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Pain Physiology Education Improves Health Status

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ORIGINAL ARTICLE
Pain Physiology Education Improves Health Status
and Endogenous Pain Inhibition in Fibromyalgia
A Double-Blind Randomized Controlled Trial
Jessica Van Oosterwijck, PT, PhD,*wz Mira Meeus, PT, PhD,*w
Lorna Paul, PT, PhD,y Mieke De Schryver, PT, MSc,* Aurelie Pascal, PT, MSc,*
Luc Lambrecht, MD, PhD,8 and Jo Nijs, PT, PhD*wz
Objectives: There is evidence that education on pain physiology can
have positive effects on pain, disability, and catastrophization in
patients with chronic musculoskeletal pain disorders. A doubleblind randomized controlled trial (RCT) was performed to examine
whether intensive pain physiology education is also effective in
fibromyalgia (FM) patients, and whether it is able to influence the
impaired endogenous pain inhibition of these patients.
Methods: Thirty FM patients were randomly allocated to either the
experimental (receiving pain physiology education) or the control
group (receiving pacing self-management education). The primary
outcome was the efficacy of the pain inhibitory mechanisms, which
was evaluated by spatially accumulating thermal nociceptive
stimuli. Secondary outcome measures included pressure pain
threshold measurements and questionnaires assessing pain cognitions, behavior, and health status. Assessments were performed at
baseline, 2 weeks, and 3 months follow-up. Repeated measures
ANOVAS were used to reveal possible therapy effects and effect
sizes were calculated.
Results: After the intervention the experimental group had
improved knowledge of pain neurophysiology (P < 0.001). Patients
from this group worried less about their pain in the short term
(P = 0.004). Long-term improvements in physical functioning
(P = 0.046), vitality (P = 0.047), mental health (P < 0.001), and
general health perceptions (P < 0.001) were observed. In addition,
the intervention group reported lower pain scores and showed
improved endogenous pain inhibition (P = 0.041) compared with
the control group.
Discussion: These results suggest that FM patients are able to
understand and remember the complex material about pain
Received for publication May 25, 2012; revised October 28, 2012;
accepted November 4, 2012.
From the *Department of Human Physiology, Faculty of Physical
Education & Physiotherapy, Vrije Universiteit Brussel;
zDepartment of Physical Medicine and Physiotherapy, University
Hospital Brussels, Brussels; wDepartment of Health Care Sciences,
Division of Musculoskeletal Physiotherapy, Artesis University
College Antwerp, Antwerp; 8Private Practice for Internal Medicine,
Gent/Aalst, Belgium; and yNursing and Health Care, School of
Medicine, University of Glasgow, Glasgow, UK.
J.V.O. is financially supported by grant no. OZR1596 from the research
council of the Vrije Universiteit Brussel, Brussels, Belgium. M.M. is
a postdoctoral research fellow of the Research Foundation Flanders (FWO). The remaining authors declare no conflict of interest.
Reprints: Jo Nijs, PT, PhD, Department of Human Physiology, Faculty of Physical Education & Physiotherapy, Vrije Universiteit
Brussel, Building L-3rd floor, Pleinlaan 2, Brussels BE-1050,
Belgium (e-mail: jo.nijs@vub.ac.be).
Supplemental Digital Content is available for this article. Direct URL
citations appear in the printed text and are provided in the HTML
and PDF versions of this article on the journal’s Website,
www.clinicalpain.com.
Copyright r 2013 by Lippincott Williams & Wilkins
Clin J Pain
Volume 29, Number 10, October 2013
physiology. Pain physiology education seems to be a useful component in the treatment of FM patients as it improves health status
and endogenous pain inhibition in the long term.
Key Words: patient education, conditioned pain modulation, spatial summation, rehabilitation, central sensitization.
(Clin J Pain 2013;29:873–882)
F
ibromyalgia (FM) is characterized by the presence of
chronic widespread pain1,2 and studies have demonstrated exaggerated pain responses after sensory stimulation of healthy tissues.3 This has led to the hypothesis
that the central nervous system is hyperexcitable in these
patients and that pain could be perceived in the absence of a
nociceptive input, due to induction of irreversible plasticity
changes in the central nervous system (CNS).4 Staud et al5,6
found evidence for this hypothesis in FM patients and
demonstrated that hypersensitivity of the CNS or central
sensitization is a characteristic of FM.
Sensitivity to pain results from the outcome of the
balance between pain facilatory and inhibitory pathways,
which either potentiate (descending facilitation) or suppress
(descending inhibition) the passage of nociceptive messages
to the brain.7 Malfunctioning of these central inhibitory
pathways seems to be responsible for abnormal spatial
summation and contributes to central sensitization in people
with chronic pain.8–10 In FM patients a disturbed and/or
impaired descending nociceptive inhibition has been observed.10 It has been shown that pain inhibitory systems are
not optimally recruited by spatial summation procedures
(SSP) using noxious conditioning stimuli in FM patients, in
contrast to chronic low back pain patients and pain-free
individuals.10,11 Although some researchers have observed
normal spatial summation responses,12 efficient activation of
the pain modulatory systems in FM12–14 has only been
established when short and/or innocuous stimuli are utilized.
The dysfunctional descending nociceptive inhibitory
mechanism as seen in FM is primarily biological, but is
influenced by negative and maladaptive thoughts, emotions,
cognitions, and behaviors like catastrophizing, hypervigilance,
avoidance behavior, and somatization.3 These negative cognitions can develop when FM patients do not understand the
origin of their generalized musculoskeletal chronic pain and
can facilitate pain. Therefore they need to be addressed during
therapy, for instance, through education.15,16
Most of the educational models have limited efficacy in
decreasing pain and disability in patients with chronic
musculoskeletal pain, and may even increase patients’ fears
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and pain.17 However, clinical studies have shown that
education concerning pain physiology is able to influence
negative, maladaptive cognitions about pain, improve pain
behavior and pain-free movement performance, and reduce
pain in chronic musculoskeletal disorders.17 Although this
type of education has been shown to reduce pain, we were
interested to know if pain physiology education is able to
directly influence endogenous pain inhibition. Although
pain physiology education has been studied in patients with
chronic low back pain,18–20 chronic whiplash,21 and chronic
fatigue syndrome in combination with widespread pain,22
studies in FM are lacking. In addition, previous studies in
patients with chronic musculoskeletal pain have only
studied immediate posttreatment effects.
The present study examined whether reconceptualisation of pain, by pain physiology education, was able to
influence (1) pain cognitions, (2) health status, and (3)
endogenous nociceptive processing in FM patients. In
addition, long-term effects of pain physiology education
were examined.
MATERIALS AND METHODS
Setting and Patients
Patients with FM were referred for study participation
from a private practise for internal medicine. To be included
into the study, participants had to (1) have FM as defined by
the criteria of the 1990 ACR,2 (2) be between 18 and 65 years
of age, and (3) have Dutch as their native language. A power
analysis was performed based on the outcomes of the perceived pain scores during a SSP procedure (similar to the
SSP procedure used in this study) from a previous study,
which examined the efficacy of pain inhibition in chronic
pain patients.23 The analysis revealed that 15 participants per
group were required to obtain a power between 0.865 and
0.985, and with a significance level of 0.01.
This double-blind, randomized controlled clinical trial
(ClinicalTrials.gov identifier NCT00857740) was conducted
between March 2009 and June 2010 at the Department of
Human Physiology, Vrije Universiteit Brussel, Belgium and
the Division of Musculoskeletal Physiotherapy, Artesis
University College Antwerp, Belgium. Because of the long
study duration (3 mo follow-up) patients were able to continue with their medication, but were asked to abstain from
analgesics and antidepressants at least 24 hours before the
assessments and not to commence any new treatments during the study. Ethical approval was obtained from the Ethics
Committee of the University Hospital Brussels/Vrije Universiteit Brussel. Patients provided written informed consent.
Measurements
At the first day of the study baseline assessments were
performed, that is, a battery of questionnaires was filled out
and pain was assessed using pressure algometry and a SSP.
After the initial education session, patients from both
groups were asked to fill out the Neurophysiology of Pain
Test and undergo pressure pain threshold (PPT) measurements once again. The patients underwent the same clinical
assessments as in baseline at 2 weeks and after 3 months
follow-up, conducted by the same blinded assessor. The
procedure of the study and the CONSORT diagram for the
patient flow through the study are presented in Figure 1.
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Volume 29, Number 10, October 2013
Primary Outcome Measures
The SSP was chosen as the primary outcome measure.
The examiner marked the patients dominant arm at the
following locations: (1) proximal interphalangeal joints, (2)
mid-palm, (3) wrist, (4) distal-third of the forearm, (5)
middle-third of the forearm, (6) elbow, (7) mid-biceps, and
(8) shoulder, dividing the limb into 8 segments as shown
in Figure 2. The dominant arm was gradually immersed
into warm circulating water (461C) starting with the fingertips (first segment) until the whole arm was immersed.
Each segment was immersed for 2 minutes. The participants
were asked to rate their pain on a score of 100, every 15
seconds of the 2-minute immersion period. The 2-minute
immersions were alternated with 5 minutes rest where
the arm was withdrawn from the water and wrapped in a
towel. This procedure was described by Marchand and
Arsenault24 who used this protocol to investigate inhibitory
mechanisms and pain perception in pain-free people.
The same procedure has been used with noxious cold or
hot water to examine the efficacy of the pain inhibitory
mechanisms in patients with FM,10 chronic low back
pain,10 and chronic fatigue syndrome with chronic widespread pain.23
Secondary Outcome Measures
Self-reported questionnaires include the Fibromyalgia
Impact Questionnaire (FIQ) (scores range from 0 to 100,
average FM patients score about 50 and severely affected
patients score >70),25 the Medical Outcomes Short Form
36 Health Status Survey (SF-36) (8 separate subscales with
scores ranging from 0 to 100, with improvement as scores
increase),26 the Pain Coping Inventory (PCI) (consisting
of 3 scales representing active coping strategies, ie, transformation, distraction, reducing demands, and 3 scales
representing passive coping strategies; ie, ruminating,
retreating, resting; with higher scores indicating more frequent application of that specific coping strategy),27 the
Pain Catastrophizing Scale (PCS) (consisting of a general
score and 3 subscales, ie, helplessness, magnification, rumination; higher scores indicating more severe catastrophic
thoughts about pain),28,29 the Pain Vigilance and Awareness
Questionnaire (PVAQ) (scores range from 0 to 80 and high
scores indicate hypervigilance for pain),30 the Tampa Scale
Kinesiophobia (TSK) (scores range from 17 to 68, with
scores >37 indicating high fear of movement),31,32 and the
Neurophysiology of Pain Test—patient version (scores
ranging from 0 to 19, with high scores representing a better
knowledge regarding pain neurophysiology).19,33 As patients
were Dutch speaking, we used the Dutch translations of the
above mentioned questionnaires. Clinical assessment comprised pressure algometry to measure PPTs bilaterally at the
spine (5 cm left and right of the spinous process of T8 and
L3),34 the upper trapezius muscle (pars descendens midway,
between the seventh cervical vertebra and the tip of the
acromion),35 the proximal third of the calf, and the web
between index finger and thumb36 using an analog Wagner
algometer (Wagner Instruments, Greenwich, CT). The
threshold was determined as the mean of the 2 last values out
of 3 consecutive measurements (10 s in between).37
Randomization
Thirty patients participated in this study and were
randomly allocated to either the experimental group
(n = 15) or the control group (n = 15) using a simple
randomization procedure.38,39 Therefore patients drew
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Intensive Pain Physiology Education for FM Patients
numbered lots that were marked either 1 (control group) or
2 (experimental group) from a bag. Neither the patients,
nor the researcher who performed the assessments (J.V.O.)
were informed about the allocation (double-blind design).
The patients were aware of participating in an experiment
in which 2 educational sessions were compared and that the
drawn lot determined the allocation, but the design and the
interventions were not explained in terms of control or
experimental groups. The researcher who delivered both the
control and the experimental intervention was blinded to
the outcomes of the measurements. However, this
researcher was aware of the study hypothesis.
At the end of the trial, the success of the blinding
procedure was examined, both among the patients and the
assessor, by asking them whether they thought the participant received the experimental or control intervention.
ENROLLMENT
Intervention
The patients in the experimental group received 2 oneon-one educational sessions about the neurophysiology of
pain, whereas the patients of the control group received 2
one-on-one educational sessions about activity self-management techniques. The sessions were delivered by a bachelor in
physiotherapy (M.D.S. educated 19 patients, March to May
2009; A.P. educated 11 patients, November 2009 to May
2012) who received training from 2 qualified physiotherapists
(J.V.O. and J.N.) with experience in providing education.
A standard PowerPoint presentation was used by the
therapist to guide the patient through the first educational
session, but the therapist tailored the education session to
the patients’ specific experiences. Pictures, examples, and
metaphors were used to maximize the intelligibility. The
session had a duration of 30 minutes.
FM-patients assessed for eligibility (n=115)
Excluded (n=85)
•
•
Not meeting inclusion criteria (n=25)
Declined to participate (n=60)
Measure 1 - Baseline:
•
Questionnaires
Pressure algometry
•
•
Spatial summation procedure
ALLOCATION
Randomized (n=30)
Experimental group (n=15)
session 1: Education about pain
neurophysiology
D
A
Y
Control group (n=15)
session 1: Education about activity
management
1
Measure 2:
• Questionnaire: the Neurophysiology of Pain Test
• Pressure algometry
Information brochure about pain
neurophysiology to read at home
Information brochure about activity
management to read at home
Session 2: Education about pain
neurophysiology (by telephone)
Session 2: Education about activity
management (by telephone)
D
A
Y
7
FOLLOW-UP
Lost to follow-up (n=3):
• Familial reason
• Lost the ability to drive the car
• Hospitalized because of a
blood cloth
D
A
Y
Measure 3:
Questionnaires
•
Pressure algometry
•
Spatial summation procedure
•
Measure 4:
Questionnaires
•
Pressure algometry
•
•
Spatial summation procedure
•
Effectiveness of blinding
14
M
O
N
T
H
Lost to follow-up (n=1):
•
Relocation
3
ANALYSIS
Experimental group analysed (n=15)
• Intention-to-treat analysis by last
observation-carried-forward approach (n=3)
Control group analysed (n=15)
• Intention-to-treat analysis by last
observation-carried-forward approach (n=1)
FIGURE 1. CONSORT diagram for the patient flow through the study protocol.
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were. Patients were motivated and coached to apply their
new insights into their daily life.
Statistical Analysis
FIGURE 2. Effect of intervention on the mean pain score slopes
from the spatial summation procedure at 3 months follow-up.
Estimated marginal means covarying for sex and medication use
(analgesics or antidepressants). Error bars represent SE of the
mean. Interaction effects between group and slope of the mean
pain scores during the spatial summation procedures were
examined using repeated measures ANOVA (P = 0.041).
The experimental group received education about pain
neurophysiology, which covers the physiology of the nervous system in general and of the pain system in particular.
Pain physiology education focuses on informing the patient
on the difference between “nociception” and “pain,” and
teaches patients that the CNS has the ability to increase or
decrease its sensitivity (neuroplasticity) to help them cope
with persistent pain.17 The content of the education sessions
and the pictures were based on the book “Explain Pain” by
Butler and Moseley40 and an overview can be found in
Table S1 (Supplemental Digital Content 1 http://links.
lww.com/CJP/A56). The control group received education
about pacing self-management techniques, teaching FM
patients how to manage their daily activities with respect to
their symptoms. This activity management strategy is used
to encourage patients to achieve an appropriate balance
between activity and rest to avoid exacerbation and to set
realistic goals for increasing activity.41 The oral education
was completed by a leaflet containing written information
about either pain neurophysiology or activity management.
Patients were asked to take the brochure home and to read
it several times.
One week after the initial education session, the
researcher that provided the education contacted the patients
for a second educational intervention session delivered by
telephone. Patients were asked whether they had read and
understood the brochure and if they had any questions that
could be answered by the researcher. In addition the questions on the Neurophysiology of Pain Test, which were
incorrectly answered after the first educational session were
explained once again to the interventional group. Patients
from both the experimental and the control groups were
asked if they had tried to apply what they had learned during
the education in their daily life and what their experiences
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All data were analyzed using IBM SPSS Statistics 19.0
for Windows (IBM Corporation, Somers, NY). Normality
of the variables was tested with the Kolmogorov-Smirnov
test and appropriate descriptive statistics were calculated.
Comparability of the groups before the intervention was
studied with the Fisher exact test and the independent
samples t test. Possible changes in the outcomes of the
questionnaires and the PPTs in response to the intervention
were examined between the 2 groups using repeated measures analysis of variance. Intervention (education about
pain physiology vs. education about pacing self-management techniques) served as the between-subjects factor and
time (baseline vs. the follow-up treatment scores) served as
the within-subjects factor.
An 8-factor repeated measures analysis of variance on
the data of the SSP (segments group interaction) was
used to identify differences between the 2 groups in pain
intensity evolution or slope during the immersion procedure. Confounding effects of sex might play an important
role in the findings of impaired pain inhibitory system
activation in patients with chronic pain, and differences in
pain modulatory responses between male and female FM
patients have been reported.8,42,43 Many participants indicated that they did not comply with the request to avoid
analgesics and antidepressants for at least 24 hours before
testing. For these reasons sex and medication (analgesics
and antidepressants) use were entered as covariates in the
repeated measures analysis of the SSP.
Four FM patients did not attend the 3-month followup assessment (experimental group, n = 3; control group,
n = 1). The reason for their absence and the patient flow
throughout the study are represented in Figure 1. We
therefore conducted intention-to-treat analysis using the
last observation-carried-forward approach.
The significance level was set at 0.05 for all statistical
tests and effect sizes were obtained by calculating Cohen’s
d.44 The Cohen’s d effect size was defined as the mean
baseline value minus the mean follow-up value divided by
the pooled SD of both. A d value around 0.20 is described
as small, around 0.50 as medium (moderate), and near 0.80
as large.44
RESULTS
As shown in Table 1 there were no significant differences for demographic and baseline characteristics between
the experimental group and the control group.
Primary Outcome Measures
Efficacy of the endogenous pain inhibitory mechanisms was assessed using the SSP and results showed no
significant differences between the experimental and the
control groups in baseline (P = 0.960) or after 2 weeks
(P = 0.521), but there was a significant difference after 3
months (P = 0.041). At 3 months follow-up, the mean pain
scores in the experimental group were lower than those in
the control group. Regarding the slope of the mean scores,
pain scores increased as the immersed surface increased in
the control group, whereas pain scores decreased slightly in
the intervention group (Fig. 2).
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Intensive Pain Physiology Education for FM Patients
TABLE 1. Patient Demographic and Baseline Characteristics
Age (y) (mean [SD])
Sex (n [%])
Male
Female
Employment status
(n [%])
Full time
Part time
Unemployed or on
disability
Onset symptom (mo)
(mean [SD])
Patients using
analgesics (n [%])
Patients using
antidepressants
(n [%])
Received academic
education about
neurophysiology
before study
participation (n [%])
Experimental
Group
(n = 15)
Control
Group
(n = 15)
45.8 (9.5)
45.9 (11.5)
3 (20)
12 (80)
1 (6.7)
14 (93.3)
BetweenGroup
Comparison
(P)
0.973
0.598
0.697
2 (13.3)
3 (20)
10 (66.7)
156 (96)
2 (13.3)
5 (33.3)
8 (53.3)
116 (46)
0.162
12 (80)
1.000
11 (73.3)
6 (40)
0 (0)
7 (46.7)
0 (0)
1.000
1.000
Secondary Outcome Measures
The experimental group and the control group were
comparable in baseline regarding the secondary outcome
measures (P < 0.05). After the intervention no significant
differences in PPTs were found (P-values between 0.323 and
0.889) between the 2 groups. However, we found significant
changes in some of the self-reported outcome measures in
response to the treatment. Scores on the Neurophysiology of
Pain Test significantly increased in response to the experimental intervention (P < 0.001), whereas no significant
effects were established in response to the control intervention (P = 0.150). When the 2 groups were compared this
resulted in a significant difference (P < 0.001) between the 2
groups, and the effect size was large (d = 1.97).
In addition, the experimental and the control groups
showed some significant changes in health status (SF-36).
Although scores for physical functioning (P = 0.046)
improved from baseline to 3 months follow-up in the
experimental group, scores declined in the control group.
Scores on the general health perceptions scale (P < 0.001)
increased between baseline and 3 months follow-up in the
experimental group, in the control group scores increased in
response to the intervention but declined at 3 months follow-up. A large effect size was established (d = 0.98). In
response to the intervention, scores on the vitality scale
(P = 0.047) slightly decreased 2 weeks posttreatment in the
experimental group, but increased at 3 months follow-up.
In the control group, a linear decrease was established and
the effect size was small. Mental health scores (P < 0.001)
increased from baseline to 2 weeks and 3 months follow-up
in the experimental group, whereas they decreased in the
control group resulting in a large effect size.
A significant change in the PCI subscales transformation
(P = 0.027) and worrying (P = 0.004) was established 2 weeks
after treatment. However, at 3 months follow-up the changes
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2013 Lippincott Williams & Wilkins
were no longer significant (transformation, P = 0.079; worrying, P = 0.141). Although the mean scores of the remaining
self-reported outcome measures, that is, PCS, PVAQ, FIQ,
and TSK decreased the changes were not significant (P-values
between .064 and .929). The mean scores and effect sizes of the
secondary outcome measures are represented in Table 2.
Efficacy of Blinding Procedure
At the end of the study, 2 of the 13 FM patients from
the experimental group thought that they had received the
experimental intervention and 11 thought that they had
received the control intervention. Six of the 14 FM patients
from the control group thought that they had received the
experimental intervention and 8 thought that they had
received the control intervention. The assessor’s assumption regarding the allocation was right in 9 from the 15
cases in the experimental group and in 8 from the 15 cases
in the control group.
DISCUSSION
The results of this study suggest that education about
pain physiology can be a useful component in the treatment
of FM patients, as it can be used to improve health status
and endogenous pain inhibition in the long term.
Influencing Descending Nociceptive Processing
The results of our study suggest that pain physiology
education had a positive effect on descending nociceptive
processing at 3 months follow-up. In pain-free individuals,
the mean pain intensity scores over the different segments
vary between 26 and 45 during the SSP, whereas in FM
patients scores between 49 and 77 have been observed.10 In
our study, FM patients from the experimental group
showed lower pain scores (varying between 52 and 58), than
patients from the control group (varying between 59 and
68), 3 months after the intervention. In the control group,
pain scores tended to augment as the immersed surface
increased, which has been observed before in FM patients10
and indicates a deficit of the endogenous pain inhibitory
systems. In the experimental group, pain perception was
not related to the stimulated surface area, which indicates
that the inhibitory efferents counterbalance the facilitatory
afferents efficiently as seen in healthy controls.24
Could it be possible that pain physiology education is
able to improve descending nociceptive processing? As
descending facilitatory pathways depart from brain areas
that are involved in the regulation of cognitive and emotional reactions, such as the limbic system, these cognitions
and emotions can modulate the activity in the descending
pathways.45 Negative cognitions and emotions, which can
develop when patients do not understand their condition or
the cause of experiencing pain, can facilitate pain through
these descending pathways. Thus on theoretical basis, one
can assume that altering maladaptive thoughts and cognitions could result in less top down pain facilitation and an
improved descending nociceptive inhibition of the CNS,
which in turn can lead to less pain and improvements in
movement performance. Indeed, the current study findings
can confirm this theory to certain extent. If pain physiology
education can be used to improve endogenous pain inhibition, as suggested by our findings, this could be a feasible
mechanism to explain previously reported improvements in
pain18,21 and (pain-free) movement performance15,21 after
pain physiology education.
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TABLE 2. Changes in Secondary Outcome Measures After the Intervention
Experimental Group
(n = 15)
Mean (SD)
Neurophysiology of pain test
Measurement 1: baseline
Measurement 2: postintervention
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
FIQ
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 physical functioning
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 role limitations due to physical pain
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 bodily pain
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 general health perceptions
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 vitality
Measurement 1: Baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 social functioning
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 role limitations due to emotional
problems
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
SF-36 mental health
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCI transformation
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCI distraction
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCI reducing demands
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCI worrying
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCI retreating
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCI resting
Measurement 1: baseline
5.5
10.9
11.4
11.3
(2.9)
(3.4)
(2.3)
(3.0)
Control Group
(n = 15)
Mean (SD)
5.9
7.1
6.8
7.2
Within-Group
Comparison
(F; P)
Cohen’s d
ES
10.3; <0.001*
1.97w
3.3; 0.079
0.36
3.3; 0.046*
0.27
1.0; 0.388
0.29
0.5; 0.602
0.28
9.2; <0.001*
0.98w
3.2; 0.047*
0.19
3.1; 0.064
0.20
1.7; 0.189
0.24
9.2; <0.001*
0.89w
2.7; 0.079
0.36
0.7; 0.929
0.14
0.2; 0.861
0.00
2.0; 0.141
0.36
0.5; 0.624
0.00
1.3; 0.269
0.16
(3.8)
(3.7)
(4.3)
(4.2)
38.7 (10.7)
34.9 (10.1)
36.5 (9.9)
59.4 (12.9)
58.7 (15.4)
60.1 (10.5)
47.7 (22.7)
51.0 (21.6)
53.7 (21.8)
49.7 (17.9)
45.7 (17.1)
45.3 (12.3)
18.3 (34.7)
25.0 (35.4)
28.3 (35.2)
13.3 (22.9)
5.0 (10.4)
15.0 (26.4)
37.1 (19.2)
45.8 (25.8)
42.5 (19.9)
40.3 (15.8)
49.2 (20.2)
52.4 (21.5)
24.7 (10.6)
32.8 (15.5)
37.7 (15.5)
31.47 (12.8)
33.3 (14.0)
28.6 (12.8)
36.3 (17.8)
35.7 (18.5)
40.0 (21.0)
42.2 (14.3)
38.5 (13.1)
35.3 (13.7)
63.1 (21.5)
63.8 (27.0)
58.1 (27.4)
48.4 (17.2)
54.9 (20.2)
61.2 (15.9)
71.1 (45.2)
60.5 (43.1)
59.9 (47.5)
42.2 (14.3)
38.5 (13.1)
35.3 (13.7)
60.8 (17.3)
61.9 (22.4)
66.7 (17.5)
62.0 (19.5)
60.1 (20.8)
48.5 (18.3)
2.1 (0.5)
1.8 (0.6)
1.9 (0.6)
1.7 (0.6)
1.9 (0.7)
1.9 (0.7)
2.2 (0.6)
2.1 (0.8)
2.1 (0.8)
2.1 (0.6)
1.9 (0.6)
2.0 (0.7)
2.2 (0.6)
2.3 (0.8)
2.2 (0.9)
2.0 (0.8)
2.0 (0.9)
2.1 (0.8)
1.7 (0.6)
1.5 (0.5)
1.5 (0.5)
1.7 (0.6)
1.7 (0.7)
1.6 (0.5)
1.7 (0.7)
1.6 (0.6)
1.7 (0.6)
1.9 (0.6)
1.9 (0.7)
1.8 (0.6)
2.1 (0.4)
1.9 (0.7)
(Continued )
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Intensive Pain Physiology Education for FM Patients
TABLE 2. (continued)
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCS helplessness
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCS magnification
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCS rumination
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PCS total
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PVAQ
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
TSK
Measurement 1: baseline
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PPT thoracic spine
Measurement 1: baseline
Measurement 2: postintervention
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PPT lumbar spine
Measurement 1: baseline
Measurement 2: postintervention
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PPT trapezius
Measurement 1: baseline
Measurement 2: postintervention
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PPT calf
Measurement 1: baseline
Measurement 2: postintervention
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
PPT hand
Measurement 1: baseline
Measurement 2: postintervention
Measurement 3: 14 d follow-up
Measurement 4: 3 mo follow-up
Experimental Group
(n = 15)
Mean (SD)
Control Group
(n = 15)
Mean (SD)
1.9 (0.6)
2.0 (0.8)
1.9 (0.7)
2.1 (0.6)
9.5 (5.3)
6.7 (6.0)
6.7 (5.8)
11.1 (5.8)
10.5 (5.6)
9.6 (5.5)
2.8 (2.4)
2.2 (2.5)
1.7 (2.1)
3.0 (2.5)
3.2 (2.1)
3.3 (2.5)
7.1 (5.0)
6.1 (3.8)
5.1 (4.2)
7.7 (2.7)
7.5 (3.3)
7.5 (4.0)
19.5 (11.8)
14.9 (11.6)
13.3 (11.6)
21.9 (9.9)
20.5 (10.2)
20.4 (12.3)
35.3 (14.5)
34.4 (11.7)
32.2 (13.7)
39.7 (12.6)
42.6 (15.1)
40.3 (14.4)
38.7 (10.7)
34.9 (10.1)
36.5 (9.9)
40.7 (8.4)
39.8 (7.1)
39.9 (8.2)
2.4
2.7
2.8
2.4
(1.5)
(1.4)
(1.7)
(1.5)
2.3
2.1
2.2
2.2
(1.8)
(2.1)
(2.2)
(2.5)
2.8
2.9
3.1
3.1
(1.8)
(1.7)
(1.8)
(2.0)
2.6
2.8
2.7
2.7
(2.3)
(2.6)
(2.7)
(2.6)
1.7
1.5
1.6
1.5
(1.2)
(0.9)
(1.1)
(1.0)
2.7
1.1
1.1
1.3
(6.0)
(1.2)
(1.3)
(1.5)
2.7
2.7
2.7
2.9
(1.5)
(1.5)
(1.7)
(1.9)
1.9
2.1
1.8
2.1
(1.0)
(1.0)
(1.1)
(1.8)
2.9
2.1
2.8
2.4
(1.6)
(1.3)
(1.9)
(1.5)
2.3
1.9
1.9
1.9
(1.4)
(1.7)
(1.7)
(1.9)
Within-Group
Comparison
(F; P)
Cohen’s d
ES
1.3; 0.265
0.53
2.3; 0.109
0.50
1.6; 0.219
0.49
1.9; 0.158
0.53
1.3; 0.279
0.21
1.0; 0.360
0.21
1.3; 0.286
0.00
0.4; 0.667
0.16
0.7; 0.409
0.18
0.1; 0.895
0.12
1.9; 0.157
0.32
Statistically significant results are marked with “*” and large ES are marked with “w”.
ES indicates effect size; FIQ, Fibromyalgia Impact Questionnaire; PCI, Pain Coping Inventory; PCS, Pain Catastrophizing Scale; PPT, pressure pain
threshold; PVAQ, Pain Vigilance and Awareness Questionnaire; SF-36, Short Form 36 Health Status Survey; TSK, Tampa Scale Kinesiophobia.
However, we did not find any evidence to support that
pain inhibition can be improved by altering negative cognitions through pain physiology education, as the observed
reductions were not significantly relevant. It is possible that
short-term alterations in pain cognitions occurred as seen in
other studies, which could have led to an improved pain
inhibition. Although it is clear that the central nervous
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system shows remarkable plasticity, we do not know how
long it takes for changes to appear. In this study, the
changes in the pain inhibitory systems could be detected
after 3 months. This indicates that changes of the CNS need
time to occur and that when examining the influence of an
intervention on descending nociceptive processing, a sufficient long follow-up is required. In contrast, we cannot
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879
Van Oosterwijck et al
exclude the possibility that the pain physiology intervention
influenced other cognitions then the ones that were measured in this study and that this contributed to the positive
treatment effects.
It has been previously shown that pain physiology
education will result in a reduction of brain activity in the
cortical pain matrix.20 This observation, together with the
current findings regarding the positive effects on descending
nociceptive inhibition, suggests that this type of education
has an influence on central pain processing. However, these
observations need to be confirmed, and future studies using
objective and sophisticated measures of pain and nociceptive processing are required to test this hypothesis. In
addition, further analysis of data from existing studies
needs to be performed to identify mediators, moderators,
and predictors of the established treatment effects, and will
provide us with insights on how pain physiology education
exactly influences central pain processing.
Understanding Pain Physiology
FM patients were able to understand and remember the
complex material about pain physiology, as shown with the
scores on the Neurophysiology of Pain Test, which increased
immediately after patients received a one-to-one educational
session about pain physiology. After the second educational
session, a further small increase in the Neurophysiology of
Pain Test scores was observed. Although it has been shown
that using only written education on pain physiology is
insufficient to change illness perceptions and health status in
FM,46 the results of this study indicate that giving FM
patients written information to read at home in addition to a
one-on-one session is a valuable part of educational therapy.
This is especially important for those patients with memory
or concentration problems. In addition, patients were
encouraged to apply what was learned in daily life, and had
the chance to discuss questions and experiences over the
telephone with the therapist. The new acquired knowledge
about pain physiology was maintained, even after 3 months.
Influencing Cognitions, Behavior, and Health
Patients reported to ruminate or worry less in response
to their pain at 2 weeks follow-up. However, we were not
able to establish any long-term effects on pain cognitions or
pain behavior. Although Meeus et al22 and Moseley15
showed improvements in pain catastrophizing due to pain
physiology education in chronic fatigue syndrome and
chronic low back pain patients, respectively, those studies
reported immediate posttreatment effects and did not
examine longer term effects. Because of the length of time
required for baseline measures (± 105 min) combined with
the educational session (± 30 min), we did not subject the
patients to immediate posttreatment measures except for
algometry and the Neurophysiology of Pain Test. It is
possible that education about pain physiology has an
influence on pain coping and catastrophizing in FM, but
that these effects are only present at short term, and that
they will lead to improvements in health status and
endogenous pain inhibition in the long term. Future studies
should try to asses immediate posttreatment effects as well
as include several follow-up assessments to study both
short-term and long-term effects.
Although pain physiology education did not have any
long-term effects on cognitions or behavior linked to pain,
there was an effect on general health perceptions, mental
health, and behavior. FM patients from the experimental
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Clin J Pain
Volume 29, Number 10, October 2013
group showed improvements in their general health perceptions and mental health with a large effect size. These
patients also reported an improved physical functioning
and more vitality. We can conclude that education about
pain physiology improves the health status of FM patients.
Strengths and Limitations
Although this study is limited by a relatively small
sample, the sample size was determined based on an a priori
power analysis. In addition, Cohen’s d effect sizes from
significantly changed outcome measures were presented and
varied from 0.19 to 1.97, representing values for the 58th to
the 98th percentile, indicating that the average person in the
experimental group scored higher than 58% to 98% of the
control group. It could seem a concern that the study
sample only included 4 males (13.3%); however, this is in
line with prevalence of FM, which is a disorder that is
predominant in females. It has been reported that 13% of
the FM patients are male, whereas 87% are female.47 One of
the strengths of this study is the control intervention, that is,
education about activity self-management techniques. Not
only was the format from the control intervention similar
then the format of the experimental intervention, it allowed
us to provide a useful intervention for all study participants.
It is a limitation that because of practical issues it was
impossible to withhold the study hypothesis from the
researcher/clinician who delivered the interventions. However, it must be clarified that the educator was aware that
the control intervention, that is, pacing activity management, has positive benefits and is often included in rehabilitation programs for FM patients, thus delivering both
interventions with the same enthusiasm.
FM patients were recruited using the 1990 ACR criteria,2 which have been used for 20 years by physicians to
diagnose FM, and these criteria have recently been
adapted.1 This was done to make the diagnosis more
practical for physicians. Besides widespread pain, the new
2010 criteria considers other important somatic symptoms
often experienced by FM patients and allow differentiation
among patients according to the level of FM symptoms.1
The new criteria were published in May 2010. The
recruitment for this study took place between March 2009
and March 2010, therefore patients were diagnosed using
the 1990 criteria. Because the 1990 criteria were more
stringent than the 2010 criteria, we believe that the conclusions of this study also apply to FM patients diagnosed
according to the 2010 criteria.
CONCLUSIONS
FM patients are able to understand and remember the
complex material about pain physiology. Education about
pain physiology in FM will lead to less worrying in
the short term, and long-term improvements in vitality,
physical functioning, mental health, and general health
perceptions. No significant changes were established in pain
catastrophizing, hypervigilance, or kinesiophobia. Although
PPTs remained the same, a positive effect was found on
endogenous pain inhibition at 3 months follow-up. Education of pain physiology seems to be a useful component
in the treatment of FM patients. Future studies should
further examine the underlying, explanatory mechanisms of
the efficacy of pain physiology education in chronic pain
patients, and the effect of pain physiology education in
conjunction with other treatment components or therapies.
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Volume 29, Number 10, October 2013
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