Artigo (4) importante para a preparação para o curso de dor lombar crônica. "Características sensoriais da dor lombar crônica inespecífica: uma investigação de subgrupos."

1. Original article
Sensory characteristics of chronic non-specific low back pain: A
subgroup investigationq
Peter O’Sullivan*, Robert Waller, Anthony Wright, Joseph Gardner, Richard Johnston,
Carly Payne, Aedin Shannon, Brendan Ware, Anne Smith
School of Physiotherapy & Exercise Science, Curtin University, GPO Box 1987, Perth, WA 6845, Australia
a r t i c l e i n f o
Article history:
Received 22 May 2013
Received in revised form
6 March 2014
Accepted 14 March 2014
Keywords:
Pain sensitivity
Chronic non-specific low back pain
Biopsychosocial
Classification
a b s t r a c t
It has been proposed that patients with chronic non-specific low back pain (CNSLBP) can be broadly
classified based on clinical features that represent either predominantly a mechanical pain (MP) or non-mechanical
pain (NMP) profile. The aim of this study was to establish if patients with CNSLBP who report
features of NMP demonstrate differences in pain thresholds compared to those who report MP char-acteristics
and pain-free controls. This study was a cross-sectional design investigating whether pressure
pain threshold (PPT) and/or cold pain threshold (CPT) at three anatomical locations differed between
patients with mechanical CNSLBP (n ¼ 17) versus non-mechanical CNSLBP (n ¼ 19 and healthy controls
(n ¼ 19) whilst controlling for confounders. The results of this study provide evidence of increased CPT at
the wrist in the NMP profile group compared to both the MP profile and control subjects, when con-trolling
for gender, sleep and depression (NMP versus MP group Odds Ratio (OR): 18.4, 95% confidence
interval (CI): 2.5e133.1, p ¼ 0.004). There was no evidence of lowered PPT at any site after adjustment for
confounding factors. Those with an MP profile had similar pain thresholds to pain-free controls, whereas
the NMP profile group demonstrated elevated CPT’s consistent with central amplification of pain. These
findings may represent different pain mechanisms associated with these patient profiles and may have
implications for targeted management.
2014 Elsevier Ltd. All rights reserved.
1. Introduction
Patients with chronic non-specific low back pain (CNSLBP) pose
a complex diagnostic and management challenge. Classification
systems (CS) that identify mechanisms that underlie the pain dis-order
have been advocated in clinical practice in order to better
target interventions (O’Sullivan, 2012a, 2005; Woolf, 2011). The
Quebec Task Force CS (Spitzer, 1987) whilst differentiating specific
pathology and radicular pain from CNSLBP, does not further
differentiate subjects with CNSLBP (Dankaerts et al., 2006). A recent
review of clinical CS’s for CNSLBP concluded that a limitation of the
majority of CS’s is that they do not consider underlying pain
mechanisms and focus largely on biomechanical assessment
(Karayannis et al., 2012).
A multidimensional CS system for LBP has been proposed that at
the first level triages people with LBP to identify red flag disorders
and specific pathology from non-specific LBP (Fig. 1). Once identi-fied,
CNSLBP disorders are further differentiated on the basis of
their pain characteristic’s reflecting a spectrum from either ‘me-chanical
pain’ (MP) to ‘non-mechanical pain’ (NMP) (Fig. 1). This is
based on routine clinical examination of the patient’s reported pain
characteristics linked to aggravating and easing factors and pain
responses to movement and loading tests (O’Sullivan, 2005, 2012b;
Vibe Fersum et al., 2009, 2012). While it is acknowledged that for
some patients there may be a mixed pain profile for others the
clinical distinction is clear. It is postulated that these groups may
have different underlying neurophysiological mechanisms, where
pain in the MP group is related to processes of peripheral sensiti-sation
and some degree of activity dependent central sensitisation,
whereas pain in the NMP group is related to more extensive
changes in central pain processing. Other dimensions such as pain
type, psychosocial, lifestyle, and movement related factors as well
as pain comorbidities are also considered in the CS (O’Sullivan,
2005, 2012b; Vibe Fersum et al., 2009). Although this CS has pre-viously
been shown to have good inter-rater reliability for identi-fication
of aspects of the CS related to movement and psychological
profiles (Vibe Fersum et al., 2009), no pain sensitivity (PS) testing
q Ethical approval for this study was granted by the Curtin University Human
Research Ethics Committee (PT0180).
* Corresponding author. Tel.: þ61 8 9266 3629; fax: þ61 8 9266 3699.
E-mail address: p.osullivan@curtin.edu.au (P. O’Sullivan).
Contents lists available at ScienceDirect
Manual Therapy
journal homepage: www.elsevier.com/math
http://dx.doi.org/10.1016/j.math.2014.03.006
1356-689X/ 2014 Elsevier Ltd. All rights reserved.
Manual Therapy 19 (2014) 311e318

2. P. O’Sullivan 312 et al. / Manual Therapy 19 (2014) 311e318
Fig. 1. Multidimensional classification of LBP disorders adapted from O’Sullivan, 2005, 2012b; Vibe Fersum et al., 2009, 2012.
has been conducted to quantify the sensory profiles associated with
these pain characteristic profiles.
Both cold hyperalgesia and widespread pressure hyperalgesia
are believed to be indicative of central hyperexcitability (Woolf,
2011). Pain Sensitivity testing is used to assess sensory pre-sentations
in various pain disorders (Rolke et al., 2006a) however
little research has investigated PS in CNSLBP disorders and con-troversy
exists regarding its value in understanding these disorders
(Hubsher et al., 2013). A recent narrative review of available liter-ature
in CLBP concluded that currently the available research
demonstrates mixed results, with some studies documenting
reduced pain thresholds suggestive of widespread or extra-segmental
hyperalgesia, other studies observe only segmental
hyperalgesia and others reporting no hyperalgesia at all (Roussel
et al., 2013). Another recent systematic review investigating the
relationship between pain thresholds and pain intensity and
disability levels in LBP and neck pain patients, concluded that pain
thresholds are a poor marker for patients pain and disability levels
(Hubsher et al., 2013). The apparent conflict between these findings
may reflect the heterogeneity of subjects in the different studies,
with the potential for different pain phenotypes in the CNSCLP
population unaccounted for by study design (Giesecke et al., 2004;
Roussel et al., 2013).
Both sensory perception and sensory testing are potentially
influenced by a number of factors other than pain, such as gender,
age, genetics, body composition, sleep and psychosocial factors
(Dunn, 1997; O’Sullivan et al., 2008; Leboeuf-Yde et al., 2009;
Heffner et al., 2011;Woolf, 2011), highlighting the need to consider
these factors when conducting research into PS. While there is
limited research investigating whether the presence of CNSLBP is
associated with PS changes independent of these factors, a recent
study reported that pressure pain threshold (PPT) was most pre-dictive
of CNSLBP independent of age, gender, body composition
and psychological factors (Neziri et al., 2012). Therefore the primary
aim of this study was to investigate whether patients with CNSLBP
who report features of NMP demonstrate differences in cold pain
threshold (CPT) and PPT compared to those who report MP char-acteristics
and pain-free controls.

3. 2. Materials and methods
2.1. Study design
A cross-sectional study design was used.
2.2. Participants
P. O’Sullivan et al. / Manual Therapy 19 (2014) 311e318 313
A total of 53 participants were included in the study; 36 par-ticipants
with CNSLBP (13 males and 23 females with a mean age of
40.7 (standard deviation (SD) 14.0)) were recruited from local
private physiotherapy clinics in the greater Perth area, and 19 pain-free
controls (8 males and 11 females with a mean age of 41.9
(SD 13.9)) recruited from the same district. Pain participants were
included if they had experienced pain for a minimum of 3 months,
reported pain intensity on a Visual Analogue Scale (VAS) of 3 or
greater on the day of testing and LBP was their primary complaint
(from T12 to gluteal fold). Control subjects were included on the
basis that they had not reported LBP or any other pain disorder in
the previous 6 months. Individuals were excluded if they had been
diagnosed with specific spinal pathology or medical causes of low
back pain, were pregnant or less than 6 months post-partum or
suffered from peripheral neuropathy. In all groups, subjects were
excluded if they did not perceive pressure pain below 1000 kPa
during PPT testing, or they did not perceive a change in cold
sensation during CPT testing. A-priori power calculation deter-mined
18 participants in each group would provide 85% power to
detect pairwise differences of at least one standard deviation in
mean CPT or PPT assuming a lognormal distribution, at a statistical
significance level of 0.05. Ethical approval for this study was
granted by the Curtin University Human Research Ethics Commit-tee
(PT0180).
2.3. Participants classification
The CNSLBP participants, identified following a triage process to
exclude red flag and specific pathology, were divided into two
groups based on clinical criteria (Fig. 1). Participants in the MP
group were included on the basis of: localised and anatomically
defined LBP associated with reports of specific and consistent
mechanical aggravating and easing factors (LBP that was more
intermittent in nature and demonstrated a proportionate pain
provocation and easing response to specific postures, activities and
movements). Participants in the NMP group were included on the
basis of: LBP was more widespread and ill defined, LBP being more
constant, non-remitting, spontaneous and where minor mechani-cal
loading factors (such as simple spinal movements) resulted in
exaggerated (severe) or prolonged (lasting hours) pain responses
(O’Sullivan, 2005). The decision to classify was based on a combi-nation
of patient report and response to routine clinical examina-tion.
Pain sensitivity testing was not part of this decision making
process.
Recruitment of the CNSLBP participants occurred across a
number of Physiotherapy practices, and consecutive patients were
invited to participate if they fulfilled the inclusion criteria. Further
screening was performed by RW (Musculoskeletal Physiotherapist
with 23 years clinical experience) and POS (Specialist Musculo-skeletal
Physiotherapist and the developer of the CS who has 25
years clinical experience) both of whom are trained in the CS to
ensure the patients fitted the clinical subgroups. A total of 3 par-ticipants
who agreed to participate were excluded as they failed to
meet all the inclusion criteria. One was excluded due to a lack of
pain response to pressure, and two had a VAS of less than 3/10 on
the day of testing.
2.4. Procedures
On the day of testing all participants completed two question-naires,
the Pittsburgh Sleep Quality Index (PSQI) and the Depres-sion
Anxiety and Stress Scale (DASS 21), which have established
reliability and validity (Buysse et al., 1989; Lovibond and Lovibond,
1995) and were used as covariates to control for the potential
confounding effect of poor sleep quality and stress on PS. Age,waist
and hip girth were also recorded. Upon agreeing to take part in the
study, participants were not asked to stop any of their regular
medications. A list of current medications taken over the week
prior to testing was documented.
Participants with NSCLBP were also asked to complete the
following to provide a clinical profile. The pain intensity level of
their LBP was measured using the VAS (Huskisson, 1974), and pain
areas were recorded using a body chart to provide total areas of
pain using the Widespread Pain Index (Wolfe et al., 2010). The
Roland Morris Disability Questionnaire (RMDQ) was used to assess
functional disability levels and is valid and reliable (Roland and
Morris, 1983; Roland and Fairbank, 2000). The StarT Back
screening tool (SBST) was used to assess risk profile (Hill et al.,
2008). The PainDETECT Questionnaire was used as a validated
self-report tool to identify neuropathic pain features. It is an
established questionnaire with high sensitivity and specificity
(Freynhagen et al., 2006).
2.5. Sensory testing
For participants with CNSLBP, the most painful side was tested.
The right side was used for those where there was no pain domi-nant
side and for the pain-free controls. Three test sites, the dorsal
aspect of the wrist joint line, the L5/SI interspinous space and the
lateral calcaneus, were tested in a standardised order and location
(Jones, 2007). Each site was tested 4 times with the first test acting
as familiarisation with the testing procedure (Wright et al., 1994;
Lewis et al., 2010). The testing protocol was strictly followed to
limit tester error (Rolke et al., 2006b). Participants were allocated to
testers according to time and location of testing, tester allocation
was distributed evenly between the three groups, and testers were
blinded to pain group allocation.
2.6. Pressure pain thresholds
PPT was defined as the moment the sensation of pressure be-comes
one of pressure and pain (Jones, 2007). The PPT was tested
using an algometer (Somedic AB, Sweden) with a contact area of
1 cm2 which was applied perpendicularly to the skin. The pressure
increased from 0 kPa at a constant rate of 40 kPa/s until PPT or a
maximum of 1000 kPa (Chien and Sterling, 2010) was reached. The
standardised instructions were, “Pressure will be applied at a
gradual rate. Allow the pressure to increase until it reaches a point
where it first feels uncomfortable and then press the button.”
Testing was performed by one of two testers (CP, BW). Prior to PPT
testing, consistency for PPT measurement between testers was
ensured.
2.7. Cold pain thresholds
An MSA Thermal stimulator (Somedic AB, Sweden) was used to
obtain the CPT. Before assessing CPT a cold detection threshold was
obtained for each site to confirm the participant’s ability to detect
cold (Mosek et al., 2001). Each test began at a baseline temperature
of 32 C, and decreased at 1C/s until reaching CPT or the automatic
minimum cut-off of 5 C (Carli et al., 2002). The standardised in-structions
were, “The temperature probe will gradually get cooler.

4. P. O’Sullivan 314 et al. / Manual Therapy 19 (2014) 311e318
Allow the temperature to drop until it reaches a point where it first
feels uncomfortably cold, and then press the button.” Following CPT
testing the subjects were asked “Did you feel a sensation other than
cold and if yes, how would you describe it?” These responses were
divided into ‘cold’ or non-noxious (pressure, nice, cold, tingling,
pleasant and numb) and ‘non-cold’ or noxious (burning, ice, sharp,
sting, gnawing and freezing) descriptors for further statistical
analysis. Previous studies have reported the reliability of CPT
measurement (Zwart and Trond, 2002; Wasner and Brock, 2008;
Moloney et al., 2012). Testing was performed by one of two tes-ters
(AS, BW).
2.8. Statistical analysis
The average of 3 trials at each site was used for statistical
analysis (Slater et al., 2005). CNSLBP subgroups were examined for
differences in clinical profile using chi-squared tests, Fisher’s exact
test, ManneWhitney U or KruskaleWallis tests as appropriate. The
association between sensory threshold measures and variables
considered as covariates (sex, age, waist/hip girth, DASS and PSQI)
were examined using chi-squared tests, analysis of variance,
ManneWhitney U or KruskaleWallis test as appropriate. Variables
with evidence for imbalance among pain groups (p 0.200) were
included in multivariable models.
CPT values were suggestive of an underlying bimodal distribu-tion
of this measure in the population (see Fig. 2), and all trans-formations
including logarithmic failed to normalise the data. For
further analysis we created a dichotomous variable based upon
visual examination of the distribution of data for the CPT measure
which supported a cut-off point of 15 C as clearly separating two
groups in the data (15 C, 15 C, see Fig. 2). This dichotomisation
was further supported by k-means cluster analysis, for which a two-cluster
solution produced two clusters of individuals, with indi-vidual
CPT measures below and above 15 C. Descriptive statistics
and chi-squared tests were used to compare differences in pro-portions
of participants with high CPT at each site between groups.
Three binary logistic regressions with high/low CPT at each of the
three sites as the outcome variable were used to assess pain group
differences adjusting for covariates gender, DASS and PSQI. Differ-ences
in frequency of use of non-cold descriptors of sensation
experienced during testing between groups were tested using a
chi-squared test.
PPT measures were log transformed to correct for positive skew.
General linear regression models with log transformed PPT mea-sures
as the outcome variable were used to assess group differences
unadjusted and adjusted for covariates gender, DASS and PSQI
(three models for three sites).
95% Confidence intervals with associated p-values are presented
for all regression coefficients. All data were analysed using the
Statistical Package for Social Sciences (SPSS) student version 18.0
Table 1
Clinical profile of CNSLBP participants.
Instrument
(max score)
(SPSS Inc., Chicago, IL, USA). Data were inputted by one researcher
(CP) and cross-checked by a second researcher (AS).
3. Results
Nineteen of the CNSLBP participants displayed NMP character-istics
(4 males and 15 females with a mean age 42.6 (SD 14.8))
and 17 displayed MP characteristics (9 male and 8 females with a
mean age of 39.4 (SD 14.2)). All subjects were screened for health
complaints and none reported other co-existing pain conditions,
diabetes, endocrine disorders, nervous system disorders or psy-chiatric
disorders. Clinical characteristics of the pain groups are
reported in Table 1. The NMP group was characterised by higher
pain levels, more pain areas, a larger proportion of neuropathic
pain as classified by PainDETECT scores, greater disability, higher
risk rating on the SBST and greater frequency of medication use.
Fig. 2 presents the untransformed individual values for CPT.
Initial univariable analyses provided evidence of group differences
in CPT at wrist, lumbar spine and heel sites, and PPT at the lumbar
spine site (Table 2). The proportions of subjects with elevated CPTs
(15 C) at the wrist were; control group 26%, MP group 24% and
NMP group 84%. There was evidence of some imbalance between
groups in DASS total, PSQI and gender, but not age orwaist-hip ratio
(Table 3), and of various associations between sex, DASS total and
Fig. 2. Untransformed individual values for CPT.
Mechanical
CNSLBP
Non-mechanical
CNSLBP
p-Value
Median (inter-quartile range), minemax
VAS (10) 4 (4), 8e17 6 (3), 10e19 0.018a
Widespread Pain
Index (19)
2 (2), 1e7 3 (3), 1e9 0.014a
RMDQ (24) 3 (6), 1e15 11 (11), 2e20 0.004a
PainDETECT (39) Number (percentage of pain group)
Nociceptive 14 of 17 (82%) 8 of 19 (42%)
Unclear 3 of 17 (18%) 6 of 19 (32%)
Neuropathic 0 5 of 19 (26%) 0.010b
StarT Back score (9)
Risk category Number (percentage of pain group)
Low 11 of 17 (65%) 2 of 19 (11%)
Medium 6 of 17 (35%) 9 of 19 (47%)
High 0 of 17 (0%) 8 of 19 (42%) 0.001b
Medication use Number (percentage of pain group)
Non-opioid 1 of 17 (6%) 6 of 19 (32%) 0.052b
NSAID 3 of 17 (18%) 8 of 19 (42%) 0.112b
Opioid 0 of 17 (0%) 5 of 19 (26%) 0.023b
Centrally acting 2 of 17 (12%) 6 of 19 (32%) 0.153b
For each questionnaire, the maximum score is given in brackets. RMDQ, the Roland
Morris Disability Questionnaire; VAS, a Visual Analogue Scale for pain on the day of
testing; CNSLBP ¼chronic non-specific low back pain.
a Statistical test for group differences is ManneWhitney U test.
b Statistical test for group differences is Fisher’s exact test.

5. P. O’Sullivan et al. / Manual Therapy 19 (2014) 311e318 315
Table 2
Cold pain threshold (CPT) and pressure pain threshold (PPT) measures by participant group.
Subgroup
Control (n ¼ 19) Mechanical (n ¼ 17) Non-mechanical (n ¼ 19) p-Value
CPT (n (%)15 C)
Wrist 5 (26.3) 4 (23.5) 16 (84.2) 0.001b
Lumbar spine 9 (47.4) 8 (47.1) 16 (84.2) 0.029b
Heel 6 (31.6) 9 (52.9) 14 (73.7) 0.034b
PPT (median (IQR), mm(Hg)) and Ln(PPT)a (mean (SD))
Wrist (untransformed) 301.3 (141.7) 302.0 (177.3) 239.7 (167.7)
Ln(PPT) 5.73 (0.27) 5.66 (0.40) 5.59 (0.31) 0.416c
Lumbar spine (untransformed) 352.7 (222.3) 288.7 (289.0) 183.0 (115.3)
Ln(PPT) 5.84 (0.40) 5.72 (0.60) 5.14 (0.71) 0.001c
Heel (untransformed) 309.3 (151.0) 315.0 (159.0) 270.3 (109.3)
Ln(PPT) 5.76 (0.36) 5.78 (0.40) 5.58 (0.34) 0.055c
Bold represent significant findings based on alpha of 0.05.
PSQI and CPT measures, and between waist:hip ratio and PPT
measures (Table 4). Therefore, DASS total, PSQI and sex were
included in multivariable models as potential confounders.
The results of the multivariable logistic regression model
adjusting for sex, DASS total and PSQI for CPT at the wrist showed
statistical evidence for group differences (Table 5). It was estimated
that those patients in the NMP group had 18.4 (95% CI: 2.5e133.1,
p¼0.004) times the odds of having an elevated (15 C) CPT to those
in the MP group. This estimate was similar to the unadjusted odds
ratio (OR) of 17.3 (p ¼ 0.001), meaning that sex, DASS total and PSQI
were not important confounders of the association between group
and CPT. CPT at the lumbar spine and heel sites was not statistically
significantly different between NMP and MP groups after adjust-ment
for covariates. At the lumbar spine, patients in the NMP group
were estimated to have 5.9 (95% CI: 0.9e38.4, p ¼ 0.064) times the
odds of having an elevated (15 C) CPT to those in the MP group
after adjustment for sex, DASS total and PSQI, with the adjusted OR
was similar in magnitude to the unadjusted estimate (6.0). At the
heel, patients in the NMP had 6.3 (95% CI: 0.9e41.5, p¼ 0.058) times
the odds of having an elevated (15 C) CPTcompared to those in the
MP group adjusting for sex, DASS total and PSQI. At this site the
adjusted OR (6.3) was larger than the unadjusted OR (2.5) which
indicates the likely presence of negative confounding by covariates.
At all sites there was no evidence that the MP group had greater or
lesser odds than the control group for elevated CPT thresholds.
The results of the linear regression models for PPT provided no
evidence for group differences at any site (Table 5). Although there
was some evidence that the NMP group had lower PPT than the MP
group at the lumbar spine for the univariable model
(difference: 0.58, 95% CI: 0.97 to 0.19, p ¼ 0.004), the model
adjusted for sex, DASS total and PSQI did not confirm a difference
existed independently of these covariates (difference: 0.37, 95%
CI: 0.83 to 0.09, p ¼ 0.117).
There were significant differences in the frequency of reporting
of non-cold descriptors (at CPT) between groups at all three sites.
Table 6 shows that the NMP group had the highest frequency of
non-cold descriptors and controls the lowest. For the wrist and
back sites the NMP group had a higher frequency than the MP
group.
4. Discussion
This study lends support to the presence of differences in PS
profile between clinically determined subgroups of CNSLBP
participants based on their pain characteristics, whilst adjusting for
potential confounding factors known to influence sensory thresh-olds.
The NMP group was estimated to have at least 2.5 times the
odds of having cold hypersensitivity, as defined by a CPT greater
than 15 C at the wrist, when compared to the MP CNSLBP group
and the pain-free control group (95% CI for OR: 2.5e133.1,
p ¼ 0.004), although the sample size was small and consequently
confidence intervals for group differences were wide. Estimates of
elevated CPT at the lumbar spine and heel were not statistically
significant meaning that the null hypothesis of no difference be-tween
groups cannot be rejected, however the pattern of larger
odds of having cold hypersensitivity in the NMP group is consistent
across all three sites, and it is possible that the lack of statistical
significance is due to the low power of the study to detect possibly
smaller effects at the lumbar spine and heel.
Whilst a lower PPT in the NMP group at the lumbar spine was
also detected, interestingly there was no statistical evidence for an
independent group difference between the MP and control group
after controlling for sex, sleep and psychological factors. These
findings suggest that the changes in PPT observed in the NMP group
may be mediated via gender differences, sleep deficits and/or
psychological distress highlighting the multidimensional nature of
PS. They also suggest that changes in PPT were limited to the
lumbar test site. These findings however are at odds with previous
reports where PPT was shown to be the best PS measure to
distinguish a group of 40 patients with CNSLBP from pain-free
controls after adjusting for age, gender, body compositions and
psychological factors (Neziri et al., 2012). The differences in the
findings may again reflect different patient profiles and methodo-logical
differences.
The findings of our study may explain some of the conflicting
and variable findings in the previous PS research into CNSLBP dis-orders
(Lewis et al., 2010; Attal et al., 2011; Blumenstiel et al., 2011;
O’Neill et al., 2011; Hubsher et al., 2013; Neziri et al., 2012; Roussel
et al., 2013), suggesting that NSCLNP is not a homogeneous group
and that patient classification is one means by which to deal with
this problem. Other authors have also proposed the need to classify
NSCLBP patients based on neurophysiological mechanisms (Nijs
et al., 2010; Smart et al., 2010; Woolf, 2011). Smart et al. (2010)
also described a group of CNSLBP patients with ‘central sensitisa-tion’,
defined by pain that is diffuse, lacks clear proportionate
mechanical characteristics and present with associated psycho-logical
factors. They defined a ‘nociceptive’ CNSLBP group by pain
that is more intermittent, localised and responds to clear
a Natural log transformation.
b Statistical test for group differences is chi-squared test.
c Statistical test for group differences is analysis of variance test.

6. P. O’Sullivan 316 et al. / Manual Therapy 19 (2014) 311e318
Table 3
Association between participant group membership and sex, age, waist:hip ratio, DASS and PSQI scores.
Subgroup
Control (n ¼ 19) Mechanical (n ¼ 17) Non-mechanical (n ¼ 19) p-Value
Female sex (n (%)) 11 (57.9) 8 (47.1) 15 (79.0) 0.132b
Age (mean (SD)) 42.6 (14.9) 39.4 (14.2) 41.9 (13.9) 0.788c
Waist:hip ratio (mean (SD)) 0.83 (0.11) 0.85 (0.09) 0.85 (0.10) 0.696c
DASS total (0e126a) (median (IQR)) 10 (14) 20 (18) 30 (34) 0.001d
PSQI (0e21a) (mean (SD)) 4.3 (2.8) 7.7 (3.5) 11.0 (3.4) 0.001c
Bold represent significant findings based on alpha of 0.05.
aggravating and easing factors (Smart et al., 2010). Although not
previously investigated against PS measures, these profiles are
similar to the NMP and MP CNSLBP groups described.
4.1. Possible pain mechanisms
It is proposed that central amplification of pain may be associ-ated
with a number of changes within the central nervous system
(CNS). These include neuronal hyperexcitability (Scott et al., 2005),
enlarged receptor fields (Kasch et al., 2005), lowered thresholds of
second order neurons (Kasch et al., 2005), reduced recruitment of
pain modulating control systems (Campbell and Edwards, 2009),
temporal summation (wind up) (Meeus and Nijs, 2007) and
neuronal reorganisation (Woolf and Mannion,1999). These changes
may be associated with a combination of factors including: sleep
dysfunction, psychosocial factors and environmental/genetic in-teractions,
influencing the immune-endocrine system and the
neuromatrix, highlighting the complex multidimensional nature of
persistent pain (O’Sullivan, 2012a). While peripheral sensitisation
and some degree of segmental activity dependent central sensiti-sation
might be anticipated for all patients with CNSLBP the
development of widespread extra-segmental pressure hyperalgesia
or the development of multi-modality sensitisation with either cold
or heat hyperalgesia implies much more extensive changes in pain
processing within the CNS. These changes are likely to involve
many of the processes outlined above. These central amplification
processes may also be linked to the presence of more constant and
persistent pain.
Interestingly therewas also a bimodal distribution for CPT in the
pain-free control group demonstrating that a number of control
subjects (26%) had elevated CPT, although their descriptors were
different to the centrally amplified group. Whether this finding
represents vulnerability in these subjects to future pain is not
known but has been hypothesised previously (Woolf, 2011).
The absence of PS differences between the MP and control group
may reflect that MP participants’ spinal structures are sensitised to
movement and/or load, but not local pressure (O’Sullivan, 2005;
Dankaerts et al., 2009), or that the site where the PPT testing was
applied was not specific to their pain location. Participants in the
MP CNSLBP group also displayed lower levels of psychosocial fac-tors
and sleep disturbance (Meeus and Nijs, 2007). Further research
is required to determine the relationship between pain character-istics
and PS to determine the role that central amplification has on
patient clinical profiles.
4.2. Clinical relevance
The classification of CNSLBP based on an underlying mechanism
has been proposed to enhance targeted management (Deyo et al.,
2009; O’Sullivan, 2012a; Woolf, 2011). While formal reliability
testing of clinicians ability to discriminate these groups was not
carried out, the results suggest that experienced physiotherapists
were able to identify patients with different PS profiles, based on
routine clinical examination (O’Sullivan, 2005; 2012b). Evaluation
of cold hyperalgesia at the wrist may be combined with clinical
assessment of patients to provide quantitative confirmation for
patients who exhibit some degree of central amplification of their
pain. Recent research in neck pain subjects indicates a pain
response 5/10 with the application of ice indicated a 90% likeli-hood
of laboratory measured CPT being 13 C (Maxwell and
Sterling, 2013). These findings may have clinical application to
the CNSLBP population described in this study, although further
research is required to confirm this.
Although speculative it would be interesting to investigate
whether patients with MP respond better to locally targeted
treatments, whereas patients with NMP require management ap-proaches
that more specifically address central pain mechanisms.
Clearly further research is required in larger populations of patients
with CNSLBP to determine the validity of the clinical profiles and
determine their predictive validity in relation to different targeted
interventions as well as the ability of less experienced clinicians to
reliably identify these patients.
4.3. Methodological considerations/limitations
This study was only powered to detect large effect sizes, and
consequently may have failed to detect smaller but still clinically
meaningful differences between groups. As a consequence of the
small sample size, the confidence intervals for the elevated odds of
cold hypersensitivity in the NMP group were very wide, limiting
a Minimum to maximum score possible.
b Statistical test for group differences is chi-squared.
c Statistical test for group differences is analysis of variance.
d Statistical test for group differences is KruskaleWallis test.
Table 4
Associations between cold (15 C, 15 C) and pressure pain (ln(PPT)) threshold
measures and sex, age, waist:hip ratio, DASS and PSQI scores.
CPT PPT
Wrist Lx Heel Wrist Lx Heel
Sex 0.116d 0.122d 0.080d 0.166c 0.236c 0.094c
Age 0.006c 0.133c L0.365c** 0.240b 0.254b 0.278b*
Waist:hip
ratio
0.001c 0.071c 0.040c 0.285a* 0.069a 0.273a*
DASS total 0.312c* 0.177c 0.038c 0.042b L0.394b** 0.110b
PSQI 0.336c* 0.290c* 0.141c 0.031a L0.400a** 0.550a
Bold represent significant findings based on alpha of 0.05.
Lx ¼ lumbar spine.
*p 0.05; **p 0.01.
a Measure of association is Pearson correlation coefficient.
b Measure of association is Spearman correlation coefficient.
c Measure of association is Point-biserial correlation coefficient.
d Measure of association is Phi correlation coefficient.

7. P. O’Sullivan et al. / Manual Therapy 19 (2014) 311e318 317
Table 5
Adjusted and unadjusted parameter estimates for group membership from univariable and multivariable binary logistic regression (CPT: 15 C, 15 C) and general linear
(ln(PPT)) models (multivariable models adjusted for gender, DASS total and PSQI).
Cold pain threshold Unadjusted Adjusted
precise estimation of this association in the population under
study. Furthermore, for PPT, testing at a generic site at the lumbar
spine may not detect local hyperalgesia. Previous authors have
successfully tested PPT in patients with CNSLBP at the site of most
severe pain and found it to be predictivewith pain, independent of
potential confounders (Neziri et al., 2012). Pain medication use
was only reported in CNSLBP participants, which precluded use of
this variable in the multivariable models presented. However,
group differences in medication use were not large (Table 6) and
current pain medication use was not associated with CPT or PPT.
Other variables only assessed in CNSLBP participants and associ-ated
with pain group membership, such as pain intensity, number
of pain areas, RMDQ and SBST, were not considered as con-founders
of the group membership/pain threshold association in
this study as they represented part of the common clinical profile
of these groups and thus consequences of differential sensory
processing. The inter-therapist reliability of the ability of Physio-therapists
to differentiate NP from NMP requires further investi-gation
and larger studies are required to verify these results.
5. Conclusion
This study provides preliminary evidence that two patient
groups with CNSLBP identified clinically, can be distinguished
based on their PS profile. When used in conjunction with sound
clinical reasoning, these profiles may help clinicians more accu-rately
identify mechanisms that underlie CNSLBP and better target
interventions. While these pain profiles have yet to be further
validated, they provide a framework for future research.
Author contributions
All authors discussed the results and contributed to the
manuscript.
References
Attal N, Perrot S, Fermanian J, Bouhassira D. The neuropathic components of chronic
low back pain: a prospective multicenter study using the DN4 questionnaire.
J Pain 2011;12:1080e7.
Blumenstiel KMD, Gerhardt AMA, Rolke RMD, Bieber CMD, Tesarz JMD,
Friederich H-CMD, et al. Quantitative sensory testing profiles in chronic back
pain are distinct from those in fibromyalgia. Clin J Pain 2011;27:682e90.
Buysse D, Reynolds C, Monk T, Berman S, Kupfer D. The Pittsburgh sleep quality
index: a new instrument for psychiatric practice and research. Psychiatry Res
1989;28:193e213.
Campbell C, Edwards R. Mindebody interactions in pain: the neurophysiology of
anxious and catastrophic pain-related thoughts. Transl Res 2009;153:97e101.
Carli G, Suman AL, Biasi G, Marcolongo R. Reactivity to superficial and deep stimuli
in patients with chronic musculoskeletal pain. Pain 2002;100:259e69.
Chien A, Sterling M. Sensory hypoaesthesia is a feature of chronic whiplash but not
chronic idiopathic neck pain. Man Ther 2010;15:48e53.
Dankaerts W, O’Sullivan P, Burnett A, Straker L. Differences in sitting postures are
associated with nonspecific chronic low back pain disorders when patients are
subclassified. Spine 2006;31:698e704.
Dankaerts W, O’Sullivan P, Burnett A, Straker L, Davey P, Gupta R. Discriminating
healthy controls and two clinical subgroups of nonspecific chronic low back
pain patients using trunk muscle activation and lumbosacral kinematics of
postures and movements. Spine 2009;34:1610e8.
Deyo RA, Mirza SK, Turner JA, Martin BI. Overtreating chronic back pain: time to
back off? J Am Board Fam Med 2009;22:62e8.
Dunn W. The impact of sensory processing abilities on the daily lives of young
children and their families: a conceptual model. Infants Young Child 1997;9:
23e35.
Freynhagen R, Baron R, Gockel U, Tolle T. painDETECT: a new screening question-naire
to identify neuropathic components in patients with back pain. Curr Med
Res Opin 2006;22:1911e20.
Giesecke T, Gracely RH, Grant MAB, Nachemson AL, Petzke F, Williams DA, et al.
Evidence of augmented central pain processing in idiopathic chronic low back
pain. Arthritis Rheum 2004;50:613e23.
Table 6
Frequency of non-cold descriptorsa cited during the cold pain testing.
Controls
(n ¼ 19)
Mechanical
CNSLBP (n ¼ 17)
Non-mechanical
CNSLBP (n ¼ 19)
p-Valueb
N (% of group)
CPT wrist 3 (15.8) 6 (35.3) 12 (63.2) 0.010
CPT L5/S1 7 (36.8) 12 (70.6) 18 (94.7) 0.001
CPT heel 3 3 (15.8) 9 (52.9) 11 (57.9) 0.017
a Non-cold descriptors used were ‘burning, ice, sharp, sting, gnawing and
freezing’. Any other descriptions were not included as non-cold descriptors. These
were ‘pressure, nice, cold, tingling, pleasant and numb’.
b Chi-squared test.
Odds ratioa (95% CI) p-Value Odds ratio (95% CI) p-Value
Wrist Non-mechanical 17.3 (3.3, 91.7) 0.001 18.4 (2.5, 133.1) 0.004
Control 1.2 (0.3, 5.3) 0.849 1.3 (0.2, 7.0) 0.759
Mechanical REF REF
Lx Non-mechanical 6.0 (1.3, 28.5) 0.024 5.9 (0.9, 38.4) 0.064
Control 1.0 (0.3, 3.8) 0.985 1.4 (0.3, 6.4) 0.637
Mechanical REF REF
Heel Non-mechanical 2.5 (0.6, 10.1) 0.201 6.3 (0.9, 41.5) 0.058
Control 0.4 (0.1, 1.6) 0.198 0.3 (0.1, 1.4) 0.134
Mechanical REF REF
Pressure pain threshold b (95% CI)b p-Value b (95% CI) p-Value
Wrist Non-mechanical 0.07 (0.29, 0.15) 0.551 0.11 (0.37, 0.15) 0.407
Control 0.08 (0.14, 0.30) 0.489 0.11 (0.13, 0.35) 0.347
Mechanical REF REF
Lx Non-mechanical 0.58 (0.97, -0.19) 0.004 0.37 (0.83, 0.09) 0.117
Control 0.12 (0.27, 0.51) 0.547 0.04 (0.38, 0.47) 0.838
Mechanical REF REF
Heel Non-mechanical 0.19 (0.43, 0.06) 0.133 0.22 (0.52, 0.08) 0.142
Control 0.01 (0.26, 0.23) 0.911 0.01 (0.27, 0.28) 0.954
Mechanical REF REF
Bold represent significant findings based on alpha of 0.05.
a The ratio of the odds for cold pain threshold 15 C for the test group (non-mechanical or control) to the reference group (mechanical pain group).
b Coefficient represents difference in the natural log of pressure pain threshold between test groups (non-mechanical or control) and the reference group (mechanical pain
group, positive value indicates higher value in test group).

8. P. O’Sullivan 318 et al. / Manual Therapy 19 (2014) 311e318
Heffner K, France C, Trost Z, Ng H, Pigeon W. Chronic low back pain, sleep distur-bance,
and interleukin-6. Clin J Pain 2011;27:35e41.
Hill JC, Dunn KM, Lewis M, Mullis R, Main CJ, Foster NE, et al. A primary care back
pain screening tool: identifying patient subgroups for initial treatment.
Arthritis Rheum 2008;59:632e41.
Hubsher M, Moloney N, Leaver A, Rebbeck T, McAuley J, Refshauge K. Relationship
between quantitative sensory testing and pain or disability in people with
spinal pain e a systematic review and meta-analysis. Pain 2013;154:1497e504.
Huskisson EC. Measurement of pain. Lancet 1974;2:1127e31.
Jones D. Testeretest reliability of pressure pain threshold measurements of the
upper limb and torso in young healthy women. J Pain 2007;8:650e6.
Karayannis NV, Jull GA, Hodges PW. Physiotherapy movement based classification
approaches to low back pain: comparison of subgroups through review and
developer/expert survey. BMC Musculoskelet Disord 2012;13:24.
Kasch H, Qerama E, Bach FW, Jensen TS. Reduced cold pressor pain tolerance in non-recovered
whiplash patients: a 1-year prospective study. Eur J Pain 2005;9:
561e9.
Leboeuf-Yde C, Nielsen J, Kyvik K, Fejer R, Hartvigsen J. Pain in the lumbar,
thoracic and cervical regions: do age and gender matter? A population-based
study of 34,902 Danish twins 20e71 years of age. BMC Musculoskelet Disord
2009;10.
Lewis C, Khan A, Souvlis T, Sterling M. Sensory characteristics of tender points in the
lower back. Man Ther 2010;15:536e41.
Lovibond S, Lovibond P. Manual for the depression anxiety stress scales; 1995.
Maxwell S, Sterling M. An investigation of the use of a numeric pain rating scale
with ice application to the neck to determine cold hyperalgesia. Man Ther
2013;18:172e4.
Meeus M, Nijs J. Central sensitization: a biopsychosocial explanation for chronic
widespread pain in patients with fibromyalgia and chronic fatigue syndrome.
Clin Rheumatol 2007;26:465e73.
Moloney NA, Hall TM, Doody CM. Reliability of thermal quantitative sensory
testing: a systematic review. J Rehabil Res Dev 2012;49:191e207.
Mosek A, Yarnitsky D, Korczyn AD, Niv D. The assessment of radiating low back pain
by thermal sensory testing. Eur J Pain 2001;5:347e51.
Neziri A, Curatolo M, Limacher A, Nüesch E, Radanov B, Andersen O, et al. Ranking
of parameters of pain hypersensitivity according to their discriminative ability
in chronic low back pain. Pain 2012;153:2083e91.
Nijs J, Van Houdenhove B, Oostendorp RAB. Recognition of central sensitization in
patients with musculoskeletal pain: application of pain neurophysiology in
manual therapy practice. Man Ther 2010;15:135e41.
O’Sullivan P. Diagnosis and classification of chronic low back pain disorders: mal-adaptive
movement and motor control impairments as underlying mechanism.
Man Ther 2005;10:242e55.
O’Sullivan P, Straker L, Smith A, Perry M, Kendall G. Carer experience of back pain is
associated with adolescent back pain experience even when controlling for
other carer and family factors. Clin J Pain 2008;24:226e31.
O’Sullivan P. It’s time for change in the management of non-specific chronic low
back pain. Br J Sports Med 2012a;46:224e7.
O’Sullivan PB. A classification-based cognitive functional approach for the man-agement
of back pain. J Orthop Sports Phys Ther 2012b;42:A17e21.
O’Neill S, Kjær P, Graven-Nielsen T, Manniche C, Arendt-Nielsen L. Low pressure
pain thresholds are associated with, but does not predispose for, low back pain.
Eur Spine J 2011;20:2120e5.
Roland M, Fairbank J. The RolandeMorris disability questionnaire and the Oswestry
disability questionnaire. Spine 2000;25:3115e24.
Roland M, Morris R. A study of the natural history of back pain. Spine 1983;8:141e4.
Rolke R, Baron R, Maier C, Tolle TR, Treede RD, Beyer A, et al. Quantitative sensory
testing in the German research network on neuropathic pain (DFNS): stan-dardized
protocol and reference values. Pain 2006a;123:231e43.
Rolke R, Baron R, Maier C, Tölle TR, Treede RD, Beyer A, et al. Quantitative sensory
testing in the German research network on neuropathic pain (DFNS): stan-dardized
protocol and reference values. Pain 2006b;123:231e43.
Roussel NAPMPT, Nijs JPMPT, Meeus MPPT, Mylius VPMD, Fayt CPMD,
Oostendorp RPMPTPT. Central sensitization and altered central pain processing
in chronic low back pain: fact or myth? Clin J Pain 2013;29:625e38.
Scott D, Jull G, Sterling M. Widespread sensory hypersensitivity is a feature of
chronic whiplash-associated disorder but not chronic idiopathic neck pain. Clin
J Pain 2005;21:175e81.
Slater H, Arendtnielsen L, Wright A, Gravennielsen T. Sensory and motor effects of
experimental muscle pain in patients with lateral epicondylalgia and controls
with delayed onset muscle soreness. Pain 2005;114:118e30.
Smart K, Blake C, Staines A, Doody C. Clinical indicators of ‘nociceptive’, ‘peripheral
neuropathic’ and ‘central’ mechanisms of musculoskeletal pain. A Delphi survey
of expert clinicians. Man Ther 2010;15:80e7.
Spitzer WO. Scientific approach to the assessment and management of activity-related
spinal disorders: a monograph for clinicians. Report of the Quebec
task force on spinal disorders. Spine 1987;12:1e59.
Vibe Fersum K, O’Sullivan PB, Kvåle A, Skouen JS. Inter-examiner reliability of a
classification system for patients with non-specific low back pain. Man Ther
2009;14:555e61.
Vibe Fersum K, O’Sullivan P, Skouen JS, Smith A, Kvåle A. Efficacy of classification
based ‘cognitive functional therapy’ in patients with Non Specific Chronic Low
Back Pain – a randomized controlled trial. Eur Pain J 2012;17(6):916e28.
Wasner GL, Brock JA. Determinants of thermal pain thresholds in normal subjects.
Clin Neurophysiol 2008;119:2389e95.
Wolfe F, Clauw D, Fitzcharles M, Goldenberg D, Katz R, Mease P, et al. The American
College of Rheumatology preliminary diagnostic criteria for fibromyalgia and
measurement of symptom severity. Arthritis Care Res 2010;62:600e10.
Woolf C, Mannion R. Neuropathic pain: aetiology, symptoms, mechanisms, and
management. Lancet 1999;353:1959e64.
Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain.
Pain 2011;152:S2e15.
Wright A, Thurnwald P, O’Callaghan J, Smith J, Vicenzino B. Hyperalgesia in tennis
elbow patients. J Musculoskelet Pain 1994;2:83e97.
Zwart J-A, Trond S. Repeatability of dermatomal warm and cold sensory thresholds
in patients with sciatica. Eur Spine J 2002;11:441e6.