ORIGINAL ARTICLE

Special Topic Series: Approach to Physical Activity in Pain:

From Theory to the Lab, From Clinic to the Patient

Overactivity in Chronic Pain, the Role of Pain-related

Endurance and Neuromuscular Activity
An Interdisciplinary, Narrative Review
Monika I. Hasenbring, PhD,*† Nicole E. Andrews, BOccThy(Hons), PhD,‡§
and Gerold Ebenbichler, MD∥

persist in activities despite severely increasing pain until a break will

Objectives: Decades of research have convincingly shown that fear of
pain and pain-related avoidance behavior are important precursors of
disability in daily life. Reduced activity as a consequence of avoidance,
however, cannot be blamed for chronic disability in all patients. A
contrasting behavior, pain-related dysfunctional endurance in a task
and overactivity has to be considered. Currently, there is a need to
better understand the psychological determinants of overactivity, dys-
functional endurance, and neurobiomechanical consequences.
Methods: This is a narrative review.
Results: The first part of this review elucidates research on self-reported
overactivity, showing associations with higher levels of pain and dis-
ability, especially in spinal load positions, for example, lifting, bending,
or spending too long a time in specific positions. In addition, measures
of habitual endurance-related pain responses, based on the avoidance-
endurance model, are related to objective assessments of physical
activity and, again, especially in positions known to cause high spinal
load (part 2). The final part reveals findings from neuromuscular
research on motor control indicating the possibility that, in particular,
overactivity and dysfunctional endurance may result in a number of
dysfunctional adaptations with repetitive strain injuries of muscles,
ligaments, and vertebral segments as precursors of pain.
Discussion: This narrative review brings together different research
lines on overactivity, pain-related endurance, and supposed neuro-
muscular consequences. Clinicians should distinguish between
patients who rest and escape from pain at low levels of pain, but
who have high levels of fear of pain and those who predominantly
Received for publication November 12, 2019; accepted November 15,
2019.
From the *Department of Medical Psychology and Medical Sociology,
Faculty of Medicine, Ruhr-University of Bochum, Bochum, Germany;
‡ The Occupational Therapy Department, Professor Tess Cramond
Multidisciplinary Pain Centre, The Royal Brisbane and Women’s
Hospital, Herston; §RECOVER Injury Research Centre, The University
of Queensland, Brisbane, QLD, Australia; ∥Department of Physical
Medicine, Rehabilitation and Occupational Medicine, General Hospital
of Vienna, Vienna Medical University, Vienna, Austria; and †Faculty of
Health Science, University of Southern Denmark, Odense, Denmark.
The authors declare no conflict of interest.
Reprints: Monika I. Hasenbring, PhD, Department of Medical Psychology
and Medical Sociology, Faculty of Medicine, Ruhr-University of
Bochum, Universitätsstraße 150, Bochum 44780, Germany (e-mail:
monika.hasenbring@ruhr-uni-bochum.de).
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
DOI: 10.1097/AJP.0000000000000785
be enforced by intolerable pain levels.
Key Words: overactivity, dysfunctional endurance, avoidance,
chronic pain, neuromuscular activity, sensory-motor control
(Clin J Pain 2020;36:162–171)
D ecades of research have shown that fear of pain and
avoidance of pain-associated activities are clear precursors
of chronic pain and pain-related disability in daily life.1 All the
more surprising, it might appear that, in contrast, overactive
behavior that leads to a severe aggravation of pain, can cause
forced phases of rest and subsequent avoidance of pain-
provoking activities. The first part of the present review eluci-
dates current qualitative and quantitative research on this
phenomenon, which builds on work from the 1970s described by
Fordyce,2 the father of the operant conditioning theory of
chronic pain. The second part of the review concerns possible
cognitive, affective, and behavioral mechanisms of pain-related
endurance that may play a crucial role in overactivity and “ flare-
ups”of pain,3 outlining the avoidance-endurance model of pain
(AEM)4,5 and presenting an update of AEM-based empirical
research. In the third part, possible mechanisms of disturbed
motor control as a response to pain and overactive behavior are
described, on the basis of basic physiological concepts of trunk
motor control.6,7 This review, for the first time, aims to deliver
biopsychosocial hypotheses explaining dysfunctional character-
istics of behavioral overactivity, patterns of endurance despite the
pain, and potential neurobiomechanical consequences that may
be responsible for the development of chronic pain and disability.
OVERACTIVITY IN THE CONTEXT OF CHRONIC
PAIN
A Historical Perspective
In 1976, Fordyce contributed to a radical shift in thinking
when he proposed the operant behavior model of chronic pain.
In his ground-breaking book “ Behavioral Methods in Chronic
Pain and Illness,”Fordyce2 outlined how targeting and reduc-
ing “ pain behaviors”in chronic pain populations can enable
individuals to become more physically active and reduce their

162 | www.clinicalpain.com Clin J Pain ! Volume 36, Number 3, March 2020

Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Pain ! Volume 36, Number 3, March 2020
dependence on pain medications. In this publication, Fordyce2
described a cohort of individuals with chronic pain who
engaged in high levels of activity, which severely aggravates
pain, forcing the individual to rest. Fordyce labeled these
individuals as “pacers”and proposed that a learned association
between periods of rest and severe pain develops. This rein-
forces the overactive behavior, as rest is then avoided.
The behavior was further described by Philips8 who
used the term “ overactivity”to refer to individuals who
habitually engage in an excessive amount of activity that is
only halted by periods of severe pain and incapacity. The
term overactivity continued to be used by others, such as
Hanson and Gerber,9 who described how habitually over-
active individuals oscillate between “ good days”and “bad
day,”and Birkholtz et al,10 who asserted that individuals
who are initially overactive can move gradually toward
longer periods of rest and activity avoidance. The term
overactivity is still used in textbooks and patient education
such as “ Manage Your Pain” 11 and “The Pain Toolkit.”12
Overactivity and Pain: Qualitative Evidence
The overactivity phenomenon has been described by a
number of individuals with chronic pain during qualitative
inquiries. A number of studies have investigated the nature
of severe pain aggravations or “ flare-ups.”Individuals with
low back pain (LBP) report that flare-ups can (1) last from
hours to weeks, (2) negatively impact on physical function,
emotions, and cognitions, and (3) can be associated with
spasms, paresthesia, or reduced motor and bladder control.3
Physical activities such as lifting and bending were identified
as the most common perceived triggers of flare-ups in a cohort
of individuals with chronic nonspecific back pain.13 Individuals
also reported severe pain aggravations from spending too long
a time in a sustained spinal position when sitting or standing.13
Andrews et al14 conducted a qualitative inquiry that
explored habitual overactivity behavior. Individuals with
chronic pain who were identified as being habitually overactive
described periods of incapacitation where they were unable to
carry out activities of daily living (eg, showering) and basic
activities (eg, walking) secondary to severe pain aggravations.
Individuals also linked negative emotions such as low mood,
frustration, and irritation to their pain exacerbations.
Overactivity and Pain: Quantitative Evidence
A number of studies have objectively investigated the
relationship between activity and pain using time-series
analyses. The results of these studies have been mixed. Geisser
et al15 found a significant 30-minute lagged relationship
between self-reported physical activity levels and pain
intensity in a sample of 25 individuals with chronic back
pain, whereby an increase in pain followed activity by
∼30 minutes. Using accelerometery, Liszka-Hackzell and
Martin16 found a significant 30-minute lagged relationship
between objective physical activity levels and pain intensity
in a small sample with acute LBP. A relationship between
objective activity and pain was, however, not found in a
chronic back pain sample.16 Schepens et al17 investigated
changes in pain following lab-based physical tasks in 35
older adults with osteoarthritis. This study failed to find a
relationship between activity and subsequent pain levels.
Conversely, Rabbitts et al18 found significant relationships
between mean objective physical activity levels and pain
intensity ratings at the end of the day, whereby higher
activity levels were associated with less pain at the end of
the day.
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Special Topic Series
There are a number of possible explanations for these
mixed results. It is possible the same type of activity affects
individuals with chronic pain differently. A large sample of
individuals with chronic (c) LBP reported disparate and varied
activities, which they perceived caused severe pain
aggravations.13 Individuals with pain are also likely to have
different activity tolerances for the activities that do exacerbate
pain. The methodology of the aforementioned studies may not
have been able to account for the complexities of the rela-
tionship between activity and pain in chronic pain populations.
The results do, however, cast doubt on the legitimacy of the
overactivity construct. Overactivity as a construct has been
derived from patients’ self-reports. Hence, individuals may,
retrospectively, attribute pain exacerbations to increased
activity levels on the basis of their beliefs about the relationship
between activity and pain, as opposed to activity engagement
causing pain exacerbations. Other factors that may contribute
to or cause a pain exacerbation, such as pain catastrophizing
and anxiety, were not controlled for in the studies that have
found a significant lagged relationship between activity
and pain.
Andrews et al19 investigated the relationship between
an individual’s self-reported overactivity behavior and
patterns of pain and activity, which were obtained through
monitoring procedures. In this study, overactivity was
operationalized as “a prolonged period of activity engage-
ment followed by a significant increase in pain.”Both high
levels of physical activity and prolonged engagement in
sedentary tasks requiring sustained spinal positions were
considered as precursors to a significant pain exacerbation.
The study found that individuals who reported more fre-
quent overactivity behavior in a self-report questionnaire
were significantly more likely to have an objective over-
activity period observed more than once in their data. This
was the first known study to establish that individuals who
report more frequent overactivity behavior are more likely
to frequently engage in activity in a way that significantly
exacerbates pain. More research is, however, warranted to
understand the relationship between activity and pain in
chronic pain populations and the overactivity phenomena.
The Association Between Overactivity and Daily
Activities
The association between overactivity and daily function
has been examined through both qualitative and quantitative
investigations. During a qualitative inquiry, individuals who
were identified as being habitually overactive reported that the
periods of incapacitation, caused by their behavior, results in a
loss of independence and unreliability, impacting on life roles.14
Individuals reported reducing their engagement in leisure/social
activities,14 an association that has also been found using
an observational study design.20 Cross-sectional quantitative
examinations have found an association between higher levels
of self-reported overactivity behavior and a more global self-
reported disability.21,22 A quantitative study that examined the
association between overactivity and specific functional activ-
ities found that self-reported overactivity is associated with a
number of self-reported difficulties of participating in daily
tasks but not with the performance skills used during these
activities (ie, walking, sitting, and standing tolerance).23 The
results of this study do not support the notion that overactivity
leads to a reduction in physical capacity over time, but do
suggest that an association between overactivity and reduced
activity participation exists.
www.clinicalpain.com | 163
Special Topic Series
Overactivity
Frequent severe pain
exacerbations
Increased pain Increased
catastophising and analgesic Sleep
fear medication disturbances and
use and reactive fatigue
pain coping
Avoidance of pain-
Negative impact
provoking
on cognition
activities
Negative impact on ability to participate in valued activity and role loss
FIGURE 1. The association between overactivity and reduced activity participation.
Individuals have also reported a number of negative
consequences of frequently severely aggravating their pain
during qualitative inquiries. Individuals have described the
negative impact that pain exacerbations have on mood.14
Cross-sectional quantitative investigations have consistently
linked higher levels of self-reported overactivity behavior to
poorer psychological functioning,21,22,24 and individuals
have described how this can impact negatively on their
relationships with others.14 Individuals have also described
the negative impact of pain exacerbations on physiological
functions including sleep and energy levels. An association
between overactivity and poorer sleep quality has been
found in 2 quantitative investigations.23,25 In addition, an
observational study revealed that higher levels of self-
reported overactivity behavior were associated with being
prescribed opioid medication, more frequent PRN (as
needed) opioid use, and taking more medication than
prescribed.25 Individuals described how their pain exacer-
bations increased reactive pain-coping such as taking extra
prescribed medications, substance use and presenting to
emergency departments.14 A graphical display of the impact
of overactivity on daily function based on the findings pre-
sented above is displayed in Figure 1.
OVERACTIVITY AND ENDURANCE-RELATED
PAIN PROCESSING
Patterns of Dysfunctional Endurance
Overactivity, as characterized by Fordyce2 and Philips,3
refers to dysfunctional aspects of physical activity shown
despite high levels of pain before, during, and following
activities, forcing the individual to rest or leading to a certain
time of incapacity. From a psychological perspective, the
question arises why some individuals may tolerate even severe
levels of pain before deciding or feeling forced to rest for
164 | www.clinicalpain.com Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Pain ! Volume 36, Number 3, March 2020
& Periods of incapacity
Loss of
Negative independence and
affect decreased
reliability
Negative impact Reduced
participation in Decreased ability
on relationship
leisure and social to maintain
with others
activities employment
a while. Adopting a self-regulation, motivational perspective,
the AEM conceptualizes patterns of cognitive, affective, and
behavioral pain processing, which are associated with over-
active behavior.4,5,26 Persistence in an ongoing activity that is
associated with an increase of pain can be understood as
planned or highly automatized behavior that is accompanied
by cognitive attempts to avoid the experience of pain to
maintain engagement in the ongoing activity. Persistence in an
activity despite pain can be seen as a possible way to solve a
conflict between the wish for immediate pain relief and the wish
to maintain in a highly valued activity. Within the AEM, the
term pain-related endurance was used and defined as “ a pattern
of attention diversion, trivializing the meaning of a pain stim-
ulus, and task persistence in the face of severe pain to facilitate
persistent movement toward a current activity.” 26 Originally
based on a series of standardized clinical interviews, 2 different
endurance-related patterns of pain processing have been
described, labeled as distress-endurance pain responses (DER)
and eustress-endurance pain responses (EER), differing pri-
marily in cognitive/affective aspects of the pain experience.
Whereas the DER pattern comprises cognitions of thought
suppression, affective distress with irritated and depressive
mood, and excessive task persistence behavior, the EER pattern
was characterized by cognitions of focused distraction from
pain or trivializing the meaning of pain, positive mood, and
high levels of persistence despite severe pain. Furthermore, an
adaptive pain response (AR) pattern has been described, sug-
gesting a flexible change between short-term avoidance and
endurance, besides a well-known fear-avoidance response pat-
tern with high levels of fear of pain and anxiety, cognitions of
catastrophizing, and high scoring in pain avoidance5 (Fig. 2).
Thought suppression has been defined by Wegner et al27
as the conscious and effortful attempt to simply “ not think
about an unwanted stimulus.” In numerous experimental
studies including healthy individuals, the instruction “ to not
think”on a specific stimulus was less successful than the so-
Clin J Pain ! Volume 36, Number 3, March 2020
Flare up of pain
Catastrophizing Thought Suppression Distraction/Ignoring
Fear/Anxiety Anxiety/Depressive Mood Positive Mood
Avoidance Behavior Endurance Behavior Endurance Behavior
Physical Inactivity Physical Overactivity Physical Overactivity
Muscular Underuse Muscular Overuse Muscular Overuse
Maintenance of pain Maintenance of pain Maintenance of pain Reduction of pain
FAR DER EER
FIGURE 2. The Avoidance-Endurance Model of pain describes
different ways of how people engage in physical activity while
experiencing a flare of pain and the respective risk of developing
or maintaining chronic pain. AR indicates adaptive responses; DER,
distress-endurance responses; EER, eustress-endurance responses;
FAR, fear-avoidance responses.
called focused distraction, wherein the instruction implied to
think on a specific other stimulus (eg, description of the living
room at home).28 Moreover, after ending the experimental
phase, a nonvoluntary occurrence of the experimental stimuli
was found significantly more often after thought suppression
than following focused distraction conditions (the “ rebound
phenomenon” ). Failures and rebound phenomena associated
with habitual thought suppression are suggested to lead to
affective distress in terms of fear, anxiety, and irritated and
depressive mood.29 There are only a few experimental studies
using tonic pain stimuli of increasing severity (eg, the cold
pressor pain) supporting the dysfunctional effects of instructed
thought suppression compared with distraction30,31 with respect
to ratings of pain intensity and affective distress. In patients
with subacute or chronic low back pain, habitual pain-related
thought suppression has been shown as the most often reported
cognitive pain response32 that mediates the relationship
between pain and depression,33,34 especially within the
context of chronic daily life stress.35,36 Pain thought sup-
pression was positive and to a moderate to a high degree
related to endurance behavior.32 In addition, pain-related
thought suppression was the most pronounced in the AEM-
based distress-endurance subgroup.37,38
In comparison, habitual pain-related focused distraction
has been shown to be positively related to pain intensity ratings
but related negatively to a self-reported disability,32 indicating
more pain but less disability with higher distraction. Moreover,
distraction was negatively related to several indicators of pain
anxiety and depression and positively associated with positive
mood reported despite the pain.32 Habitual distraction was
also positively and to a moderate degree correlated with
endurance behavior, which was highest pronounced in the
AEM-based eustress-endurance subgroup.37 The question
arises, whether pain-related endurance, associated with cogni-
tive disengagement in terms of thought suppression or focused
distraction, appears as adaptive or maladaptive with respect to
the maintenance of pain and disability.
Pain-related endurance might be adaptive, at least
under certain circumstances, for example, when it ascertains
high-performance levels in valued activities and pain
increases only temporarily, not leading to phases of forced
incapacity. This may be the case in high-performance
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Special Topic Series
professionals such as musicians or athletes.39 Similar con-
ditions may be relevant in laypersons who persist in an
activity of daily living, that is, in the household, in leisure
time activities, or at work. From an operant view, cognitive
disengagement from pain and endurance in an activity
despite pain may be positively reinforced by the realization
Coping-Signal of good performance, that is, good training times in the case
of an athlete, praise by a supervisor at work, or happy
Balance of break
and activity
children when mother bakes a birthday cake. Pain-related
endurance may be reinforced negatively when high endur-
Flexible ance at work leads to the avoidance of critique from a
balance of load supervisor or to the completion of self-criticism.
However, in the case, endurance leads to an intolerable
intensity of pain, and a period of rest will be compelled; several
AR psychological and physiological consequences will arise. Rest-
ing behavior will be negatively reinforced by a decrease in pain.
Repeated experiences of such rest-pain reduction cycles may
lead to a maintenance of resting behavior and prolonged
physical inactivity.2 Moreover, adopting the concept of self-
efficacy,11 persisting in an activity until the pain gets intolerably
high, the experience of being forced to quit this activity may
increase feelings of ineffectiveness and helplessness. Bio-
mechanically, the AEM suggests that prolonged physical
activity despite high levels of pain will cause an overload of
physical structures that may be responsible for a further
increase in pain. Possible consequences of overactivity and
excessive endurance from the perspective of motor function and
control will be outlined in part 3 of this review.
Endurance and Pain Intensity
During the past 2 decades, accumulative evidence from
clinical studies indicates that high-endurance behavior shown
despite high levels of pain is positively related to the intensity of
pain. Using the continuous information of self-reported scales
measuring task persistence behavior despite pain cross-sectional
studies revealed low but positive relationships with pain.32,40
Results of a few prospective studies indicate task persistence or
endurance behavior as predictive for the development of future
pain. Hasenbring et al,41 for example, found baseline levels of
self-reported endurance despite pain as a predictor of higher
pain intensity scores at the discharge of conservative medical
treatment in patients with subacute sciatic pain. Ignoring pain
sensations, a cognitive part of pain-related endurance, was
predictive of pain intensity at a 6-month follow-up.41
Inspecting patient subgroups showing DER and EER
pattern due to the AEM, evidence from prospective studies
in patients with acute or subacute pain indicates the devel-
opment of higher pain intensity levels in both subgroups
compared with an adaptive group.37,38,42 Hasenbring38
reported higher pain intensity scores at a 6-month follow-up
after a stationary nonsurgical therapy in 111 patients with
acute sciatic pain and a DER or EER pattern compared
with patients with an AR pattern. Grebner et al42 found
patients with a DER and an EER pattern predictive of
retirement due to pain 6 months after a lumbar disk surgery.
Both patterns have further been shown as predictive for
future pain intensity in a sample of subacute nonspecific
LBP.37 In phases of chronic pain, interestingly, evidence
from different prospective studies indicate that especially
patients with a DER pattern, revealed higher pain scores
than AR patients, in some studies, before and after
treatment,43 in others, only after treatment,44,45 whereas
patients with an EER pattern revealed a reduction of pain
comparable to that of the AR patients. To note, in subacute
samples, the DER and EER pathways differ with respect to
www.clinicalpain.com | 165
Special Topic Series
their pain-related cognitions and their affective pain
responses. Although patients with a DER pattern predom-
inantly revealed cognitions of thought suppression and
increased pain-related affective distress, cognitions of
humor/distraction and increased positive mood despite pain
have been shown as most prevalent in EER pathways.37
Thought suppression, the pure attempt to “ not think”on
pain or unwanted thoughts in general, is known as an
important precursor of affective distress due to the fact that
trying to not do something is prone to failure and, more
important, to a so-called rebound phenomenon, wherein
nonvolitional thoughts and sensation come into the mind.27
In contrast, cognitive distraction has been shown to increase
positive mood, 2 features predominantly present in patients
with an EER pattern.37 It can be speculated that these dif-
ferences between EER and DER pattern might be respon-
sible for their different rates of recovery in the chronic pain
samples. There is a lack of data on these psychological
features in patients with chronic states of pain, indicating a
need for more research in chronic pain.
Pain-related Endurance: Self-reported Disability
and Quality of Life Versus Objective Activity
In contrast to measures of pain intensity, research on the
linear association between pain-related endurance and self-
reported pain disability and quality of life mostly revealed low to
moderate relations of a negative direction, indicating a more
functional value of endurance.32,43 The more pain persistence
behavior an individual reported the less disability and the more
quality of life were experienced. Interestingly, inspecting sub-
groups of patients with the 2 endurance-related response pat-
terns, merely patients with an EER pattern displayed low dis-
ability and high quality of life, while patients showing a DER
pattern had lower quality of life scores43 and higher disability
compared with AR patients,37,43 even despite higher levels of
accelerometer-based measures of physical activity.46,47 In the
Plaas’s study,47 both subgroups, DER and EER patients,
revealed a higher number of physical postures such as sitting or
standing in an upright or forward bent position, which is known
to cause specific strain to spine-related structures.48 Both sub-
groups also have reported higher pain intensity scores than the
AR group. Nevertheless, the DER group not only displayed
higher depression and distress than EER and AR patients but
also higher disability due to pain. The authors speculated that
patients showing the DER pattern may have shown far higher
levels of physical activity and strain positions before developing
chronic pain than all other subgroups, which is why they now
experience impairments of daily activities despite still high levels
of objectively assessed activity.49 Patients with a DER pattern
also revealed higher scores on avoidance behavior compared
with AR patients,37 underlining this hypothesis.
It is of interest, trying to interpret the findings of high pain-
related endurance and also relatively high avoidance, seen in
patients with a DER pattern. Inspecting the items of the
respective subscales of the Avoidance-Endurance Questionnaire
(AEQ),32 some of them are concerned with behavior at work,
others with leisure time activities, such as meeting with friends or
visiting a concert. It might be plausible that high scores on
endurance trace back on the work-related items, whereas high
scores on avoidance items, go back on leisure activities. High
endurance and avoidance may further be based on a specific
modality; a patient might try to solve the conflict between
reducing pain, on the one hand, to endure in a valued activity on
the other.26 Imagine a patient who experiences pain in the back
and the right leg, which increases while trying to walk in a quick
166 | www.clinicalpain.com Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Pain ! Volume 36, Number 3, March 2020
manner to do the daily shopping for the family. The patient
decides to humble, taking off the load from the right leg while
instead overloading the left leg, to maintain the quick style of
walk. Thus, the valued activity (to hustle while shopping) was
maintained despite severe pain, while severe aggravations of pain
are avoided during humbling. That also means that specific
health-promoting behaviors (to walk in a calm manner, spread-
ing burden on the legs equally, taking a break) will be avoided to
finalize shopping in a fixed time frame. In the end, we can
speculate that patients showing a DER pattern may be over-
active until high levels of pain force them to rest and to avoid
strenuous activities that would cause intolerable pain.
OVERACTIVITY AND THE NEUROMUSCULAR
SYSTEM IN LBP
Movement Behavior in Patients With LBP
Individuals who experience pain in their backs move dif-
ferently when compared with pain-free individuals. The percep-
tion of pain in the back appears a potent stimulus to change
motor control and movement behavior. Despite enormous
empirical efforts toward a more scientifically based under-
standing of how motor control may adapt to the perception of
LBP, the underlying mechanisms of observed impairments are
still incompletely understood. This may, in part, be due to the
restricted investability of the motor control system in humans
and/or a lack of distinguishability between motor adaptations
that may occur reflexively to pain and those due to pain-related
altered attention, mood, and movement-related fear, as evi-
denced from leg muscles.50–52 In addition, innumerable muscles
and fascicles of the back extensors overlap in function and thus
allow for considerable redundancy when moving and stabilizing
the spine throughout a movement trajectory.6 Such redundancy
within the motor control of the trunk would allow multiple
adaptive and compensatory motor control strategies intended to
protect the painful/injured structure in the back.53 This would be
supported by discrepant findings from measurable outcomes of
the motor control system, which suggest that the changes in
motor control in consequence to LBP would not follow one
stereotype, but vary widely within individuals (variability with
the performance of a task) and particularly between
individuals.54,55 Things become even more complex if long-term
consequences of automatic “ reflexive”and anticipated adapta-
tions that may drive acute adaptations of and reorganization
within the motor control system in LBP53,55 are investigated in
relation to divergent bodily movement behaviors of an individual
with LBP—the respective extremes would represent bodily
overactivity and avoidance behavior, respectively.
In fact, if an acute back pain episode does not resolve and
is becoming chronic when often a single cause of pain is difficult
to identify, the initial pain-related adaptations within the motor
control system may persist, and secondary adaptive alterations
within the motor control system and passive structures of the
spine could be driven through the movement behavior of the
individual despite the perception of back pain. Accordingly, an
inactive, avoidant behavior would thus drive disuse-related
muscle weakness and deconditioning along with metabolic
changes in the musculoskeletal structures and the central
nervous system (CNS),56 thereby fueling a vicious circle of
peripheral and central sensitization, thus disposing the indi-
vidual to increased pain perception, more inactivity and dis-
ablement, and reduced mood and spirits as well.1 By contrast,
in bodily overactive individuals with LBP, inadequate muscle
force and force rate generation might expose the vertebral
Clin J Pain ! Volume 36, Number 3, March 2020
joints, ligaments, and connective tissues within and around
muscles to increased stress and repetitive strain, thus causing
microdamages, laxity (with decrease in segmental stability),
inflammation, and reparation in these tissues, despite a pro-
tective stiffening of the spine.57,58 This would, in further con-
sequence, facilitate secondary adaptations and reorganizations
in the already altered motor control system, fuel a vicious cycle
with increased peripheral and central sensitization through
repetitive passive tissue strain, and further a chronic back pain
overuse syndrome.
To facilitate the understanding of the mechanisms that
may occur with bodily overactivity in individuals with LBP,
this part of the article is intended to discuss in brief (1) some
physiologic aspects of trunk motor control, (2) structural
and functional changes that may occur in individuals with
LBP compared with healthy pain-free controls, and (3)
possible consequences to the neuromuscular system caused
by an overactive movement behavior on pre-existing pain-
related adaptations observed in individuals with LBP.
Physiology of Trunk Motor Control
Because of the multisegmental nature of the spine, the
physiology of motor control of the trunk is complex. If
an individual follows a movement trajectory, innumerous
local and global muscles and fascicles of the spine require
appropriate spatial and temporal activation and fine-
coordination to provide all a harmonious movement pattern,
continuous stability in the vertebral segments, and permanent
control over the body’s position for the purpose of balance and
orientation.6,55 Voluntary movements are elicited through
intentionally induced motor commands that are generated and
processed in the cerebral cortex, basal ganglia, and cerebellum.
These motor commands project via the extrapyramidal
descending pathways and via the pyramidal tract to the spinal
cord. The planning and preparation of a movement command is
a higher cognitive process that utilizes motor engrams and
multisensory information from the different sensors of the
human body, including proprioceptive, somatosensory ves-
tibular, visceral and visual sensation.59 The sensory feedback
may provide both cognitive and emotional references to the
cerebral cortex and limbic system, thereby modulating the motor
command through projections from the limbic hypothalamus to
the brain stem and spinal cord.59,60 The descending extrapyr-
amidal and pyramidal input and its reflexive modulation would
result in a net excitatory common input to the motor neuron
pool (muscles and muscle spindles) within the different segments
of the spinal cord. The motor units of the back/trunk muscles are
activated following a hierarchical order according to the size of
motor units and the principle of common drive,61,62 the latter
referring to the synchronous modulation of the motor neuron
pool within a given muscle/fascicles of a muscle, synergistically,63
and, if coactivated, to voluntarily stabilize a joint between
antagonistically activated muscles.64 Noteworthy differences in
muscle spindle density between superficial polysegmental
(movement coordination) and local monosegmental to oligo-
segmental muscles (main segmental stabilizers)65,66 of the spine
may influence the thresholds of recruitment and derecruitment
and the maximum firing rate of motor units within these muscles
and fascicles in a significant way.67
Target-oriented movement commands always integrate
and convey automatic processes of postural control that
include balance adjustments and muscle tone regulation
(feed-forward control of posture). If the balance is per-
turbed, automatic postural responses would regain balance.6
The permanent real-time feedback to the higher subcortical
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Special Topic Series
and cortical centers of the CNS, in particular, via the spi-
nocerebellar tract, seems to play a major role in the auto-
matic regulation of motor control. On the spinal cord level,
specially tuned neural network pattern generators for gait/
cyclic movements and posture allow for basic automatic
motor/movement patterns. If complex nonrepetitive or
novel movements are to be learned, then these processes
change to cognitive movement and posture control that is
dependent on the cognition of self-body information and
spatial localization of objects in the extrapersonal space.59
Changes in Motor Control Observed With LBP
The notion that back pain–related adaptations in
motor control would affect gait and trunk movement patterns
appears well-supported by findings from studies that sought
to investigate the kinematics and movement patterns of
weight-bearing multijoint everyday movements, such as
walking, lifting, or moving the trunk. Individuals with LBP
were observed with a tendency toward a reduced preferred
walking speed if tested on a treadmill68 or to move their trunks
slower and within a smaller range of motion than pain-free
individuals.69 During gait, LBP individuals revealed more
stiffness in their lumbopelvic region with less counter-rotation
of the pelvis and thorax, lower ground reaction forces, and a
higher stride to stride variability.68 If individuals with LBP are
required to walk at higher speeds or move their trunk quickly,
the adaptability in motor output was suggested to be impaired
if joints and vertebral segments are stiffened.68 With respect to
maintaining posture, feed-forward control of movements was
found diminished repeatedly,70,71 and, based on findings from
a recent motor learning study in experimental leg pain,72 a shift
toward increased reliance in feedback control in individuals
with LBP may be assumed.
Observations from cross-sectional studies that sought to
investigate adaptive changes in motor control with back pain
and back injury relative to pain-free, healthy individuals revealed
that both functional and structural impairments may occur in
any source of the system; but the impairments may vary
considerably.55,73 Functional alterations in the responsiveness of
receptors and alterations in the central processing of the afferent
information were found—in addition to nociception per se—to
impair proprioceptive input with the provision of less accurate
and inappropriate feedback to the CNS. This would induce
motor cortical adaptations and alter the motor output.74 Con-
sistent with this, the motor cortical representations were found
altered, as the discrete differential organization in motor cortical
inputs to the local (deep, monosegmental to oligosegmental,
stabilizing) and the more global (multisegmental, coordinating)
back extensor muscles disappeared when compared with pain-
free controls.75,76 Likewise, the neuromuscular activation of the
trunk muscles was found to be altered to a variable extent with
LBP. Despite a broad variety of findings, with some studies
demonstrating inhibition and others overexcitability of trunk
muscles if individuals are affected with LBP,54 the deep stabi-
lizing trunk muscles tended to be more consistently inhibited,
whereas the polysegmental more superficial trunk muscles
appeared relatively over-activated.55
Findings from structural changes in individuals with
chronic LBP when compared with pain-free controls revealed a
preferential decrease in the cross-sectional area and an
increased muscle fat content within the multifidus muscles,77,78
or a higher than normal proportion of glycolytic muscle fibers
in the medial back extensors, the latter being indicative of a
decreased muscle capability.79,80 Impairments in back muscle
capability in LBP were also evidenced by a considerable
www.clinicalpain.com | 167
Special Topic Series Clin J Pain ! Volume 36, Number 3, March 2020

number of studies that observed early back extensor muscle
fatigue using the median frequency surface electromyographic
method recorded during static, sustained back extensions at
high submaximal voluntary efforts.81,82
The consideration of all the heterogeneous and partly
contradictory findings from adaptations in motor control in
association with LBP led to a theory that would propose 2
principle phenotypes of pattern changes representing the
extremes of a wide spectrum of possible adaptations. One of
these would refer to a “
tight”control over trunk movement type
and the other one to a “ loose”trunk control type.55 “ Tight
control”is postulated to result from increased stiffness due to
co-contraction, elevated reflex gains, and enhanced attentive
movement control.53,83 In contrast, “ loose control”would relate
to decreased motor excitability in consequence of a protective
adaptation mechanism intended to reduce pain provocation and
reduce tissue loading related to large muscle forces or resulting
compressive spine loading.55 With the occurrence of a back pain
attack, the primary pain-associated adaptations within the
motor control system are assumed to be facilitated through
reinforcement learning processes. These would be driven by
both the minimizing of movement-related pain and the
regaining of active control over the trunk movement.83 In our
opinion, a loose trunk control type could also represent the
long-term result of a primarily tight control type wherein the
LBP individual has—despite the persistence of pain—
adopted or maintained an overactive movement behavior.
Neuromuscular Consequences of Overactivity in
Individuals Affected With LBP
The role of bodily activity in LBP appears enigmatic.
On the one hand, bodily activity is a proven intervention
intended to treat chronic LBP. On the other hand, bodily
activity, in particular, overactivity may drive further changes
and adaptations in the motor control system that could result
in increased pain and disablement in these individuals.58,84 A
graphical display of the possible neurophysiological mecha-
nisms is shown in Figure 3.
We propose that, in overactive individuals with LBP,
inappropriate muscle strength and strength rate (power) gen-
eration in reaction to sudden load increases and unexpected
movements of the trunk may—despite a tonic “ protective”
stiffening of the spine—overstrain the passive tissues of the spine,
thus leading to instability. Such a hypothesis would reasonably
apply, in particular, to individuals with an excessive task per-
sistence behavior associated with thought suppression, anxiety,
and depressive mood (DER) but also to those with focused pain
distraction or trivializing the meaning of pain (EER).
One of the mechanisms proposed for insufficient force
generation in stiffened spine muscles would refer to the
occurrence of plateau potentials, as evidenced from studies of
motor unit trains.85 Plateau potentials refer to a self-sustained
firing of low-threshold, fatigue-resistant motor units, with a
consecutive increase in force output of the fibers, and would be
expected as a complementary mechanism to contribute to
tonic stiffening of spine stabilizing, antagonistic muscles in
addition to reflexive neuromuscular hyperexcitation of motor
neurons in consequence to nociception. Plateau potentials were
indeed observed in antagonistic pairs of the deep stabilizing
back extensor muscles and may spatially rotate between dif-
ferent motor units.85 Plateau potentials appear elicited by
excessive monoaminergic stimulation through reticulospinal
descending axons86 and thus are likely activated through
projections from the extrapyramidal descending motor path-
ways and emotional projections from the limbic hypothalamus
to the brain stem. Plateau potentials are limited in rate coding,
that is, are less responsive to further excitatory input to the
motor neuron pool. If the trunk is suddenly loaded, an

Stiffness of trunk & Altered/adapted movement

Low Back Pain lumbopelvic region altered behavior

Inadequate force rate generation

Plateau potentials; doublet/triblet motor unit discharge
Bodily Overactivity Early fatigue of high threshold motor units
Altered neuromuscular coordination
Failure of neuromuscular compensation

Insufficient neuromuscular Strain to connective tissues of

stabilization of spine Strain to individual motor ligaments, discs, fascia, and to
units/muscle fibers cartilage
segments

Muscle fiber membrane

leaks contracture; Inflammation
Insufficient blood supply to
Altered blood flow
muscle fibers –
consecutive inflammatory
response

Sensitization

Pain

FIGURE 3. Physiological mechanisms that may explain an increase of pain in individuals with LBP and bodily overactivity behavior.
Doublets/triplets refer to electromyographical motor unit discharges with short interspike intervals of a few milliseconds (2-20 ms). LBP
indicates low back pain.

168 | www.clinicalpain.com Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Pain ! Volume 36, Number 3, March 2020
adequate generation in the trunk muscles’ torque and power
would thus need to be achieved through the progressive
recruitment of higher threshold motor units rather than an
increase in firing rate. However, if the net excitatory drive to
the high-threshold motor units is insufficiently high to reach
the recruitment threshold, particularly of the very high-
threshold motor units, an inadequate increase in trunk muscle
torque/power would be generated only. Consequently, the
force and power generation of the trunk muscles would fail to
actively stabilize the spine. Findings of increased intramuscular
fat content preferably within the spine stabilizing back exten-
sors in chronic low back pain would indirectly be proof of
evidence for the unrecruitability of some muscle fibers.77,78 In
addition, hybrid muscle fibers would be expected to shift from
an aerobic to an anaerobic, glycolytic phenotype, if not acti-
vated for a longer period of time.87 Even if all the high-
threshold motor units were recruitable, their muscle fibers
would tend to fatigue early. Consequently, with the duration
of the bodily activity, inadequate torque and power demands
would fail to actively stabilize the spinal segments in individ-
uals with LBP due to early muscle fatigue. Compared with
healthy controls, early muscle fatigue in back extensors of
individuals with LBP was repeatedly observed,61,81 and even
occurred in high-level sport-performing rowers,88 or if the
trunk was exposed to relatively low loads only.89
Inappropriate trunk muscle force generation with bodily
overactivity would transfer the reactive forces that act on the
spine to the passive tissues. The reactive forces on passive tissues
would even be augmented through decreased shock absorption
in consequence of increased stiffness of the spine.90,91 Thus,
bodily overactivity would impose through (1) inadequate active
spine stabilization throughout the movement trajectory and (2)
an increased rate of stress and strain to the connective tissues,
inducing creep laxity and inflammation, resulting, at last, tem-
porarily in spinal instability.58
Another mechanism that may drive secondary adaptations
and reorganizations in motor control in overactive back pain
individuals would relate to the formation of motor unit duplets
and triplets in trunk muscles. This mechanism would particularly
come into effect if trunk movements that require quick force
adaptations are performed by individuals with LBP and, par-
ticularly, if they would be classified as “ loose trunk control”
types.55 Increased rates of force development and shortening
velocities were repeatedly suggested to relate to motor unit dis-
charges at short interspike intervals, so-called doublets, and
triplets, at the beginning of a motor unit train,84,92 and were
proposed as a compensatory mechanism to bypass the slow
contractile twitch properties of low-threshold motor unit muscle
fibers.84 Doublets at the beginning but also with the duration of a
motor unit train were observed in paraspinal muscles.85 Doublets
within a motor unit train are expected to contribute to the
maintenance of higher levels of force production and particularly
involve fast-twitch, fast fatiguing motor units.93,94 With bodily
overactivity, the regular occurrence of doublets and triplets could
impair metabolic and intracellular calcium homeostasis with a
consecutive breakdown of sarcolemma inflammation and stim-
ulation of nociceptive free nerve endings,95 a mechanism that was
also suggested for the generation of myofascial trigger points.96
In addition, the development of muscle fatigue was found
accelerated in motor units adjacent to myofascial trigger points.97
Consequently, an overactive movement behavior would be
independent of the initial motor adaptation with LBP and
induce long-term adaptations in motor control. This might
present the LBP individual with a relatively well-preserved
bodily fitness, despite episodes of increased pain and imbalanced
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Special Topic Series
homeostasis of the motor control system that is reorganized and
adapted in association with LBP to maintain bodily activities.
Despite an increased stiffness of the trunk, the long-term con-
sequences of impaired force and power generation in the trunk
muscles in bodily overactive individuals would dispose the trunk
and adjacent joints of the pelvis and lower extremities to an
increased susceptibility for repetitive strain injury of the con-
nective tissues of muscles, ligaments, and the vertebral segments,
thereby facilitating the chronification of the pain syndrome. This
would, in further consequence, facilitate all segmental insta-
bility, early degeneration in vertebral segments of the lumbar
spine, and in adjacent joints of the pelvis, hips, and knees.
SUMMARY AND CONCLUSION
This narrative review focuses on the role of high levels of
physical activity despite severe pain, possible cognitive-behavioral
determinants, and neuromuscular consequences in patients with
chronic pain. The concept of “ overactivity”opens the view for a
new understanding of pain-related avoidance: resting and escape
from pain-provoking activities may occur as a consequence of
continuing persistence in an activity despite an increase (flare-up)
of pain. A pause was enforced by intolerable high levels of pain,
presumably inducing loss of control and feelings of helplessness,
affective distress, fear of injury, and, in the long-term, low self-
esteem. Helplessness has been shown as the main predictor of
pain and disability not only in patients with chronic back pain
but also in physically highly active athletes.98 Helplessness is
positively correlated with thought suppression, one critical cog-
nitive response to pain among endurance-related pathways,32,98
and acts as an important mediator between pain and depres-
sion.33,34,99 Thus, treatment regimen should distinguish between
patients who rest and escape from pain at low levels of pain—but
who have high levels of fear of pain—and those who predom-
inantly persist in activities despite severely increasing pain until a
break will be enforced by intolerable pain levels. Understanding
cognitive-affective and behavioral mechanisms of overactivity
may help to develop educational tools for effective prevention
and treatment. Not least, educational programs should further
provide an understanding of the complexity of neuromuscular
consequences with peripheral and central pathways of sensitiza-
tion that are probably highly different for patients showing fear
and avoidance with and without preceding overactivity.
REFERENCES
1. Vlaeyen JWS, Linton SJ. Fear-avoidance model of chronic
musculoskeletal pain: 12 years on. Pain. 2012;153:1144–1147.
2. Fordyce WE. Behavioral Methods for Chronic Pain and Illness.
St. Louis, MO: Mosby; 1976.
3. Setchell J, Costa N, Ferreira M, et al. What constitutes back
pain flare? A cross sectional survey of individuals with low back
pain. Scand J Pain. 2017;17:294–301.
4. Hasenbring MI, Verbunt JA. Fear-avoidance and endur-
ance-related responses to pain: new models of behavior and their
consequences for clinical practice. Clin J Pain. 2010;26:747–753.
5. Hasenbring MI, Chehadi O, Titze C, et al. Fear and anxiety in
the transition from acute to chronic pain: there is evidence for
endurance besides avoidance. Pain Manag. 2014;4:363–374.
6. Ebenbichler GR, Oddsson LI, Kollmitzer J, et al. Sensory-
motor control of the lower back: implications for rehabilitation.
Med Sci Sports Exerc. 2001;33:1889–1898.
7. Hodges PW, Moseley GL. Pain and motor control of the
lumbopelvic region: effect and possible mechanisms. J Electro-
myogr Kinesiol. 2003;13:361–370.
8. Philips C. The Psychological Management of Chronic Pain.
New York, NY: Springer; 1988.
www.clinicalpain.com | 169
Special Topic Series
9. Hanson R, Gerber K. Coping With Chronic Pain: a Guide to
Patient Self Management. New York, NY: Guilford Press; 1990.
10. Birkholtz M, Aylwin L, Harman RM. Activity pacing in
chronic pain management: one aim, but which method? Part
one: introduction and literature review. Br J Occup Ther. 2004;67:
447–452.
11. Nicholas M, Molloy A, Tokin L, et al. Manage Your Pain. Sydney,
Australia: ABC Books; 2011.
12. Moore P, Cole F. The Pain Toolkit. London, UK: NHS; 2008.
13. Suri P, Saunders KW, Von Korff M. Prevalence and character-
istics of flare-ups of chronic nonspecific back pain in primary
care: a telephone survey. Clin J Pain. 2012;28:573–580.
14. Andrews NE, Strong J, Meredith PJ, et al. “ It’s very hard to
change yourself” : an exploration of overactivity in people with
chronic pain using interpretative phenomenological analysis.
Pain. 2015;156:1215–1231.
15. Geisser ME, Robinson ME, Richardson C. A time series
analysis of the relationship between ambulatory EMG, pain,
and stress in chronic low back pain. Biofeedback Self Regul.
1995;20:339–355.
16. Liszka-Hackzell JJ, Martin DP. An analysis of the relationship
between activity and pain in chronic and acute low back pain.
Anesth Analg. 2004;99:477–481.
17. Schepens SL, Kratz AL, Murphy SL. Fatigability in osteo-
arthritis: effects of an activity bout on subsequent symptoms
and activity. J Gerontol A Biol Sci Med Sci. 2012;67:1114–1120.
18. Rabbitts JA, Holley AL, Karlson CW, et al. Bidirectional
associations between pain and physical activity in adolescents.
Clin J Pain. 2014;30:251–258.
19. Andrews NE, Strong J, Meredith PJ. Overactivity in chronic
pain: is it a valid construct? Pain. 2015;156:1991–2000.
20. Andrews NE, Strong J, Meredith PJ, et al. Approach to activity
engagement and differences in activity participation in chronic pain:
a five-day observational study. Aust Occup Ther J. 2018;65:575–585.
21. Cane D, Nielson WR, McCarthy M, et al. Pain-related activity
patterns: measurement, interrelationships, and associations
with psychosocial functioning. Clin J Pain. 2013;29:435–442.
22. Kindermans HPJ, Roelofs J, Goossens MEJB, et al. Activity
patterns in chronic pain: underlying dimensions and associations
with disability and depressed mood. J Pain. 2011;12:1049–1058.
23. Andrews NE, Strong J, Meredith PJ. The relationship between
approach to activity engagement, specific aspects of physical
function, and pain duration in chronic pain. Clin J Pain. 2016;
32:20–31.
24. Esteve R, Ramirez-Maestre C, Peters ML, et al. Development
and initial validation of the activity patterns scale in patients
with chronic pain. J Pain. 2016;17:451–461.
25. Andrews NE, Strong J, Meredith PJ, et al. Association between
physical activity and sleep in adults with chronic pain: a momentary,
within-person perspective. Phys Ther. 2014;94:499–510.
26. Hasenbring MI, Kindermanns HPJ. Avoidance and endurance
in chronic pain. A self-regulation perspective. In: Karoly P,
Crombez G, eds. Motivational Perspectives on Chronic Pain.
New York, NY: Oxford University Press; 2018:287–314.
27. Wegner DM, Schneider DJ, Carter SR, et al. Paradoxical effects
of thought suppression. J Pers Soc Psychol. 1987;53:5–13.
28. Wegner DM. Ironic processes of mental control. Psychol Rev.
1994;101:34–52.
29. Wegner DM, Zanakos S. Chronic thought suppression. J Pers.
1994;62:615–640.
30. Cioffi D, Holloway J. Delayed costs of pain. J Pers Soc Psychol.
1993;64:274–282.
31. Masedo AI, Exteve MR. Effects of suppression, acceptance and
spontaneous coping on pain tolerance, pain intensity and
distress. Behav Res Ther. 2007;45:199–209.
32. Hasenbring MI, Hallner D, Rusu AC. Fear-avoidance- and
endurance-related responses to pain: development and validation
of the Avoidance-Endurance Questionnaire (AEQ). Eur J Pain.
2009;13:620–628.
33. Klasen BW, Bruggert J, Hasenbring M. Role of cognitive pain
coping strategies for depression in chronic back pain. Path
analysis of patients in primary care. Schmerz. 2006;5:398–410.
170 | www.clinicalpain.com Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Pain ! Volume 36, Number 3, March 2020
34. Hülsebusch J, Hasenbring MI, Rusu AC. Understanding pain
and depression in back pain: the role of catastrophizing, help-/
hopelessness, and thought suppression as potential mediators.
Int J Behav Med. 2016;23:251–259.
35. Konietzny K, Chehadi O, Streitlein-Böhme I, et al. Mild
depression in low back pain: the interaction of thought suppression
and stress plays a role, especially in female patients. Int J Behav Med.
2018;25:207–214.
36. Konietzny K, Chehadi O, Levenig C, et al. Depression and
suicidal ideation in high-performance athletes suffering from
low back pain: the role of stress and pain-related thought
suppression. Eur J Pain. 2019;23:1196–1208.
37. Hasenbring MI, Hallner D, Klasen B, et al. Pain-related
avoidance versus endurance in primary care patients with
subacute back pain: psychological characteristics and outcome
at a 6-month follow-up. Pain. 2012;153:211–217.
38. Hasenbring M. Endurance strategies-a neglected phenomenon in the
research and therapy of chronic pain? Schmerz. 1993;7:304–313.
39. Deroche T, Woodman T, Stephan Y, et al. Athletes’ inclination to
play through pain: a coping perspective. Anxiety Stress Coping.
2011;24:579–587.
40. Andrews NE, Strong J, Meredith PJ. Activity pacing,
avoidance, endurance, and associations with patient function-
ing in chronic pain: a systematic review and meta-analysis. Arch
Phys Med Rehabil. 2012;93:2109–2112.
41. Hasenbring M, Marienfeld G, Kuhlendal D, et al. Risk factors
of chronicity in lumbar disc patients. A prospective inves-
tigation of biologic, psychologic, and social predictors of
therapy outcome. Spine. 1994;19:2759–2765.
42. Grebner M, Breme K, Rothoerl R, et al. Coping und
Genesungsverlauf nach lumbaler Bandscheibenoperation [Coping
and convalescence course after lumbar disk operations]. Schmerz.
1999;13:19–30.
43. Scholich SL, Hallner D, Wittenberg RH, et al. Pilot study on
pain response patterns in chronic low back pain. The influence
of pain response patterns on quality of life, pain intensity and
disability. Schmerz. 2011;25:184–190.
44. Fehrmann E, Tuechler K, Kienbacher T, et al. Comparisons in
muscle function and training rehabilitation outcomes between
avoidance-endurance model-subgroups. Clin J Pain. 2017;33:
912–920.
45. Cane D, Nielson WR, Mazmanian D. Patterns of pain-related
activity: replicability, treatment-related changes, and relation-
ship to functioning. Pain. 2018;159:2522–2529.
46. Hasenbring MI, Plaas H, Fischbein B, et al. The relationship
between activity and pain in patients 6 months after lumbar disc
surgery: do pain-related coping modes act as moderator
variables? Eur J Pain. 2006;10:701–709.
47. Plaas H, Sudhaus S, Willburger R, et al. Physical activity and
low back pain: the role of subgroups based on the avoidance-
endurance model. Disabil Rehabil. 2014;36:749–755.
48. Stokes IAF, Iatridis JC. Mechanical conditions that accelerate
intervertebral disc degeneration: overload versus immobiliza-
tion. Spine. 2004;29:2724–2732.
49. Bousema EJ, Verbunt JA, Seelen HA, et al. Disuse and physical
deconditioning in the first year after the onset of back pain.
Pain. 2007;130:279–286.
50. Tucker KJ, Hodges PW. Changes in motor unit recruitment
strategy during pain alters force direction. Eur J Pain. 2010;14:
932–938.
51. Tucker K, Larsson AK, Oknelid S, et al. Similar alteration of
motor unit recruitment strategies during the anticipation and
experience of pain. Pain. 2012;153:636–643.
52. Gallina A, Salomoni SE, Hall LM, et al. Location-specific
responses to nociceptive input support the purposeful nature of
motor adaptation to pain. Pain. 2018;159:2192–2200.
53. Hodges PW, Tucker K. Moving differently in pain: a new
theory to explain the adaptation to pain. Pain. 2011;152(suppl):
90–98.
54. van Dieën JH, Selen LP, Cholewicki J. Trunk muscle activation
in low-back pain patients, an analysis of the literature. J
Electromyogr Kinesiol. 2003;13:333–351.
Clin J Pain ! Volume 36, Number 3, March 2020
55. van Dieën JH, Reeves NP, Kawchuk G, et al. Motor control
changes in low-back pain: divergence in presentations and
mechanisms. J Orthop Sports Phys Ther. 2018;6:370–379.
56. Verbunt JA, Smeets RJ, Wittink HM. Cause or effect? Decondi-
tioning and chronic low back pain. Pain. 2010;149:428–430.
57. Solomonow M. Ligaments: a source of work-related musculoskel-
etal disorders. J Electromyogr Kinesiol. 2004;14:49–60.
58. Solomonow M. Neuromuscular manifestations of viscoelastic
tissue degradation following high and low risk repetitive lumbar
flexion. J Electromyogr Kinesiol. 2012;22:155–175.
59. Takakusaki K. Functional neuroanatomy for posture and gait
control. J Mov Disord. 2017;10:1–17.
60. Horak FB. Postural orientation and equilibrium: what do we
need to know about neural control of balance to prevent falls?
Age Ageing. 2006;35(suppl 2):ii7–ii11.
61. Da Silva RA, Vieira ER, Cabrera M, et al. Back muscle fatigue
of younger and older adults with and without chronic low back
pain using two protocols: a case-control study. J Electromyogr
Kinesiol. 2015;25:928–936.
62. Ebenbichler GR, Unterlerchner L, Habenicht R, et al. Estimating
neural control from concentric vs. eccentric surface electromyo-
graphic representations during fatiguing, cyclic submaximal back
extension exercises. Front Physiol. 2017;8:299.
63. De Luca CJ, Erim Z. Common drive of motor units in
regulation of muscle force. Trends Neurosci. 1994;17:299–305.
64. De Luca CJ, Mambrito B. Voluntary control of motor units in
human antagonist muscles: coactivation and reciprocal activa-
tion. J Neurophysiol. 1987;58:525–542.
65. Amonoo-Kuofi HS. The number and distribution of muscle
spindles in human intrinsic postvertebral muscles. J Anat. 1982;135:
585–599.
66. Amonoo-Kuofi HS. The density of muscle spindles in the
medial, intermediate and lateral columns of human intrinsic
postvertebral muscles. J Anat. 1983;136:509–519.
67. De Luca CJ, Kline JC. Influence of proprioceptive feedback on
the firing rate and recruitment of motoneurons. J Neural Eng.
2012;9:016007.
68. Koch C, Hänsel F. Chronic non-specific low back pain and
motor control during gait. Front Psychol. 2018;92236.
69. Laird RA, Gilbert J, Kent P, et al. Comparing lumbo-pelvic
kinematics in people with and without back pain: a systematic
review and meta-analysis. BMC Musculoskelet Disord. 2014;15:229.
70. Hodges PW. Changes in motor planning of feedforward
postural responses of the trunk muscles in low back pain. Exp
Brain Res. 2001;141:261–266.
71. Silfies SP, Mehta R, Smith SS, et al. Differences in feedforward
trunk muscle activity in subgroups of patients with mechanical
low back pain. Arch Phys Med Rehabil. 2009;90:1159–1169.
72. Bouffard J, Salomoni SE, Mercier C, et al. Effect of experimental
muscle pain on the acquisition and retention of locomotor
adaptation: different motor strategies for a similar performance.
J Neurophysiol. 2018;119:1647–1657.
73. Hodges P, van den Hoorn W, Dawson A, et al. Changes in the
mechanical properties of the trunk in low back pain may be
associated with recurrence. J Biomech. 2009;42:61–66.
74. Tong MH, Mousavi SJ, Kiers H, et al. Is there a relationship
between lumbar proprioception and low back pain? A systematic
review with meta-analysis. Arch Phys Med Rehabil. 2017;98:
120–136.
75. Tsao H, Danneels LA, Hodges PW. ISSLS prize winner:
Smudging the motor brain in young adults with recurrent low
back pain. Spine. 2011;36:1721–1727.
76. Schabrun SM, Elgueta-Cancino EL, Hodges PW. Smudging of
the motor cortex is related to the severity of low back pain.
Spine. 2017;42:1172–1178.
77. Sions JM, Coyle PC, Velasco TO, et al. Multifidi muscle
characteristics and physical function among older adults with
and without chronic low back pain. Arch Phys Med Rehabil.
2017;98:51–57.
Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.
Copyright r 2019 Wolters Kluwer Health, Inc. All rights reserved.
Special Topic Series
78. Goubert D, Oosterwijck JV, Meeus M, et al. Structural changes
of lumbar muscles in non-specific low back pain: a systematic
review. Pain Physician. 2016;19:E985–E1000.
79. Mannion AF, Weber BR, Dvorak J, et al. Fibre type
characteristics of the lumbar paraspinal muscles in normal
healthy subjects and in patients with low back pain. J Orthop
Res. 1997;15:881–887.
80. Demoulin C, Crielaard JM, Vanderthommen M. Spinal muscle
evaluation in healthy individuals and low-back-pain patients: a
literature review. Joint Bone Spine. 2007;74:9–13.
81. Roy SH, De Luca CJ, Emley M, et al. Classification of back
muscle impairment based on the surface electromyographic
signal. J Rehabil Res Dev. 1997;34:405–414.
82. Sung PS, Lammers AR, Danial P. Different parts of erector
spinae muscle fatigability in subjects with and without low back
pain. Spine J. 2009;9:115–120.
83. Van Dieën JH, Flor H, Hodges PW. Low-back pain patients
learn to adapt motor behavior with adverse secondary
consequences. Exerc Sport Sci Rev. 2017;45:223–229.
84. Søgaard K, Sjøgaard G. Physical activity as cause and cure of
muscular pain: evidence of underlying mechanisms. Exerc Sport
Sci Rev. 2017;45:136–145.
85. Lothe LR, Raven TJ, Eken T. Single-motor-unit discharge
characteristics in human lumbar multifidus muscle. J Neuro-
physiol. 2015;114:1286–1297.
86. Heckman CJ, Lee RH. The role of voltage-sensitive dendritic
conductances in generating bistable firing patterns in moto-
neurons. J Physiol Paris. 1999;93:97–100.
87. Pette D. What can be learned from the time course of changes in
low-frequency stimulated muscle? Eur J Transl Myol. 2017;27:6723.
88. Roy SH, De Luca CJ, Snyder-Mackler L, et al. Fatigue,
recovery, and low back pain in varsity rowers. Med Sci Sports
Exerc. 1990;22:463–469.
89. Larivière C, Gagnon D, Gravel D, et al. The assessment of
back muscle capacity using intermittent static contractions. Part
I—validity and reliability of electromyographic indices of
fatigue. J Electromyogr Kinesiol. 2008;18:1006–1019.
90. Cholewicki J, Silfies SP, Shah RA, et al. Delayed trunk muscle
reflex responses increase the risk of low back injuries. Spine.
2005;30:2614–2620.
91. McCook DT, Vicenzino B, Hodges PW. Activity of deep
abdominal muscles increases during submaximal flexion and
extension efforts but antagonist co-contraction remains
unchanged. J Electromyogr Kinesiol. 2009;19:754–762.
92. Cheng AJ, Place N, Bruton JD, et al. Doublet discharge
stimulation increases sarcoplasmic reticulum Ca2+ release and
improves performance during fatiguing contractions in mouse
muscle fibres. J Physiol. 2013;591:3739–3748.
93. Zehr EP, Sale DG. Ballistic movement: muscle activation and
neuromuscular adaptation. Can J Appl Physiol. 1994;19:363–378.
94. Mrówczyński W, Celichowski J, Raikova R, et al. Physiological
consequences of doublet discharges on motoneuronal firing and
motor unit force. Front Cell Neurosci. 2015;9:81.
95. Søgaard K, Olsen HB, Blangsted AK, et al. Single motor unit firing
behavior in the right trapezius muscle during rapid movement of
right or left index finger. Front Hum Neurosci. 2014;8:881.
96. Mense S. Differences between myofascial trigger points and
tender points. Schmerz. 2011;25:93–103.
97. Ge HY, Arendt-Nielsen L, Madeleine P. Accelerated muscle
fatigability of latent myofascial trigger points in humans. Pain
Med. 2012;13:957–964.
98. Gajsar H, Titze C, Levenig C, et al. Psychological pain responses
in athletes and non-athletes with low back pain: avoidance and
endurance matter. Eur J Pain. 2019;23:1649–1662.
99. Fahland RA, Kohlmann T, Hasenbring MI, et al. Which route
leads from chronic back pain to depression? A path analysis on
direct and indirect effects using the cognitive mediators catastroph-
izing and helplessness/hopelessness in a general population sample
[article in German]. Schmerz. 2012;26:685–691.
www.clinicalpain.com | 171