 5min post-intervention.
Significant increase in PPT bilaterally in the cervical SM group compared to thoracic SM. Significant increase in pain-free grip strength in both groups.
(Molina-Ortega et al. 2014)
N=30 (16 male) Asymptomatic, mean age 25.8-29.8yrs
Participants randomised to one of: 1) Right or left C5-C6 HVLA SM 2) T4 HVLA SM 3) Control, simulated C5-C6 SM without tension or thrust
PPT bilaterally at the C5-C6 joint, lateral epicondyle, and tibialis anterior muscles. Serum substance P and nitric oxide concentrations. Measured baseline, and immediately and 2hrs post-intervention.
Significant increase in PPT bilaterally at C5-C6 and lateral epicondyle in cervical SM group immediately but not at 2hrs, compared to other groups. No change to tibialis anterior PPT. Significant increase in substance P in cervical SM group compared to other groups.
(Bishop, Beneciuk, and George 2011)
N=90 (24 male) Asymptomatic, mean age 22.9yrs
Participants randomised to one of: 1) HVLA SM to upper thoracic region 2) ‘Chin tuck’ cervical exercise 3) Control, supine, 5min quiet rest
PPT bilaterally at dorsal web space of 1st and 2nd fingers and 1st and 2nd toes. Thermal ‘first pain’ sensitivity bilaterally at the anterior forearm and posterior upper calf. Temporal sensory summation bilaterally at the thenar eminence and dorsal foot. Measured baseline and immediately post-intervention.
PPT increased significantly within all groups. No significant changes in PPT between groups. No significant changes in thermal ‘first pain’ between groups. Significant decrease in temporal sensory summation in the SM group compared to the exercise and control groups.
(de Oliveira et al. 2013) N=148 (39 male) Chronic non-specific LBP, mean age 46yrs
Participants randomised to either: 1) Upper thoracic HVLA SM 2) Lumbar HVLA SM
PPT bilaterally at the L3 and L5 paraspinal muscles and tibialis anterior muscle. Subjective pain intensity. Measured baseline and immediately post-intervention.
Significant increase in PPT at all lumbar levels within the thoracic SM group only, but no significant between-group differences. Pain intensity decreased significantly in both groups.
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Reference Participants Intervention/s Outcome Measures Main Findings
(Gay et al. 2014) N=24 (17 male) Asymptomatic, mean age 21.6yrs
Participants completed exercise protocol to induce LBP, then randomised to receive one of: 1) Lumbar HVLA SM 2) Lumbar mobilisation 3) Therapeutic touch to the lumbosacral region
PPT bilaterally at the L1, L5, and S2 paraspinal muscles, and at the dorsal web space of 1st and 2nd fingers and 1st and 2nd toes. Brain functional connectivity using MRI. Subjective pain intensity. Measured baseline and immediately post-intervention.
No significant changes to PPT occurred in any group. Various significant changes in functional connectivity occurred. Statistically significant decrease in subjective pain intensity in all groups.
(Oliveira-Campelo et al. 2010)
N=122 (31 male) MTrPs in the masseter muscle, mean age 20yrs
Participants randomised to one of: 1) Bilateral C0-C1 HVLA SM 2) Soft tissue therapy to suboccipital muscles 3) Control, supine, 2min quiet rest
PPT bilaterally at MTrPs in the masseter and temporalis muscles. Active mouth opening in millimetres. Measured baseline and 2min post-intervention.
Significant increase in PPT at masseter muscles in SM group compared to soft tissue therapy and control. Significant increase in PPT at temporalis muscles in SM and soft tissue therapy groups compared to control. Significant increase in active mouth opening in SM group compared to others.
(Mansilla-Ferragut et al. 2009)
N=37 (0 male) Mechanical neck pain, mean age 35yrs
Participants randomised to either: 1) Bilateral C0-C1 HVLA SM 2) Placebo, simulated C0-C1 SM with full passive cervical rotation
PPT bilaterally at the sphenoid bone. Pain-free maximal mouth opening in millimetres. Measured baseline and 5min post-intervention.
Statistically significant increase in PPT and in maximal mouth opening in the SM group compared to placebo.
(Packer et al. 2014) N=32 (0 male) Temporomandibular pain and neck pain, mean age 23.5-26yrs
Participants randomised to either: 1) T1 HVLA SM 2) Placebo, simulated T1 SM without tension or thrust
PPT bilaterally at masseter and temporalis muscles and the temporomandibular joint. Subjective pain intensity. Measured baseline, immediately post-intervention, and 48-72hrs post-intervention.
No statistically significant changes seen in either group for any outcome measure.
Abbreviations: HVLA = high-velocity low-amplitude, LBP = lower back pain, PPT = pressure pain threshold SM = spinal manipulation.
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1.3.1.4. Asymmetric Effects
A limited number of studies specifically investigate whether SM causes changes to PPT that are
bilateral, asymmetrical, or unilateral. Each of the studies found increases in PPT were bilateral
(Fernández-Carnero, Cleland, and Arbizu 2011; Fernández-Carnero, Fernández-de-las-Peñas,
and Cleland 2008; Fernández-de-las-Peñas et al. 2008; Fernández-de-las-Peñas et al. 2007;
Maduro de Camargo et al. 2011). Three of these studies found that PPT increased more on the
ipsilateral side following right cervical SM, though all participants were right-hand dominant
(Fernández-Carnero, Cleland, and Arbizu 2011; Fernández-Carnero, Fernández-de-las-Peñas,
and Cleland 2008; Maduro de Camargo et al. 2011). Fernández-de-las-Peñas et al. (2008) and
Fernández-de-las-Peñas et al. (2007) found that right PPT increased more than left in right-hand
dominant participants, regardless of which side of the cervical spine was manipulated. The
evidence thus suggests that SM affects PPT bilaterally, but there may be asymmetry related to
the participant’s dominant side, the side of SM, or another unknown factor. No studies have
directly compared right- to left-hand dominant participants. As these articles involve only
cervical SM, no assumptions can be made about whether such effects also occur in the lumbar
spine.
1.3.1.5. Other Factors
Overall, the duration of changes in PPT remains unclear. Few studies assessed short-term PPT
changes beyond ten minutes. One found increases in PPT that were present at five minutes but
not at 30 minutes (Hamilton, Boswell, and Fryer 2007), and another found changes that
persisted to 15 minutes but did not measure beyond this (Srbely et al. 2013). Another study
identified PPT changes immediately but not two hours post-SM (Molina-Ortega et al. 2014).
Three further studies measured beyond ten minutes, but failed to find changes in PPT at any
time point (Cote, Mior, and Vernon 1994; Orakifar et al. 2012; Packer et al. 2014). The study by
Schiller (2001) applied up to six interventions of thoracic SM over a three week period, in
participants with mechanical thoracic spine pain. It was found that PPT in the thoracic spine (the
20
specific location is not identified) increased at the final treatment and at follow-up one month
later compared to baseline, but not compared to sham ultrasound. However, the study is at risk
of committing type II error (falsely accepting a null hypothesis) due to low power. Shearar,
Colloca, and White (2005) compared four sessions of sacroiliac joint HVLA SM or mechanical
sacroiliac joint SM over two weeks in a population with sacroiliac joint syndrome. PPT at the
sacroiliac joints showed no changes in either group when measured before the third treatment
visit, or at the follow-up visit within one week of the final treatment. Any short-term changes in
PPT would have been missed. A variety of subjective measures improved significantly in both
groups. Thus we have no clear evidence regarding how long changes in PPT might last for, and
there is a definite need to investigate this systematically.
Based on the current literature, it is unclear if the magnitude or duration of PPT changes are
dose related as this specific relationship does not appear to have been studied. Importantly, the
clinical implications of the observed increases in PPT following SM is limited at this stage as no
studies correlate changes in PPT to changes in clinical outcomes. However, it is tempting to
hypothesise that mechanisms that result in increases in PPT may cause part or all of the
subjective pain relief associated with SM. This relationship needs further investigation.
The studies discussed variably use asymptomatic or symptomatic populations. No literature was
identified comparing the effects of SM on PPT between asymptomatic and symptomatic
populations. It is possible that there are differences in the responses of these two groups based
on pain sensitisation mechanisms and is an area for future research.
The majority of the above studies use the occurrence of a cavitation during the SM procedure
as an indicator of success. If a cavitation is not heard, a second attempt is typically performed.
As discussed in section 1.2.3, it appears that a cavitation is not a necessary element of a
successful SM procedure.
21
1.3.2. Pinprick Sensitivity
No studies were identified that assessed changes to PPS following SM. As such this is a novel
and potentially valuable topic for future research.
1.3.3. Thermal, Chemical, and Electrical Pain Stimuli
There are a number of studies that assess other measures of pain sensitivity following SM,
including thermal, chemical and electrical stimulus thresholds, summarised by Coronado et al.
(2012). This topic also lacks robustness in the literature.
The effect of SM on thermal sensitivity has been investigated in a few studies. An immediate
reduction in thermal sensitivity has been observed in the leg but not the arm following lumbar
HVLA SM in LBP (Bialosky et al. 2009b) and asymptomatic (Bialosky et al. 2008; George et al.
2006) participants, when compared to exercise interventions. The same has also been observed
in both the upper and lower limb immediately following upper thoracic HVLA SM but not
exercise or rest in 90 healthy individuals (Bishop, Beneciuk, and George 2011). All four of these
studies specifically found that temporal sensory summation (TSS) was reduced, thought to be
mediated by C-fibre pathways, but found no changes to thermal pain thresholds, thought to be
mediated by Aδ-fibre pathways (Anderson et al. 2013; Weiss et al. 2008). TSS is believed to
represent a measure of the wind-up phenomenon, where repetitive nociceptive stimulation
leads to excitation of the dorsal horn, which may be involved in central sensitisation (Anderson
et al. 2013). The findings of Fernández-Carnero, Fernández-de-las-Peñas, and Cleland (2008) are
in line with this pattern, showing no change to thermal pain thresholds following cervical HVLA
SM in participants with lateral epicondylalgia. TSS was not tested in this study. As increased TSS
has been observed in several chronic pain conditions compared to healthy populations
(Anderson et al. 2013), the finding that TSS appears to be reduced following SM has implications
for the treatment of chronic pain conditions that deserve investigation. Only one of the above
studies looked at TSS in a symptomatic population, LBP sufferers with an average symptom
22
duration of 222 weeks (Bialosky et al. 2009b). Future research in this area should investigate
different populations, and whether there is a correlation between changes to TSS and clinical
outcomes following SM.
Other experimental pain stimuli have also been investigated. Mohammadian et al. (2004) is the
only study identified which has taken a preliminary look at chemically-induced pain, using
capsaicin cream on the forearm. The group that received cervical SM exhibited immediate
reductions in the size of the area (which was exposed to capsaicin cream) experiencing allodynia,
or pain in response to a stimulus that should not be painful, and hyperalgesia, an excessive pain
response, as well as the intensity of spontaneous pain compared to the control group. In
addition, an increase in electrical pain tolerance has been noted in a population of 50
chiropractic students, for ten minutes following thoracic SM, compared to controls (Terrett and
Vernon 1984).
These studies provide preliminary evidence that SM not only results in mechanical hypoalgesia,
but possibly also hypoalgesia to thermal, chemical and electrical stimuli. More research in this
area is needed.
1.3.4. Biomechanical Factors
SM is essentially a mechanical impulse applied to the spine, with resulting biomechanical effects
on the body (Triano 2005). Thus it is generally accepted that part of the therapeutic benefit of
SM arises from the biomechanical impact (Triano 2005). Our understanding to date of the
biomechanical impacts of SM is limited, but forms an important element in our understanding
of how SM achieves clinical results.
It has been found that both HVLA and mechanical SM result in significant displacement or
translation of the spinal segment being targeted, as well as of the adjacent segments (Colloca,
23
Keller, and Gunzburg 2004; Colloca et al. 2006; Gál et al. 1994a, b, 1997; Keller, Colloca, and
Gunzburg 2003). Several studies using mechanical SM also found that this vertebral
displacement was temporally related to the initiation of action potentials, recorded in the dorsal
horn of the targeted segment (Colloca, Keller, and Gunzburg 2003, 2004; Colloca et al. 2000).
It has been hypothesised that stretch of the facet joint capsule and surrounding structures
occurs during a SM procedure (Pickar 2002). We know that facet joint capsules are innervated
with a variety of low- and high-threshold mechanoreceptors and some nociceptors, and that
capsule stretch within the physiologic range stimulates mechanoreceptors (Lu et al. 2005;
McLain and Raiszadeh 1995). Beyond the physiologic range nociceptive signals become
prevalent (Lu et al. 2005; McLain and Raiszadeh 1995). It has been documented in human
cadaver studies that mechanical lumbar SM does strain the facet joint capsule at the site and
distal to the site of manipulation (Ianuzzi and Khalsa 2005a, b). The capsule strain does not
exceed that noted during normal physiological movements, though the particular characteristics
of the strain and loading that occur during SM are suggested to trigger novel, non-physiologic
afferent stimulation (Ianuzzi and Khalsa 2005a). A study using a feline model found that different
directions of SM loading produced somewhat unique responses in lumbar facet capsule
mechanoreceptors, lending strength to this theory (Pickar and McLain 1995). Further studies in
feline models have shown that muscle spindle responses occur following mechanical SM, and
that the responses to rapid loading (like those during HVLA SM) are greater than responses
during slower loading (Pickar and Kang 2006; Pickar et al. 2007). This was further characterised
in humans, with the finding that faster thrust speeds led to greater thoracic paraspinal muscle
electromyographic activity (Pagé et al. 2014). This evidence supports the notion that facet
capsule and paraspinal muscle stretch does occur during SM, and that the mechanical
characteristics of SM may lead to unique afferent signals. This unique input to the nervous
system may help to account for some of the clinical and physiological effects associated with
SM, including hypoalgesia.
24
1.3.5. Neurophysiological Factors
A variety of studies have investigated the effects of SM on neurophysiology by specifically
observing changes to central nervous system functions and processing. This is a broad area, and
the research at present is very limited in scope and applicability, but is highly interesting
nonetheless.
Reed et al. (2014) found, in rats which received mechanical lumbar SM, that a higher thrust
magnitude resulted in an increase in the threshold of nociceptive lateral thalamic neurons to
mechanical stimuli (i.e. decreased sensitivity). A smaller-magnitude thrust resulted in no change.
The lateral thalamic nuclei are responsible for relaying and integrating sensory information as it
ascends to the cortex and other regions of the brain (Patestas and Gartner 2006). It also appears
to have a relationship with descending pain control circuits, as discussed in section 1.3.7.1. Thus
it is interesting to consider that a sufficient mechanical stimulus to the spine may affect the
sensitivity of nociception processing in the thalamus. This warrants further research in human
subjects, and may help in our currently limited understanding of how SM results in hypoalgesia.
There is some early experimental evidence that suggests SM could possibly have an effect on
aspects of central pain and the processing and integration of sensory information. A variety of
intra- and inter-hemispheric changes to functional connectivity between regions of the brain
involved in pain processing have been observed following lumbar SM, mobilisation, and
therapeutic touch interventions (Gay et al. 2014). Some changes were unique to each
intervention, while others were common to all groups and may represent natural history or
effects shared by the three manual therapies. This study was previously described as it also
measured PPT and pain scores; PPT did not change in any group but pain scores improved in all
groups. It is suggested by the authors that the intervention-dependent changes to functional
connectivity may help elucidate the mechanisms of pain relief associated with the interventions,
though this is highly speculative.
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1.3.6. Biochemical Factors
In an attempt to determine the mechanism behind the hypoalgesia associated with SM, the
effects of SM on various pain-related biochemicals have been investigated.
1.3.6.1. -endorphins
A number of studies have measured changes to serum -endorphin levels following SM. -
endorphins are endogenous opioids with a potent pain-relieving function, acting to inhibit
peripheral somatosensory fibres, among other roles (Hartwig 1991). The studies show mixed
results, with Christian et al. (1988) and Sanders et al. (1990) reporting no changes to -endorphin
levels in symptomatic and asymptomatic populations following SM and compared to sham. In
contrast, Vernon et al. (1986) noted a small (8%) but significant increase in -endorphin levels
five minutes but not 10 or 30 minutes after cervical SM, compared to sham and control groups.
However there are concerns about the assay techniques used in each study, which bring into
question their results. The current studies on this topic are of insufficient quality to make any
conclusions regarding the effect of SM on serum -endorphin levels, so it remains unclear
whether the opioid system contributes to the hypoalgesia observed following SM. It may be that
HVLA SM does not stimulate the release of -endorphins, that the three studies to date have
failed to detect a change, or that serum -endorphins are an inappropriate measure. There are
similarly conflicting results from studies on other forms of manual therapy, reviewed by Bender
et al. (2007).
1.3.6.2. Substance P
Substance P is mainly involved in the transmission of slow nociceptive signals from peripheral
neurons to the dorsal horn (Snijdelaar et al. 2000; Todd 2010). Four studies have looked at
plasma substance P levels following SM. In a subset of participants studied by Brennan et al.
(1991), there were no significant changes to substance P levels in the group who received
thoracic SM group compared to sham SM. There was an increasing trend, but nine of the 30
26
participants had levels below the detection limit of the assay technique, so the remaining data
was underpowered (Brennan et al. 1991). Another subset in the same study compared SM to
baseline only, and found a statistically significant increase in substance P at 15 minutes post-SM
(Brennan et al. 1991). Brennan et al. (1992) also studied a subset of 30 participants, of whom
nine subjects’ blood samples could not be used due to technical difficulties, and found a
statistically significant increase in the levels of substance P 15 minutes after a thoracic SM,
though it is not stated if the data loss affected the statistical power of this finding. Teodorczyk-
Injeyan, Injeyan, and Ruegg (2006) compared thoracic SM to a ‘sham’ thoracic SM involving a
thrust but not eliciting a cavitation, and to venipuncture control. They investigated a variety of
biochemicals, measuring them 20 minutes and two hours after intervention. No significant
changes in substance P levels were noted in any group. Finally, Molina-Ortega et al. (2014)
demonstrated that serum substance P levels increased significantly immediately and two hours
after cervical SM but not thoracic SM and sham cervical SM, in an asymptomatic population. The
thoracic SM group did show a trend toward an increase, but with only ten participants per group,
there may have been insufficient power. Although generally accepted as having a pro-
nociceptive role, some have suggested substance P can also be involved in hypoalgesia (Molina-
Ortega et al. 2014). Given that Molina-Ortega et al. (2014) found a positive correlation between
substance P levels and PPT, this may be plausible. The significance of this is, however, uncertain,
and given that the four studies above show conflicting results it is perhaps unlikely that
substance P plays a significant role in post-SM hypoalgesia.
1.3.6.3. Cortisol
Salivary and serum cortisol levels have been investigated as a marker of stress responses to SM
in both symptomatic and asymptomatic populations. Four studies failed to find any significant
changes to cortisol levels immediately or at up to 5 weeks post-intervention (Christian et al.
1988; Padayachy et al. 2010; Tuchin 1998; Whelan et al. 2002). One study found cortisol levels
were significantly increased immediately but not 30 minutes after cervical HVLA SM in
27
asymptomatic participants compared to thoracic HVLA SM and control (Plaza-Manzano et al.
2014). It is conceivable that anxiety in anticipation of receiving SM, especially in naïve
participants, may affect cortisol levels, which could explain the short-lived change in cortisol
found in one study. Cortisol release is primarily stimulated by adrenocorticotropic hormone
(ACTH) via the hypothalamic-pituitary-adrenal axis (Tsigos and Chrousos 2002). In agreement
with the apparent lack of changes to cortisol following SM, Christian et al. (1988) also observed
no overall changes to the levels of ACTH following SM in the useable data they collected (almost
half of subjects had ACTH levels below the minimum detection level of the assay). It appears
unlikely that cortisol is involved in SM-induced hypoalgesia.
1.3.6.4. Other Biochemicals
In the study by Plaza-Manzano et al. (2014) serum levels of neurotensin, oxytocin, and orexin A
were observed following cervical or thoracic HVLA SM in asymptomatic subjects. Levels of
neurotensin and oxytocin were significantly increased in participants immediately after SM
compared to controls, but this did not persist at two hours post-intervention. Orexin A levels
remained unchanged. Each of the hormones investigated are known to have an analgesic role
in the body. Neurotensin’s analgesic function is independent of the opioid system, but can also
cause hyperalgesia in lower concentrations (St-Gelais, Jomphe, and Trudeau 2006). Oxytocin-
induced analgesia may involve direct stimulation of GABAergic spinal interneurons to inhibit Aδ-
and C-fibres, or indirectly through the endogenous opioid system (Millan 2002; Rash, Aguirre-
Camacho, and Campbell 2014). It is also plausible that the mood-enhancing and stress-reducing
effects of oxytocin contribute to its analgesic effect (Rash, Aguirre-Camacho, and Campbell
2014). Orexin A has a non-opioid analgesic mechanism and also potentially interplays with the
opioid system (Chiou et al. 2010). Nitric oxide is another chemical that is involved in nociception,
investigated by Molina-Ortega et al. (2014). Serum nitric oxide levels did not change following
either cervical SM, thoracic SM, or sham.
28
1.3.7. Theories for Post-Manipulation Hypoalgesia
Several theories may help to explain post-SM hypoalgesia (Bialosky et al. 2009a; Potter,
McCarthy, and Oldham 2005):
1. Activation of descending inhibitory pain control mechanisms
2. Activation of the pain gate mechanism
3. Altered spinal cord dorsal horn excitability
4. The placebo effect and psychosocial factors
1.3.7.1. Descending Inhibitory Pain Control Theory
A prominent theory is that SM produces activation of descending pain inhibition pathways.
Preliminary evidence suggests this may be mediated by serotonergic and noradrenergic, but not
opioidergic or GABAergic, pathways.
The descending pain pathways are highly complex, may inhibit or facilitate nociceptive signals,
and involve a variety of neurotransmitters including opioids, GABA, serotonin, and
noradrenaline (Millan 2002). Of particular relevance is the periaqueductal gray (PAG), situated
within the mesencephalon of the brainstem. It has been demonstrated that specific activation
of the PAG (particularly the dorsal portion) can result in mechanical hypoalgesia, altered
sympathetic tone and motor facilitation (Bandler and Shipley 1994, Benarroch 2012). The PAG
is activated in response to direct nociceptive and non-nociceptive inputs from the spinal cord,
and from a variety of supraspinal inputs (Benarroch 2012). It has projections to two areas of the
brainstem known to play an important role in descending pain modulation, the rostral ventral
medulla and dorsolateral pons (Benarroch 2012). Neurons from these areas modulate
nociceptive signals from dorsal horn neurons using serotonin and noradrenaline respectively
(Benarroch 2012, Millan 2002). This is simplistically illustrated in Figure 1.3. Additionally,
autonomic regions in the spinal cord receive significant innervation from related serotonergic
and noradrenergic descending pathways (Millan 2002).
29
Skyba et al. (2003) found that serotonergic and
noradrenergic inhibitory pathways were at least
partly responsible for the hypoalgesia following
knee mobilisation in rats, but opioids and GABA
did not appear to be involved. It is, however,
unclear whether joint mobilisation under
anaesthesia, in rodents, induces similar
biochemical changes to SM and thus these
results cannot be extrapolated to SM. Similar
human studies are limited, with three finding
that opioids are not involved in generating the
hypoalgesia following elbow mobilisation
(Paungmali et al. 2004), or spinal manual
therapy (by Vicenzino et al. 2000 and Zusman et
al. 1989, cited in Paungmali et al. 2004).
Alongside the mechanical hypoalgesia, altered autonomic tone has been observed following SM
in various studies. Decreased blood pressure and altered heart rate variability (predominantly
increased parasympathetic activity) has been noted (Mangum, Partna, and Vavrek 2012, Shafiq,
McGregor, and Murphy 2014, Win et al. 2015). Decreased skin blood flow, decreased skin
temperature, and increased skin conductance, following mobilisation has also been
demonstrated (Chu et al. 2014).
Skyba et al. (2003) postulate that afferent mechanical stimulation from joint manipulation
stimulates the PAG, which in turn activates the descending serotonergic and noradrenergic
pathways to inhibit nociceptive stimuli at the dorsal horn and alter autonomic output. This could
theoretically cause the observed post-manipulation hypoalgesia.
Figure 1.3. Serotonergic and noradrenergic
descending pain control pathways.
30
There is also some animal-model evidence that SM may alter pain processing in the lateral
thalamus (Reed et al. 2014). Since the PAG and thalamus have direct connections and exhibit a
reciprocal relationship related to pain modulation (Wu et al. 2014), it is postulated that SM may
affect pain processing in the thalamus via the PAG (Reed et al. 2014).
PAG-mediated hypoalgesia has been noted to primarily inhibit dorsal horn neurons relaying C-
fibre stimuli but not Aδ-fibre stimuli (Benarroch 2012). As highlighted in section 1.3, PPT
activates both C-fibres and Aδ-fibres, and thus would be expected to change following activation
of the PAG, while PPS stimulates only Aδ-fibres and thus would not be expected to change. It
has also been shown that SM elicits a reduction in TSS (see section 1.3.3), which is again
mediated by C-fibres, though thermal pain thresholds, mediated by Aδ-fibres, do not change.
We must also consider other biochemical research (see section 1.3.6). There is conflicting
evidence regarding serum β-endorphin (an opioid) levels following SM, though neurotensin and
oxytocin serum levels may increase. The release of oxytocin in the brainstem is modulated by
serotonergic and noradrenergic pathways, though its hypoalgesic effect is dependent upon
GABA and opioids in the dorsal horn (Millan 2002). Neurotensin, with its dual non-opioid hyper-
and hypo-algesic roles, is not well understood though is known to interplay with the
serotonergic system (Millan 2002; St-Gelais, Jomphe, and Trudeau 2006).
At present, early evidence from animal models and human studies, as well as basic science
research, fail to refute, and even support, the proposed serotonergic and noradrenergic
descending inhibitory pain control theory for post-SM hypoalgesia. More human studies to
determine if this is actually the case would be highly valuable and it is a promising direction for
future research.
31
1.3.7.2. Pain Gate Theory
The pain gate mechanism proposes that the transmission of nociceptive afferent impulses via
the dorsal horn can be inhibited by stimulating large-diameter fibres carrying non-nociceptive
afferent signals (muscle spindles, joint and cutaneous mechanoreceptors), essentially closing
the ‘gate’ and preventing nociceptive stimuli from reaching the brain (Melzack and Wall 1965).
Though details of the theory have altered over time with new research, this basic tenet is still
largely valid (Mendell 2014). It has been proposed that SM may activate the pain gate by
stimulating non-nociceptive receptors through muscle and/or facet joint stretch to generate
hypoalgesia (Potter, McCarthy, and Oldham 2005). No experimental research was identified to
support or refute this theory, though it is known (as discussed in section 1.3.4) that SM does
stimulate large-fibre mechanical afferent fibres that would be expected to activate the pain gain
mechanism. The pain gate is only a temporary mechanism to decrease transmission of
nociceptive signals while a concurrent non-nociceptive signal is being applied, so this is unlikely
to explain hypoalgesia that lasts beyond the actual treatment.
1.3.7.3. Altered Spinal Cord Dorsal Horn Excitability
Alteration of the excitability of neurons in the dorsal horn of the spinal cord (responsible for the
transmission of sensory information) in response to mechanical input has also been proposed
as a mechanism to explain post-SM hypoalgesia (Bialosky et al. 2009a). This primarily relates to
the findings of reduced TSS following SM (see section 1.3.3), which is considered to represent
reduced excitability of dorsal horn neurons (Anderson et al. 2013). This altered excitability could
theoretically affect transmission of nociceptive signals to the central nervous system and thus
mediate decreased pain sensitivity (Bishop, Beneciuk, and George 2011).
32
1.3.7.4. Placebo and Psychosocial Factors
The placebo effect is well known to occur with many interventions, and it is suggested by Potter,
McCarthy, and Oldham (2005) that SM is particularly susceptible to producing it. Maigne and
Vautravers (2003) discussed why:
A feeling that the vertebra has been returned to its normal position, a perception that
the cracking sound indicates effectiveness, and the manual contact preceding the
manipulation all contribute to the placebo effect. ... Finally, patients may perceive the
explanations supplied by SMT [spinal manipulative therapy] practitioners as more
satisfactory than those given by physicians [44].
Given that pain is a highly subjective experience, it is highly plausible that the placebo effect
may account for at least some of the hypoalgesia observed following SM. In addition,
expectation and other psychosocial factors such as fear can be involved (Bialosky et al. 2009a).
The current sham-controlled studies agree in finding greater hypoalgesia following SM than
sham (see section 1.3.1.3), which is encouraging for a real effect. It is however known to be
difficult to truly blind participants to manual therapies (Kawchuk, Haugen, and Fritz 2009).
1.4. State of the Literature
At present, there are significant gaps in our understanding of hypoalgesia following SM. We can
say with confidence that cervical SM leads to at least short term hypoalgesia. It appears that this
hypoalgesia is both local and remote, most likely only in locations with a direct neurological
connection to the site receiving SM. Thoracic SM may also produce hypoalgesia, while lumbar
SM seems not to alter local or remote pain sensitivity based on weaker evidence. The reason for
the conflicting findings between the cervical and lumbar spine remains unexplored. In addition,
research into the duration of hypoalgesia (particularly beyond 10 minutes), asymmetry, a dose-
response relationship, and differences between various populations (e.g. chronic pain vs.
33
asymptomatic) are scarce and no conclusions can be made in these areas. All of this research is
based upon PPT, and PPS remains unstudied in relation to SM. SM probably reduces TSS, and
maybe reduces chemical and electrical pain sensitivity as well.
Multiple theories for this hypoalgesia exist, and the explanation is likely complex and a
combination of factors (Bialosky et al. 2009a). Descending inhibitory pain control mechanisms,
pain gait mechanisms, altered spinal cord dorsal horn excitability, placebo and psychosocial
factors may each be involved.
The present study aims to add to the limited body of research looking at the effect of lumbar
SM on local and remote hypoalgesia to help clarify whether any effect occurs, if any effect is
local or remote, and if remote, whether it is segmental or non-segmental in nature. This study
also sets out to explore some of the current gaps by following pain sensitivity for 30 minutes,
longer than the majority of studies, and investigating any asymmetry in hypoalgesia.
As such, the research questions under investigation are:
1) Does lumbar SM affect pain sensitivity (deep and superficial) at local and remote
locations?
2) Do changes last for at least 30 minutes?
3) Are any changes related to the side of manipulation (i.e. bilateral symmetric or
asymmetric)?
2. Methods
This study followed a single-blind randomised parallel trial design. It was registered with the
Australian New Zealand Clinical Trials Registry (registration number: ACTRN12614000682640,
available at www.anzctr.org.au/ACTRN12614000682640.aspx).
34
2.1. Power Calculation
G*Power 3.1 software (University of Düsseldorf, Germany) was used for a power analysis. A
sample of 34 participants and an estimated effect size of 0.4 provides 80% power to detect a
significant difference for within and between group changes in PPT and PPS. The sample size
was limited by the time available to complete the study, thus the large effect size of 0.4 satisfied
80% power and maintained an achievable sample size.
2.2. Participant Recruitment
Participants were recruited from the student population at Murdoch University through oral
announcements during classes, flyers around the Murdoch University Campus, and the general
public via personal contacts of the first investigator.
Participants were required to be between 18 and 45 years of age, and were precluded from the
study if any of the following exclusion criteria were met:
1. Current chronic pain condition
2. Current acute or sub-acute LBP
3. Existing contraindication/s to lumbar spinal manipulation (WHO 2005), which included:
Lumbar spine fracture/dislocation, lumbar instability, lumbar intervertebral disc
or other injury, or lumbar spine surgery.
Spinal infection, spine or spinal cord tumour, rheumatologic disease,
neurological disease, lower limb neurologic symptoms, bleeding disorder, anti-
coagulant therapy, recent onset severe headache, recent infection, generalised
hypermobility, or low bone density.
4. Qualified chiropractor or student in 4th or 5th year of chiropractic university degree
5. Taken pain-relieving medication in the previous 24 hours
6. Had alcohol within the previous 12 hours
35
Upon commencement of data collection, chiropractic students at all stages of study were
excluded from participation in the interest of reducing expectancy bias among participants.
Significant difficulty in recruiting participants led to a change in the exclusion criteria, allowing
chiropractic students in their 1st, 2nd and 3rd year of study to participate. These students had yet
to receive formal lectures on the neurological effects of spinal manipulation, and thus presumed
to be less likely to introduce expectancy bias.
2.3. Randomisation
Participants were randomly assigned to group 1 or 2. Group 1 received the intervention on the
right, while group 2 received the intervention on the left. A randomisation list consisting of equal
numbers of 1s and 2s was created using the GraphPad random number generator (available at
www.graphpad.com/quickcalcs/randomN1/), and placed in sequentially numbered, opaque,
sealed envelopes by the second investigator (providing the intervention). The second
investigator used these envelopes to allocate participants to their groups immediately prior to
the intervention. Due to the nature of the intervention, participants were unable to be blinded.
2.4. Procedure
Data was collected in a designated research room at the Murdoch University campus. The
participant completed a relevant medical history form (Appendix A) to ensure eligibility, and was
then provided with an Information Letter to read (Appendix B) followed by informed consent
(Appendix C). The participants’ dominant hand was also recorded. The participant was
requested to wear appropriate clothing on the day, to allow access to the areas under
investigation. If clothing prevented access to the skin at these sites, the participant was asked
to don a clean clinical examination gown for the duration of the study.
The following points were then marked bilaterally on the participant’s skin with a non-
permanent marker by the first investigator (Figure 2.1):
36
2cm lateral and inferior to the root
of the spine of the scapula, over the
infraspinatus muscle,
2cm lateral to the L5 spinous
process, over the lumbar
paraspinal muscles,
Half way down the medial head of
the gastrocnemius muscle, and
The frontal eminence of the frontal
bone.
The scapular site was chosen as an easily
accessible remote location that has no neurological connection with the region of the spine
receiving manipulation. The lumbar site is local, being directly adjacent to the site of
manipulation. The gastrocnemius site was chosen as it is innervated by L5/S1, thus is
segmentally related to the site of manipulation. The frontal eminence site was chosen as it is
remote and lies within the cranial nerve distribution. These were chosen to allow us to
determine whether any effects of lumbar spinal manipulation were purely local, segmental, or
centrally driven.
The PPT and PPS measures were taken by the first investigator, at the above locations. The
procedure for measuring PPT and PPS was explained to the participant, and baseline
measurements taken at the eight sites. The intervention was then applied to the participant by
the second investigator, while the first investigator left the room (thus blinded to the side of
intervention). PPT and PPS were then measured by the first investigator at each site immediately
after the intervention, and at 10 minutes, 20 minutes and 30 minutes post-intervention. The
participant was then free to leave.
Figure 2.1. Testing sites.
37
2.5. Pressure Pain Threshold
PPT was measured using a Wagner FDIX pressure
algometer with a 1cm2 rubber probe. This was
standardised and calibrated against a Kistler force
plate prior to taking outcome measures. The
participant was instructed on the procedure, and
asked to say “Yes” when the sensation of pressure
from the algometer first changed to pain. The
algometer was placed perpendicular to the skin and
increasing pressure applied at a rate of 500g/s until the participant said “Yes”, at which point
the investigator removed the algometer and the maximum was pressure recorded (Figure 2.2).
This technique was described and validated by Fischer (1987). Two practice measurements on
the back of the hand were performed first, to ensure the participant understood the procedure.
Actual measurements were performed three times at each site, following a circuit to allow
sufficient rest time between measures at each site. The participant lay prone, having the first
measure at the gastrocnemius, lumbar and infraspinatus sites on each side (left then right) taken
in succession. The participant was then asked to lay supine to take the first forehead
measurements. This was repeated twice more to achieve a total of three measures per site. This
method was validated by Bisset, Evans, and Tuttle (2015). The average of the second and third
measures was used for analysis, found to be reliable by Lacourt, Houtveen, and van Doornen
(2012). The cut-off point was set at 10kg/cm2 for the forehead and infraspinatus sites (Lacourt,
Houtveen, and van Doornen 2012), and at 12.5kg/cm2 for the lumbar and gastrocnemius sites
as this was the upper measurement limit of the algometer. If the pressure reached this value
without the participant saying “Yes”, the cut off value was taken as the value for that
measurement and no further pressure applied.
Figure 2.2. Wagner algometer.
38
2.6. Pinprick Sensitivity
PPS was measured by determining
the intensity of a pinprick
sensation, using the Neuropen
(Owen Mumford 2014) with
Neurotips™ (Figure 2.3). This device
is designed to consistently exert 40g of force when the Neurotip™ is pressed into the skin (Owen
Mumford 2014), though no reliability studies exist. An 11-point Numerical Rating Scale (NRS)
was used where 0 = not sharp, and 10 = extremely sharp, as used previously in an experimental
trial (Vo and Drummond 2013). The Neurotip™ was placed perpendicular to the skin and pressed
in until the guiding markers on the Neuropen were aligned, maintained for one second and then
the Neurotip™ removed. The participant was asked to verbally report the severity of the
sharpness using the NRS. Two practice measurements on the muscle bulk at the base of the
thumb were performed first. Actual measurements were performed once at each site,
immediately following the completion of all PPT measures. A new Neurotip™ was used for each
participant, with used tips being discarded into a sealable sharps container.
2.7. Spinal Manipulation
HVLA SM was applied to the L5-S1 spinal segment. A technique commonly used by chiropractors,
referred to as the hypothenar mammillary push (Bergmann and Peterson 2011, 253-254), was
used (Figure 2.4). The second
investigator (with 15 years of
clinical and academic experience)
applied the SM with the participant
in the side-lying position, taking a
contact upon the L5 mamillary
process on the appropriate side of
Figure 2.3. Neuropen with semi-sharp tip.
Figure 2.4. Right-sided L5 spinal manipulation technique.
39
the participant, based on their randomisation. For example, if the participant was randomised
to group 1, they were asked to lie on their left-hand side and the SM was applied to the right
side of the lumbar spine. The success of the procedure was subjectively determined by the
investigator, and not based upon the occurrence of a cavitation which seems to be unimportant
(see section 1.2.3).
2.8. Data Analysis
The algometer used in this study was standardised against a standard Kistler force plate prior to
collecting data. Pearson’s coefficient of correlation (two-tailed) and the mean of the differences
was determined using SPSS version 23.
Pain sensitivity data was entered into and analysed using the statistical package SPSS Version
23. The data was checked for implausabilities and outliers, and five random samples were
examined for data entry errors. A repeated measures analysis of variance was conducted for
PPT and for PPS, at each location (calf, lumbar spine, scapula, and forehead). Each had factors
of Time (baseline, immediately after intervention, 10min, 20min and 30min), Side
(measurement taken on right or left side of the body), and Group (participants received either
right lumbar SM [R-SM] or left lumbar SM [L-SM]). Simple contrasts between baseline and each
subsequent time point were included in the analyses to investigate effects of the intervention
at each time point. Further interactions were investigated using paired t-tests. Mean PPT or PPS
values and standard deviations (SD) are reported for each significant interaction. Effect sizes are
reported in the form of partial Eta squared (ηP2), where ≥0.10, ≥0.25, and ≥0.50 are considered
to represent small, moderate and large effect sizes respectively (Richardson 2011).
40
3. Results
3.1. Algometer Standardisation
The Wagner FDIX algometer was standardised against a Kistler Force Plate prior to data
collection. The correlation was 0.99, which is significant at the p = 0.01 level (2-tailed). The line
of best fit had a slope of y = 0.11+0.97*x (Figure 3.1). There is however, a mean difference in the
readings between the two instruments of 0.30kg/cm2 (SD 0.10). It was determined that the
Wagner algometer was a reliable and valid instrument for the purposes of this study.
Kistler vs. Wagner pressure correlation
Kistler force plate measurement (kg/cm2)
0 1 2 3 4 5 6 7 8 9 10
Wa
gn
er
alg
om
ete
r m
ea
su
rem
en
t (k
g/c
m2)
1
2
3
4
5
6
7
8
9
10
Figure 3.1. Correlation between Wagner algometer and Kistler force plate pressure measurements.
3.2. Pain Sensitivity Results
In total, 34 participants (20 male) completed data collection and were included in analysis
(Figure 3.2), with an average age of 22.56 years (SD 3.99, range 18 - 36 years). Data was collected
between October 2014 and June 2015, and recruitment ended when 34 participants had
successfully completed data collection. Baseline characteristics of the participants are reported
in Table 3.1. No harms were reported during or after the follow-up period.
41
Figure 3.2. Flow diagram of trial, investigating right vs. left lumbar spinal manipulation for pressure
pain threshold and pinprick sensitivity.
Table 3.1. Baseline characteristics.
R-SM L-SM
Actual difference
(% difference)
Gender 8 female, 9 male 6 female, 11 male -
Age (mean age in years) 22.59 (SD 3.10) 22.53 (SD 4.81) 0.06 (0.27)
Dominant hand 11 right, 6 left 16 right, 1 left -
Calf PPT (kg/cm2) 5.10 (SD 2.23) 4.48 (SD 1.87) 0.62 (12.16)
Lumbar Spine PPT (kg/cm2) 7.12 (SD 2.88) 5.89 (SD 2.64) 1.23 (17.28)
Scapula PPT (kg/cm2) 5.05 (SD 1.89) 4.13 (SD 1.85) 0.92 (18.22)
Forehead PPT (kg/cm2) 2.83 (SD 0.96) 2.38 (SD 0.95) 0.45 (15.90)
Calf PPS (0-10 scale) 4.12 (SD 2.18) 5.12 (SD 2.36) 1.00 (19.53)
Lumbar Spine PPS (0-10 scale) 4.32 (SD 1.60) 5.26 (SD 2.14) 0.94 (17.87)
Scapula PPS (0-10 scale) 3.24 (SD 1.69) 4.53 (SD 2.01) 1.29 (28.48)
Forehead PPS (0-10 scale) 4.35 (SD 1.79) 5.26 (SD 2.35) 0.91 (17.30)
Abbreviations: SD = standard deviation, PPT = pressure pain threshold, PPS = pinprick sensitivity.
42
Two cells had missing data, the first due to an algometer error and the second due to a recording
error. These two missing values were Left Scapula PPT at Baseline for participant six, and Right
Lumbar PPT Immediately after Intervention for participant 19. For participants with complete
data, the second and third PPT measures at the specific location and time point were averaged
to arrive at a given cell’s value, with the first PPT measure remaining unused. Since the cells of
interest were missing the second and third, respectively, of their PPT measures, the data for
those cells were imputed by substituting just the remaining third or second measure
respectively, into the cell. This imputed value was decided to be most appropriate as t-tests
revealed that the means of the second and third PPT measures in each participant were very
similar (Table 3.2). The differences in the means between the first and second, and first and third
measures were non-significant in participant 6 (but with a greater mean difference than second
vs. third), and significantly different in participant 19. Thus it was concluded that imputing the
data in this conservative manner as described above was likely to give the closest estimate of
the true value.
Table 3.2. Comparison of first, second and third PPT measures in participants with missing data.
p-value (mean PPT difference in kg/cm2)
Participant 6
scapula
Participant 19
lumbar spine
First vs. second .172 (0.636) .013* (1.43)
Second vs. third .846 (-0.05) .729 (-0.18)
First vs. third .279 (0.30) .026* (1.26)
Abbreviations: PPT = pressure pain threshold, * = p ≤ .05.
The Shapiro-Wilk test for normality indicated numerous deviations from a normal distribution
(see Appendix D). The repeated measures ANOVA is generally considered to be fairly robust to
deviations from normality, unless the deviations are extreme or the sample size particularly low
(Norman and Streiner 2008). Visual inspection of the data’s histograms and Q-Q plots revealed
only mild to moderate deviations from a normal distribution. Thus it was concluded that the
repeated measures ANOVA was an appropriate test to use for this data.
43
3.2.1. Calf Pressure Pain Threshold
There was a significant main effect for Time (p = .034 [with Greenhouse-Geisser correction])
with a weak effect size (ηP2 = .09). Post-hoc tests revealed a trend that approached statistical
significance between calf PPT at baseline and 10min, and significant differences between
baseline and 20min, and baseline and 30min, each with weak effect sizes. There was no
significant difference between baseline and immediately after SM. These data indicate an
increase in calf PPT over time, which was significant at 20min and 30min, of 9.6% and 9.0%
respectively (Table 3.3 and Figure 3.3).
Table 3.3. Mean calf PPT at baseline, immediately after intervention, and at 10, 20, and 30 minutes.
Mean calf PPT, kg/cm2
Actual difference
compared to Baseline in
kg/cm2 (% difference)
p-value for difference
compared to Baseline
Baseline 4.79 (SD 2.05) - -
Immediate 5.05 (SD 2.23) 0.26 (5.4%) .111 (ηP2 .08)
10min 5.14 (SD 2.18) 0.35 (7.3%) .053 (ηP2 .11)
20min 5.25 (SD 2.17) 0.46 (9.6%) .017* (ηP2 .17)
30min 5.22 (SD 2.00) 0.43 (9.0%) .027* (ηP2 .14)
Abbreviations: PPT = pressure pain threshold, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
Calf, lumbar spine, scapula and forehead PPT over time
Time
Baseline Immediate 10min 20min 30min
PP
T (
kg
/cm
2)
0
1
2
3
4
5
6
7
8
* * *
* *
Lumbar
spine
Calf
Scapula
Forehead
Figure 3.3. Mean calf, lumbar spine, scapula and forehead PPT at baseline, immediately after
intervention, and at 10, 20, and 30 minutes. Abbreviations: PPT = pressure pain threshold, * = p ≤ .05.
44
There was a significant main effect for Side (p = .001) with a moderate effect size (ηP2 = .32). Calf
PPT had a mean of 5.37 kg/cm2 (SD 2.17) on the right, and 4.81 kg/cm2 (SD 2.02) on the left.
These data indicate that the right calf had a significantly higher PPT than the left calf, with a
difference of 0.56 kg/cm2.
There was no significant overall effect for Time by Side by Group (p = .201, ηP2 = .05). However,
within-subject contrasts revealed a significant difference with weak effect size between baseline
and 10min, and a trend toward significance between baseline and 20min. There were no
differences between baseline and immediately after SM, or baseline and 30min. The difference
between the right and left calf PPT measures appears to increase by 0.45 kg/cm2 after R-SM, but
decrease by 0.19 kg/cm2 after L-SM, when comparing baseline to 10min (Table 3.4 and Figure
3.4).
Table 3.4. Mean calf PPT on the right and left sides in each group, at baseline, immediately after
intervention, and at 10, 20, and 30 minutes.
Mean calf PPT, kg/cm2 p-value for
difference
compared to
Baseline R-SM group L-SM group
Baseline Right 5.30 (SD 2.49) Right 4.79 (SD 1.77) -
Left 4.90 (SD 2.17) Left 4.17 (SD 2.06)
Immediate Right 5.65 (SD 2.29) Right 4.95 (SD 2.60) .207 (ηP
2 .05) Left 5.07 (SD 1.82) Left 4.55 (SD 2.39)
10min Right 5.76 (SD 2.56) Right 5.16 (SD 2.19) .032* (ηP
2 .14) Left 4.91 (SD 2.01) Left 4.73 (SD 2.22)
20min Right 5.78 (SD 1.99) Right 5.21 (SD 2.51) .061 (ηP
2 .11) Left 5.06 (SD 1.92) Left 4.93 (SD 2.52)
30min Right 5.70 (SD 1.98) Right 5.39 (SD 2.35) .157 (ηP
2 .06) Left 4.90 (SD 1.73) Left 4.87 (SD 2.24)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
45
Calf PPT Time by Side by Group
Time
Baseline Immediate 10 min 20 min 30 min
PP
T (
kg
/cm
2)
0
2
3
4
5
6
7
R-SM Right Calf
R-SM Left Calf
L-SM Right Calf
L-SM Left Calf
Figure 3.4. Mean calf PPT on the right and left sides in each group, at baseline, immediately after
intervention, and at 10, 20, and 30 minutes. Abbreviations: PPT = pressure pain threshold, R-SM = right-
sided spinal manipulation, L-SM = left-sided spinal manipulation.
There were no significant effects for Group (p = .550, ηP2 = .01), Time by Group (p = .520, ηP
2 =
.03), Side by Group (p = .459, ηP2 = .02), or Time by Side (p = .699, ηP
2 = .02) for calf PPT.
3.2.2. Lumbar Spine Pressure Pain Threshold
There was a significant main effect for Time (p = .003 [with Greenhouse-Geisser correction])
with a weak effect size (ηP2 = .15). Post-hoc tests revealed significant differences with weak
effect sizes between lumbar PPT at baseline and 10min, baseline and 20min, and baseline and
30min, but not between baseline and immediately after SM. These data indicate a significant
increase in lumbar spine PPT from baseline to 10min, 20min and 30min of 7.2%, 9.2% and 11.8%
respectively (Table 3.5 and Figure 3.3).
46
Table 3.5. Mean lumbar spine PPT at baseline, immediately after intervention, and at 10, 20, and 30
minutes.
Mean lumbar spine
PPT, kg/cm2
Actual difference compared to Baseline in
kg/cm2 (% difference)
p-value for difference compared to Baseline
Baseline 6.50 (SD 2.79) - -
Immediate 6.74 (SD 2.72) 0.24 (3.7%) .247 (ηP2 .04)
10min 6.97 (SD 2.53) 0.47 (7.2%) .033* (ηP2 .13)
20min 7.10 (SD 2.66) 0.6 (9.2%) .011* (ηP2 .19)
30min 7.27 (SD 2.61) 0.77 (11.8%) .007* (ηP2 .21)
Abbreviations: PPT = pressure pain threshold, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
There was a significant main effect for Side (p = .006) with a weak effect size (ηP2 = .21). Lumbar
PPT had a mean of 7.11 kg/cm2 (SD 2.71) on the right, and 6.72 kg/cm2 (SD 2.51) on the left.
These data indicate that the right lumbar spine had a significantly higher PPT than the left lumbar
spine, with a difference of 0.39 kg/cm2.
There was an effect approaching significance for Side by Group (p = .057) with a weak effect size
(ηP2 = .11). The difference between right and left lumbar PPT was greater after R-SM than after
L-SM, but this did not reach significance (Table 3.6).
Table 3.6. Mean lumbar spine PPT on right and left sides in each group.
Mean lumbar spine PPT, kg/cm2 Actual difference
between sides in
kg/cm2 (% difference) Right side Left side
R-SM group 7.85 (SD 2.59) 7.19 (SD 2.43) 0.66 (8.4%)
L-SM group 6.38 (SD 2.70) 6.25 (SD 2.57) 0.13 (2.0%)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, SD = standard deviation.
There was no main effect for Group (p = .178, ηP2 = .06), and no significant effects for Time by
Group (p = .975, ηP2 = .00), Time by Side (p = .340, ηP
2 = .03), or Time by Side by Group (p = .245,
ηP2 = .04) for lumbar spine PPT.
47
3.2.3. Scapula Pressure Pain Threshold
There were no main effects for Time (p = .705 [with Greenhouse-Geisser correction], ηP2 =
.01)(Table 3.7 and Figure 3.3), Side (p = .865, ηP2 = .00), or Group (p = .098, ηP
2 = .08) for scapula
PPT.
Table 3.7. Mean scapula PPT at baseline, immediately after intervention, and at 10, 20, and 30
minutes.
Mean scapula PPT,
kg/cm2
Actual difference compared to Baseline in
kg/cm2 (% difference)
p-value for difference compared to Baseline
Baseline 4.59 (SD 1.90) - -
Immediate 4.58 (SD 2.03) -0.01 (0.2%) .881 (ηP2 .00)
10min 4.70 (SD 2.05) 0.11 (2.4%) .450 (ηP2 .02)
20min 4.71 (SD 1.95) 0.12 (2.6%) .439 (ηP2 .02)
30min 4.68 (SD 1.71) 0.09 (2.0%) .581 (ηP2 .01)
Abbreviations: PPT = pressure pain threshold, SD = standard deviation, ηP2 = effect size.
There was no overall significant effect for Time by Side (p = .271 [with Greenhouse-Geisser
correction], ηP2 = .04). Within-subject contrasts revealed a significant difference with weak effect
size between baseline and immediately after SM, but not between baseline and 10min, baseline
and 20min, or baseline and 30min. These data indicate that there was a significant difference
where at baseline, right scapula PPT was higher than the left, but immediately following the SM,
right scapula PPT was lower than the left. The actual differences, however, were small (Table
3.8).
Table 3.8. Mean scapula PPT on the right and left sides at baseline, immediately after intervention,
and at 10, 20, and 30 minutes.
Mean scapula PPT, kg/cm2 Actual difference
between sides in
kg/cm2 (% difference)
p-value for diff-
erence compared
to Baseline Right side Left side
Baseline 4.65 (SD 2.03) 4.54 (SD 1.92) 0.11 (2.4%) -
Immediate 4.50 (SD 2.14) 4.65 (SD 2.07) -0.15 (3.3%) .032* (ηP2 .14)
10min 4.75 (SD 2.24) 4.64 (SD 1.99) 0.11 (2.3%) .992 (ηP2 .00)
20min 4.75 (SD 2.10) 4.66 (SD 1.94) 0.09 (1.9%) .797 (ηP2 .00)
30min 4.66 (SD 1.76) 4.69 (SD 1.81) -0.03 (0.6%) .403 (ηP2 .02)
Abbreviations: PPT = pressure pain threshold, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
48
The Time by Side by Group interaction was nearing significance (p = .064, ηP2 = .07). Contrasts
revealed a significant difference between baseline and 20min with a weak effect size, but not
between baseline and immediately after SM, baseline and 10min, or baseline and 30min. After
R-SM, the difference between the right and left scapula PPT measures appears to increase from
baseline to 20min, with the right remaining higher than the left. After L-SM, scapula PPT is
almost identical at baseline, with the left PPT becoming higher than the right at 20min (Table
3.9 and Figure 3.5).
Table 3.9. Mean scapula PPT on the right and left sides in each group, at baseline, immediately after
intervention, and at 10, 20, and 30 minutes.
Mean scapula PPT, kg/cm2 p-value for
difference
compared to
Baseline R-SM group L-SM group
Baseline Right 5.17 (SD 2.13) Right 4.13 (SD 1.83) -
Left 4.94 (SD 1.83) Left 4.14 (SD 1.97)
Immediate Right 5.27 (SD 2.12) Right 3.74 (SD 1.94) .145 (ηP
2 .07) Left 5.12 (SD 1.69) Left 4.18 (SD 2.35)
10min Right 5.48 (SD 2.38) Right 4.03 (SD 1.89) .987 (ηP
2 .00) Left 5.25 (SD 2.03) Left 4.03 (SD 1.82)
20min Right 5.36 (SD 1.98) Right 4.13 (SD 2.09) .030* (ηP
2 .14) Left 4.88 (SD 1.63) Left 4.45 (SD 2.24)
30min Right 5.19 (SD 1.70) Right 4.14 (SD 1.71) .620 (ηP
2 .01) Left 5.18 (SD 1.77) Left 4.21 (SD 1.77)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
49
Scapula PPT Time by Side by Group
Time
Baseline Immediate 10 min 20 min 30 min
PP
T (
kg
/cm
2)
0
2
3
4
5
6
R-SM Right Scapula
R-SM Left Scapula
L-SM Right Scapula
L-SM Left Scapula
Figure 3.5. Mean scapula PPT on the right and left sides in each group, at baseline, immediately after
intervention, and at 10, 20, and 30 minutes. Abbreviations: PPT = pressure pain threshold, R-SM = right-
sided spinal manipulation, L-SM = left-sided spinal manipulation.
There were no significant effects for Time by Group (p = .255, ηP2 = .04) or Side by Group (p =
.235, ηP2 = .04) for scapula PPT.
3.2.4. Forehead Pressure Pain Threshold
There were no main effects for Time (p = .668 [with Greenhouse-Geisser correction], ηP2 =
.01)(Table 3.10 and Figure 3.3), Side (p = .641, ηP2 = .01), or Group (p = .256, ηP
2 = .04) for
forehead PPT.
Table 3.10. Mean forehead PPT at baseline, immediately after intervention, and at 10, 20, and 30
minutes.
Mean forehead PPT,
kg/cm2
Actual difference compared to Baseline, kg/cm2 (% difference)
p-value for difference compared to Baseline
Baseline 2.61 (SD 0.97) - -
Immediate 2.67 (SD 1.06) 0.06 (2.3%) .399 (ηP2 .02)
10min 2.67 (SD 1.08) 0.06 (2.3%) .446 (ηP2 .02)
20min 2.66 (SD 0.99) 0.05 (1.9%) .582 (ηP2 .01)
30min 2.69 (SD 1.03) 0.08 (3.1%) .344 (ηP2 .03)
Abbreviations: PPT = pressure pain threshold, SD = standard deviation, ηP2 = effect size.
50
The interaction Time by Side was nearing significance (p = .059, ηP2 = .07). Contrasts revealed a
significant difference with weak effect size between baseline and 20min, but no significant
differences between baseline and immediately after SM, baseline and 10min, or baseline and
30min. The data indicate that at baseline, forehead PPT on the right was higher than the left,
however at 20min, the left was higher than the right. The differences were very small (Table
3.11).
Table 3.11. Mean forehead PPT on the right and left sides at baseline, immediately after intervention,
and at 10, 20, and 30 minutes.
Mean forehead PPT, kg/cm2 Actual difference
between sides in
kg/cm2 (% difference)
p-value for diff-
erence compared
to Baseline Right side Left side
Baseline 2.64 (SD 1.04) 2.57 (SD 0.93) 0.07 (2.7%) -
Immediate 2.67 (SD 1.15) 2.67 (SD 1.00) 0.00 (0.0%) .214 (ηP2 .05)
10min 2.71 (SD 1.18) 2.64 (SD 1.03) 0.07 (2.6%) .947 (ηP2 .00)
20min 2.63 (SD 1.04) 2.69 (SD 0.98) -0.06 (2.3%) .014* (ηP2 .18)
30min 2.72 (SD 1.10) 2.66 (SD 0.98) 0.06 (2.2%) .721 (ηP2 .00)
Abbreviations: PPT = pressure pain threshold, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
There was no significant overall Time by Side by Group interaction (p = .180, ηP2 = .05), but
contrasts revealed a significant difference with weak effect size between baseline and
immediately after SM. There were no significant differences between baseline and 10min,
baseline and 20min, or baseline and 30min. The difference between the right and left forehead
PPT measures appears to decrease after R-SM, but increase after L-SM, when comparing
baseline to immediately after SM (Table 3.12 and Figure 3.6). However, the differences were
quite small, between 0.05 - 0.11kg/cm2.
51
Table 3.12. Mean forehead PPT on the right and left sides in each group, at baseline, immediately
after intervention, and at 10, 20, and 30 minutes.
Mean forehead PPT, kg/cm2 p-value for
difference
compared to
Baseline R-SM group L-SM group
Baseline Right 2.91 (SD 1.05) Right 2.38 (SD 0.98) -
Left 2.75 (SD 0.90) Left 2.39 (SD 0.96)
Immediate Right 2.82 (SD 0.97) Right 2.53 (SD 1.32) .017* (ηP
2 .17) Left 2.86 (SD 0.87) Left 2.47 (SD 1.10)
10min Right 2.91 (SD 1.08) Right 2.50 (SD 1.26) .354 (ηP
2 .03) Left 2.82 (SD 1.01) Left 2.46 (SD 1.05)
20min Right 2.83 (SD 0.94) Right 2.42 (SD 1.11) .216 (ηP
2 .05) Left 2.88 (SD 0.88) Left 2.50 (SD 1.05)
30min Right 2.94 (SD 0.96) Right 2.50 (SD 1.21) .465 (ηP
2 .02) Left 2.84 (SD 0.82) Left 2.49 (SD 1.12)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
There were no significant effects for Time by Group (p = .953, ηP2 = .01) or Side by Group (p =
.671, ηP2 = .01) for forehead PPT.
Forehead PPT Time by Side by Group
Time
Baseline Immediate 10 min 20 min 30 min
PP
T (
kg
/cm
2)
0
1
2
3
4
R-SM Right Forehead
R-SM Left Forehead
L-SM Right Forehead
L-SM Left Forehead Figure 3.6. Mean forehead PPT on the right and left sides in each group, at baseline, immediately after
intervention, and at 10, 20, and 30 minutes. Abbreviations: PPT = pressure pain threshold, R-SM = right-
sided spinal manipulation, L-SM = left-sided spinal manipulation.
52
3.2.5. Calf Pinprick Sensitivity
There was a significant main effect for Time (p = .008) with a weak effect size (ηP2 = .10). Within-
subject contrasts revealed a significant difference between baseline and 20min, and baseline
and 30min, each with a weak effect size. There were no significant differences between baseline
and immediately after SM, or baseline and 10min. These data indicate that calf PPS scores
decreased over time, which was significant when comparing baseline to 20min and 30min, with
11.5% and 13.6% change respectively (Table 3.13 and Figure 3.7).
Table 3.13. Mean calf PPS at baseline, immediately after intervention, and at 10, 20, and 30 minutes.
Mean calf PPS, 0-10
scale
Actual difference compared to Baseline (%
difference)
p-value for difference compared to Baseline
Baseline 4.62 (SD 2.29) - -
Immediate 4.60 (SD 2.07) 0.02 (0.4%) .943 (ηP2 .00)
10min 4.47 (SD 2.41) 0.15 (3.2%) .514 (ηP2 .01)
20min 4.09 (SD 2.22) 0.53 (11.5%) .039* (ηP2 .13)
30min 3.99 (SD 2.21) 0.63 (13.6%) .021* (ηP2 .16)
Calf PPS over time
Time
Baseline Immediate 10min 20min 30min
PP
S (
0-1
0 s
ca
le)
0
1
2
3
4
5
6
7
8
* *
Figure 3.7. Mean calf PPS at baseline, immediately after intervention, and at 10, 20, and 30 minutes
with standard deviation bars. Abbreviations: PPS = pinprick sensitivity, * = p ≤ .05.
Abbreviations: PPS = pinprick sensitivity, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
53
There was a significant main effect for Side (p = .049) with a weak effect size (ηP2 .12). The mean
right calf PPS (4.45 [SD 2.08]) was significantly higher than the mean left calf PPS (4.25 [SD 2.15]),
with a mean difference of 0.2.
There was no overall interaction for Time by Side (p = .291, ηP2 = .04). However, contrasts
revealed a significant difference between baseline and 20min with weak effect size. There were
no significant differences between baseline and immediately after SM, baseline and 10min, or
baseline and 30min. These data indicate that there was a significant difference, where the
difference between right and left calf PPS at baseline was significantly smaller than the
difference at 20min (Table 3.14).
There was no significant main effect for Group (p = .218, ηP2 = .05). There were no significant
interactions for Time by Group (p = .944, ηP2 = .01), Side by Group (p = .287, ηP
2 = .04), or Time
by Side by Group (p = .506, ηP2 = .03).
Table 3.14. Mean calf PPS on the right and left sides at baseline, immediately after intervention, and
at 10, 20, and 30 minutes.
Mean calf PPS, 0-10 scale Actual difference
between sides (%
difference)
p-value for diff-
erence compared
to Baseline Right side Left side
Baseline 4.68 (SD 2.16) 4.56 (SD 2.54) 0.12 (2.6%) -
Immediate 4.62 (SD 2.16) 4.59 (SD 2.23) 0.03 (0.6%) .798 (ηP2 .00)
10min 4.47 (SD 2.55) 4.47 (SD 2.40) 0.00 (0.0%) .679 (ηP2 .01)
20min 4.38 (SD 2.40) 3.79 (SD 2.14) 0.59 (13.5%) .042* (ηP2 .12)
30min 4.12 (SD 2.13) 3.85 (SD 2.52) 0.27 (6.6%) .563 (ηP2 .01)
Abbreviations: PPS = pinprick sensitivity, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
3.2.6. Lumbar Spine Pinprick Sensitivity
There was a significant main effect for Time (p = .000), with a weak effect size (ηP2 = .21). Post-
hoc testing revealed a significant difference between all levels, baseline and immediately after
SM, 10min, 20min, and 30min, each with weak to moderate effect sizes. These data indicate
54
that lumbar spine PPS decreased over time from baseline to each time point by 13.4%, 18%,
17.1% and 22.5% at 10min, 20min and 30min respectively (Table 3.15 and Figure 3.8).
There were no main effects for Side (p = .910, ηP2 = .00) or Group (p = .255, ηP
2 = .04). There were
no significant interactions for Time by Group (p = .575, ηP2 = .02), Side by Group (p = .279 , ηP
2 =
.04), Time by Side (p = .600, ηP2 = .02), or Time by Side by Group (p = .753, ηP
2 = .02).
Table 3.15. Mean lumbar spine PPS at baseline, immediately after intervention, and at 10, 20, and 30
minutes.
Mean lumbar spine
PPS, 0-10 scale
Actual difference compared to Baseline (%
difference)
p-value for difference compared to Baseline
Baseline 4.79 (SD 1.92) - -
Immediate 4.15 (SD 2.11) 0.64 (13.4%) .003* (ηP2 .24)
10min 3.93 (SD 2.35) 0.86 (18.0%) .001* (ηP2 .30)
20min 3.97 (SD 1.99) 0.82 (17.1%) .001* (ηP2 .29)
30min 3.71 (SD 2.16) 1.08 (22.5%) .000* (ηP2 .42)
Abbreviations: PPS = pinprick sensitivity, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
Lumbar PPS over time
Time
Baseline Immediate 10min 20min 30min
PP
S (
0-1
0 s
ca
le)
0
1
2
3
4
5
6
7
8
* **
*
Figure 3.8. Mean lumbar spine PPS at baseline, immediately after intervention, and at 10, 20, and 30
minutes with standard deviation bars. Abbreviations: PPS = pinprick sensitivity, * = p ≤ .05.
55
3.2.7. Scapula Pinprick Sensitivity
There was no significant main effect for time (p = .127, ηP2 = .054). Post-hoc testing revealed a
significant difference between baseline and 10min, and baseline and 20min with weak effect
sizes, but not between baseline and immediately after SM, or baseline and 30min. The data
indicate that scapula PPS decreased from baseline to 10min and 20min by 12.4% and 9.8%
respectively (Table 3.16 and Figure 3.9).
Table 3.16. Mean scapula PPS at baseline, immediately after intervention, and at 10, 20, and 30
minutes.
Mean scapula PPS, 0-
10 scale
Actual difference compared to Baseline
(% difference)
p-value for difference compared to Baseline
Baseline 3.88 (SD 1.94) - -
Immediate 3.62 (SD 2.07) 0.26 (6.7%) .278 (ηP2 .04)
10min 3.40 (SD 1.91) 0.48 (12.4%) .025* (ηP2 .15)
20min 3.50 (SD 2.07) 0.38 (9.8%) .035* (ηP2 .13)
30min 3.54 (SD 1.95) 0.34 (8.8%) .111 (ηP2 .08)
Abbreviations: PPS = pinprick sensitivity, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
Scapula PPS over time
Time
Baseline Immediate 10min 20min 30min
PP
S (
0-1
0 s
ca
le)
0
1
2
3
4
5
6
7
8
* *
Figure 3.9. Mean scapula PPS at baseline, immediately after intervention, and at 10, 20, and 30
minutes with standard deviation bars. Abbreviations: PPS = pinprick sensitivity, * = p ≤ .05.
There was a significant main effect for Group with a weak effect size (p = .041, ηP2 = .12), where
the R-SM group had a mean scapula PPS of 2.94 (SD 1.38), and the L-SM group had a mean of
56
4.24 (SD 2.09). This is likely explained by baseline differences in scapula PPS, which were
substantially lower after R-SM than L-SM (Table 3.1).
There was a significant interaction for Side by Group (p = .028) with a weak effect size (ηP2 = .14).
The data indicate that there was a significant difference where after R-SM, right scapula PPS was
lower than the left, but after L-SM, right scapula PPS was higher than the left (Table 3.17).
Table 3.17. Mean scapula PPS on right and left sides in each group.
Mean scapula PPS, 0-10 scale Actual difference
between sides Right side Left side
R-SM group 2.81 (SD 1.47) 3.07 (SD 1.41) -0.26 (9.3%)
L-SM group 4.44 (SD 2.25) 4.04 (SD 2.01) 0.40 (9.0%)
Abbreviations: PPS = pinprick sensitivity, R-SM = right-sided spinal manipulation, L-SM = left-sided spinal
manipulation, SD = standard deviation.
There was no significant main effect for Side (p = .625, ηP2 = .01). There were no significant
interactions for Time by Group (p = .982, ηP2 = .00), Time by Side (p = .373, ηP
2 = .03), or Time by
Side by Group (p = .468, ηP2 = .03).
3.2.8. Forehead Pinprick Sensitivity
There was a significant main effect for Time (p = .018 [with Greenhouse-Geisser correction])
with a weak effect size (ηP2 = .10). Post-hoc tests revealed significant differences with weak
effect sizes between forehead PPS at baseline and 10min, baseline and 20min, and baseline and
30min, but not between baseline and immediately after SM. The data indicate that forehead
PPS decreased significantly over time from baseline to 10min, 20min and 30min, by 10.8%,
14.8% and 13.1% respectively (Table 3.18 and Figure 3.10).
57
Table 3.18. Mean forehead PPS at baseline, immediately after intervention, and at 10, 20, and 30
minutes.
Mean forehead PPS, 0-
10 scale
Actual difference compared to Baseline
(% difference)
p-value for difference compared to Baseline
Baseline 4.81 (SD 2.11) - -
Immediate 4.68 (SD 2.17) 0.13 (2.7%) .447 (ηP2 .02)
10min 4.29 (SD 2.03) 0.52 (10.8%) .039* (ηP2 .13)
20min 4.10 (SD 1.98) 0.71 (14.8%) .007* (ηP2 .20)
30min 4.18 (SD 2.26) 0.63 (13.1%) .049* (ηP2 .12)
Abbreviations: PPS = pinprick sensitivity, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
There was a significant main effect for Side (p = .001) with a moderate effect size (ηP2 = .29). The
mean forehead PPS on the right was 4.63 (SD 2.09), and on the left was 4.19 (SD 1.85). This
indicates that forehead PPS was significantly higher on the right than the left, with a difference
of 0.44.
Forehead PPS over time
Time
Baseline Immediate 10min 20min 30min
PP
S (
0-1
0 s
ca
le)
0
1
2
3
4
5
6
7
8
* * *
Figure 3.10. Mean forehead PPS at baseline, immediately after intervention, and at 10, 20, and 30
minutes with standard deviation bars. Abbreviations: PPS = pinprick sensitivity, * = p ≤ .05.
There was no significant interaction for Time by Side (p = .405, ηP2 = .03). However, contrasts
revealed a significant difference between baseline and 30min with a weak effect size. There
were no significant differences between baseline and immediately after SM, baseline and
58
10min, or baseline and 20min. The data indicate that there was a significant difference where
the difference between right and left forehead PPS at baseline was significantly smaller than the
difference at 30min (Table 3.19).
Table 3.19. Mean forehead PPS on the right and left sides at baseline, immediately after intervention,
and at 10, 20, and 30 minutes.
Mean forehead PPS, 0-10 scale Actual difference
between sides (%
difference)
p-value for diff-
erence compared to
Baseline Right side Left side
Baseline 4.94 (SD 2.24) 4.68 (SD 2.06) 0.26 (5.3%) -
Immediate 4.88 (SD 2.31) 4.47 (SD 2.21) 0.41 (8.4%) .439 (ηP2 .02)
10min 4.44 (SD 2.31) 4.15 (SD 1.93) 0.29 (6.5%) .899 (ηP2 .00)
20min 4.38 (SD 2.19) 3.82 (SD 1.96) 0.56 (12.8%) .248 (ηP2 .04)
30min 4.50 (SD 2.37) 3.85 (SD 2.25) 0.65 (14.4%) .043* (ηP2 .12)
Abbreviations: PPS = pinprick sensitivity, SD = standard deviation, ηP2 = effect size, * = p ≤ .05.
There was no main effect for Group (p = .177, ηP2 = .06). There were no significant interactions
for Time by Group (p = .820, ηP2 = .01), Side by Group (p = .178, ηP
2 = .06), or Time by Side by
Group (p = .837, ηP2 = .01).
3.2.9. Ipsilateral vs. Contralateral Changes
The relationship between the side of SM and changes to the ipsilateral and contralateral side
were analysed using paired t-tests, comparing baseline to each time point.
In the calf, there was a trend toward greater increases in PPT on the side ipsilateral to the side
of SM in both groups (Table 3.20 and Figure 3.11). After R-SM, no differences reached
significance, though the mean increases in PPT were consistently greater on the ipsilateral side
than the contralateral side. After L-SM, the ipsilateral calf PPT increased significantly from
baseline to all time points. The contralateral side also tended to increase, but was not significant.
59
Table 3.20. Paired t-test results for calf PPT in each group on the ipsilateral and contralateral sides,
comparing baseline to immediately after intervention, and to 10, 20, and 30 minutes.
p-value (PPT mean difference in kg/cm2)
R-SM group L-SM group
Ipsilateral, right
calf
Contralateral, left
calf
Ipsilateral, left
calf
Contralateral, right
calf
Baseline vs. Immediate
.090 (0.34) .513 (0.16) .049* (0.38) .657 (0.16)
Baseline vs. 10min
.109 (0.45) .980 (0.01) .006* (0.57) .153 (0.37)
Baseline vs. 20min
.115 (0.48) .576 (0.16) .007* (0.76) .198 (0.42)
Baseline vs. 30min
.178 (0.39) .999 (0.00) .010* (0.71) .058 (0.60)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, * = p ≤ .05.
Calf PPT per group, side and time (ipsilateral vs. contralateral)
R-SM Ipsi Calf R-SM Contra Calf L-SM Ipsi Calf L-SM Contra Calf
PP
T (
kg
/cm
2)
0
1
2
3
4
5
6
7
Baseline Immediate 10min 20min 30min
**
* *
Figure 3.11. Mean calf PPT after R-SM on the ipsilateral side (right calf), R-SM on the contralateral side
(left calf), L-SM on the ipsilateral side (left calf), and L-SM on the contralateral side (right calf), at
baseline, immediately after intervention, and at 10, 20, and 30 minutes, with standard error bars.
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, Ipsi = ipsilateral, Contra = contralateral, * = p ≤ 0.05.
In the lumbar spine, the trend was less clear. After R-SM, ipsilateral lumbar spine PPT increased
significantly from baseline to 20min and 30min. The contralateral side also tended to increase,
but this was not significant and the increases were smaller than ipsilateral PPT. After L-SM, both
sides of the lumbar spine increased by similar amounts, reaching significance on the ipsilateral
60
side at 30min, and on the contralateral side at 20min and 30min. So for R-SM, lumbar spine PPT
tended to increase more on the ipsilateral than contralateral side, while L-SM resulted in similar
increases on both the ipsilateral and contralateral side of the lumbar spine (Table 3.21 and
Figure 3.12).
Table 3.21. Paired t-test results for lumbar spine PPT in each group on the ipsilateral and contralateral
sides, comparing baseline to immediately after intervention, and to 10, 20, and 30 minutes.
p-value (PPT mean difference in kg/cm2)
R-SM L-SM
Ipsilateral, right
lumbar spine
Contralateral, left
lumbar spine
Ipsilateral, left
lumbar spine
Contralateral, right
lumbar spine
Baseline vs. Immediate
.110 (0.55) .706 (-0.14) .381 (0.30) .437 (0.21)
Baseline vs. 10min
.142 (0.67) .624 (0.14) .073 (0.61) .178 (0.47)
Baseline vs. 20min
.043* (0.92) .343 (0.39) .117 (0.48) .008* (0.60)
Baseline vs. 30min
.048* (0.99) .313 (0.50) .033* (0.69) .019* (0.90)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, * = p ≤ .05.
Lumbar PPT per group, side and time (ipsilateral vs. contralateral)
R-SM Ipsi Lumbar R-SM Contra Lumbar L-SM Ipsi Lumbar L-SM Contra Lumbar
PP
T (
kg
/cm
2)
0
1
2
3
4
5
6
7
8
9
10
Baseline Immediate 10min 20min 30min
* *
* **
Figure 3.12. Mean lumbar spine PPT after R-SM on the ipsilateral side (right lumbar spine), R-SM on
the contralateral side (left lumbar spine), L-SM on the ipsilateral side (left lumbar spine), and L-SM on
the contralateral side (right lumbar spine), at baseline, immediately after intervention, and at 10, 20,
and 30 minutes, with standard error bars. Abbreviations: PPT = pressure pain threshold, R-SM = right-
sided spinal manipulation, L-SM = left-sided spinal manipulation, Ipsi = ipsilateral, Contra = contralateral,
* = p ≤ 0.05.
61
After R-SM, scapula PPT increases were quite small overall, and tended to be slightly greater on
the contralateral side. After L-SM, there was a significant ipsilateral increase from baseline to
20min, but otherwise the differences were small and inconsistent for both ipsilateral and
contralateral scapula PPT changes. No real trends can be identified for scapula PPT (Table 3.22
and Figure 3.13).
Table 3.22. Paired t-test results for scapula PPT in each group on the ipsilateral and contralateral
sides, comparing baseline to immediately after intervention, and at 10, 20, and 30 minutes.
p-value (PPT mean difference in kg/cm2)
R-SM group L-SM group
Ipsilateral, right
scapula
Contralateral, left
scapula
Ipsilateral, left
scapula
Contralateral, right
scapula
Baseline vs.
Immediate .621 (0.09) .190 (0.18) .786 (0.05) .080 (-0.38)
Baseline vs.
10min .314 (0.31) .225 (0.31) .527 (-0.10) .380 (-0.10)
Baseline vs.
20min .506 (0.19) .824 (-0.06) .043* (0.31) .984 (-0.00)
Baseline vs.
30min .971 (0.01) .400 (0.24) .741 (0.07) .928 (0.02)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation, * = p ≤ .05.
Scapula PPT per group, side and time (ipsilateral vs. contralateral)
R-SM Ipsi Scapula R-SM Contra Scapula L-SM Ipsi Scapula L-SM Contra Scapula
PP
T (
kg
/cm
2)
0
1
2
3
4
5
6
7
Baseline Immediate 10min 20min 30min
*
Figure 3.13. Mean scapula PPT after R-SM on ipsilateral side (right scapula), R-SM on contralateral
side (left scapula), L-SM on ipsilateral side (left scapula), and L-SM on contralateral side (right
scapula), at baseline, immediately after intervention, and at 10, 20, and 30 minutes, with standard
error bars. Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM =
left-sided spinal manipulation, Ipsi = ipsilateral, Contra = contralateral, * = p ≤ 0.05.
62
At the forehead, there were no significant PPT differences in either group, and ipsilateral and
contralateral changes tended to be very small (Table 3.23).
Table 3.23. Paired t-test results for forehead PPT in each group on the ipsilateral and contralateral
sides, comparing baseline to immediately after intervention, and at 10, 20, and 30 minutes.
p-value (PPT mean difference in kg/cm2)
R-SM group L-SM group
Ipsilateral, right
forehead
Contralateral, left
forehead
Ipsilateral, left
forehead
Contralateral, right
forehead
Baseline vs.
Immediate .335 (-0.09) .299 (0.10) .430 (0.09) .316 (0.15)
Baseline vs.
10min .989 (-0.00) .634 (0.07) .451 (0.07) .377 (0.12)
Baseline vs.
20min .508 (-0.07) .332 (0.13) .459 (0.11) .801 (0.04)
Baseline vs.
30min .798 (0.04) .546 (0.09) .397 (0.10) .368 (0.12)
Abbreviations: PPT = pressure pain threshold, R-SM = right-sided spinal manipulation, L-SM = left-sided
spinal manipulation.
No ipsilateral vs. contralateral trends were noted for PPS in the calf, lumbar spine, scapula or
forehead (Tables 3.24 – 3.27).
Table 3.24. Paired t-test results for calf PPS in each group on the ipsilateral and contralateral sides,
comparing baseline to immediately after intervention, and at 10, 20, and 30 minutes.
p-value (PPS mean difference [0-10 scale])
R-SM group L-SM group
Ipsilateral, right
calf
Contralateral, left
calf
Ipsilateral, left
calf
Contralateral, right
calf
Baseline vs.
Immediate .548 (0.18) .868 (0.6) .999 (0.00) .517 (-0.29)
Baseline vs.
10min .854 (-0.06) .791 (-0.12) .868 (-0.06) .370 (-0.35)
Baseline vs.
20min .275 (-0.41) .083 (-0.71) .064 (-0.82) .636 (-0.18)
Baseline vs.
30min .385 (-0.29) .043* (-0.77) .158 (-0.65) .120 (-0.82)
Abbreviations: PPS = pinprick sensitivity, R-SM = right-sided spinal manipulation, L-SM = left-sided spinal
manipulation, * = p ≤ .05.
63
Table 3.25. Paired t-test results for lumbar PPS in each group on the ipsilateral and contralateral sides,
comparing baseline to immediately after intervention, and at 10, 20, and 30 minutes.
p-value (PPS mean difference [0-10 scale])
R-SM group L-SM group
Ipsilateral, right
lumbar spine
Contralateral, left
lumbar spine
Ipsilateral, left
lumbar spine
Contralateral, right
lumbar spine
Baseline vs.
Immediate .110 (-0.65) .616 (-0.18) .018* (-0.82) .011* (-0.94)
Baseline vs.
10min .049* (-0.82) .024* (-1.06) .038* (-0.77) .034* (-0.82)
Baseline vs.
20min .060 (-0.88) .086 (-0.59) .060 (-0.88) .004* (-0.94)
Baseline vs.
30min .019* (-1.00) .065 (-0.88) .003* (-1.29) .006* (-1.18)
Abbreviations: PPS = pinprick sensitivity, R-SM = right-sided spinal manipulation, L-SM = left-sided spinal
manipulation, * = p ≤ .05.
Table 3.26. Paired t-test results for scapula PPS in each group on the ipsilateral and contralateral
sides, comparing baseline to immediately after intervention, and at 10, 20, and 30 minutes.
p-value (PPS mean difference [0-10 scale])
R-SM group L-SM group
Ipsilateral, right
scapula
Contralateral, left
scapula
Ipsilateral, left
scapula
Contralateral, right
scapula
Baseline vs.
Immediate .064 (-0.82) .636 (0.18) .783 (-0.12) .483 (-0.29)
Baseline vs.
10min .090 (-0.82) .743 (-0.12) .029* (-0.71) .311 (-0.29)
Baseline vs.
20min .037* (-0.65) .999 (0.00) .203 (-0.47) .203 (-0.41)
Baseline vs.
30min .124 (-0.71) .999 (0.00) .311 (-0.29) .332 (-0.35)
Abbreviations: PPS = pinprick sensitivity, R-SM = right-sided spinal manipulation, L-SM = left-sided spinal
manipulation, * = p ≤ .05.
Table 3.27. Paired t-test results for forehead PPS in each group on the ipsilateral and contralateral
sides, comparing baseline to immediately after intervention, and at 10, 20, and 30 minutes.
p-value (PPS mean difference [0-10 scale])
R-SM group L-SM group
Ipsilateral, right
forehead
Contralateral, left
forehead
Ipsilateral, left
forehead
Contralateral, right
forehead
Baseline vs.
Immediate .608 (-0.12) .332 (-0.24) .605 (-0.18) .999 (0.00)
Baseline vs.
10min .132 (-0.53) .046* (-0.59) .347 (-0.47) .227 (-0.47)
Baseline vs.
20min .203 (-0.47) .126 (-0.59) .037* (-1.12) .069 (-0.65)
Baseline vs.
30min .227 (-0.47) .018* (-0.94) .210 (-0.71) .436 (-0.41)
Abbreviations: PPS = pinprick sensitivity, R-SM = right-sided spinal manipulation, L-SM = left-sided spinal
manipulation, * = p ≤ .05.
64
4. Discussion
The key results are summarised in Table 4.1, and the significance of our findings is discussed
here-in.
Table 4.1. Summary of key results.
Pressure Pain Threshold
1. Calf PPT increased significantly at 20 and 30 minutes.
2. Lumbar spine PPT increased significantly at 10, 20 and 30 minutes.
3. Scapula and forehead PPT showed no significant change.
4. Trend toward greater ipsilateral increase in PPT at the calf and lumbar spine.
Pinprick Sensitivity
1. Calf PPS decreased significantly at 20 and 30 minutes.
2. Lumbar spine PPS decreased significantly immediately, and at 10, 20 and 30 minutes.
3. Scapula PPS decreased significantly at 10 and 20 minutes.
4. Forehead PPS decreased significantly at 10, 20 and 30 minutes.
5. No differences in ipsilateral vs. contralateral PPS changes.
Abbreviations: PPT = pressure pain threshold, PPS = pinprick sensitivity.
4.1. Baseline Characteristics
Several baseline differences between groups were noted in the present study. Firstly, the
proportion of right- and left-hand dominant participants was different between groups.
Secondly, scapula PPS was higher by 1.3 (on an NRS) in the L-SM group. As no significantly
relevant between-group differences were observed, these are considered unlikely to be of
importance.
Across all participants, baseline asymmetry was observed in PPT and PPS, which is inconsistent
with previous literature. Limited research has found no systematic differences in PPT between
the right and left sides of the body, and no differences related to hand dominance (Cathcart and
Pritchard 2006; Fischer 1987; Park et al. 2011). The differences we observed could relate to
participant handedness or methodological decisions (e.g. the left side was always measured
before the right). Only seven of 34 participants in the present study were left-hand dominant,
65
thus we were unable to reasonably explore the relationship between handedness and baseline
pain sensitivity, or changes following SM.
The baseline PPT measures in the present study are mostly consistent with other literature. Calf
muscle PPT was slightly higher than that found in the all-female population studied by Lacourt,
Houtveen, and van Doornen (2012), though PPT tends to be lower in females than in males
(discussed in section 1.3). Lumbar paraspinal muscle PPT at baseline was similar to several prior
studies (Cote, Mior, and Vernon 1994; de Oliveira et al. 2013; Lacourt, Houtveen, and van
Doornen 2012), but was lower compared to two others (Gay et al. 2014; Potter, McCarthy, and
Oldham 2006). Park et al. (2011) reports an almost identical infraspinatus baseline PPT, and a
systematic review by Andersen et al. (2015) found similar but slightly higher forehead PPT
compared to the present study. There does not appear to be any literature with baseline PPS
measures to compare to our data.
4.2. Pressure Pain Threshold
Increases in PPT over time were observed at both the calf and the lumbar spine. At both sites,
PPT tended to continue to increase successively at each time point, becoming significant
compared to baseline at 20 and 30 minutes at the calf, and at 10, 20, and 30 minutes in the
lumbar spine. This suggests that apparent hypoalgesia developed over a period of 10 - 20
minutes in the lower limb and lumbar spine, and was maintained at 30 minutes.
However, the increases were small with weak effect sizes. The minimum detectable change
(MDC) for PPT has been calculated in several studies. For within-day change in spinal muscles,
an MDC of 3.00 kg/cm2 (35 - 40% change) has been proposed (Potter, McCarthy, and Oldham
2006). For two non-spinal muscles an MDC of 1.16 - 1.57 kg/cm2 (roughly 45% change) is
reported, though this is for between-day measures (Walton et al. 2011). Similarly, Bisset, Evans,
and Tuttle (2015) report an MDC of 1.64 kg/cm2 (35 - 50% change) based on inter-rater
66
measurements. The absolute MDC varies depending on the region being tested (Walton et al.
2011), thus percentage changes may represent a more appropriate indicator of change. We
noted increases over time that were well below the suggested actual and percentage MDCs, of
between 0.43 and 0.77 kg/cm2 (7.2 - 11.8% change). This suggests the observed changes in PPT
could be due to chance or measurement error, or real but small changes.
The absence of a control group limits the strength of the conclusions. However, PPT has been
shown to be robust to repeated measurement and reliable within-day to change (Potter,
McCarthy, and Oldham 2006). That we observed increased PPT following SM in the calf and
lumbar spine, but not in the scapula or forehead, supports the argument for a treatment effect
in this study even when considering the limitations (discussed further below).
In comparison to other literature, the PPT changes we observed are consistent with changes
seen following cervical SM. Cervical SM consistently produces hypoalgesia locally (in the cervical
spine) and in the upper limb, but not the lower limb (Coronado et al. 2012). Thus our study
supports the notion of local and segmental hypoalgesia in response to SM, i.e. at the site of
manipulation and at peripheral sites innervated by that spinal area.
However, our results conflict with similar studies in the lumbar spine. Others found no significant
changes to lumbosacral or lower limb PPT following lumbar SM (Cote, Mior, and Vernon 1994;
de Oliveira et al. 2013; Gay et al. 2014; Thomson, Haig, and Mansfield 2009), or a small but
significant decrease (Orakifar et al. 2012). There is little consistency in the site of PPT testing,
and variably involved the lumbar paraspinal muscles, over a lumbar spinous process, the
sacroiliac joint, or sacrum. This may account for some of the differences compared to the
present study. Other possible explanations include differing sample populations (e.g. chronic
LBP), a potential confounding effect of other outcome measures, and a particularly small sample
size in one study.
67
As we found no significant immediate increases in PPT at the calf and lumbar spine (though there
is an upward trend), our study suggests that changes in PPT following lumbar SM develop over
a 10 - 20 minute period. Three of the five studies in the lumbar spine measured only immediate
PPT changes so this effect may have been missed. Cote, Mior, and Vernon (1994) did show an
upward trend in PPT over time, which did not reach significance. Orakifar et al. (2012) found
that PPT decreased at 10 and 15 minutes, which is contrary to any other studies in the lumbar
or cervical spine, and this could possibly be explained as a confounding effect of measuring the
Hoffman reflex, involving electrical stimulation of a peripheral nerve, prior to measuring PPT.
Two cervical spine studies showed increases in PPT were not sustained at 30 minutes or two
hours (Hamilton, Boswell, and Fryer 2007; Molina-Ortega et al. 2014). The present study adds
to this literature by suggesting that lumbar SM leads to a gradual increase in PPT over time that
is maintained at 30 minutes.
The significant disparity observed in studies of PPT following cervical SM vs. lumbar SM is
curious. Our study is the first to refute such disparity, and the reason for the differences in other
studies remains speculative. Orakifar et al. (2012) have suggested various possibilities, including
differences in the density of mechanoreceptors and nociceptors in the cervical and lumbar
regions, differences in baseline PPT between regions, and region-specific differences in the
physiologic response to SM. Methodologic decisions may also play a role.
More broadly, it appears that mobilisation of spinal and extremity joints also elicits a hypoalgesic
response that is local and possibly remote to the site of intervention (Voogt et al. 2015),
including following lumbar mobilisation (Krouwel, Hebron, and Willett 2010; Willett, Hebron,
and Krouwel 2010). This lends strength to the theory that lumbar SM does in fact cause
hypoalgesia, as suggested by our findings.
68
The trend toward greater PPT increases at the calf and lumbar spine ipsilateral to the SM is in
contrast to the limited literature in this area (see section 1.3.1.4). At present it appears that PPT
tends to increase more on the same side as the participant’s dominant hand based on limited
studies. The actual changes in PPT we observed were small, and there may have been
insufficient power to accurately detect asymmetry between groups in this manner, so the
present findings should be regarded with caution. As already stated, we recruited insufficient
left-hand dominant participants to investigate the effect of hand dominance on pain sensitivity
changes.
4.3. Pinprick Sensitivity
The observed decreases to PPS represent a reduction in pain sensitivity, seen at all sites at
various times. As PPS is a novel and unvalidated measure of superficial pain sensitivity, the
observed changes may represent a global treatment effect, a learned effect, or an
acclimatisation to PPS measurements. The pattern of change suggests a non-specific effect
unrelated to the SM.
For PPS, there is no defined MDC with which to compare our results. A 30% change in PPS may
be a reasonable approximation based on prior research investigating the minimum clinically
important difference of self-reported pain intensity using a numeric rating scale (Hawker et al.
2011). It may also be reasonable to expect changes of a similar magnitude to PPT MDC, in the
vicinity of 35-50% change. Our study observed PPS to decrease between 9.8 and 22.5%, which
reaches neither of these estimations. The effect sizes were weak to moderate. For the above
reasons, we speculate that PPS is not a relevant measure of hypoalgesia following SM.
4.4. Interpretation
A significant hurdle is that the clinical relevance of PPT and PPS is as yet unclear. Reduced PPT
has been observed in numerous painful conditions and is thought to represent an individual’s
69
sensitivity to pain; it thus may be likely to relate to clinical features such as self-reported pain
intensity and disability (Hübscher et al. 2013). A recent systematic review and meta-analysis
concluded that there was no significant correlation between pain thresholds and pain intensity
or disability, across a variety of factors including pain condition (e.g. LBP, neck pain), acute or
chronic status, and local or remote testing site (Hübscher et al. 2013). Studies published since
have found conflicting results (Fernández-Pérez et al. 2012; Gonçalves et al. 2015; Uddin et al.
2014). Variable findings may reflect differing aetiologies, chronicity, and other factors. Two
studies have however suggested that PPT may be adequately responsive to change for use as a
clinical outcome measure in some situations (Goolkasian, Wheeler, and Gretz 2002; Walton et
al. 2014). PPS does not appear to have been studied in this capacity.
It is thus unclear whether PPT may be used clinically as a valid and reliable tool in
musculoskeletal pain. Determining the clinical implications of PPT in particular, which is widely
used in manual therapy research, is of paramount importance. It should be determined if any
correlations do in fact exist between PPT and self-reported pain or disability in various painful
conditions, or if there are correlations with other clinical features such as symptom pattern, as
well as whether PPT can be used reliably as a clinical outcome measure.
Though direct evidence is lacking, we speculate that the selective hypoalgesia we observed
following SM helps to explain some of the clinical pain relief associated with SM. Short- or
medium-term hypoalgesia is potentially highly valuable in patients receiving SM, where we often
wish to encourage early return to activity in order to aid recovery. Segmental hypoalgesia could
also be beneficial in the management of painful conditions in the upper and lower limb, allowing
us to use targeted SM to enhance pain relief.
When considering the neurophysiological theories, our results are consistent with the theory
suggesting descending inhibitory pain control systems are involved in post-SM hypoalgesia. As
70
discussed in section 1.3.7.1, activation of the PAG appears to inhibit C-fibre nociceptive signals,
leaving Aδ-fibre signals unaffected. PPT (which is mediated by both fibre types) revealed
hypoalgesia in response to SM, while PPS (mediated only by Aδ-fibres) showed a global change
that we speculate is unrelated to the SM. In addition, Moss, Sluka, and Wright (2007) point out
that such supraspinal mechanisms are likely to produce a more widespread response, not just
local to the inciting stimulus. Thus the changes we observed are consistent with the mechanism
through which descending pain inhibition is carried out.
It is known that the descending pain control system is involved in the development of chronic
pain states and central sensitisation through imbalance of descending facilitatory and inhibitory
signals (Heinricher et al. 2009). Additionally, C-fibre inputs contribute to dorsal horn neuron
sensitisation (Heinricher et al. 2009). If, as speculated, SM triggers descending inhibition that
suppresses C-fibre activity, SM could play a valuable role in treating and preventing chronic pain
states.
The pain gate theory (see section 1.3.7.2) likely only accounts for short-term hypoalgesia, as the
gating effect only lasts for as long as the non-nociceptive stimulus is present (Kotzé and Simpson
2008). Primarily C-fibre nociceptive signals are inhibited, but as we observed local and lower
limb PPT changes that persisted for at least 30 minutes, the pain gate is a less likely explanation
for this.
Why hypoalgesia was observed locally in the lumbar spine and segmentally in the lower limb,
but not at the shoulder or forehead, is unclear from a neurophysiologic perspective. Some dorsal
horn neurons receiving sensory input from the lumbar spine and lower limb would be expected
to be anatomically close to one another (in the spinal cord), while those receiving input from
the shoulder and forehead are anatomically remote. Thus it is possible that the underlying
neurophysiologic mechanism alters pain processing regionally in the spinal cord.
71
It is known that the descending pathways are capable of acting on select regions of the dorsal
horn (Millan 2002), and that serotonin and noradrenaline mediate inhibition primarily through
volume transmission (the diffusion of neurotransmitters from a synapse to remote sites) which
results in more widespread effects (Todd 2010). Thus once again the descending inhibitory pain
pathways may offer a plausible explanation for the observed phenomena.
4.5. Limitations
There are various limitations to the present study. Firstly, it is possible that measuring PPS had
a confounding effect upon PPT. PPS was always measured after PPT, followed by a period of rest
before the next follow-up measures were taken, though a confounding effect may still have
occurred. Anxiety is a known confounder to pain (Rhudy and Meagher 2000), which was not
controlled for in this study other than with a thorough informed consent process and by assuring
participants that the SM procedure was unlikely to cause pain. Participants may have
experienced anxiety in relation to the induction of experimental pain or to receiving SM
(especially in those who had not had SM previously). Alternatively, some participants may have
been experiencing anxiety for unrelated reasons.
The use of young asymptomatic participants limits the generalisability of the results to
symptomatic and older populations, and future research should explore this. In particular,
chronic pain patients may respond differently as a result of central sensitisation. The lack of a
sham group also means some of the effect may be explained by placebo or other effects, such
as the positioning involved in the SM procedure or physical touch. These could each have a
confounding effect, hence a non-thrust manual contact control group would have been valuable
to account for some of this effect. Finally, the study was adequately powered to detect large
main effects at each location, however the study is likely underpowered to adequately detect
72
small changes, and changes for the more complex two- and three-way interactions. Thus we
may be committing some type II errors.
5. Conclusion
This study set out to investigate the effects of lumbar SM on local and remote pain perception
using two measures of experimental pain. As a commonly used manual therapy technique for
musculoskeletal pain, understanding the neurophysiologic effect of SM is imperative. Thus, we
sought to answer the following questions:
1) Does lumbar SM affect pain sensitivity (deep and superficial) at local and remote
locations?
2) Do changes last for at least 30 minutes?
3) Are any changes related to the side of manipulation (i.e. bilateral symmetric or
asymmetric)?
We conclude that lumbar SM does lead to increased PPT (reduced deep pain sensitivity) in the
lumbar spine and in the lower limb for at least 30 minutes, with no changes at superior sites,
despite the limitations. This implies a local and segmental selective hypoalgesia in response to
lumbar SM. The hypoalgesia may be slightly greater on the side ipsilateral to the SM, but this is
unclear.
We also conclude that PPS, considered to represent superficial pain sensitivity, does not change
as a specific response to lumbar SM.
Our findings align with the theory that post-SM hypoalgesia is mediated by supraspinal
mechanisms, namely descending inhibitory pain control. Activation of the pain gate mechanism,
altered dorsal horn excitability, and placebo and psychosocial factors may also be involved.
73
The findings may explain some of the clinical value of SM, and highlight intriguing potential for
the targeted use of SM for painful conditions including chronic pain states. It is particularly
important now that the clinical relevance of PPT be established in order to enhance the clinical
application of SM. If any relationships do exist between PPT and clinical features, it is a
potentially valuable clinical outcome measure.
As the first study to observe post-SM hypoalgesia in the lumbar spine, we highlight the
importance of future research to clarify whether lumbar SM has a similar effect on pain
sensitivity as cervical SM.
Studies following PPT beyond 30 minutes, and comparing whether responses differ between
symptomatic and asymptomatic populations would also be valuable. Additionally, it is important
that the neurophysiologic mechanism for post-SM hypoalgesia is determined as direct human
evidence is lacking.
74
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Appendix A – Participant Checklist and Medical History Questionnaire
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Appendix B – Information Letter
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Appendix C – Consent Form
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Appendix D – Shapiro-Wilk tests for Normality Results
1. Tests of Normality for Pressure Pain Threshold
Group (side of manipulation)
Shapiro-Wilk
Statistic df Sig.
PPT Left Calf at Baseline Right .935 17 .266
Left .853 17 .012*
PPT Right Calf at Baseline Right .885 17 .039*
Left .932 17 .239
PPT Left Lumbar at Baseline Right .916 17 .124
Left .828 17 .005*
PPT Right Lumbar at Baseline Right .945 17 .385
Left .810 17 .003*
PPT Left Shoulder at Baseline Right .914 17 .116
Left .895 17 .057
PPT Right Shoulder at Baseline Right .929 17 .207
Left .959 17 .616
PPT Left Forehead at Baseline Right .940 17 .318
Left .968 17 .787
PPT Right Forehead at Baseline Right .921 17 .152
Left .922 17 .160
PPT Left Calf at Immediate Right .947 17 .418
Left .808 17 .003*
PPT Right Calf at Immediate Right .913 17 .112
Left .812 17 .003*
PPT Left Lumbar at Immediate Right .955 17 .538
Left .907 17 .090
PPT Right Lumbar at Immediate Right .919 17 .144
Left .832 17 .006*
PPT Left Shoulder at Immediate Right .957 17 .568
Left .841 17 .008*
PPT Right Shoulder at Immediate Right .919 17 .144
Left .894 17 .054
PPT Left Forehead at Immediate Right .911 17 .105
Left .887 17 .041*
PPT Right Forehead at Immediate Right .962 17 .669
Left .790 17 .001*
PPT Left Calf at 10min Right .885 17 .038*
Left .810 17 .003*
PPT Right Calf at 10min Right .906 17 .087
Left .922 17 .158
PPT Left Lumbar at 10min Right .899 17 .066
Left .947 17 .411
PPT Right Lumbar at 10min Right .915 17 .121
Left .889 17 .045*
PPT Left Shoulder at 10min Right .958 17 .598
Left .898 17 .064
PPT Right Shoulder at 10min Right .885 17 .038*
Left .917 17 .134
PPT Left Forehead at 10min Right .937 17 .283
Left .902 17 .072
PPT Right Forehead at 10min Right .974 17 .890
Left .825 17 .005*
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PPT Left Calf at 20min Right .911 17 .106
Left .798 17 .002*
PPT Right Calf at 20min Right .962 17 .671
Left .873 17 .024*
PPT Left Lumbar at 20min Right .928 17 .202
Left .904 17 .080
PPT Right Lumbar at 20min Right .916 17 .124
Left .875 17 .026*
PPT Left Shoulder at 20min Right .940 17 .316
Left .916 17 .127
PPT Right Shoulder at 20min Right .909 17 .095
Left .933 17 .240
PPT Left Forehead at 20min Right .945 17 .377
Left .878 17 .029*
PPT Right Forehead at 20min Right .970 17 .815
Left .821 17 .004*
PPT Left Calf at 30min Right .899 17 .066
Left .779 17 .001*
PPT Right Calf at 30min Right .930 17 .220
Left .897 17 .061
PPT Left Lumbar at 30min Right .917 17 .131
Left .931 17 .224
PPT Right Lumbar at 30min Right .947 17 .407
Left .871 17 .023*
PPT Left Shoulder at 30min Right .943 17 .351
Left .960 17 .624
PPT Right Shoulder at 30min Right .926 17 .185
Left .971 17 .839
PPT Left Forehead at 30min Right .974 17 .886
Left .926 17 .185
PPT Right Forehead at 30min Right .946 17 .392
Left .852 17 .012*
Abbreviations: PPT = pressure pain threshold, * = significant (≤ .05).
2. Tests of Normality for Pinprick Sensitivity
Group (side of manipulation)
Shapiro-Wilk
Statistic df Sig.
PPS Left Calf at Baseline Right .939 17 .308
Left .961 17 .656
PPS Right Calf at Baseline Right .888 17 .043*
Left .931 17 .225
PPS Left Lumbar at Baseline Right .869 17 .021*
Left .946 17 .391
PPS Right Lumbar at Baseline Right .937 17 .285
Left .952 17 .483
PPS Left Shoulder at Baseline Right .893 17 .052
Left .946 17 .401
PPS Right Shoulder at Baseline Right .869 17 .021*
Left .949 17 .445
PPS Left Forehead at Baseline Right .960 17 .631
Left .922 17 .157
PPS Right Forehead at Baseline Right .952 17 .484
Left .929 17 .213
PPS Left Calf at Immediate Right .914 17 .115
89
Left .952 17 .487
PPS Right Calf at Immediate Right .960 17 .639
Left .913 17 .110
PPS Left Lumbar at Immediate Right .946 17 .402
Left .902 17 .074
PPS Right Lumbar at Immediate Right .892 17 .050*
Left .961 17 .642
PPS Left Shoulder at Immediate Right .910 17 .102
Left .930 17 .219
PPS Right Shoulder at Immediate Right .924 17 .172
Left .906 17 .087
PPS Left Forehead at Immediate Right .939 17 .305
Left .962 17 .679
PPS Right Forehead at Immediate Right .911 17 .103
Left .955 17 .539
PPS Left Calf at 10min Right .883 17 .036*
Left .926 17 .183
PPS Right Calf at 10min Right .930 17 .215
Left .948 17 .426
PPS Left Lumbar at 10min Right .946 17 .404
Left .893 17 .051*
PPS Right Lumbar at 10min Right .922 17 .160
Left .924 17 .173
PPS Left Shoulder at 10min Right .910 17 .101
Left .910 17 .100
PPS Right Shoulder at 10min Right .916 17 .124
Left .933 17 .240
PPS Left Forehead at 10min Right .942 17 .337
Left .962 17 .663
PPS Right Forehead at 10min Right .950 17 .449
Left .968 17 .774
PPS Left Calf at 20min Right .887 17 .042*
Left .896 17 .058
PPS Right Calf at 20min Right .910 17 .101
Left .958 17 .593
PPS Left Lumbar at 20min Right .953 17 .513
Left .966 17 .741
PPS Right Lumbar at 20min Right .910 17 .101
Left .961 17 .657
PPS Left Shoulder at 20min Right .913 17 .111
Left .918 17 .136
PPS Right Shoulder at 20min Right .925 17 .180
Left .973 17 .875
PPS Left Forehead at 20min Right .928 17 .202
Left .950 17 .454
PPS Right Forehead at 20min Right .951 17 .475
Left .965 17 .727
PPS Left Calf at 30min Right .823 17 .004*
Left .919 17 .142
PPS Right Calf at 30min Right .920 17 .146
Left .934 17 .257
PPS Left Lumbar at 30min Right .905 17 .082
Left .911 17 .103
PPS Right Lumbar at 30min Right .917 17 .131
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Left .955 17 .539
PPS Left Shoulder at 30min Right .906 17 .087
Left .918 17 .137
PPS Right Shoulder at 30min Right .866 17 .019*
Left .909 17 .096
PPS Left Forehead at 30min Right .951 17 .467
Left .946 17 .402
PPS Right Forehead at 30min Right .943 17 .356
Left .961 17 .658
Abbreviations: PPT = pressure pain threshold, * = significant (≤ .05).