Management of the Individual With
Pain: Parts 1 and 2
John L Echternach, PT, EdD, ECS, FAPTA
Objectives
After reading part 1 of this continuing education article,
you will be able to:
• Describe theories on how pain is perceived and
transmitted.
• Identify key elements of the examination of the
patient with pain.
• Discuss various tests and measures used to
quantify pain, including the reliability and validity
of the measurements.
After reading part 2, you will be able to:
• Discuss the integration of behavioral management
techniques into a traditional physical therapy
program.
• Describe how the pain intensity data obtained
from the examination and evaluation can be used
to develop the plan of care.
• Apply the above concepts to the management of a
hypothetical patient who had a hyperextension
injury to the knee and developed complex regional
pain syndrome.
This article is the updated version of “Management of
the Individual With Pain, Parts 1 and 2” (PT
Magazine, November-December 1996), written by
John L Echternach, PT, EdD, ECS, FAPTA,
Professor and Eminent Scholar, School of Physical
Therapy, Old Dominion University, Va.
PART 1—PHYSIOLOGY AND
EXAMINATION
Introduction/Perception of Pain
One of the most challenging and rewarding experiences of
a physical therapist's career is the successful management
of the patient with pain. Many-perhaps most-patients are
referred to physical therapists because of pain and
associated dysfunction.
Perception of Pain
The International Association for the Study of Pain has
defined pain as “an unpleasant sensory and emotional
experience associated with actual or potential tissue
damage or described in terms of such damage.”1 The
sensory component of the pain experience depends on the
activation of peripheral receptors (often in response to
tissue injury or death), the transmission of afferent
impulses to the spinal cord, and the processing of this
information within the central nervous system (CNS).
Events in the Periphery
Pain receptors in the periphery have been identified as free
nerve endings that respond to stimuli occurring secondary
to imminent or actual tissue damage or destruction. These
free nerve endings are associated with small-diameter
afferent fibers, which transmit sensory information
associated with noxious stimuli to the dorsal horn of the
spinal cord. Free nerve endings, located primarily in the
skin and linings of the mouth and anus, are associated with
small, myelinated A delta fibers.2 They are most sensitive
to high-intensity mechanical stimulation, although the
transmission of cold and hot impulses also occurs along
these fibers.3,4 Impulses travel along the A delta fibers to
the dorsal horn at speeds of 5 to 15 m/s. Most sensations
associated with A delta activity are described as sharp,
pricking, well-localized (or “fast”) pain; however, A delta
fibers are capable of transmitting non-noxious information
as well.3
Other free nerve endings, called polymodal nociceptors,
transmit information along small, unmyelinated C fibers.
The polymodal nociceptors are located predominantly in
the deep layers of the dermis and virtually every other
tissue in the body, except for the nervous system. The
polymodal nociceptors have small, homogeneous receptive
fields and respond to noxious levels of mechanical,
thermal, and chemical stimulation (hence the name
“polymodal”). They are believed to respond to chemical
substances, such as histamine and bradykinin, that are
released in response to tissue damage. The C fibers
transmit information more slowly (about 1 m/s) than the
myelinated A delta fibers do. Burning pain (often referred
to as “second” pain) related to tissue damage is most often
associated with C-fiber activation.5-8 Gybels et al8 have
shown, however, that nonpainful sensations are also
reported following cutaneous activation of C-fiber
polymodal units.
Events in the Dorsal Horn of the
Spinal Cord
The gray matter of the spinal cord is divided into 10
laminae, or layers, based on the anatomic orientation of
the cells within each layer.9 These laminae receive a variety
of inputs from the periphery and transmit a great deal of
information to higher centers. In addition, significant
interneuronal communication occurs both within and
between cells of each lamina.
Lamina II (substantia gelatinosa, labeled “SG” on Fig. 1)
and outer zones. The outer zone receives input from C
fibers associated with high-threshold thermal nociceptors,
whereas the inner zone receives information from low-
threshold A delta mechanoreceptors.10,11 In addition, other
C-fiber and A-delta fiber inputs also synapse in lamina II.
Activation of cells in lamina II results in both excitation
and inhibition of postsynaptic neurons involved in the
transmission of noxious information to the higher centers.
Gate Control Theory
Lamina II is of particular interest to physical therapists
because it plays an important role in the gate control theory of
pain.12 This theory helps clarify the effect of the substantia
gelatinosa on pain perception and modulation, and it has
been used to explain the analgesic effects of many of the
interventions used by physical therapists.
In 1965, Melzack and Wall12 theorized that sensory
perception is the result of activation of transmission cells
(labeled “T” on Fig. 1) in the dorsal horn of the spinal
cord, which in turn results from a balance of peripheral
input along large-diameter (A alpha and A beta fibers) and
small-diameter (A delta and C fibers) afferent nerve fibers
(Fig. 1). The denseness of the interneuronal connections in
the dorsal horn provide evidence to support the gate
control theory.13 Activity from both large- and small-
diameter afferent neurons directly activates the
transmission cell. However, noxious input, transmitted via
small-diameter fibers, also restrains inhibitory interneurons
in the dorsal horn, thus decreasing the effect of
presynaptic inhibition on the transmission cell from the
interneurons. Ultimately, this results in a net increase in
perception of painful input.
In contrast, activity traveling along large-diameter afferent
fibers triggers the inhibitory interneurons, thus facilitating
presynaptic inhibition of the transmission cell. Ultimately,
this results in a “closing of the spinal gate” or a decrease in
the perception of sensory activity. In the early 1970s,
transcutaneous electrical nerve stimulation (TENS) was
viewed as a form of comfortable peripheral sensory input
that could decrease pain perception by preferentially
increasing the input from large-diameter afferent fibers
and aiding the presynaptic inhibition of the transmission
2
cell, thus decreasing conscious pain perception. For
instance, TENS has been demonstrated to be effective in
relieving pain associated with postherpetic neuralgia, a
disease that results in degeneration of large-diameter
afferent fibers,14 and has been recommended as part of the
management of postherpetic neuralgia.15,16
Although TENS continues to be used in patients with
postherpetic neuralgia, it is often combined with other
interventions.17 Currently, there seems to be no one
effective treatment for postherpetic neuralgia, and
evidence to support any one particular approach is not
available.
When applied to the painful region or to a segmentally
related region in which the population of large-diameter
fibers remains intact, conventional TENS effectively
controls the pain associated with postherpetic neuralgia. It
does this by activating the remaining large-diameter
afferent fibers that lie in close proximity to the
pathologically active small-diameter afferent neurons in the
CNS.18 Other analgesic interventions, including massage or
vibration, may also be explained by this theory.
The gate control theory was criticized for failing to (1)
account for a variety of painful conditions in which small-
diameter afferents were preferentially destroyed and (2)
consider the role of the higher centers in conscious pain
perception.18-20 In 1968, Melzack and Casey21 modified the
gate control theory to account for activation of the higher
centers. They added the limbic and reticular systems, both
of which are known to influence pain perception, affect,
and motor responses (Fig. 2). Higher centers in the
neocortex also monitor painful afferent input by
“comparing” it with past experiences and learned
responses. Melzack and Casey suggested that a “central
control trigger,” activated by input to these higher centers,
might influence activity in the dorsal horn through
descending systems and also might contribute to pain
modulation. Thus, a mechanism for pain control
through distraction, meditation, or relaxation was
discovered (Fig. 2).
The gate control theory as proposed by Melzack and Wall
has undergone continuous revision over the past several
years, retaining the important features of the theory and
adding features such as the possibility of both inhibitory as
well as excitatory links from the substantia
gelatinosa. Expanded versions of the central controls
exhibited downwardly in the system continue to be added
(Fig. 3). In 1999, Melzack22 wrote about gate control
theory and its incorporation into newer theories. In an
expansion of the gate control model, Melzack22-24
theorized that the brain possesses a neural network—the
“body-self neuromatrix”—that integrates multiple inputs
to produce an output pattern that evokes pain (Fig. 4). He
argued that this neuromatrix is comprised of widely
distributed neural networks that include: (1) the parallel
somatosensory and thalamocortical components that serve
the sensory discriminative function and (2) parallel
components for the affective motivational and evaluative
cognitive dimensions of the pain experience. Melzack
believed that this elaboration from the gate control theory
to the neuromatrix would help explain the characteristics
of chronic pain, incorporate the concepts of
neuroplasticity of the nervous system, and demonstrate
how our understanding of pain has evolved from the
concept of a one-to-one relationship between injury and
pain.
He believed that the neuromatrix theory provides a
framework for explaining both the central, downward
control of pain mechanisms and the existence of cognitive
aspects of pain in addition to the traditional sensory
inputs. Melzack argued that recent research indicates the
great complexity of the mechanisms involved in pain and
that the perception of pain does not simply involve our
immediate reaction to noxious inputs but involves a
dynamic process that may be influenced by past
experiences.22-24 By understanding the changes in the
central nervous system that are induced by peripheral
injury or noxious stimulation, Melzack and colleagues25
argued that clinicians should be able to improve clinical
treatment to relieve and prevent pathologic pain.
Modulation of Pain
Stimulation-Produced Analgesia
Stimulation-produced analgesia (SPA), which involves the
production and utilization of endogenous opiates (eg,
endorphins and enkephalins) is one of the theories
developed to explain pain modulation. In 1978, Basbaum
and Fields26 proposed a negative feedback loop
mechanism to account for analgesia resulting from low-
frequency, high-intensity (acupuncture-like) TENS. They
suggested that the noxious input associated with
acupuncture-like TENS activates ascending pathways,
leading to the awareness of pain. Along these pathways,
certain axons synapse within medullary reticular formation
nuclei. Input from these nuclei then is transmitted to the
periaqueductal gray regions of the midbrain and thalamus,
regions that have high concentrations of endogenous
opiates and opiate receptors. When these regions are
activated, efferent axons synapse within nuclei in the raphe
magnus and reticularis gigantocellularis. Output from these
nuclei descends through the spinal cord and makes
enkephalinergic synapses that inhibit spinal transmission of
substance P, which is suspected of being a
neurotransmitter that conveys noxious information
between axons. Thus, the application of acupuncture-like
TENS may activate a negative feedback loop that
ultimately blocks further transmission of noxious
information.
3
Because activation of endorphin-mediated analgesia may
be blocked by naloxone, an opiate antagonist, analgesic
procedures that are suspected of being mediated by
endorphins can be identified. Administration of naloxone
will reverse this analgesia or lower an elevated pain
threshold to pretreatment values.27 Use of low-frequency,
high-intensity electrical stimulation of acupuncture points
and remote anatomical sites as an endorphin-mediated
analgesia has been confirmed by some investigators28-31
and refuted by others.32,33
Recent work in the area of electroacupuncture and TENS
stimulation suggests the release of endorphins by these
methods. After summarizing a group of studies that they
conducted, Ulett and colleagues34 concluded that both
low- and high-frequency electroacupuncture was successful
in producing analgesia. An earlier study by Wang et al,35
which used a rat as the experimental model, revealed that
there was no difference in the analgesic effects produced
by either electroacupuncture or TENS; both were
successful in producing an analgesic affect.
Proctor et al36 conducted a systematic review of the effects
of TENS and acupuncture for primary dysmenorrhea.
They reviewed the literature on this topic to see if high-
and low-frequency TENS were more effective than
acupuncture. They also compared these interventions with
placebo TENS, no treatment, or medical treatment for
primary dysmenorrhea. They found 9 articles that met
their review criteria. Overall, Proctor et al concluded that
high-frequency TENS was more effective for pain relief
than placebo TENS and that low-frequency TENS was be
no more effective in reducing pain than placebo TENS.
They reported conflicting results on whether high-
frequency TENS was more effective than low-frequency
TENS. Their final conclusion was that, in a number of
small trials, high-frequency TENS was found to be
effective for the treatment of dysmenorrhea. According to
Proctor et al, there was insufficient evidence to determine
the effectiveness of acupuncture in reducing
dysmenorrhea. This review noted that both TENS and
acupuncture were pain relief methods that had no direct
effect on uterine contractions but were thought to work by
altering the body’s ability to receive or perceive pain
signals. Proctor et al stated that they conducted this review
because they felt that these two nonpharmacological
methods had the potential for fewer side effects.
Analgesia resulting from acupuncture, acupressure, or
cognitive interventions (eg, distraction, imagery, hypnosis)
also has been associated with an endorphin-mediated
mechanism.37 As methods of histochemical and
electrophysiological data acquisition become more
sophisticated, knowledge of additional neurophysiological
mechanisms (as well as confirmation or refutation of
current ones) will add to our understanding of pain
perception and modulation.
Response to Pain
Motivational and Affective Components
Motivational and affective components influence a
person’s perception of and response to pain. These
components include age, sex, ethnicity, culture, religious
background, attention and distraction levels, environment
(eg, who’s watching), and the response of others to his or
her behavior.38 In addition, behavioral responses to pain
depend on previous experience with pain, responses
learned from others, and perception of control over the
cause of the pain.
Acute Pain Versus Chronic Pain
Acute pain is often described as pain of less than 6 months’
duration for which an underlying pathology can be
identified. Tissue inflammation, damage, or destruction is
often related somatically or, in a referred distribution, to
the location and intensity of the person’s pain report. Pain
is well localized, and the patient with acute pain is able to
define it. Medication intake and other medical
interventions usually are appropriate for the degree of
pathology identified.
Acute pain is mediated through pathways that include
rapidly conducting systems, such as the dorsal column
postsynaptic system, spinocervical tract, and
neospinothalamic tract.39 Acute pain is also associated with
increases in muscle reflex activity (often called spasticity),
heart rate, blood pressure, skin conductance, and other
manifestations of increased sympathetic nervous system
activity. In contrast, chronic pain appears to be mediated
through slowly conducting fibers in the
paleospinothalamic tract and spinoreticular formation, and
it is often associated with insomnia, loss of appetite and
libido, and feelings of helplessness and hopelessness,
rather than with increased sympathetic nervous system
activity.39
Chronic pain is often of longer than 6 months’ duration. An
underlying pathology is no longer identifiable and may
never have been present. The patient’s description of pain
is less defined and is poorly localized, and the examination
data are inconclusive. The patient’s verbal description of
the pain may contain words associated with emotional or
motivational characteristics, in contrast to the
predominance of sensory descriptors associated with acute
pain. The patient may indicate suffering through facial
grimacing, stooped posture, antalgic gait, and verbal
complaints that are out of proportion to the degree of
pathology that may be identified. Often, self-imposed
limited activity—a disrupted lifestyle and avoidance of
work, interaction with others, and sexual activity—is
evident. Secondary gains—such as monetary benefit,
sympathy and attention from significant others, or
avoidance of undesirable employment—are present.
4
Progressive inactivity, depression, anxiety, misuse of
prescription drugs, and increased dependence on the
health care system are all associated with chronic pain.
Bond40 described physical pain as having characteristics
analogous to those of acute pain. He labeled the poorly
defined chronic pain experience as psychogenic pain,
emphasizing that physical pain is usually alleviated once
the underlying pathology has been identified and treated,
whereas psychogenic pain is often unresponsive to
physiological interventions.
The perception of pain involves many complex
interactions among the patient, the cause of the pain, and
the surrounding environment. As described earlier, the
distinction between acute and chronic pain can be made
relatively simply. The distinctions between chronic pain
and the psychological aspects of pain, however, cannot
always be made clearly. In nearly all instances, patients
with chronic pain have a psychological component to their
pain. This is not to suggest that their pain is not real or that
they are not experiencing pain as part of their problem.
Patients with chronic pain will nearly always benefit if they
and the clinicians treating them understand that there is a
psychological component to their pain problem. This is a
difficult concept for both patients and therapists who are
used to understanding things in a more simple context of a
medical model of injury and disease. Chronic pain involves
not only the problem of pain but the problem of the
patient’s reaction to his or her health care provider. These
patients may feel that they have been ignored or
mismanaged by health care professionals, and there may be
an anger component in patients with chronic pain that
clinicians must handle. Physical therapists, however, may
not be prepared to manage the psychological aspects of
pain, except as part of a team.
Behavioral Manifestation of Pain
A pictorial representation comparing the degree of
physiological pathology with the behavioral manifestation
of pain is helpful in understanding patients with pain
(Fig. 5).41 “Patient A” displays a high degree of pain
behavior in response to a severe physiological disruption,
such as a burn. Our society views this patient as
responding appropriately and provides sympathy,
encouragement, and support, confident that the patient’s
pain behavior will diminish as the burn heals. “Patient B”
displays a great deal of pain behavior associated with little
physiological disruption and represents the patient with
chronic pain. “Patient C” displays a low degree of pain
behavior despite having a great deal of physiological
disruption. This patient may be thought of as a “stoic” and
may have learned to hide feelings from others. This patient
also may be distracted, concentrating on other things in
the environment, and therefore is not “perceiving” pain to
a degree associated with the pathology. Finally, “patient
D” represents the average, well-adjusted person who
displays pain behavior appropriate to the degree of
physiological disruption.
Fordyce41 described a pain experience in which an
underlying pathology can be identified through the
medical/disease model (Fig. 6). Health care professionals
may be comfortable with and capable of managing patients
whose pain experience is represented by this model. The
patient’s symptoms are directly related to the underlying
pathology, and, once that pathology has been identified
and treated, the patient’s symptoms and pain behaviors are
removed. In contrast, a patient who has symptoms and
pain behaviors that are not associated with an underlying
pathology presents a much greater challenge to health care
professionals. When no underlying pathology can be
identified, traditional medical intervention cannot be as
effective in modifying the patient’s symptoms and pain
behavior. The patient’s behavior has been learned (perhaps
in response to an initial underlying pathology), has been
reinforced (by the attention and sympathy from others, by
financial gain, or by avoidance of unpleasant activities),
and persists even in the absence of an underlying
pathology or noxious stimulus (Fig. 7).41
In the medical/disease model, the patient displays a
respondent behavior, one that depends on the presence of an
underlying pathology or noxious stimulus (Fig. 8, top).42
Once the noxious stimulus is removed, the behavior
ceases. In the learning model, the patient exhibits operant
behavior (ie, a set of responses to a noxious stimulus that
are initially reinforced and persist as long as ongoing
reinforcement is available, even when the noxious stimulus
has been removed) (Fig. 8, middle and bottom). Clearly,
treatment in the second case must be directed at the
dysfunctional operant behaviors—by removing the
reinforcement of negative behaviors and by replacing these
behaviors with positive (healthy) ones.
There are patients who will not respond to traditional
treatment and whose functional disability appears to be
much greater than it would be on the basis of their
examination findings alone.43 In some patients with
chronic pain conditions, their persistent pain does not
seem to be related to changes or progression of their
disease. To manage these patients, a biopsychosocial
model or paradigm has been proposed.44-46 This model
combines the biologic, psychologic, social, and cultural
influences responsible for maintaining or exacerbating the
patient’s pain condition, and its purpose is to reduce the
dichotomy between organic and psychogenic sources of
pain. The changes that occur in patients with chronic pain
can be partially explained by the interaction of these
factors (which include social and cultural factors), and the
patient’s perception of pain and the distress expressed as a
response to pain.43
5
Understanding these interrelationships has become
extremely important in the care of patients by
interdisciplinary teams. Many health care professionals
understand that this new model demonstrates that the role
of psychological factors in chronic pain is more complex
and involves more psychological factors than originally
thought.44-46 The relationship between chronic pain and
depression as well as the relationship between the response
of individuals to chronic pain and the failure of coping
mechanisms now are better understood.44-46
The importance of identifying whether behavioral
manifestation of a pain experience is operant or
respondent is critical to the successful interdisciplinary
management of the patient with pain. Clinicians may state
that they are concerned about the underlying problem
rather than about the patient’s pain, believing that if the
underlying problem can be altered, the pain situation will
also be altered. This is not always the case. There are
patients whose underlying problems no longer seem to
exist but whose significant pain symptoms seem to
continue.47 The integration of behavioral management
techniques into a traditional physical therapy program will
be discussed in part 2.
Examining the Patient With Pain
The careful, detailed examination of the patient with pain
is critical to the accurate identification of the causes
(underlying pathology) and sources of pain and to the
accurate assessment of treatment effectiveness.
Matching Experimental and Clinical Pain
Various methods have been identified to evaluate and
quantify the sensory aspects of experimental pain with a
high degree of reliability and validity. When these
experimental methods are applied to the evaluation of
clinical pain, however, the validity of the measurements is
compromised because they do not reflect the multiple
components of the pain experience.
Sternbach48 described the tourniquet pain test, in which
the patient attempts to correlate clinical pain intensity with
the pain intensity perceived from experimentally induced
ischemia in the upper extremity. A pain ratio—comparing
the clinical pain with the maximum ischemic pain
tolerated—is derived, and the clinical pain is described as a
percentage of the ischemic pain tolerance of the patient.
The tourniquet pain test reportedly correlates well with
clinical pain estimates reported on a visual analog scale
(VAS).48
In a study of the sensitivity of the tourniquet pain test,
Sternbach et al49 concluded that the variability of
tourniquet pain test scores was too great to determine
differences in response to analgesics. However, they felt
that the tourniquet techniques would continue to be useful
until more accurate measures of the severity of clinical
pain were available.
Modified tourniquet techniques continue to be used to
match a painful stimulus experimentally and to study the
effects of various interventions on a painful stimulus
created by ischemia. Moore and colleagues50 described the
use of a submaximal effort tourniquet test as it was used to
evaluate experimental and chronic pain. They believed that
variation in the application of the test was great and that
the exercise portion of the test was not always applied in a
standard manner. In their opinion, the lack of a
standardized way to apply the test could limit its use in the
study of experimental and chronic pain.
Rosenblatt and Hetherington51 found that TENS did not
alleviate experimental tourniquet pain. They could not
obtain a significant increase in the duration of the ischemia
that was tolerated by subjects when they were exposed to
either single-channel or dual-channel TENS compared
with a control situation.
In a study of the effects of TENS on experimentally
induced ischemic pain, Walsh et al52 used 2 different
frequencies of TENS under what they considered to be
double-blind conditions. They used a submaximal effort
tourniquet technique and also obtained subject responses
to a VAS and the McGill Pain Questionnaire. They found
that the lower-frequency TENS showed a greater effect
than the higher frequency TENS. They believed that their
findings confirmed that TENS had a analgesic effect on
experimental ischemic pain.
Another study using the submaximal effort tourniquet
technique was done by Johnson and Tabasam.53 They
conducted a single-blind, placebo-controlled study to
examine the analgesic effects of interferential currents on
experimentally induced ischemic pain. Thirty volunteers
received the active treatment of the interferential current
(IFC), a sham treatment of IFC, or no treatment. There
were 10 subjects in each group. Their analysis revealed
differences among the groups, with a significant reduction
of pain intensity for the IFC group when compared with
the control groups that received sham IFC or no
treatment. Gracely54 reported a high degree of intrasubject
reliability when patients matched the intensity of their
clinical myofascial pain to experimentally induced pain
from an electrical stimulus.
Since the 1950s, thermal stimuli, applied and quantified
with a dolorimeter, have been used to evaluate clinical pain
as well as the analgesic effects of various drugs.55 Kast56
attempted to quantify clinical pain by inducing pain in a
patient’s fingertip with an air-pressure device and asking
the patient to match the intensity of the experimentally
induced pain to that of the clinical pain. Kast’s method
6
correlated highly with the other pain matching methods
described above.
Perkins et al57 described an inexpensive device to help
determine radiant heat pain thresholds in a clinical
environment in people without impairments. The device
was adapted from the dolorimeter developed by Hardy et
al55 and, according to the authors, is a nonclinical method
for evaluating pain threshold in research environments.
They established that measurements obtained from this
device were reliable from session-to-session with 2 groups
of adults.
In a more recent example of the use of the dolorimeter,
Pienimaki and colleagues58 used this device to measure
pressure pain thresholds. Their study used a VAS to
compare the responses of subjects with medial
epicondylitis and subjects with lateral epicondylitis to pain
pressure thresholds at defined points and to various
conditions.58 Subjects in this study were shown to have less
pain under strain if they had chronic medial epicondylitis
than if they had lateral epicondylitis. Those subjects with
lateral epicondylitis showed greater impairment of arm
function in a variety of tests, including tests of muscle
force, grip, and work. The authors considered their use of
a structured interview to assess the patient’s pain problems
to be helpful; however, they pointed out that clinicians
should follow the patient’s lead (ie, let them explain their
pain in a way that is meaningful to them) when using a
structured approach if the patient describes pain in
unexpected ways.58
Several problems may affect the validity of matching
experimental and clinical pain intensity levels. First, in
order to accurately match the 2 types of pain, the subject
must experience clinical pain at the same time that the
experimental pain is induced. The clinical pain may be so
severe, however, that the introduction of experimental
pain would be both ethically unacceptable and
physiologically impossible to duplicate. Second, pain
matching requires the subject’s concentration and
cooperation and therefore is limited to patients who are
oriented, alert, cooperative, and have relatively mild clinical
pain. Finally, the experimental pain experience ignores the
motivational, affective, and learned behavioral components
of clinical pain and does not account for the lack of
control that a subject may perceive, particularly as part of a
chronic pain experience.
The dilemma of accurately evaluating the multiple
components of clinical pain persists. The various
components of a comprehensive evaluation of the patient
with pain seek to optimize validity (ie, do our measures
reflect that which we intend to measure?) and reliability (ie,
can the measures be accurately reproduced for one patient
by a variety of evaluators?). Alternative measurement tools
for examination are described below.
The Bases for Examining the
Patient’s Problem
The clinician examines the patient’s pain problems for two
important reasons. The first reason is to determine the
underlying cause or causes of the pain. Erickson59 stated
that pain should be categorized initially as either
nociceptive or deafferentation pain. In addition, he stated
that chronic pain is significantly different from acute pain
because it is carried on different pathways. He also noted
that any form of nerve injury that alters somatic sensation,
whether in the peripheral nervous system or in the CNS,
might lead to chronic pain. Erickson59 defined this chronic
pain, which is secondary to neurotrauma, as deafferentation
pain. He stated that this form of pain is the result of
reverberating neuronal circuits that are set up by
hyperactive pools of neurons, pools that may be quite
remote from the original site of the lesion. He further
stated that deafferentation pain is typified by a wide range
of sensory phenomena and that nociceptive pain is the
sensation that is related to ongoing tissue damage detected
by thermal receptors and mechanoreceptors of the gamma
and C-fiber neurons. He believed that both deafferentation
and nociceptive pain can be increased by stress.
Erickson described 4 categories of pain:
• Projected pain is the pain transmitted along the
course of the nerve that is either segmental (eg,
along the intercostal nerve) or peripheral (eg,
along the ulnar nerve). Other examples are
trigeminal neuralgia and brachial plexus neuralgia.
• Referred pain has been related to irritation of deep
somatic or visceral structures that may cause the
sensation of pain in distant regions that are
innervated by the same neurosegment (eg, angina
referred to the left arm or the jaw, pain referred to
the spine in the case of a duodenal ulcer).
• Reflex pain (causalgic pain) is marked by
hyperalgesia, hyperesthesia, and vasomotor,
sudomotor, and trophic changes (eg, reflex
sympathetic dystrophy).
• Non-organic pain is related primarily to
psychological factors that affect pain sensation
and may be related to anxiety states, depression,
and conversion syndromes.
As suggested by Erickson,59 using this scheme may help
the physical therapist to have an initial idea of what type of
pain problem a patient may have. This examination
establishes the baseline level of the pain problem.
The second reason for evaluating a patient’s pain problem
is to determine whether the intervention that the clinician
is using has altered the pain in significant ways. Obviously,
the two reasons are very closely related. If the intervention
is not planned in a way that will alter the patient’s pain
7
problem, obtaining information about the patient’s pain is
essentially meaningless.
Patient History
During the initial interview, the clinician should ascertain
the patient’s chief complaint or medical diagnosis, the
onset or mechanism of injury, the relevant medical and
surgical history, previous and current treatments that have
been directed at the underlying pathology or sources of
pain, and current and recent medications. In addition, the
clinician should take a careful family, social, and vocational
history to (1) learn the patient’s perception of the effects
that the pain and dysfunction have on these important
areas and (2) identify how pain behavior in the absence of
underlying pathology might be reinforced.
When taking the patient’s history, the clinician should ask
questions to determine whether the pain varies and under
what conditions. The interview includes questions about
the intensity, quality, temporal aspects, and physical
characteristics of the pain. The therapist should attempt to
find out about these 4 pain characteristics by asking the
patient to describe each of them.60
Intensity of pain relates to its severity, whereas quality of
pain relates to characteristics such as whether the pain is
burning, pinching, or pulsing. The temporal aspect of pain
refers to whether pain is constant or whether there are
periodic, intermittent, or brief attacks of pain. Physical
characteristics refer to the location where the pain is
experienced and whether the pain is localized, radiating, or
diffused. Other questions about pain will often require the
patient to determine whether various positions or activities
make the pain worse. The patient also should be asked if
there are some activities that lessen the pain.47,60
A detailed history and a detailed examination may be the
most important aspects of understanding and managing a
patient’s pain problems. Analysis of the pain situation can
be accomplished by asking questions about pain that are
specific and in logical sequence. This method of
questioning helps to develop hypotheses about the cause
of the patient’s pain. The purpose of this reasoning
process is to plan the treatment of the underlying causes
and the symptoms of the patient’s pain. Treatment of
these underlying causes may require consultation or
referral to another health care professional. Leading the
patient through the interview to gain an understanding of
the pain problem also establishes a baseline for future
comparison.20,21,26,47,60
Tests and Measures: Pain Intensity
Physical therapists should be aware of what the Interactive
Guide to Physical Therapist Practice (Guide) says about
pain.61 The “Tests/Measures” section lists a number of
tests and measures that can be used to measure: (1) pain,
soreness, and nociception and (2) pain in specific body
parts. It also provides references to studies of reliability
and validity for many tests and measures and links to the
abstracts in PubMed. The Guide also describes the types
of interventions that physical therapists provide.
According to the Guide, in examining patients with pain,
the clinician may need to measure aerobic
capacity/endurance; circulation; cranial and peripheral
nerve integrity; gait, locomotion, and balance;
integumentary integrity; joint integrity and mobility; muscle
performance (including strength, power, and endurance);
posture; sensory integrity; and ventilation and
respiration/gas exchange. Intact sensation and circulation
are critical to the safe and effective application of many
physical therapy interventions. Sensory or circulatory
dysfunction will often dictate the need for careful selection
of interventions and vigilant observation of safety
precautions. For the purposes of this CE article, the focus
is on the measurement of pain intensity.
Careful, consistent evaluation of the patient’s perception
of the intensity, quality, and distribution of their pain—and
of the variation of pain level related to posture, activity,
medication intake, or time of day—is important in the
assessment of treatment outcomes. Several methods of
pain evaluation are used in the clinical setting.
Verbal, Visual, and Numerical Scales
One method is the simple descriptive scale (SDS), also
called the verbal pain report, uses a 4- or 5-point scale
based on the patient’s selection of a word that best
describes current pain intensity or pain associated with
specific activities or time of day (Fig. 9). The value of this
scale, however, is limited by its lack of sensitivity in
detecting small changes in pain intensity.62,63
The visual analog scale is a 10-cm line, oriented vertically
or horizontally, with one end representing “no pain” and
the other end representing “pain as bad as it can be”
(Fig. 10). The patient is asked to mark a place on the line
corresponding to the current pain intensity.
The numerical rating scale (NRS), shown in Figure 11, is a
verbal or written determination of a pain level on a scale
from 0 to 10, in which 0 represents no pain and 10
represents excruciating pain. Sternbach48 has expanded the
NRS into a pain estimate, based on a numerical rating of 0
to 100, in which 0 is defined as no pain and 100 is defined
as pain “so severe you’d commit suicide if you had to
endure it for more than a minute or two.” The patient is
then asked to describe current or average pain intensity as
a percentage of 100. According to a study by Downie et
al,62 the NRS provides better discrimination of small
changes in pain intensity than the SDS does.
8
The continued use of the NRS seems to show clinicians’
preference for scales that have 11 points or more and
seems to indicate that they believe that rating scales that
have 4 or 5 points are not as reliable.64 When comparing
the VAS with the NRS, some investigators have found that
the NRS is not as sensitive to patients’ ability to express
distress. These investigators, therefore, recommend using
the VAS because it is better suited to parametric analysis
and because it provides a continuous score.63
In a study comparing an 11-point NRS with a VAS in an
emergency room environment, the investigators found that
the NRS could be used by more subjects and showed
better discriminant power than the VAS, particularly in
patients with trauma.65 There was no difference in the
results of the NRS compared with the VAS in patients
without trauma who were seen in the emergency room.65 A
study compared patients’ ratings on a VAS to a 5-point
NRS because these 2 methods are considered to be
equivalent in some environments. The equivalence is based
on the idea that a score of 2 on the 5-point scale would be
seen as a score of 4 on a 10-cm VAS. When the results
were compared, the researchers found that the VAS
ratings were lower than the NRS ratings and that more
than three-fourths of the patients provided ratings that
were not mathematically equivalent, which brought the
interchangeability of the 2 scales into question.66
In a study of the maximum number of levels needed for
pain intensity measurement, Jensen and
colleagues67 compared a 101-point NRS with 11- or 21-
point rating scales. They concluded that the 11- and 21-
point scales provided sufficient levels of discrimination for
patients with chronic pain.67 Ferraz et al68 compared the
use of a VAS and an NRS in 2 groups of patients with
chronic pain—one group was illiterate and one group was
literate—and they found that both groups were able to use
these methods in a reliable fashion, but the NRS had
higher reliability in both groups of patients.
Downie and colleagues62 evaluated the degree of
agreement among the SDS, NRS, and VAS in patients with
rheumatic diseases and found a high correlation among the
3 scales. The scales are simple to understand and do not
demand a high degree of literacy or sophistication on the
part of the patient, unlike other pain measurement tools,
such as the semantic differential scales described below.
The NRS, SDS, and VAS are simple and quick to
administer, and they may be used before, during, and
following treatment to evaluate changes in the patient’s
perception of pain related to treatment. The scales also
may be completed throughout the course of a day to assess
change in pain intensity related to activity or time of day.
Semantic Differential Scales
Semantic differential scales comprise word lists and
categories developed by physicians, students, and patients
that represent the sensory, affective, and evaluative
components of the pain experience.69,70 Words are
categorized by whether they describe temporal, spatial,
pressure, or thermal characteristics of pain (sensory); fear,
anxiety, and tension in the pain experience (affective); and
the overall cognitive experience of pain based on previous
experience and learned behaviors (evaluative). Words
within each category are rank-ordered in terms of intensity.
One of the most commonly used word lists was developed
by Melzack and Torgerson69 for the McGill Pain
Questionnaire (Fig. 12).71 Patients are asked to select a
word in any of 20 categories that best describes their pain
experience. The patient does not have to select all
categories. Several numerical indexes regarding the scope,
quality, and intensity of the pain experience can be
calculated from this inventory. A number-of-words-chosen
score (0-20) is calculated simply by adding up the number
of words selected by a patient. A pain rating index can be
calculated by adding the rank sums of the assigned
intensity values for each of the 3 categories selected or for
all of the categories together.
Semantic differential scales are difficult and time
consuming to complete and demand a sophisticated
literacy level, a sufficient attention span, and a normal
cognitive state. They, therefore, are less convenient to use
in the clinical environment, but they are valuable when a
more detailed analysis of a patient’s perception of pain is
needed, such as in a pain clinic or clinical research setting.
Reliability and Validity of Measurements
Obtained Using Pain Scales
Measurements of phenomena such as pain are often
referred to as a “subjective measurements” when they are
actually measurements of a subjective phenomenon. On
the other hand, if what is being measured has an external
manifestation, such as range of motion or the force a
muscle generates, people often refer to this as an
“objective” measurement when they should be calling it
measurement of an objective phenomenon. Pain,
therefore, is a subjective phenomenon, but if it is measured
reliably, the quality of the measurement would be
objective.72
We can have objective measurements of objective and
subjective phenomena, and we can also have subjective
measurements of subjective and objective phenomena.
The most important issue is that the measurement have as
little error as possible and that means having as much
reliability as possible. The more reliable a measurement,
the more objective the measurement. When the
measurement is not reliable, even if it is of observable
phenomena such as range of motion or muscle force, the
measurement is then subjective. Figure 12 shows how the
quality of the measurement may be either subjective or
9
objective and how a phenomenon being measured may be
subjective or objective.
If the reliability of a measurement is known, the objectivity
of that measurement can be discussed. Frequently,
assumptions are made about objectivity of
measurements.72 Readers should examine the definitions of
subjective measurement and objective measurement found
in APTA’s Standards for Tests and Measurements in Physical
Therapy Practice.73
The issue of reliability has been addressed in numerous
reports,71,74-78 particularly for the VAS and the McGill Pain
Questionnaire. These reports, however, do not lead to a
consensus on the reliability of these measurements. They
suggest that reliability varies based on the patient groups
that were examined for pain. Reliability therefore becomes
an issue of “reliable in whose hands?” Reliability of many
of the pain measurement methods have not been
confirmed beyond that found by the original developers of
the tests and measures.71,74,75(pp63-198),76-78
An expert working group assembled under the auspices of
the research network of the European Association of
Palliative Care reviewed the status of current pain
measurements, and, in their opinion, visual analog scales,
numerical rating scales, and verbal rating scales were all
considered to be valid for measuring pain intensity in
clinical trials and in other types of studies.79 This group
also stated that the McGill Pain Questionnaire, both the
standard form and the long form, were valid because they
were available in many multilingual versions.79
Visual analog scale. Reliability and validity of the VAS
continue to be examined. In a study of reliability and
validity of VAS for acute abdominal pain, subjects were
tested upon admission to the emergency department, 1
minute later, and then in 30-minute increments over a 2-
hour period.80 The subjects were also asked to respond to
a 5-point graded verbal descriptor scale. Validity in this
study was examined by comparing the VAS scores to the
graded verbal descriptor scores. The investigators found
that the scores were closely associated and measured
changes in a linear fashion. There also were assessments of
the VAS scores that were taken 1 minute apart and those
that were taken at 30-minute intervals. Reliability was
reported to be high, with interclass correlation coefficients
of .99 for the 1-minute comparison. The investigators also
found that the minimally clinical significant difference in
acute abdominal pain was 16 mm on the scale. They
concluded that VAS measurements in this study were both
valid and reliable.80
Questions about reliability of the VAS continue to center
on the patient population in which they are used. In
general terms, VAS measurements have been found to be
both valid and reliable. In many studies,80-82 the VAS has
been considered to be the most easily used and is believed
to provide the most reliable measurements of pain
intensity. It therefore has been used to compare new
methods for examining pain or to revalidate currently used
methods.
McGill Pain Questionnaire. Melzack and Katz83 wrote
that the McGill Pain Questionnaire is probably the most
frequently used self-rating instrument for the measurement
of pain in both clinical and research settings. They argued
that research has continued to show that the McGill Pain
Questionnaire provides reliable, valid, and consistent
measurements. The short form also has proven to provide
reliable and valid measurements in those instances when
the intensity of pain is the primary subject of the
examination. These same authors observed that the VAS is
one of the most frequently used measures of pain intensity,
and they felt it also had demonstrated validity and
reliability for the measurement of pain intensity.83
In a study by McDonald and Weiskopf,84 patients were
asked to examine their postoperative pain using the short
form of the McGill Pain Questionnaire. These patients
also were interviewed about their pain. The results of this
study showed that patients used almost exactly the same
words in the interview as they did on the short form. The
authors believed that these results continued to show the
usefulness and reliability of this test for patients to
describe their pain intensity as well as an affective
component of pain.
Faces Pain Scale. In either its original version or in
various revised versions, the Faces Pain Scale (FPS) has
become the most widely used method of assessing pain in
children and is a valuable method for evaluating pain in
children from the age of 4 and upward. In 1990, Bieri et
al85 published their report on the FPS. Their subjects were
children between the ages of 6 and 9 years, and their first
step was to have children perform drawings of facial
expressions of pain. From this beginning, the authors
developed a 7 Faces Scale. By the time they completed
their series of studies, they were convinced that the 7
Faces in their instrument had the properties of a scale, that
the intervals between points were essentially equal, and
that the test/retest data suggested that the instrument
provided reliable measurements. Hunter and McDowell,86
testing the FPS in children who were between preschool
age and 6½ years of age, believed that even young children
could comprehend the scale and that the scale possessed
the ability to discriminate levels of pain.
Various attempts to revise the FPS have been carried out.
Hicks et al87 suggested revising the original number of
faces from 7 to 6. They felt this change made it easier to
compare the FPS with other self-rating and observational
scales that were based on a 0-to-5 or 0-to-10 scaling
matrix. They found a strong correlation when they
10
compared the new 6 Faces Pain Scale with the VAS. They
concluded that the revised FPS was appropriate for use
with children from age 4 and above, particularly with
children in acute pain.
Chambers and Craig88 were concerned that the neutral
point (or the anchor) for children’s pain scales may affect
how children will respond to the pain scale. Pain scales
currently have either of two anchors: a neutral face as the
“no pain” anchor and a smiling face as the “no pain”
anchor. The study concluded that the smiling faces anchor
may affect the child’s concept of pain and, therefore,
prompt a different response to the FPS than the neutral
face anchor.
Chambers and colleagues89 compared the measurement of
pediatric pain using the FPS and parents’ ratings. The
results of this study showed that the smiling pain anchor
causes children to rate their pain at a higher level than the
neutral anchor. These results were similar in parents when
they used the smiling face anchor versus the neutral face
anchor. This study also showed that girls gave a similar
pain experience a higher level of pain than boys and that
the correlations between children’s pain scores and
parents’ pain scores on the same event were low. Both
children and parents in this study showed a preference for
the FPS that they perceived to be happy and cartoon-like.89
In a commentary on this research, Wong and
Baker90 agreed with Chambers and colleagues that
different facial scales may produce several differences in
pain reports; however, they felt that the important thing
was that the FPS allowed children to provide health care
professionals with information about their pain in an
effective manner.
Chambers et al91 also studied the agreement between
children’s and parents’ reports of pain with patients who
were 7 to 12 years old who underwent surgery. This study
showed that parents tend to underestimate their children’s
pain on the day of surgery and the day following surgery,
but on the second day after surgery, there was agreement
between parent and child on pain ratings. The authors
were concerned that the parents’ underestimation of their
child’s pain may contribute to inadequate pain control for
children.
Herr and colleagues92 decided that the FPS might be a
useful measure of pain intensity when used with an elderly
population. They studied a group of community-dwelling
elderly people who were 65 years of age or older. The
subjects were asked to rank-order the faces in the scale to
expected pain levels, and the investigators found that the
ability of the subjects to do this was supported at a higher
level. Subjects were asked to rate the degree of perceived
pain from a vividly remembered painful experience using
the FPS, and then they were asked to rate the same
experience 2 weeks later. In this part of the experiment,
the FPS demonstrated strong reproducibility, with a
Spearman rho correlation coefficient of .94. The authors
concluded that this result supported the idea that the use
of the FPS with the elderly would provide reliable
measurements; however, they were not sure that the
equality of the intervals in the FPS have been fully
supported in older adults. They stated that further
investigation of the use of FPS with the elderly was
justified.
The quest for pain questionnaires continues unabated. In
1995, Sullivan and colleagues93 developed a Pain
Catastrophizing Scale (PCS). A factor analysis of the PCS
by van Damme et al94 looked at what factors were
important in this scale. The validation study was done on 3
Dutch-speaking samples: 550 were students who were free
of pain, 162 were patients with chronic low back pain, and
100 were patients with fibromyalgia. The three factors they
found were labeled “rumination,” “magnification,” and
“helplessness.” They believed that all 3 factors were
present across all samples. They felt that there was more
work to be done linking castrophizing as a psychological
concept to the experience of pain.
A lack of clear reliability information should not prevent
the clinician from using these methods, but clinicians
should be aware that a particular measurement may not be
reliable with a particular patient or a group of patients. The
clinician also should ensure that health care professionals
who use the measurements for their own purposes will be
aware of the limitations of these measurements.47
A difficult aspect of reliability is that the patient may have
developed a different understanding of the pain problem
and may give a different response from one examination
to the next. It is equally important for examiners to ask
themselves whether the interpretation of the patient’s
responses differs from one examination to the next. Both
of these factors affect the reliability of the data being
gathered.47
Logs
The patient’s rating of pain relative to changing postures,
activities of daily living, work, recreation, and social
activities, and time of day is important in identifying
factors that aggravate or relieve pain and may help identify
the functional or structural sources of pain that can then
be treated. Patients can complete daily activity or pain logs
and medication intake records before beginning treatment,
and they can maintain these logs both during an episode
of care and after discharge from services. Improvement in
a patient’s performance of activities is at least as important
as improvement in pain rating, particularly in documenting
efficacy of treatment for reimbursement.95 These logs also
can reveal causes of exacerbations of pain or signs of
malingering in the face of otherwise effective treatment.
11
Spatial Distribution of Pain
The patient may indicate the spatial distribution of pain by
filling in a body diagram (Fig. 13). Different colored
pencils or symbols may be used to distinguish superficial
pain from deep pain or sharp pain from dull pain. These
diagrams help determine the etiology and structural
sources of pain, and they may be used to document the
location for the application of certain modalities (eg,
electrode placements for electroanalgesic
interventions).75(pp190-197) Although the diagrams may be
used to indicate certain bony landmarks to help patients
accurately describe the location of pain, they should not be
labeled with dermatome, myotome, or peripheral nerve
distributions, because these labels can often lead the
patient to fill in a specific distribution that may not
necessarily reflect the true location of the pain.
In part I of the McGill Pain Questionnaire, the patient is
asked to indicate where on the body diagram the pain is
located and is asked to place an “E” or an “I” to indicate
whether the pain is external or internal (indicating deep
somatic pain).
One observation about patient-generated pain diagrams is
that the amount of time and care that the patient takes may
indicate something about the psychological overtones of
pain for the patient.2,71,74 Some investigators,96-100 therefore,
have used pain diagrams to distinguish symptoms and
signs of physical disease from signs of distress and illness
behavior. Eggebricht et al,101 however, believed that the
pain drawing provides an excellent way to assess where the
patient experiences pain, and they have recommended that
pain drawings be used to document the location of the
patient’s pain and the amount of surface area involved in
the pain rather than to measure psychopathology.101
Those investigators who advocate the latter view feel that,
through the patient’s pain diagram, the clinician can (1)
gain information about the stability of a patient’s pain over
time and (2) assess the effectiveness of treatment. In
addition to having the patient mark “E” or “I” to indicate
external or internal pain, some investigators have asked
patients to use intensity markings of 1 to 10, with 1 being
the least amount of pain and 10 indicating the most pain.
Still others have asked patients to use a variety of symbols
to indicate different characteristics of pain, such as zeros
for “pins and needles,” dashes for “numbness,” and Xs for
“burning” pain.75
Barrack et al96 conducted a study to determine the
frequency of pain that patients attributed to their hip after
a total hip arthroplasty. Patients did a pain drawing to
localize the area of their symptoms, and the degree of pain
was quantified using a VAS.96 A great deal of other patient
data was collected, including clinical and radiographic data
and data about age, sex, and activity level, to see whether
anything other than the total hip arthroplasty correlated
with the pain drawing. The results of this study indicated
that the type of stem fixation from the total hip
arthroplasty was the only parameter that was statistically
correlated with a higher incidence of thigh pain. Patients
with proximally coated stems were more than twice as
likely to report pain than patients with a fully coated or
cemented hip. Although the incidence of thigh pain was
significantly higher in this group, the severity of pain was
not significantly higher. The results of this study appear to
indicate that a higher percentage of patients who received
proximal coated stems perceived pain originating in the
hip.
Ohnmeiss et al97 examined the relationship between
patient self-report measures—Oswestry Low Back Pain
Disability Questionnaires (ODQ) and pain drawings—and
functional testing using an isokinetic dynamometer.97
Subjects in this study were patients who were entering a
physical rehabilitation program. They found that patients
with greater scores on pain drawings, particularly those
with unusual pain patterns, performed more poorly during
the isokinetic testing than those with normal drawings.
The authors believed that the use of pain drawings
combined with the ODQ showed that the isokinetic test
values were significantly influenced by the patient’s self-
reported disability and pain expression as demonstrated by
these 2 measures.
Ohnmeiss98 also did a study of the repeatability of pain
drawings on a patient population with low back pain. The
subjects in this study were patients who were considered to
have chronic low back pain. The subjects completed a pain
drawing at the beginning of their interventions and
repeated the pain drawing at some time in the future. The
mean time between the first and second drawings was 244
days. The authors reported that the pain drawings
completed on these widely separated occasions were highly
repeatable, and they felt that this supported the reliability
of pain drawings for the use with patients with chronic low
back pain.
Ohnmeiss et al99 also studied the relationship between pain
location on a pain drawing and disk pathology. A group of
patients who were to undergo computed tomography for
the 3 lowest lumbar levels for diagnostic purposes filled
out a pain drawing on the day of the test. The analysis of
Ohnmeiss et al showed that the pain drawings are helpful
in identifying which specific disk areas are associated with
pain complaints. They also noted that, as with any other
method of examination, these drawings should be
considered only in combination with findings from other
tests and measures. For example, the percentage of
patients who reported pain in the posterior thigh or leg but
not in the anterior leg on their pain drawing and who had a
positive discographic finding for the L5-S1 disk was
greater than or equal to 75%. In contrast, Rankine and
colleagues100 found that a pain drawing correctly classified
12
only 58% of patients with nerve compression. They
concluded that pain drawings are not a good predictor of
nerve compression in patients who are examined by
magnetic resonance imaging for back and leg pain.
Pain drawings continue to be used primarily in
musculoskeletal problems, and they appear to be used
frequently with patients who have low back pain with or
without radiating pain. Because of the contradictory nature
of the studies on reliability and validity, clinicians who wish
to use pain drawings will need to have a fairly good idea of
the consistency of the patient in reporting pain overall (eg,
from other tests) before they can determine whether this
method is helpful.
Pain Inventories
Several pain inventories that combine the variety of pain
measurements described above are available for clinical
use. The McGill Pain Questionnaire is a widely used pain
inventory that combines pain intensity rating scales,
semantic differential scales, spatial diagrams, and open-
ended interview questions.71 A short form of this
questionnaire was published to make it easier to
use.102 Mannheimer and Lampe75(pp190-197) also suggested
components of a pain inventory for convenient clinical
use; however, no data about this instrument have been
published in the current literature.
Psychological Factors
As understanding of psychological factors in pain has
expanded, so has the investigation of these factors. Two
brief examples will suffice. First, the use of the concept of
locus of control, which has been helpful in understanding
people’s health behavior, has been expanded to examine
the relationship of locus of control to responses to
pain.103 Second, the factors of introversion and
extroversion as personality types and a person’s responses
to pain based on these factors have been examined.104 As
the understanding of the psychological aspects of pain and
the use of the biopsychosocial model expands, physical
therapists need to understand these interrelationships,
particularly if they are working in an interdisciplinary
framework in the treatment of pain.
The locus of control has been studied in a variety of
situations.105,106 The original studies of locus of control
were primarily of the person’s overall psychology. This
concept was then expanded to include the healthy locus of
control. The study of back pain management by Layell107
looked particularly at patient satisfaction with the services.
This study showed that subjects who had a stronger
internal locus of control had a more positive outlook on
the outcome of their treatment and were more satisfied
with services that were provided.
Coughlin et al108 studied whether a multidisciplinary
treatment of patients with pain could change their locus of
control. They used an instrument called the Pain Locus of
Control Scale (PLCS). Seventy-three patients with chronic,
nonmalignant pain completed questionnaires before and
after treatment in the comprehensive, multidisciplinary
pain management program. Two of the objectives of the
pain management program were to see if a patient’s
perceptions of personal control over pain could be
increased from the pretreatment to the posttreatment time
and to see if a patient’s perception of external control over
pain, such as fate or powerful people, decreased from
pretreatment to posttreatment. The study concluded that
patients’ beliefs about pain could be altered to increase
their “self-efficacy” in control of pain and to decrease their
attribution of their pain problems to external sources.
Gibson and Helme109 reported on a study of the use of the
PLCS in older people. One of their objectives was to
compare the responses of older people to this scale
compared with those of younger people. One hundred
sixty-nine older patients who were attending a pain
management clinic completed the PLCS scale along with
several other psychometric tests at admission. During the
time the patients were in the treatment program, they were
encouraged to orient their locus of control internally. The
results of this study showed that the orientation of
patients’ locus of control was related to their use of coping
strategies and their expression of levels of pain and
depression. The authors stated that cognitive factors
seemed to be of importance in older patients with chronic
pain and that the use of this scale might lead to better
understandings of the cognitive behavioral models of pain
and how older patients with chronic pain fit into these
models.
Evaluation
After completing the examination—including a history, a
systems review, and selecting and administering tests and
measures—to gather information about the patient,
physical therapists begin the evaluation (ie, making a
clinical judgment based on the data that has been gathered
during this examination).61 These 2 processes are essential
before the process of diagnosis and prognosis begins. The
diagnostic and prognostic process is often cautious in
patients with pain because of the great abundance of
information gathered and because the origin of the
patient’s pain is sometimes unclear.
There has been a gradual shift in how physical therapists
approach certain pain problem areas.110,111 This is most
evident in the area of low back pain. Because low back
pain is one of the more common problems seen by many
physical therapists, it is probably worth discussing the
trends in thinking in this area. There has been increasing
interest in using classification systems rather than
pathologic diagnosis for categorizing patients with low
13
back pain.110,111 Classification systems are designed for a
variety of purposes that may include determining the
appropriate intervention, assisting in prognosis, identifying
pathology, or placing a patient into a homogeneous group
based on selected variables. In a review of the literature
and an analysis of systems of classification, Riddle111
suggested that further research will be needed before the
usefulness of classification systems can be determined.
New or existing systems may be helpful in managing
patients with low back pain. Fritz110 reported on the use of
a classification system to guide the treatment of 3 patients
with low back syndrome. She concluded that the
identification of the appropriate classification of the
patient led to the use of appropriate intervention and that
classification systems based on these 3 cases showed
promise of being helpful in patient management.110
Another trend in pain management is the use of functional
outcomes measures rather than assessing the
characteristics of the patient’s pain in isolation.112-117 Many
investigators112-116 have suggested the use of a variety of
instruments—including the Roland-Morris Disability
Questionnaire, the Oswestry Low Back Pain Disability
Questionnaire and its modified version, and the Quebec
Back Pain Disability Scale—to assess improvements in
people with low back pain. In addition to these methods,
the Resumption of Activities of Daily Living Scale has
been applied to patients with acute low back pain.117 These
scales and questionnaires show that, in some ways, the
focus of the examination of patients with pain is shifting
toward the examination of the patient’s function during
and following interventions by physical therapists.
Part 2 addresses using the examination and evaluation
results to develop the plan of care, with a case example
that focuses on a patient who had a hyperextension injury
to the knee and developed complex regional pain
syndrome (CRPS), formerly called reflex sympathetic
dystrophy syndrome (RSDS).
References
1 IASP terminology page. International Association for the
Study of Pain Web site. Available at: http://www.iasp-
pain.org/terms-p.html. Accessed October 22, 2003.
2 Bowsher D. Nociceptors and peripheral nerve fibers. In:
Wells PE, Frampton V, Bowsher D, eds. Pain Management in
Physical Therapy. Norwalk, Conn: Appleton & Lange; 1988:18-21.
3 Nolan MF. Anatomic and physiologic organization of neural
structures involved in pain transmission, modulation, and
perception. In: Echternach JL, ed. Pain. New York, NY:
Churchill Livingstone Inc; 1987:8-9.
4 Basebaum AI, Jessell TM. The perception of pain. In: Kandel
ER, Schwartz JH, Jessell TM. Principles of Neural Science. 4th
ed. New York, NY: McGraw-Hill; 2000:473-491.
5 Price DD, Hu JW, Dubner R, Gracely RH. Peripheral
suppression of first pain and central summation of second pain
evoked by noxious heat pulses. Pain. 1977;3:57-68.
6 Torebjork HE. Afferent C units responding to mechanical,
thermal, and chemical stimuli in human non-glabrous skin. Acta
Physiol Scand. 1974;92:374-390.
7 Van Hees J, Gybels J. C nociceptor activity in human nerve
during painful and non-painful skin stimulation. J Neurol
Neurosurg Psychiatry. 1981;44:600-607.
8 Gybels J, Handwerker HO, Van Hees J. A comparison
between the discharges of human nociceptive nerve fibers and
the subject’s ratings of his sensations. J Physiol. 1979;292:193-
206.
9 Rexed B. The cytoarchitectonic organization of the spinal
cord in the cat. J Comp Neurol. 1952;96:415-495.
10 Light AR, Perl ER. Reexamination of the dorsal root
projection to the spinal dorsal horn including observations on
the differential termination of coarse and fine fibers. J Comp
Neurol. 1979;186:117-131.
11 Light AR, Perl ER. Differential termination of large-diameter
and small-diameter primary afferent fibers in the spinal dorsal
gray matter as indicated by labeling with horseradish peroxidase.
Neurosci Lett. 1977;6:59-63.
12 Melzack R, Wall PD. Pain mechanisms: a new theory. Science.
1965;150:971-979.
13 Wall P. The dorsal horn. In: Wall PD, Melzack R, eds.
Textbook of Pain. New York, NY: Churchill Livingstone Inc;
1984:80.
14 Nathan PW, Wall PD. Treatment of post-herpetic neuralgia
by prolonged electrical stimulation. Br Med J. 1974;3:645-657.
15 Niv D, Ben-Ari S, Rappaport A, et al. Postherpetic neuralgia:
clinical experience with a conservative treatment. Clin J Pain.
1989;5:295-300.
16 Thorsteinsson G. Chronic pain: use of TENS in the elderly.
Geriatrics. 1987;42:75-77, 81-82.
17 Carmichael JK. Treatment of herpes zoster and postherpetic
neuralgia. Am Fam Physician. 1991;44:203-210.
18 Nathan PW, Rudge P. Testing the gate-control theory of pain
in man. J Neurol Neurosurg Psychiatry. 1974;37:1366-1372.
19 Kerr FW. Pain: a central inhibitory balance theory. Mayo Clin
Proc. 1975;50:685-690.
20 Iggo A. Critical remarks on the gate control theory. In: Payne
JP, Burt RAP, eds. Pain. London, England: J&A Churchill;
1972:127.
14
21 Melzack R, Casey KL. Sensory, motivational, and central
control determinants of pain. In: Kenshalo DR, ed. The Skin
Senses: Proceedings of the International Symposium on Skin Senses,
1966, Florida State University. Springfield, Ill: Charles C Thomas
Publisher; 1968:423-443.
22 Melzack R. Pain: an overview. Acta Anaesthesiol Scand.
1999;43:800-884.
23 Melzack R. From the gate to the neuromatrix. Pain.
1999;suppl 6:S121-S126.
24 Loeser JD, Melzack R. Pain: an overview. Lancet.
1999;353:1607-1609.
25 Melzack R, Coderre TJ, Katz J, Vaccarino AL. Central
neuroplasticity and pathological pain. Ann NY Acad Sci.
2001;933:157-174.
26 Basbaum AI, Fields HL. Endogenous pain control
mechanisms: review and hypothesis. Ann Neurol. 1978;4:451-462.
27 Mayer DJ, Price DD, Rafii A. Antagonism of acupuncture
analgesia in man by the narcotic antagonist naloxone. Brain Res.
1977;121:368-372.
28 Sjolund B, Terenius L, Ericksson M. Increased cerebrospinal
fluid levels of endorphins after electro-acupuncture. Acta Physiol
Scand. 1977;100:382-384.
29 Sjolund BH, Ericksson MB. The influence of naloxone on
analgesia produced by peripheral conditioning stimulation. Brain
Res. 1979;173:295-301.
30 Salar G, Job I, Mingrino S, et al. Effect of transcutaneous
electrotherapy on CSF beta-endorphin content in patients
without pain problems. Pain. 1981;10:169-172.
31 Facchinetti F, Sandrini G, Petraglia F, et al. Concomitant
increase in nociceptive flexion reflex threshold and plasma
opioids following transcutaneous nerve stimulation. Pain.
1984:19:295-303.
32 O’Brien WJ, Rutan FM, Sanborn C, Omer GE. Effect of
transcutaneous electrical nerve stimulation on human blood
beta-endorphin levels. Phys Ther. 1984;64:1367-1374.
33 Hansson P, Ekblom A, Thomsson M, Fjellner B. Influence of
naloxone on relief of acute oro-facial pain by transcutaneous
electrical nerve stimulation (TENS) or vibration. Pain.
1986;24:323-329.
34 Ulett GA, Han S, Han JS. Electroacupuncture: mechanisms
and clinical application. Biol Psychiatry. 1998;44:129-138.
35 Wang JQ, Mao L, Han JS. Comparison of antinociceptive
effects induced by electroacupuncture and transcutaneous
electrical stimulation in the rat. Int J Neurosci. 1992;65:117-129.
36 Proctor ML, Smith CA, Farquhar CM, Stones RW.
Transcutaneous electrical nerve stimulation and acupuncture for
primary dysmenorrhoea. Cochrane Database Syst Rev.
2002;(1):CD002123.
37 Han JS, Terenius L. Neurochemical basis of acupuncture
analgesia. Ann Rev Pharmacol Toxicol. 1982;22:193-220.
38 Zborowski M. People in Pain. San Francisco, Calif: Jossey-Bass;
1969.
39 Melzack R, Dennis SG. Neurophysiological foundations of
pain. In: Sternbach RA, ed. The Psychology of Pain. New York, NY:
Raven Press; 1978:1-26.
40 Bond MR. Psychological and psychiatric aspects of pain.
Anaesthesia. 1978;33:355-361.
41 Fordyce WE. Pain viewed as learned behavior. In: Bonica JJ,
ed. International Symposium on Pain, 1973,
Issaquah, Washington. New York, NY: Raven Press; 1974:417.
Advances in Neurology; vol 4.
42 Fields HL. Pain: Mechanisms and Management. New York, NY:
McGraw-Hill Inc; 1987:150, 251-303, 309, 319-320, 327.
43 Weisberg MB, Clavel AL. Why is chronic pain so difficult to
treat? Pyschological considerations from simple to complex care.
Postgrad Med. 1999;106:141-142, 145-148, 157-160.
44 Michel TH. Evaluation of chronic pain patients. In: Wittink
H, Michel TH, eds. Chronic Pain Management for Physical
Therapists. Boston, Mass: Butterworth-Heinemann; 1997:chap 4.
45 Materson RS. Techniques for assessing and diagnosing pain.
In: Weiner RS, exec ed. Pain Management: A Practical Guide for
Clinicians. Vol 1. 5th ed. Boca Raton, Fla: St Lucie Press;
1998:chap 6.
46 Biewen PC. A structural approach to low back pain: a
thorough evaluation is the key to effective treatment. Postgrad
Med. 1999;106:102-107, 111-114.
47 Echternach JL. Clinical evaluation of the patient in pain.
Physical Therapy Practice. 1993;2:14-26.
48 Sternbach RA. Pain Patients: Traits and Treatment. New
York, NY: Academic Press Inc; 1974.
49 Sternbach RA, Deems LM, Timmermans G, Huey LY. On
the sensitivity of the tourniquet pain test. Pain. 1977;3:105-110.
50 Moore PA, Duncan GH, Scott DS, et al. The submaximal
effort tourniquet cast: its use in evaluating experiemental and
chronic pain. Pain. 1979;6:375-382.
51 Rosenblatt RM, Hetherington A. Failure of transcutaneous
electrical stimulation to alleviate experiemental tourniquet pain.
Anesth Analg. 1981;60:720-722.
15
52 Walsh DM, Liggett C, Baxter D, Allen JM. A double-blind
investigation of the hypoalgesic effects of transcutaneous
electrical nerve stimulation upon experimentally induced
ischemic pain. Pain. 1995;61:39-45.
53 Johnson MI, Tabasam G. A single-blind placebo-controlled
investigation into the analgesic effects of interferential current
on experimentally induced ischemic pain in healthy subjects. Clin
Physiol Funct Imaging. 2002;22:187-196.
54 Gracely RH. Pain research and therapy. In: Bonica JJ,
Ventafridda V, Fink BF, et al, eds. International Symposium on Pain
of Advanced Cancer, 1978, Venice, Italy. New York, NY: Raven
Press; 1979:805-824. Advances in Pain Research and Therapy; vol 3.
55 Hardy JD, Wolff HG, Goodell H. Pain Sensations and
Reactions. Baltimore, MD: Williams & Wilkins; 1952.
56 Kast EC. An understanding of pain and its measurement. Med
Times. 1966;94:1501-1503.
57 Perkins KA, Grobe JE, Jennings JR, et al. A technique for
rapid reliable assessment of thermal pain threshold in humans.
Behavior Research Methods, Instruments and Computers. 1992;24(1);60-
66.
58 Pienimaki TT, Siira PT, Vanharanta H. Chronic medical and
lateral epicondylitis: a comparison of pain, disability, and
function. Arch Phys Med Rehabil. 2002;83:317-321.
59 Erickson RK. The physical examination of the patient in pain.
In: Camic PM, Brown FD, eds. Assessing Chronic Pain: A
Multidisciplinary Clinic Handbook. New York, NY: Springer-Verlag;
1989:71-90.
60 Echternach HL. Evaluation of pain in the clinical
environment. In: Echternach JL, ed. Pain. New York, NY:
Churchill Livingstone Inc; 1987:37-72.
61 Interactive Guide to Physical Therapist Practice, With Catalog of Tests
and Measures. Version 1.1. Alexandria, Va: American Physical
Therapy Association; 2003.
62 Downie WW, Leatham PA, Rhind VM, et al. Studies with
pain rating scales. Ann Rheum Dis. 1978;37:378-381.
63 Good M, Stiller C, Zauszniewski JA, et al. Sensation and
Distress of Pain Scales: reliability, validity, and sensitivity. J Nurs
Meas. 2001;9(3):219-238.
64 Raphael J, Southall J, Gnanadurai T, et al. Long-term
experience with implanted intrathecal drug administration
systems for failed back syndrome and chronic mechanical low
back pain. BMC Musculoskele Disord. 2002;3(1):17.
65 Berthier F, Potel F, Leconte P, et al. Comparative study of
methods of measuring acute pain intensity in an ED. Am J Emerg
Med. 1998;16:132-136.
66 Carpenter JS, Brockopp D. Comparison of patients’ rating
and examination of nurses’ responses to pain intensity rating
scales. Cancer Nurs. 1995;18:292-298.
67 Jensen MP, Turner JA, Romano JM. What is the maximum
number of levels needed in pain intensity measurement? Pain.
1994;58:387-392.
68 Ferraz MB, Quaresma MR, Aquino LR, et al. Reliability of
pain scales in the assessment of literate and illiterate patients
with rheumatoid arthritis. J Rheumatol. 1990;17:1022-1024.
69 Melzack R, Torgerson WS. On the language of pain.
Anesthesiology. 1971;34:50-59.
70 Tursky B. The development of a pain perception profile: a
psychophysical approach. In: Weisenberg M, Tursky B, eds. Pain:
New Perspectives in Therapy and Research. New York, NY: Plenum
Press; 1976:171.
71 Melzack R. The McGill Pain Questionnaire: major properties
and scoring methods. Pain. 1975;1:277-299.
72 Rothstein JM, Echternach JL. Primer on Measurement: An
Introductory Guide to Measurement Issues. Alexandria, Va: American
Physical Therapy Association; 1993.
73 Standards for Tests and Measurements in Physical Therapy
Practice. Phys Ther. 1991;71:589-622.
74 Melzack R. The McGill Pain Questionnaire. In: Melzack R,
ed. Pain Measurement and Assessment. New York, NY: Raven Press;
1983:41-47.
75 Mannheimer JS, Lampe GN. Clinical Transcutaneous Electrical
Nerve Stimulation. Philadelphia, Pa: FA Davis Co; 1984:63-198,
406.
76 Sternbach RA. The tourniquet pain test. In: Melzack R, ed.
Pain Measurement and Assessment. New York, NY: Raven Press;
1983:27-32.
77 Grossman SA, Sheidler VR, McGuire DB, et al. A
comparison of the Hopkins Pain Rating Instrument with
standard visual analogue and verbal descriptor scales in patients
with cancer pain. J Pain Symptom Manage. 1992;7:196-203.
78 Anton F, Euchner I, Handwerker HO. The psychophysical
examination of pain induced by defined CO2 pulses to the nasal
mucosa. Pain. 1992;49:53-60.
79 Caraceni A, Cherny N, Fainsinger R, et al. Pain measurement
tools and methods in clinical research in palliative care:
recommendations of an expert working group of the European
Association of Palliative Care. J Pain Symptom Manage.
2002;23:239-255.
80 Gallagher EJ, Bijur PE, Latimer C, Silver W. Reliabiity and
validity of a visual analog scale for acute abdominal pain in the
ED. Am J Emerg Med. 2002;20:287-290.
16
81 Lingjaerde O, Foreland AR. Direct assessment of
improvement in winter depression with a visual analog scale:
high reliability and validity. Psychiatry Res. 1998;81:387-392.
82 Singer AJ, Thode HC Jr. Determination of the minimal
clinically significant difference on a patient visual analog
satisfaction scale. Acad Emerg Med. 1998;5:1007-1011.
83 Melzack R, Katz J. The McGill Pain Questionnaire: appraisal
and current status. In: Turk DC, Melzack R, eds. Handbook of
Pain Assessment. 2nd ed. New York, NY: Guilford Press; 2001.
84 McDonald DD, Weiskopf CS. Adult patients’ postoperative
pain descriptions and responses to the Short-Form McGill Pain
Questionnaire. Clin Nurs Res. 2001;10:442-452.
85 Bieri D, Reeve RA, Champion GD, et al. The Faces Pain
Scale for the self-assessment of the severity of pain experienced
by children: development, initial validation, and preliminary
investigation for ratio scale properties. Pain.1990;42:139-150.
86 Hunter M, McDowell L, Hennessy R, Cassey J. An evaluation
of the Faces Pain Scale with young children. J Pain Symptom
Manage. 2000;20:122-129.
87 Hicks CL, von Baeyer CL, Spafford PA, et al. The Faces Pain
Scale–Revised: toward a common metric in pediatric pain
measurement. Pain. 2001;93:173-183.
88 Chambers CT, Craig KD. An intrusive impact of anchors in
children’s Faces Pain Scales. Pain. 1998;78:27-37.
89 Chambers CT, Giesbrecht K, Craig KD, et al. A comparison
of faces scales for the measurement of pediatric pain: children’s
and parents’ ratings. Pain. 1999;83:25-35.
90 Wong DL, Baker CM. Smiling faces as anchor for pain
intensity scales [letter to the editor]. Pain. 2001;89:295-300.
91 Chambers CT, Reid GJ, Craig KD, et al. Agreement between
child and parent reports of pain. Clin J Pain. 1998;14:336-342.
92 Herr KA, Mobily PR, Kohout FJ, Wagenaar D. Evaluation of
the Faces Pain Scale for use with the elderly. Clin J Pain.
1998;14:29-38.
93 Sullivan MJL, Bishop SO, Pivele J. The Pain Catastrophizing
Scale: development and validation. Psychol Assess. 1995;7:524-532.
94 van Damme S, Crombez G, Bijllebeir P, et al. A confirmatory
factory analysis of the Pain Catastrophizing Scale. Pain.
2002;96(3):325-328.
95 Nolan MF. Documenting patient care with transcutaneous
electrical nerve stimulation: suggestions for reducing
reimbursement denials. Clinical Management in Physical Therapy.
1988;8(4):16-19.
96 Barrack RL, Paprosky W, Butler RA, et al. Patients’
perception of pain after total hip arthroplasty. J Arthroplasty.
2000;15:590-596.
97 Ohnmeiss DD, Vanharanta H, Estlauder AM, Jamsen A. The
relationship of disability (Oswestry) and pain drawings to
functional testing. Eur Spine J. 2000;9:208-212.
98 Ohnmeiss DD. Repeatability of pain drawings in a low back
pain population. Spine. 2000;25:980-988.
99 Ohnmeiss DD, Vanharanta H, Ekholm J. Relation between
pain location and disc pathology: a study of pain drawings and
CT/discography. Clin J Pain. 1999;15:210-217.
100 Rankine JJ, Fortune DG, Hutchinson CE, et al. Pain
drawings in the assessment of nerve root compression: a
comparative study with lumbar spine magnetic resonance
imaging. Spine. 1998;23:1668-1676.
101 Eggebricht DB, Bautz MT, Brenny ID, et al. Psychosomatic
evaluation. In: Camic PM, Brown FD, eds. Assessing Chronic Pain:
A Multidisciplinary Clinic Handbook. New York, NY: Springer-
Verlag; 1989:71-90.
102 Melzack R. The short-form McGill Pain Questionnaire. Pain.
1987;30:191-197.
103 Seville JL, Roberson AB. Locus of control in the patient
with chronic pain. In: Gatchel RJ, Weisberg JN, eds. Personality
Characteristics of Patients With Pain. Washington, DC: American
Psychological Association; 2000:chap 7.
104 Phillips JM, Gatchel RJ. Extroversion-introversion and
chronic pain. In: Gatchel RJ, Weisberg JN, eds. Personality
Characteristics of Patients With Pain. Washington, DC: American
Psychological Association; 2000:chap 8.
105 Nyland J, Johnson DL, Caborn DN, Brindle T. Internal
health status belief and lower perceived functional deficit are
related among anterior cruciate ligament deficient patients.
Arthroscopy. 2000;18:515-518.
106 Rybarczyk B, DeMarco G, DeLaCruz m, et al. A classroom
mind/body wellness intervention for older adults with chronic
illness: comparing immediate and 1-year benefits. Behav Med.
2001;27:15-27.
107 Layzell M. Back pain management: a patient satisfaction
study of services. Br J Nurs. 2001;10:800-807.
108 Coughlin AM, Badura AS, Fleischer TD, Guck TP.
Multidisciplinary treatment of chronic pain patients: its efficiency
in changing patient locus of control. Arch Phys Med Rehaibl.
2000;81:739-740.
109 Gibson SJ, Helme RD. Cognitive factors and the experience
of pain and suffering in older persons. Pain. 2000;85:375-383.
17
110 Fritz JM. Use of a classification approach to the treatment
of 3 patients with low back syndrome. Phys Ther. 1998;78:766-
777.
111 Riddle DL. Classification and low back pain: a review of the
literature and critical analysis of selected systems. Phys Ther.
1998;78:708-737.
112 Stratford PW, Binkley JM, Riddle DL, Guyatt GH.
Sensitivity to change of the Roland-Morris Back Pain
Questionnaire: part 1. Phys Ther. 1998;78:1186-1196.
113 Riddle DL, Stratford PW, Binkley JM. Sensitivity to change
of the Roland-Morris Back Pain Questionnaire: part 2. Phys Ther.
1998;78:1197-1207.
114 Delitto A. Subjective measures and clinical decision making.
Phys Ther. 1989;69:585-589.
115 Fairbank JC, Couper J, Davies JB, O’Brien JP. The Oswestry
Back Pain Disability Scale. Physiotherapy. 1980;66:271-273.
116 Kopec JA, Esdaile JM, Abrahamowicz M, et al.
The Quebec Back Pain Disability Scale: measurement properties.
Spine. 1995;20:341-352.
117 Williams RM, Myers AM. A new approach to measuring
recovery in injured workers with acute low back pain:
Resumption of Activities of Daily Living Scale. Phys Ther.
1998;78:613-623.
MANAGEMENT OF THE
INDIVIDUAL WITH PAIN:
PART 2—TREATMENT
Introduction/Eradicating the Source of
Pain
Careful, consistent examination of the patient with pain—
which was discussed in detail in part 1—is the cornerstone
of identifying the underlying pathology or source of pain.
Once this source has been identified, a plan of care can be
devised to eradicate the source of pain, promote healing of
injured tissues, and help the patient achieve an optimal
level of physiological and psychological function. If the
source of pain involves a nonmodifiable condition (eg,
ankylosing spondylitis, phantom limb pain following
amputation), the primary foci of treatment are (1)
modifying the patient’s perception of what constitutes a
reasonable amount of discomfort and (2) maximizing
function within the physical limitations imposed by the
source of pain.
The Joint Commission on the Accreditation of Health
Care Organizations (JCAHO) recently issued new
standards for pain assessment and pain management in
accredited health care organizations, including hospitals
and hospice and home care settings.1,2 The standards
underline the needs of patients with pain in all areas and
include the following:
• patients have the right to appropriate assessment
and management of pain,
• all patients are examined for the existence of pain,
• the health care organization records pain
assessments and treatment in a manner that will
lead to regular follow-up care,
• the health care organization determines and
ensures staff competency in pain assessment and
management and that the orientation of all new
staff includes the ability to address pain
assessment and management,
• patients and their families are educated about
effective pain management.
The JCAHO standards on pain care are a response to the
rising concern that certain groups are not having their pain
management problems addressed.3 These groups include
not only patients at the end of their life, but also patients at
risk, including newborns, children, and the elderly. Some
have said that the new standards have made pain the fifth
vital sign.4
Eradicating the Source of Pain
Frequently, the underlying pathology can be directly
addressed by medical, surgical, or rehabilitation
interventions. For example, pain secondary to appendicitis
is eliminated once the infected appendix has been
surgically removed. Similarly, pain secondary to a tumor or
neuroma impinging on a nerve can be eliminated by
removal of the offending tissue. Pain resulting from soft
tissue injuries or fractures can be reduced by realignment
of the injured tissues, followed by rest, reduction of
inflammation, and promotion of healing. Reduction of
inflammation and promotion of healing may be achieved
through a variety of pharmaceutical and physical therapy
interventions.
In other cases, the source of pain may be structural
malalignment (eg, poor posture, scoliosis, sacroiliac joint
separation) or movement dysfunction (eg, faulty body
mechanics, gait deviations secondary to structural or
functional abnormalities). Although the optimal treatment
to alleviate pain in these cases is correction of the
structural or functional deficit, it may be necessary to
address pain directly before the patient is able to
participate in a rehabilitation program. In these cases, pain
may result from abnormal pressure on peripheral nerves,
muscle spasm and associated impaired circulation,
accumulation of tissue irritants, or local inflammation of
18
the acutely or chronically injured structures. The specific
causes of pain are identified and treated before, or
simultaneously with, the correction of the structural or
functional deficit. Treatment outcomes are assessed using
the various pain evaluation measures described in part 1 as
well as by physical and functional assessments of muscle
force, mobility, endurance, and performance of daily
activities.
It is beyond the scope of this article to describe in detail all
of the sources of pain and all of the treatment
interventions available to the physical therapist. Several
common sources of pain and suggested treatment
interventions, however, are discussed below to aid the
reader’s development of treatment planning.
Pain Secondary to Inflammation, Vascular
Congestion, or Muscle Spasm (Acute
Muscular Strain)
Pain secondary to acute soft tissue injury is usually
exacerbated by an accumulation of tissue irritants,
including bradykinin and histamine, that are released
locally in response to injury. These irritants excite free
nerve endings that transmit pain along small-diameter
afferent fibers to the central nervous system (CNS). In
addition, histamine is a potent vasodilator, and its presence
results in an initial increase in circulation to the injured
area. Blood and lymph fluid accumulate in the injured
tissues, and edema results. Muscles are resistant to
movement, and additional pain is caused by splinting to
immobilize and protect the injured tissues and an
accumulation of fluid and tissue irritants. This pain-spasm
cycle is a common target of early physical therapy
interventions and may be addressed in several ways.
Normal metabolic balance and circulation may be restored
by a variety of techniques. If edema is identified as a
source of pain secondary to pressure on nerves, the
physical therapist may minimize capillary leakage and
blood flow into the area by applying superficial cold
modalities, compression, and elevation of the body part
above the heart to aid passive venous return. The body
part often is immobilized to minimize metabolic demand
and further reduce blood flow into the region.
After the first 24 to 48 hours after the injury, capillary
leakage usually is not a major concern, and the foci of
treatment are restoration of normal metabolic
homeostasis, removal of tissue irritants through the
promotion of blood flow through the region, and
relaxation of muscle spasm. If the injured tissues lie within
the most superficial centimeter of skin, superficial heat—in
the form of hot packs, whirlpool therapy, paraffin, or
infrared radiation—may be applied to accelerate blood
flow into and out of the region. Manual massage of the
soft tissues helps move fluid and tissue irritants out of the
area and helps relax muscles in spasm by providing
comfortable sensory input and by relieving pain as
hypothesized by the gate control theory of pain. (See
Part 1).
If the injured tissues lie under the first centimeter of skin,
deep-heating modalities, including ultrasound and
diathermy, may be indicated to improve local circulation
and remove tissue irritants. The application of
electroanalgesic modalities also may be indicated to relieve
pain (as hypothesized by the gate control theory or
through stimulation-produced analgesia) and prepare the
patient for active participation in exercise or functional
activities. Electrical stimulation of motor nerves in the area
may aid muscle contraction and enhance venous return.
Clinicians, however, should take care to avoid passively
exercising acutely injured tissues using electrical
stimulation, if activity may result in additional injury. Some
evidence indicates that some forms of electrical
stimulation, including high-voltage pulsed current (HVPC)
and microamperage stimulation, enhance circulation and
aid wound healing.5-12 These mechanisms may account for
the pain relief often reported by patients who undergo
these treatments. It should be emphasized, however, that
the analgesic properties of microamperage electrotherapy
have not been validated by well-controlled clinical studies.
There has been considerable controversy on whether the
evidence shows that electrical stimulation speeds the
healing of wounds. The controversy, however, has not
addressed the topic of whether electrical stimulation of
wounds relieves pain from the wound. It would seem
obvious, however, that whatever helps speed the healing of
the wound would help hasten the day when the wound
was no longer a cause of pain for the patient. The Center
for Medicare and Medicaid Services (CMS) recently issued
a decision on the use of electrical stimulation in
wounds.13 The CMS decision basically said that the use of
electrical stimulation on chronic stage-3 and stage-4
pressure ulcers, arterial ulcers, diabetic ulcers, and venous
ulcers would be covered under Medicare. Chronic ulcers
were defined as ulcers that did not heal within 30 days of
occurrence. Under the ruling, electrical stimulation will not
be covered as the initial treatment modality. Instead, it will
be covered as an adjunct to therapy only after there are no
measurable signs of healing for at least 30 days of
treatment with standard wound therapy. The CMS
decision was the result of a controversy with the American
Physical Therapy Association and other groups that
supported the use of electrical stimulation in wound care
that lasted for more than 5 years.
In 1999, Gardner and colleagues14 reported the results of a
meta-analysis of articles on the effects of electrical
stimulation on chronic wound healing. After examining 15
studies, they found that patients who received electrical
stimulation showed an average rate of healing per week
19
that was far greater than the average rate of healing in the
control subjects. They concluded that electrical stimulation
produced a substantial improvement in the healing of
chronic wounds, but they did not believe that there was
any evidence to say which type of electrical stimulation
device was the most effective in promoting wound healing.
In a review article on the role of the physical therapist in
managing patients with wounds, McCulloch15 argued that
physical therapists should remain involved in wound care
and that they were a major untapped resource in this area.
In addition to providing physical agents for the treatment
of wounds, McCulloch said that physical therapists’
background knowledge of biomechanics would enhance
the services of any wound care team, because they could
advise the team about the need to redistribute pressure or
relieve pressures for patients who are confined to bed or a
wheelchair or who are ambulatory but have loss of
sensation in their feet.
Once pain is adequately relieved, the patient may be
directed to actively participate in an exercise or other
rehabilitation program to restore soft tissue strength,
flexibility, and integrity and to prevent further injury.
Pain Secondary to Structural
Malalignment or Movement Dysfunction
Once the structural or functional deficit has been
identified as the source of pain, the primary focus of
physical therapy is to correct the deficit. This may be done
through active exercise, passive tissue elongation,
positioning with orthotic devices (eg, shoe inserts or lifts),
instruction in proper kinesiological movement (eg, gait
training, assessment and correction of biomechanical
problems in the workplace), intermittent or static spinal
traction to elongate paraspinal tissues and relieve
impingement on nerve roots, or mobilization to restore
proper accessory motion in joints, thus allowing correct
kinesiological function. Pain associated with these deficits
may be addressed before, or simultaneously with, an active
rehabilitation program using some of the treatments
described above. Ultimately, the responsibility for
restoration and maintenance of optimal function through
ongoing conditioning and appropriate activity should rest
with the patient. Patient education, motivation, and
compliance are key elements in this type of treatment
scheme.
Pain Secondary to Peripheral Nervous
System Pathology (Phantom Limb Pain,
Complex Regional Pain Syndrome, and
Sensory Deprivation Syndromes Such as
Peripheral Neuropathies or Nerve
Injuries)
Pain associated with peripheral nervous system pathology
often occurs because of hyperactivity along small-diameter
afferent fibers or hypoactivity along the large-diameter
afferent fibers. According to the gate control theory,16 pain
reaches the higher centers and is perceived as a result of
the imbalance between comfortable and noxious impulses
reaching the dorsal horn. The afferent information that
ultimately reaches the sensory cortex and is perceived as
painful may be modified at the peripheral level by
augmenting large-diameter fiber activity and “closing the
gate,” minimizing small-diameter afferent activity by
treating the source of pain or modifying the neurological
information anywhere along the afferent pathways in the
CNS.
A variety of treatment interventions augment comfortable
sensory input along large-diameter afferent fibers. These
interventions include electroanalgesic methods (eg,
transcutaneous electrical nerve stimulation [TENS],
HVPC), massage, and comfortable tactile stimulation,
including superficial heat, tapping, or vibration.
Modification of pain perception at the CNS level may
include redirecting the patient’s attention away from the
pain and toward another thought or activity, teaching the
patient autogenic (self-directed) relaxation through
electromyographic or temperature biofeedback, imagery,
or hypnosis.
Phantom limb pain illustrates the importance of identifying
the source as well as neurophysiological mechanisms of
the pain experience to optimally modify pain perception
and enhance rehabilitation potential. Phantom limb pain
provides an excellent example of a source of pain that
originates as a peripheral nervous system (sensory
deprivation) problem but is exacerbated by hyperactivity of
the sympathetic nervous system. Phantom limb pain is
more likely to occur in patients who have had a traumatic
amputation or a therapeutic amputation following
prolonged and painful trauma than in patients with
congenital malformations. The pain may appear to occur
anywhere in the absent limb and also has been reported
following any interruption of the afferent pathway between
the periphery and the sensory cortex (eg, spinal cord
injury, peripheral nerve injury). Pain is described as
jabbing, stabbing, piercing, burning, or electrical and may
be aggravated by fatigue, anxiety, ischemia, fear, urination,
defecation, and ejaculation.17
It follows that pain relief may be provided by
augmentation of comfortable sensory input and reduction
20
of sympathetic nervous system activity. Indeed, patients
with phantom limb pain report a reduction in pain
associated with rubbing, tapping, and vibration of the
residual limb or contralateral limb.17 Transcutaneous
electrical nerve stimulation has also been used successfully
in the management of phantom limb pain.18-20
Kawamura and colleagues21 reported on the use of TENS
in relieving phantom limb pain. In their study, the
contralateral limb was stimulated in the same area where
the patients reported pain in the amputated limb. The
authors studied 10 subjects—8 had lower-extremity
amputations and 2 had upper-extremity amputations—
who had severe phantom limb pain that hampered
prosthetic use and ambulation training. The average length
of treatment was 9 weeks, and subjects reported significant
changes in their visual analog scale ratings from
pretreatment to posttreatment times. Patients stated that
not only was the degree and duration of their pain
reduced, the area of the pain also was reduced. These
effects led to having better use of their prostheses and
improved the time spent in walking activities.
Halbert et al22 conducted a systematic review of the
evidence for the optimal management of acute and chronic
phantom pain. Their search identified 12 published from
1966 to 1999 trials that included 375 patients with follow-
ups ranging from 1 week to 2 years. Of these 12 trials, 3
used TENS as part of their treatment. Halbert et al
concluded that 70% of patients have phantom limb pain
after amputation, but they found little evidence from
randomized trials about the most appropriate treatment.
They concluded that a gap exists between research and
practice in the treatment of phantom limb pain, which
underlines the need for continued research, especially
randomized controlled studies.
Patients who undergo immediate postoperative fitting of a
pylon and early preprosthetic training also increase
comfortable afferent input and report milder phantom
limb pain and a less frequent incidence of pain. Patients
also report that redirection of attention, relaxation,
avoidance of anxiety-producing situations, and stress
reduction contribute to reduction of phantom limb pain.
In this case, pain relief may be considered a means to an
end. If the patient is free of pain, he or she is more likely
to be active and participate in a rehabilitation program.
Increased activity levels also increase comfortable afferent
input, thus “closing the gate” and perpetuating analgesia.
Pain Secondary to Underlying Pathology
That Cannot Be Modified With Treatment
Patients with pain secondary to incurable diseases or
nonmodifiable conditions may be taught to have
alternative responses to their pain. The focus of treatment
is a change in the patient’s behavior (eg, providing
alternative responses to the pain experience). The patient is
taught to cope with pain by understanding its course and
by avoiding responses that may aggravate the pain, such as
tension, stress, or anger. The patient is instructed in
relaxation techniques, often using imagery or
electromyographic or temperature biofeedback, to change
his or her response from one of fear or anxiety
(sympathetically mediated) to one of relaxation and
control.23 Redirection of attention, distraction,
psychotherapy, and hypnosis provide additional
alternatives. If the patient can learn to reduce the
sympathetically mediated response to pain, the
accompanying muscle spasm and increases in vasomotor
tone—which often exacerbate the pain—may be reduced,
and the patient may perceive a degree of control over pain.
Pain reduction associated with these interventions may be
explained by the important role that descending pain
inhibitory pathways play in pain perception and
modulation.24
The role of biopsychosocial assessment in the treatment of
painful conditions has received a lot of attention recently.
A review article by Keefe et al25 reviewed research on
patients with osteoarthritis and rheumatoid arthritis. Some
of the topics that were reviewed in this article included
coping with pain, handling stress, dealing with depression,
and dealing with a patient who has learned that
“helplessness” gets them something. The article also
reviewed the efficacy of the biopsychosocial treatment
approaches for these conditions. Keefe noted that patients
with arthritis vary in their involvement in self-management
efforts. Some research that Keefe examined has suggested
that patients with arthritis can be distributed into
subgroups that may predict their willingness to participate
in pain coping skills training, exercise interventions, and
other forms of self-management. He also felt that there
was a relationship between the stage of the patient’s
arthritis and his or her willingness to be involved in self-
management of pain. Keefe suggested that spouse-assisted
coping skills interventions in patients with osteoarthritis
may be a way to improve their coping with their disease as
well as to improve self-efficacy. There were individual
differences spouse assisted coping skills training noted
over the long term, which may have been related to the
couples’ marital satisfaction. Research has apparently
shown that there is a relationship between the perceived
effectiveness of pain coping and the patient’s most recent
experiences of daily pain and mood. Both of these factors
are related to self-efficacy ratings collected from patients
with arthritis.
A great deal of attention has been paid in the literature to
the problems of patients with chronic work-related
musculoskeletal pain disability, particularly patients with
low back pain. Dersh and colleagues26 pointed out that the
majority of the patients with chronic work-related
musculoskeletal pain disability have an associated
psychiatric disorder. The psychiatric disorders in fact are
21
diagnosable, and this population is different than the
general population in many ways. Clinicians who are
working with these patients should be prepared to refer
these patients to a mental health professional. The
biopsychosocial approach is a multidisciplinary approach
that includes psychological treatment as well as treatment
by pain specialists and physical therapists.
According to Turk and Okifuji,27 research has
demonstrated the importance of coping in maintaining
quality of life and decreasing disability in chronic pain.
They further state that the biopsychosocial model of
chronic pain helps patients in the self-management of their
pain and other related problems. These authors argue that
psychologists can make an important contribution to the
treatment of these patients in a multidisciplinary
environment.
Eccleston,28 in reviewing the role of psychology in pain
management, discussed the concept of cognitive
behavioral therapy (CBT), and he emphasized the
importance of a team approach. His model includes
anesthesiologists, clinical psychologists, and physical
therapists. Part of CBT is directed at creating an
environment that minimizes situations where patients’ pain
behaviors are reinforced. The emphasis in CBT is on the
positive reinforcement of “well behavior” and not on the
reinforcement of “sick behavior.” Eccleston also reviewed
some of the evidence on the use of CBT with chronic pain
available in reviews and meta-analyses. In one meta-
analysis of 25 studies that he cited, CBT produced positive
effects in all domains that were measured compared with
control groups that received no treatment.29 Compared
with other treatments, CBT produced significant effects
for the domains of pain coping and pain behavior. The
meta-analysis concluded that this amounts to good
evidence for the effectiveness of CBT for chronic pain
management in adult patients.
Others have reviewed the effectiveness of the
biopsychosocial approach. A systematic review by
Guzman and colleagues30 looked at the multidisciplinary
rehabilitation of chronic low back pain. In reviewing 10
randomized controlled trials that reported 12 randomized
comparisons of multidisciplinary treatment in a controlled
condition, they found strong evidence that intensive
multidisciplinary biopsychosocial rehabilitation improved
function when it was compared with inpatient or
outpatient treatments that were not multidisciplinary.
Guzman et al also stated that there was moderate evidence
that intensive multidisciplinary biopsychosocial
rehabilitation with functional restoration reduces pain to a
greater extent than outpatient rehabilitation that was not
multidisciplinary or “usual” care. They also noted that less
intensive outpatient psychosocial treatments did not
improve pain or function when compared with outpatient
therapy that was not multidisciplinary. They also stated
that there were few trials that looked at the effects of
treatment on quality of life.
Nielson and Weir31 came to similar conclusions in looking
at biopsychosocial approaches in the treatment of chronic
pain. They suggested that future studies, in order to clarify
the effectiveness of these treatments, should be condition-
specific rather than include patients with different pain
conditions in the same study group. Because these subject
groups were not homogeneous and because outcome
measurements were similarly variable, the researchers felt
that comparison of studies was difficult.
A systematic review of the effects of biopsychosocial
rehabilitation of upper-limb strain injuries in working-age
adults was conducted by Karjalainen et al.32 They
concluded that there was little scientific evidence for the
effectiveness of the biopsychosocial rehabilitation on
repetitive strain injuries. They further stated that high-
quality trials in this area are needed. The same
authors33 also reported on a systematic review of the
biopsychosocial rehabilitation of neck and shoulder pain
among working-age adults, and they reached the same
conclusion. They found little scientific evidence on the
effectiveness of multidisciplinary biopsychosocial
rehabilitation compared with other rehabilitation methods
in relieving neck and shoulder pain.33 They concluded that
there also was a need for high-quality trials in this area.
Both biofeedback and hypnosis continue to be used by
some clinicians in managing patients with chronic pain. A
recent article by Deepak and Behari34 looked at the
problem of hand dystonia and the effects of
electromyographic (EMG) biofeedback on this condition.
Deepak and Behari34 found that EMG was effective in
reducing the abnormal EMG values in 10 of 13 patients.
Pain was assessed by a visual analog scale as well as the
ability to improve handwriting. Only one patient did not
show any improvement.
Wickramasekera,35 in discussing the relationship between
biofeedback and clinical symptoms, stated that the
reduction in clinical symptoms was related not to the
magnitude of the change in physiological factors (eg,
EMG, electroencephalogram, temperature), but to other
factors. He stated that, if both the patient and the therapist
believe in the efficacy of the therapy, then the therapy has
a chance of being more effective. He also talked about the
response of the patients based on “hypnotic ability.” He
said that the biofeedback could be hypothesized as most
effective in reducing clinical symptoms in subjects who
had low to moderate hypnotic ability and that those who
have high hypnotic ability should be instructed in
autogenic training, progressive muscle relaxation, and
other methods that allow them to control their pain
symptoms.
22
Montgomery et al36 conducted a meta-analysis of 18
studies on the effectiveness of hypnosis-induced analgesia.
They found a moderate to large hypnoanalgesic effect and
concluded that these techniques were useful in pain
management. They suggested that there should be broader
application of hypnoanalgesic techniques in treatment of
patients with pain.
Pain in the Absence of an Identified
Source
When a patient experiences pain and portrays pain
behavior in the absence of an underlying pathology,
treatment is directed toward modification of the pain
symptoms and behaviors. An illness behavior syndrome
has been identified in patients with chronic pain.37,38 The
concept of illness behavior seems to be well established
and is discussed in general terms in current texts on pain
topics.39-41 Components of this syndrome include (1)
dramatization of complaints, which leads to overtreatment
and overmedication; (2) progressive dysfunction, which
leads to decreased physical activity and often compounds
pre-existing musculoskeletal or circulatory dysfunction; (3)
drug misuse; (4) progressive dependency on others,
including health care professionals, that leads to overuse of
the health care system; and (5) income disability, in which
the patient’s illness behavior is perpetuated by the desire
for financial gain.39,42
Behavior modification—using principles of operant and
respondent conditioning to alter a patient’s perception of,
and response to, pain—is often the treatment of choice for
patients displaying illness behavior syndrome. The goals of
behavior modification are to decrease the incidence of pain
behaviors by removing all positive reinforcements for
these behaviors and to increase the incidence of wellness
behaviors by providing and selectively reinforcing a
repertoire of healthy, socially acceptable, and beneficial
behaviors.
A behavioral pain therapy program is implemented in
several steps.43 Spanswick and Parker41 described
interdisciplinary approaches to pain management in a
variety of settings. First, the patient’s resistance to
behavioral change is identified and defused by education,
counseling, support, and sometimes psychotherapy. The
patient and family members are then provided information
to help them identify the multifaceted nature of the pain
experience. They learn that pain is not only physical
(sensory) in nature, but that it also has behavioral, social,
verbal, and financial components. They begin to identify
the components that positively reinforce illness behaviors
and how this reinforcement perpetuates the pain. The
patient and family are then helped to set realistic short-
term goals—steps toward normalization of behavior.
These goals may include reduction in pain medication
intake, increased recreational and vocational activity levels,
increased socialization time, and other behaviors
associated with health and well-being. The patient then
must be taught wellness behaviors to substitute for pain
behaviors. The patient is taught coping skills to help
change his or her responses to pain. The patient may be
taught somatic relaxation through biofeedback, imagery,
self-hypnosis, or other cognitive means. A realistic activity
or exercise program may be prescribed in which the
patient is expected to participate daily. Dietary
modifications may be suggested. A medically supervised
narcotic detoxification program is often included in a
comprehensive pain therapy approach.
The positive reinforcements that previously has
perpetuated pain behaviors are withdrawn. This may be
accomplished through strategies such as family education
regarding appropriate display of caring and concern
without sympathetic support of pain behaviors. Disability
income may be reduced or withdrawn. Positive
reinforcement, in the form of family praise, support,
receipt of a massage, or other pleasant treatment, follows
the patient’s consistent display of wellness behaviors (eg,
increases in activity, decrease in medication intake) and
thus perpetuates wellness behaviors. To be effective, a
positive reinforcement must be something that is valued by
the patient. Finally, the patient is provided the opportunity
to practice wellness behaviors and coping skills in
environments other than the health care facility. The
patient and family are encouraged to integrate the practices
learned in the pain therapy program within the home and
vocational environment. Reinforcement for wellness
behaviors rather than for illness behaviors should continue
in these environments until the patient is able to reinforce
healthy attitudes and responses on his or her own.
It is useful to integrate the principles of behavior
modification into the traditional medical model of
treatment and, in many patients, perhaps prevent the
development of chronic pain behavior. Pain medications
are usually prescribed on a pain-contingent basis (ie, the
patient is instructed to take pain medication as needed).
Therefore, the patient perceives pain in order to take the
medication. To modify the requirement of pain,
medication should be prescribed on a time-contingent
basis (ie, medication should be taken every so often,
whether or not the patient is experiencing pain). The
schedule of medication should be based on the source and
severity of pain and should be prescribed often enough so
that the patient does not feel significant pain before taking
more medication. As the physical source of pain is treated
or heals, the dosage or its frequency can be diminished.
Physical therapists often prescribe exercise or activity
programs that are too challenging, and the patient often
refuses to participate. Exercise programs should be
23
established that are well within the patient’s capabilities in
order for the patient to successfully complete a program
and feel good about his or her accomplishments. Success
within a program that requires some work but that can be
successfully completed encourages continued participation
in exercise, activity, and other wellness behaviors.
Physical therapists are in the position to provide excellent
positive reinforcement for successful completion of tasks
or improved wellness behavior. The physical therapist can
provide the patient with comfortable treatments, such as
heat or massage, following completion of a prescribed activity
rather than preceding the activity. In this way, the therapeutic
intervention serves as a positive reinforcement for wellness
behaviors—not for pain behaviors. The clinician’s
enthusiastic but realistic praise for a patient’s successful
completion of a task is also a powerful reinforcement and
ultimately will be replaced by the patient’s own sense of
satisfaction and self-worth.
The Pain Clinic
Frequently, pain therapy programs are organized within a
pain clinic. The pain clinic approach involves a health care
team consisting of a physician, a psychologist, a social
worker, a nurse, and possibly a vocational rehabilitation
counselor, physical therapist, occupational therapist, or
recreational therapist. The patient and his or her family are
also members of the pain clinic team. The team is
responsible for patient examination, establishment of
realistic goals, education and treatment leading to
attainment of these goals, and follow-up once the patient
has been discharged from the pain clinic environment.
Pain clinics may be inpatient or outpatient environments.
In order to provide the patient with 24-hour supervision
and medical attention, most narcotic detoxification
programs are part of inpatient pain clinics. Many pain
clinics, however, are outpatient-based to allow the patient
to practice coping skills and wellness behaviors in the
home environment from the beginning of the
rehabilitation process.
The physical therapist in the pain clinic may be responsible
for evaluating the physical capabilities of the patient; for
establishing, instructing, and supervising exercise and
activity protocols in which the patient participates; and for
providing positive reinforcement for successful
completion of these challenges.
Additional Interventions
Placebo
The term “placebo” is derived from the Latin verb placere
(“to please”). In clinical terms, a placebo is defined as a
sham treatment that resembles an actual treatment but is
known to be ineffective for the patient’s condition.44 The
patient’s favorable response to a placebo may be
accounted for by the factors of hope and expectation
inherent in the treatment process.45 Placebo treatments are
used as control interventions in clinical trials to determine
the efficacy of a therapeutic intervention. They may also be
used therapeutically to facilitate a patient’s belief that he or
she is “feeling better” or “healing” when an active
treatment may not be in the patient’s best interest or when
it is contraindicated.
For a placebo to be effective, patients must believe that
they are receiving an actual treatment. This may involve
substituting an inert substance for actual medication in a
capsule or pill or applying electrodes from
electrotherapeutic equipment without activating the
current source.
Several factors influence the placebo response. Some
patients will respond to placebo analgesia in certain
situations and not in others. Increases in pain intensity or
related anxiety have been shown to increase the likelihood
of a favorable response, perhaps because the motivation to
respond favorably is increased.46-48 In the treatment of
patients with pain, placebo effects have been discussed.
Generally speaking, there has been difficulty in defining
placebo satisfactorily. Some authors49 have held that in a
clinical trial placebos are generally control treatments with
a similar appearance to the intervention or research
treatment but without the same specific activity. Some
authors35 have noted that placebo effects occur in nearly
any treatment situation, particularly if both the patient and
the practitioner administering the treatment believed in the
treatment.
In an article evaluating the importance of placebo effects
in pain treatment and research, Turner et al47 came to the
following conclusions. They stated that placebo effects
influence patients’ outcomes after any treatment, including
surgery, and that this led both the patient and the clinician
to believe that treatments were effective. They also stated
that placebo effects, combined with a natural tendency for
conditions to improve, often result in high rates of
successful outcomes and that these could be misattributed
to specific treatment effects. They argued that there was an
inadequate number of randomized clinical trials to know
the true cause of improvement in pain treatment.
In a controlled study of chronic low back pain, Marchand
and colleagues46 evaluated whether TENS effects were
purely placebo effects. They assigned patients randomly to
24
3 groups: a group that received TENS, a group that
received placebo TENS, and a control group that received
no treatment. Pain ratings on a visual analog scale were
taken before and after each treatment session. At the end
of the experiment, Marchand et al concluded that TENS
was significantly more effective than placebo TENS in
reducing pain intensity. They also found an additive effect
in the TENS group—as patients received repeated
treatment sessions, there was a greater decrease in pain
intensity and the relative unpleasantness of pain in the
TENS group than in the placebo TENS group. Patients
were evaluated in their home environment at the end of
the experiment rather than in the clinic environment 1
week after treatment had been discontinued. They found
that the TENS group continued to have significant
reduction in pain intensity compared with the placebo
TENS group. This, however, was not true 3 and 6 months
later.
Ernst and Resch,48 discussing the topic of true and
perceived placebo effects, commented that placebos
repeatedly have been shown to have greater effects on pain
than on other symptoms. They also stated that many
clinical trials lack a clear distinction between placebo
groups and control groups that receive no treatment. They
felt that the placebo response, when it is described in a
trial, should take into account the natural course of the
disease, the regression toward the mean of the
characteristic under investigation, and other nonspecific
effects. They also stated that the placebo effect is highly
variable and that the inclusion of a second untreated
control group to compare it with a placebo control group
is desirable if there are no ethical objections.
A study by Hrobjartsson and Gotzsche49 reported in the
New England Journal of Medicine raised the question of
whether placebos are as powerful as has been supposed in
the past and has started a new debate about the role and
usefulness of placebo treatments. These authors conducted
a systematic review of clinical trials in which patients were
randomly assigned to either placebo or no treatment
groups. The study groups included pharmacologic,
physical, and psychological placebos. One hundred and
thirty trials met their inclusion criteria. In the trials that
used a physical placebo, the procedure that was performed
most frequently was a treatment with a machine that was
turned off (eg, sham TENS). As the authors examined the
results of their study, they stated that only the 27 trials
concerning the treatment of pain showed significant
effects of placebo compared with no treatment. They also
stated that small trials reported that the placebo had the
greatest effect. Overall, they found little evidence that
placebos have powerful clinical effects in general.
In an editorial, Bailar50 argued that Hrobjartsson and
Gotzsche perhaps were too sweeping in their
interpretation of their findings and that, as long as
placebos provided relief of pain in some patients, they
could not be condemned as a treatment method wholesale.
Bailar, however, also noted that there should be a careful
justification for use of placebos, particularly in the clinical
setting. The author also wondered about the difference in
placebo effects in a research setting and in clinical settings.
Expectation of analgesia, based on a patient’s past
experience with a related treatment or on enthusiastic
suggestion of success by the clinician, will enhance the
placebo response. Other factors that enhance the placebo
response include associated side effects (eg, nausea,
dizziness, or sedation) and a high-powered, technologically
advanced professional environment. Finally, testimonials
of treatment efficacy from valued health care
professionals, family, friends, or celebrities also add
credence to the placebo treatment.
There certainly is an element of placebo response with any
treatment administered by a caring, concerned clinician
who communicates enthusiastic belief in the efficacy of
treatment. The placebo response is an efficacious
component of patient management and may be used
ethically and effectively as long as it is identified and the
placebo administration is in the best interest of the patient.
Neurosurgical Interventions for Pain
Neurosurgery directed specifically at alleviating pain, rather
than at treating its source, has met with varying degrees of
success. Neurosurgical electrical stimulation of pain-
inhibitory sites along peripheral nerves, on the dorsal
columns, and in the deeper regions of the brain (ie,
periventricular gray matter of the caudal diencephalon,
sensory portion of the thalamus) carries with it the risks of
infection and leakage of the cerebrospinal fluid. Although
the effectiveness of this intervention has been impressive
in animal models, surgeons have found it difficult to
isolate and stimulate strictly pain-inhibitory centers. The
long-term benefit of this surgery has been poor.51(p319-320) A
review of surgical treatment of intractable pain was
conducted by Davis and colleagues52 noted that a variety
of both ablative and stimulation procedures have relieved
pain. Tasker53 observed that pharmacological approaches
and the advent of deep brain stimulation have decreased
the number of destructive neurosurgical lesions.
A brief review of the literature on neurosurgical
approaches to pain management reveals rather uneven
results of these procedures in different areas. In a study of
extradural sensory rhizotomy in the management of
chronic lumbar radiculopathy, Wetzel and
colleagues54 found that, 6 months after surgery, 28 of the
51 patients in their study believed that they had good
results, whereas the remainder felt that they had poor or
failed outcomes. At a 2-year follow-up, only 19% of the 37
patients available for follow-up felt that they had
maintained good or excellent outcomes. The authors
25
concluded that the results of the rhizotomy procedures
deteriorated over time and that they could not recommend
with confidence that this procedure would have successful
outcomes.
Neurosurgery continues to be utilized as a method of pain
relief. A variety of methods have been tried and spinal
cord stimulation seems to be gaining favor for use in
chronic and neuropathic pain. A variety of studies using
spinal cord stimulation for relief of pain have been
conducted.55-61 With a small sample of 29 patients, Kavar
et al55 found that 50% of their patients felt that they had
received benefit in their chronic pain syndrome from this
procedure. Spinal cord stimulation has been used for
nonspecific limb pain as well as neuropathic pain.56 Kim
and colleagues57 defined success as a greater than 50%
reduction in pain for 1 year. In a series of patients they
studied who received spinal cord stimulation, this
reduction occurred in 83% of patients with nonspecific leg
pain, in 89.5% of patients with limb pain associated with
root injury, and in 73.9% of patients with neuropathic
nerve pain. They concluded that spinal cord stimulation
was as effective in treating nonspecific limb pain as it was
for treating neuropathic pain including limb pain
associated with nerve root damage.
In a review article on spinal cord stimulation for chronic
pain, Deer58 believed that the method was gaining favor as
a first-line therapy to control pain produced by many
conditions. In his opinion, this development occurred
because the intervention had no addictive component or
systemic side effects. He also noted that there have been
technological advances in how spinal cord stimulation is
being done and that the use of multilead or multielectrode
arrays has improved the results. He also noted that the
technique has been used for a variety of conditions, from
complex regional pain syndrome to radiculopathies,
angina, and ischemic extremity pain.
Several other studies have found that patients derive
significant pain relief from spinal cord stimulation but a
certain number of patients require surgical revisions
because of technological and biological factors. One
study59 reported that complication rates from spinal cord
stimulation for chronic pain have declined to
approximately 8% and that re-operation was necessary in
approximately 4% of patients. According to North and
Wetzel,60 spinal cord stimulation provided an important
treatment option for patients that was chronic pain with
mostly neuropathic in origin and had a topographical
distribution involving the extremities. It also has been
noted that spinal cord stimulation should be used only
when less costly therapies have failed to provide the
appropriate relief from pain.61
Neurosurgical ablation of structures along the pain
pathways also has had limited success. Ablation of the
peripheral nerve sensory root ganglion has been attempted
for relief of intractable pain; however, this procedure did
not account for additional nociceptive input or
augmentation from higher centers, other peripheral
regions, sympathetic activation, or deficits in the
descending pain-inhibitory systems.51 Similarly, ablation of
the second-order neurons of the lateral spinal thalamic
tract has failed to produce permanent analgesia because of
incomplete ablation of all of the fibers of the tract.
Ablation of higher centers active in pain perception,
including thalamotomy, prefrontal lobotomy, and
cordectomy, has resulted in pain relief for some patients
with intractable pain from cancer. This very invasive
procedure carries with it the significant risk of disability
and is used only in patients with a limited life expectancy;
therefore, duration of analgesia has not been adequately
evaluated.51
Analgesic Medications
It is beyond the scope of this article to review in detail the
wide variety of pharmaceutical agents used in managing
patients with pain. However, it is important for the
physical therapist to (1) identify which medications a
patient may be taking, (2) have a solid understanding of the
medication’s target regions, (3) identify significant,
common side effects that affect, impede, or contraindicate
physical therapy interventions, and (4) be aware of the
risks associated with certain medications. Ciccone’s44 text
offers excellent information about the major categories of
medication used to manage pain and identifies target
tissues, common side effects, and risks.
Other Interventions
Additional case reports are available in the literature that
demonstrate other approaches to pain relief utilized by
physical therapists.62,63 One of these reports describes the
treatment of neuropathic pain in a patient with diabetic
neuropathy using TENS applied to the skin of the lumbar
region.62 This case report addresses an area in which
physical therapists have thought that effective treatment
was not available. One of the primary benefits outlined in
the report was that the patient was able to sleep through
the night without being awakened by pain in her lower
extremities.62
Case Example
The principles described in the examination and
intervention sections of this article are applied below to a
case history describing a patient with complex regional
pain syndrome (CRPS).
Complex Regional Pain Syndrome
CRPS is a condition that may occur following injury,
especially to an extremity.64 This condition encompasses a
group of symptoms that have been called reflex
26
sympathetic dystrophy (RSD) and, on occasion, also
known as causalgia when there has been nerve injury. In
1993, the International Association for the Study of Pain
determined that the term CRPS would be preferable to the
terms used at that time.65 This syndrome is a devastating
pain condition in which a limb is often rendered useless by
intractable pain and associated trophic changes. Although
not always the case, CRPS frequently occurs following a
partial or complete nerve injury (causalgia) and includes
trauma, associated pain, and immobilization (either
imposed or volitional). A hallmark of CRPS is the obvious
disruption of a normal balance of sympathetic nervous
system activity in the area of the injury, possibly triggered
by abnormal synapses (ephapses) that form between
primary afferent nerve fibers and sympathetic efferent
fibers in close proximity with each other.51(p150),66
As CRPS progresses, the limb becomes exceedingly painful
and hyperesthetic, with the patient protecting the limb
from all stimuli and functional activity. The condition is
marked by hyperactivity of the sympathetic efferents,
resulting in local vasoconstriction, cyanosis, lowered skin
temperature, hyperhidrosis, disruption of hair and nail
growth, and associated skin, muscle, and bony
atrophy.51(p150) Indeed, near-normal characteristics of
function of the limb of patients with CRPS have been
restored by the blocking of sympathetic efferent activity,
either by temporary sympathetic ganglion block or
sympathectomy.67 The final phase of CRPS is
characterized by a decrease in pain, with a predominance
of bony and muscular atrophy, rendering the limb
essentially useless.
CRPS has been divided into 2 separate categories: type 1
and type 2. The type 1 category refers primarily to
conditions that were exhibited under RSD and includes the
presence of 4 characteristics:
(1) the presence of an initiating event such as a painful
injury or immobilization of a body part because of
injury
(2) continuing pain or hyperalgesia that is
disproportionate to the event that caused it
(3) evidence of edema, changes in skin blood flow, and
abnormal pseudomotor activity in the painful region
after the initial injury
(4) diagnosis is excluded by the existence of conditions
that would otherwise account for the degree of pain
and dysfunction.65
According to the International Association for the Study
of Pain, 3 of the 4 characteristics—specifically
characteristics 2, 3, and 4—should be present. Type 2
CRPS has essentially the same 3 characteristics mentioned
above, without the presence of an initiating noxious event
or cause for immobilization of the extremity. For type 2
designation, all 3 characteristics must be present.65
The first concern of a treating practitioner in dealing with
CRPS is prevention, which usually includes directing
treatment to the site of the injury and prevention of
secondary infection if necessary.68 Early and effective
analgesia for the area involved and, unless the severity of
the injury indicates immobilization, active motion are
desirable in mild and moderate trauma. Harden68 has noted
that early and aggressive treatment is often helpful and
that, with proper treatment, the syndrome may be kept
from progressing.
Some physicians69 suggest using sympathetic blockade,
particularly with lidocaine or intravenous regional
sympathetic blockade when indicated, to manage this
condition. The intervention should be performed under
the supervision of a physician, most likely an
anesthesiologist, experienced in this technique.69 A variety
of medications have been used in the treatment of patients
with CRPS. The discussion of the different classes of
medications used to treat this condition is beyond the
scope of this article; however, it has been recommended
that narcotics be avoided because of their addictive
potential.69
It has been noted that TENS might provide pain control
in the early phases of CRPS.70 If the patient has a long-
term problem, however, TENS may lose its effectiveness.
Some patients with a problem respond to a team approach
as evidenced by pain centers that offer a chronic pain
rehabilitation program.71 Some authors68,69 have noted that
spontaneous remission of CRPS is rare. They do state,
however, that many cases will subside in weeks to months,
especially with proper and early treatment. A timely
diagnosis of the condition and early intervention to
prevent the problem from progressing is important.
The Reflex Sympathetic Dystrophy Syndrome Association
of America has published clinical practice guidelines for
the management of CRPS on their Web
site.65 Harden68 recently cited the fact that clinical
treatment or interventions with CRPS are often
complicated by a lack of diagnostic precision. In addition,
the use of many interventions is seriously hindered by the
lack of evidence-based information on effectiveness and
efficacy. Harden also pointed out that few scientific trials
of any particular therapy or medication have been
conducted that are specifically directed at determining the
best approach to CRPS.
Vacariu69 reviewed the current concepts of CRPS and
noted that the pathophysiologic mechanisms in this
disorder are still doubtful. In fact, he questioned whether
sympathetic hyperactivity in the development of the
syndrome could be confirmed. He also pointed out that no
diagnostic test specific for the diagnosis of CRPS exists
and that a diagnosis continues to depend on clinical
findings and the exclusion of other conditions that could
27
account for the degree of pain and dysfunction that the
patient experiences. The only common element in the
literature on CRPS is that early definition and early
intervention is essential in preventing this condition from
becoming severe and progressive.
Examination
A 34-year-old woman sustained a hyperextension injury to
the left knee when she tripped while walking down a gravel
driveway in August. She initially reported pain and stiffness
and demonstrated slight edema in the patellar tendon. Pain
was exacerbated during weight-bearing and stair climbing
as well as during active knee flexion. Pain increased over
the next few days, and the patient sought medical
treatment.
Radiological evaluation revealed no significant bony or soft
tissue injuries. The injury was diagnosed by her primary
care physician as a strain of the patellar tendon, and the
patient was placed in a long-leg knee-extension brace for 3
weeks and allowed to bear full weight during ambulation.
At this time, the patient reported being unable to bear
weight on the limb without pain, which was localized at
the lateral joint line. She was referred by her primary care
physician for examination by an orthopedic surgeon, who
confirmed the diagnosis and encouraged the patient to
ambulate without the knee brace and to begin muscle
strengthening and range-of-motion exercises to restore
normal knee function.
Seven weeks after sustaining the injury, the patient was
referred by the orthopedic surgeon to a physical therapist
for examination and an exercise program with the goals of
strengthening the quadriceps femoris and hamstring
muscles and restoring normal knee mobility. She
demonstrated an antalgic gait, with decreased stance time
on the left leg, and reported pain in the subpatellar region
and lateral joint line. An extension lag of 10 to 15 degrees
was observed during active straight leg raising. Soft tissue
evaluation for ligamentous discontinuity was negative. Skin
tone, color, and temperature were equivalent to the
uninvolved extremity. A manual muscle test of the knee
musculature revealed 5/5 (normal) strength of the
hamstring muscles and 3/5 (fair) strength of the
quadriceps femoris muscle group. Mobility measurements
and isometric evaluation results on the isokinetic
evaluation apparatus are listed in the Table. The
circumference of the vastus medialis muscle was 2 cm less
in the involved lower extremity than that in the uninvolved
lower extremity, indicating that disuse atrophy had
occurred.
Evaluation
Diagnosis. The physical therapist made the diagnosis of
“Impaired Joint Mobility, Motor Function, Muscle
Performance, and Range of Motion Associated With
Connective Tissue Dysfunction” (Preferred Physical
Therapist Practice Pattern 4D).72 The therapist planned the
interventions using the broad suggestions from the Guide to
Physical Therapist Practice and taking into account all that the
therapist understood about the patient’s condition.
Intervention
The patient participated in a physical therapy program
consisting of isometric and isokinetic exercises for the
hamstring and quadriceps femoris muscles, passive
mobilization of the knee joint, and management of pain
and joint stiffness with ultrasound, ice, massage, and
whirlpool therapy. She ambulated with crutches, bearing
only partial weight on her affected leg, because she did not
trust the knee’s ability to take her full weight. Pain
continued to be the major obstacle to regaining normal
biomechanical function.
Ten weeks after the injury, the patient underwent an
arthroscopic examination by the orthopedic surgeon to
conclusively rule out any bony or soft tissue derangement
in the knee. This examination was done because of the
lack of progress in resolving the patient’s pain. No such
injury was identified, and the patient resumed the physical
therapy program 10 days following surgery. At this time,
the treating physical therapist consulted another physical
therapist to evaluate the pain component of the patient’s
dysfunction. Trophic changes—including increased skin
temperature, cyanosis, tautness, increased sweating,
decreased hair growth, and slight edema—were
now observed around the affected knee joint when
compared with the unaffected knee. In light of the
patient’s history of long-standing painful dysfunction and
immobilization, the consulting physical therapist suspected
a secondary complication of CRPS. After consulting the
Guide, the patient’s diagnostic classification remained the
same. Conventional TENS was initiated to attempt to
restore the balance of sympathetic nervous system activity
as well as to provide electroanalgesia. Electrodes from one
channel were placed paraspinally at the third lumbar nerve
root level, and those from a second channel were placed
along the fibular (peroneal) nerve, at the popliteal fossa,
and posterior to the lateral malleolus to stimulate
peripheral nerves subserving the painful area. Pulse rate
was set at 100 pps and pulse duration at 0.060 ms; intensity
was set by the patient to evoke a strong paresthesia in the
area of pain, without concomitant muscle contraction. The
patient underwent stimulation for 4 to 5 hours per day, at
first under the supervision of a physical therapist and then
in a home program.
Beneficial outcomes of the intervention were observed
during and immediately following the first treatment. Skin
quality, color, and temperature were normal. The patient
reported immediate pain relief during weight-bearing,
active knee motion, and resisted knee extension. Adequate
pain control with TENS allowed the patient to participate
28
fully in her rehabilitation program, and she regained full
function of her injured knee within 4 weeks following
initiation of TENS. She was able to ambulate bearing full
weight on each extremity and discontinued using crutches.
She was discharged from physical therapy at that time.
Over the next 6 months, the patient reported occasional
discomfort and slight edema in the knee when she
overused it, but she easily controlled these symptoms with
ice and elevation of the limb. Symptoms of CRPS did not
recur.
This case example illustrates that accurate identification of
the sources of pain is essential to the successful treatment
of pain with TENS or any other analgesic agent. In the
early management of this patient, the source of pain was
assumed to be the same as the source of dysfunction, (ie,
an ill-defined soft tissue injury). If indeed the soft tissue
injury was the only source of pain, the patient should have
responded well to the initial treatments of rest and
temporary immobilization, followed by modalities and
exercise. Once the actual source of pain (CRPS) was
identified, the syndrome was easily managed with
conventional TENS, applied in the manner recommended
by Mannheimer and Lampe.73(p406) If the patient had not
responded favorably to conventional TENS, application of
acupuncture-like, modulated, or burst TENS could have
been attempted, with electrodes placed on acupuncture
points that more readily affect circulatory insufficiency or
the sympathetic nervous system.74
The application of TENS has been highly successful in the
management of CRPS, particularly during the second
phase of the syndrome.74-81 Both conventional TENS and
low-frequency stimulation of acupuncture points related to
systemic circulation have been applied successfully.
Summary
In physical therapist practice, there is a concern about
using evidence for both the choice of examination
procedures and for interventions. Systematic reviews have
been conducted in a variety of areas of both interventions
and tests and measures; however, these systematic reviews
rarely provide convincing evidence for the uses of the tests
and measures or interventions. Systematic reviews
generally consider randomized controlled trials to be the
best evidence for using an examination technique or
intervention. Several examples can be found in the
literature. The use TENS for chronic pain was reviewed by
the Cochrane Collaboration.70 In this study, 18 reports
were evaluated. These reports included only small numbers
of subjects and described generally poor outcomes. The
TENS treatment and controls were often poorly defined.
The reviewers also pointed out that few studies looked at
the long-term analgesic effectiveness of TENS. They also
pointed out that single-dose evaluations of TENS are not
helpful in making clinical decisions about using TENS in
managing chronic pain. The reviewers concluded that the
published trials do not provide information on the
stimulation parameters that were the most likely to provide
optimal pain relief and did not answer questions about
long-term effectiveness. The authors of this study
suggested that multicenter randomized controlled trials of
TENS in chronic pain are urgently needed.70
Another Cochrane review examined 85 studies of
therapeutic ultrasound for treating patellofemoral pain
syndrome.71 Only 8 of these were considered potentially
relevant and only 1 was a randomized controlled trial. The
reviewers concluded that ultrasound did not have a
clinically important effect on pain in patients with
patellofemoral pain syndrome. The studies they examined
were found to be of low methodological quality, and they
could not draw any conclusions concerning the use or
nonuse of ultrasound for treating patellofemoral pain
syndrome. Their final comment was that more well-
designed studies were needed.
At this point, physical therapists are unable to say that
many of the pain interventions they use are based on the
best evidence because randomized control trials and
systematic reviews are lacking.71,82-86 This lack of evidence
should not necessarily discourage the physical therapist
from using these methods for pain relief in their patients.
It does point out, however, that physical therapists should
participate in appropriate studies so that evidence can be
collected about these interventions. Physical therapists
should participate fully in the movement to evidence-based
practice because this can only benefit both the patient and
the profession.
The Cochrane reviews are only one source of systematic
reviews. Other sources of systematic reviews also are
available to the physical therapist. The database that
probably contains the most information about physical
therapy interventions is the Physiotherapy Evidence
Database (PEDro) developed by the Centre for Evidence-
Based Physiotherapy in Australia.
Physical Therapy has created the “Evidence in Practice”
series, which contains articles about evidence-based
practice and how a physical therapist may obtain evidence
about particular subjects. In addition, the American
Physical Therapy Association recently began Hooked On
Evidence, a project to develop a database to provide
physical therapists with easy access to the most recent and
best evidence on interventions.
The pain experience continues to challenge health care
professionals. This multidimensional symptom and its
attendant behaviors are unique to each person, and,
therefore, the pain experience eludes clear, universal
definition, explanation, and intervention. The purpose of
this two-part lesson was to provide a multifocal
29
understanding of this complex experience. The
physiological and behavioral components of the pain
experience were reviewed, and some of the current
anatomical and physiological elements of pain perception
and modulation were described. A detailed scheme for
evaluation of the patient with pain was suggested in part 1,
and a variety of interventions for pain of specific etiology
were reviewed in part 2. In addition, components of
behavioral pain therapy were explored, and alternative
methods of pain management were reviewed.
Additional Resources
Ashburn MA, Rice LJ. eds. The Management of Pain. New
York, NY: Churchill Livingstone; 1998.
This edited volume covers a broad base of topics related to pain,
with sections on fundamental aspects, chronic and acute pain,
pain in terminal disease, and pediatric pain considerations.
Basbaum AI, Jessel TM. The perception of pain. In:
Kandel ER, Schwartz JH, Jessell TM, eds. The Principles
of Neural Science. 4th ed. New York, NY: McGraw-Hill,
Health Professions Division; 2000.
This chapter covers the basic concepts of pain perception
including the role of central mechanisms in pain control.
Bishop B. Pain: its physiology and rationale for
management, parts I–III. Phys Ther. 1980;60:13-37.
Part I: neuroanatomical substrate of pain
Part II: analgesic systems of the CNS
Part III: consequences of current concepts of pain
mechanisms related to pain management
A comprehensive review of the anatomical and physiological
organization of pain perception and modulation, with
consideration of its impact on physical therapy management of
the patient with pain.
Bonica JJ, ed. International Symposium on Pain,
1973, Issaquah, Washington. New York, NY: Raven Press;
1974. Advances in Neurology; vol 4.
A compendium of work presented at the International
Symposium on Pain. Contributions cover a variety of
neurophysiological, behavioral, and clinical aspects of pain
perception, modulation, and management.
Bonica JJ, Albe-Fessard DG, eds. Proceedings of the First
World Congress on Pain. New York, NY: Raven Press;
1976. Advances in Pain Research and Therapy; vol 1.
A detailed group of presentations covering all aspects of pain
research and therapy. Subsequent proceedings have also been
published.
Cailliet R. Pain: Mechanisms and
Management. Philadelphia, Pa: FA Davis Co; 1993.
This relatively brief text covers several aspects of pain, including
neuroanatomy of pain, sympathetic nerve system aspects,
psychological testing in patients with pain, and a great variety of
interventions for pain. One of the strengths of this volume is the
coverage of mechanisms of pain in specific anatomical regions.
Discussions of special concerns with chronic pain, cancer pain,
and pain in children also are included.
Cailliet R. Soft Tissue Pain and Disability. 3rd
ed. Philadelphia, Pa: FA Davis Co; 1996.
This volume reviews the clinical aspects of pain secondary to
soft tissue injury. Mechanisms of tissue inflammation and repair
are reviewed and applied to the evaluation and treatment of a
variety of common pain syndromes. These syndromes are
organized by anatomical region for easy reference. Clear,
comprehensive illustrations augment the reader’s understanding
of this text.
Camic PM, Brown FD, eds. Assessing Chronic Pain: A
Multidisciplinary Clinic Handbook. New York, NY:
Springer-Verlag; 1989.
This handbook stresses the multidisciplinary approach to pain
assessment and management. Chapters in this text discuss the
physical, psychological, and psychometric evaluation of pain.
Several approaches to pain management are discussed. There is a
section on management of temporomandibular joint disorders
also.
Ciccone CD. Pharmacology in Rehabilitation. 3rd
ed. Philadelphia, Pa: FA Davis Co; 2002.
A comprehensive, detailed review of the principles of
pharmacology that is presented at a level appropriate for the
clinician, student, and educator. Specific chapters address the
mechanisms of action, indications, effects, side effects, and
toxicity of specific groups of pharmacological agents, with
special attention to the implications that the medications may
have rehabilitation. This important text fills a major void in
physical therapy literature.
Echternach JL, ed. Pain. New York, NY: Churchill
Livingstone; 1987.
An excellent review of the subject of pain for the physical
therapist. Nolan’s chapter on the anatomic and physiologic
organization of pain modulation is clear and comprehensible.
General evaluation and treatment approaches are reviewed, and
special topics, including movement dysfunction, foot pain, and
selected treatment approaches, are presented.
Fields HL. Pain: Mechanisms and Management. New
York, NY: McGraw-Hill; 1987.
A careful, complete, comprehensive, and understandable review
of the pain experience. Fields clearly reviews pain perception,
modulation, evaluation, and treatment in a concise manner. The
chapters on pharmaceutical management of pain provide an
excellent basis of understanding for the clinician.
Fordyce WE. Behavioral Methods for Chronic Pain and
Illness. St Louis, Mo: Mosby; 1976.
Fordyce provides clinicians with an excellent basis for
understanding and integrating behavioral modification methods.
Gatchel RJ, Weisburg JN, eds. Personality Characteristics
of Patients With Pain. Washington, DC: American
Psychological Association; 2000.
This text views the psychological aspects of pain beginning with
a historical perspective. Topics covered include personality
testing of patients with chronic pain and a variety to topics
related to personality, both nonpathologic characteristics and
personality disorders, in relationship to chronic pain.
30
Gersh MR. Electrotherapy in
Rehabilitation. Philadelphia, Pa: FA Davis Co; 1992.
A detailed review of clinical electrophysiology and
electrotherapy. Hanegan reviews the neurophysiology of
nociception in detail. Applications of electroanalgesic procedures
are discussed in several chapters. Substantial reference lists
follow each chapter.
Kingdon RT, Stanley KJ, Kizior RJ. Handbook for Pain
Management. Philadelphia, Pa: WB Saunders; 1998.
The handbook format is useful for quick access to information
about pain. The book makes use of tables, key points, and a
section called “Clinical Accountabilities” at the end of clinical
chapters. There are chapters covering topics such as pain in
children and pain in the older adult.
Main CJ, Spanswick CC, eds. Pain Management: An
Interdisciplinary Approach. New York, NY: Churchill
Livingstone; 2000.
A comprehensive text with sections of several chapters covering
an introduction to pain management, assessment, the pain
management program, issues in delivery and examination, and
new directions in pain management. The interdisciplinary aspects
of pain in health care are emphasized.
Mayer DJ, Price DD. Neural mechanisms of pain. In:
Robinson AJ, Snyder-Mackler L, eds. Clinical
Electrophysiology. 2nd ed. Baltimore, Md: Williams &
Wilkins; 1995:211-278.
A current, comprehensive review of pain perception and
modulation with a vast reference list.
McQuay H, Moore RA. An Evidence-Based Resource for
Pain Relief. New York, NY: Oxford University Press; 1998.
Part I of the text is devoted to the methodology of evidence-
based practice in pain management. Parts II and III are devoted
to evidence-based reviews in acute pain and chronic pain. In
addition to the reviews of pharmacological approaches to pain,
there are reviews of transcutaneous electrical nerve stimulation
and spinal cord stimulation approaches.
Michlovitz SL, ed. Thermal Agents in Rehabilitation. 3rd
ed. Philadelphia, Pa: FA Davis Co; 1998.
This volume, part of the Contemporary Perspectives in Rehabilitation series,
provides a foundation for the application of thermal agents to the
management of pain, inflammation, and tissue injury. Mechanisms of
injury and pain are reviewed, and detailed descriptions of specific
treatments are provided, along with a review of the literature evaluating
the efficacy of each modality. Case studies practically illustrate
applications for the clinician.
Mullens PA. Reflex sympathetic dystrophy. In: Stanley BG,
Tribizi SM, eds. Concepts in Hand
Rehabilitation. Philadelphia, Pa<: FA Davis Co; 1992:446-
471.
Mullens discusses the history of reflex sympathetic dystrophy
(RSD), classification of RSD, and the characteristics of each
classification. The author also discusses the symptoms and signs,
stages and the disease process, and etiologic factors and
describes treatment approaches in detail.
Nolan MF. A Chronological Indexing of the Clinical and
Basic Science Literature Concerning Transcutaneous
Electrical Nerve Stimulation (TENS): 1967- return to work issues, spiritual and behavioral aspects, and legal
1987. Alexandria, Va: American Physical Therapy aspects.
Association, Section on Clinical Electrophysiology; 1988.
This chronological listing provides a complete reference of Wells PE, Frampton V, Bowsher D, eds. Pain Management
topics related to electroanalgesia, stimulation-produced analgesia, in Physical Therapy. 2nd ed. Norwalk, Conn: Appleton &
and current theories of pain perception and modulation. Lange; 1994.
A clear, comprehensive, readable text that covers the
Physician’s Desk Reference. Montvale, NJ: Thomson PDR; neurobiology of pain, specific physical therapy interventions for
published annually. patients with pain, and special applications including
A detailed listing of all pharmaceutical agents, listed by generic postoperative, cancer, and obstetric and gynecologic pain. Text is
and manufacturer name, with detailed descriptions of actions, well organized, well referenced, and easy to use on a topic-by-
indications, contraindications, warnings, side effects, and drug topic basis.
interactions. All clinicians should have ready access to the PDR
at their place of employment. Available on the Internet at Wittink H, Michel TH, eds. Chronic Pain Management for
www.pdr.net. Physical Therapists. 2nd ed. Boston, Mass: Butterworth-
Heinemanm; 2001.
Salerno E, Willens JS, eds. Pain Management Handbook: Written with the physical therapist in mind, this text has several
An Interdisciplinary Approach. St Louis, Mo: Mosby; 1996. useful chapters on chronic pain concepts. Coverage includes
This handbook is divided into three sections. Section 1 covers management of some specific problems such as head and neck
introductory material concerning pain, including identifying and pain and low back pain. A chapter on documentation is also
perceiving pain and cultural aspects of pain. Section 2 looks at a included.
great variety of therapeutic approaches to pain and includes a
section on team management of pain. Section 3 discusses the
clinical application of pain management and covers a wide range
Resources on Pain Management for
of topics from acute pain to discussions of pain in geriatrics, Health Care Professionalsa
pediatrics, and a variety of special situations. The text has several
useful algorithms to guide the clinician. The appendixes also American Academy of Craniofacial Pain
include useful information about drugs and reactions to drugs 516 W Pipeline Rd
used in pain management. Hurst, TX 76053
800/322-8651 or 817/282-1501
Fax: 817/282-8012
Snyder-Mackler L. Electrical stimulation for pain E-mail: central@aacfp.org
modulation. In: Robinson AJ, Snyder-Mackler L, eds. www.aacfp.org
Clinical Electrophysiology. 2nd ed. Baltimore, Md: Membership is geared to dissemination of information to
Williams & Wilkins; 1995:279-310. professionals who have devoted a portion of their practice to
Snyder-Mackler reviews facets of pain assessment, modes of diagnosis and treatment of head, neck, and facial pain and
electrical stimulation, and characteristics of stimulators. The temporomandibular joint dysfunction.
application of specific types of electrical stimulation within
studies are reviewed in an easy-to-understand manner.
American Academy of Orofacial Pain
19 Mantua Rd
Turk DC, Meichenbaum D, Gemest M. Pain and Mount Royal, NJ 08061
Behavioral Medicine: A Cognitive-Behavioral 856/423-3629
Perspective. New York, NY: Guilford Press; 1983. Fax: 856/423-3420
A wide variety of psychological, behavioral, and cognitive www.aaop.org
approaches to pain evaluation and management are reviewed. An organization of health care professionals dedicated to
Clear applications are presented for use by clinicians. alleviating pain through education, research, and patient
education; online tutorial available on temporomandibular
Waddell G, ed.The Back Pain Revolution. Philadelphia, Pa: disease; full text of latest issue and some back issues of AAOP
Churchhill Livingstone; 1998. News available online.
This text provides an integrated and comprehensive
biopsychosocial approach to management of low back pain. The American Academy of Pain Management
text provides information on illness behavior, psychological 13947 Mono Way, Ste A
aspects of low back pain and social factors related. Also contains Sonora, CA 95370
practice guidelines from a variety of sources. 209/533-9744
E-mail: aapm@aapainmanage.org
Weiner RS, exec ed. Pain Management: A Practical Guide www.aapainmanage.org
for Clinicians. Vols 1 and 2. 6th ed. Boca Raton, Fla: St A membership organization composed of pain clinicians from
Lucie Press; 1998. many disciplines; operates an outcomes measurement system
The two volumes contain many short chapters covering a great (the National Pain Data Bank) used by more than 100 pain
variety of pain management topics. Volume 1 focuses on management programs; this growing database contains
multidisciplinary approaches to pain management. Volume 2 information on more than 12,000 patients and may be sifted to
covers a broad spectrum of pain related topics, including acute obtain statistics in specific areas of research; pain program
and chronic pain, speciality concerns about pain management,

31
accreditation offered; links to CME sites available; current International Association for the Study of Pain
edition of newsletter The Pain Practitioner included. 909 NE 43rd St, Ste 306
Seattle, WA 98105-6020
American Academy of Pain Medicine 206/547-6409
4700 W Lake Ave Fax: 206/547-1703
Glenview, IL 60025 E-mail: iaspdesk@juno.com
847/375-4731 www.asp-pain.org
Fax: 847/734-8750 A professional nonprofit association of 6,300 members from 86
www.painmed.org countries dedicated to furthering research on and improving care
The only pain organization with representation in the AMA of patients with pain; membership open to scientists, physicians,
House of Delegates; mission is to provide quality care to patients dentists, psychologists, nurses, physical therapists, and other
with pain through education and training of physicians, research, health professionals actively engaged in pain research or with a
and advancement of the specialty of pain medicine; members special interest in diagnosis and treatment of pain; objectives
receive The Clinical Journal of Pain and a newsletter containing include fostering research on pain mechanisms, improving
information about the specialty, the academy and its members, management of acute and chronic pain, and advising agencies on
and upcoming events. standards relating to use of drugs, appliances, and other pain
treatment procedures.
American Pain Foundation
201 N Charles St, Ste 710 National Forum of Independent Pain Clinicians
Baltimore, MD 21201-4111 279 E Kennedy St
E-mail: info@painfoundation.org Spartanburg, SC 29302
www.painfoundation.org 864/583-0053
Includes links to consensus and public policy statements on Fax: 864/583-0390
prescribing for chronic pain; instructions on keeping a pain E-mail: somervillejudson@netscape.net
diary; calendar of events; press release page. www.painforum.org
Provides a forum for pain clinicians in independent practice to
raise concerns, exchange ideas, and work out solutions to
American Pain Society
problems; members receive a quarterly newsletter, can attend
4700 W Lake Ave
open symposiums, and can develop a network with colleagues.
Glenview, IL 60025-1485
847/375-4715
Fax: 877/734-8758 National Foundation for the Treatment of Pain
E-mail: info@ampainsoc.org 1330 Skyline Dr, #21
www.ampainsoc.org Monterey, CA 93940
A multidisciplinary educational and scientific organization 831/655-8812
founded as national chapter of International Association for the Fax: 831/655-2823
Study of Pain; includes more than 3,200 physicians, nurses, www.paincare.org
psychologists, dentists, scientists, pharmacologists, physical A resource for medical professionals and attorneys concerned
therapists, and other professionals who research and treat pain with legal issues regarding treatment of pain.
and act as patient advocates.
Pain Net, Inc
Chronic Pain Rehabilitation Program 1680 Water Mark Dr
James A. Haley Veterans Affairs Medical Center Columbus, OH 43215
13000 Bruce B Downs Blvd 614/481-5960
Tampa, FL 33612-4798 Fax: 614/481-5964
813/972-2000, ext 7112 or 7114 E-mail: info@painnet.com
Fax: 813/903-4847 www.painnet.com
www.vachronicpain.org Developed by physicans, educators, and business professionals
Started in 1988 as an inpatient treatment program to help to provide education and support to US health care
veterans with chronic pain, the program has evolved into a professionals in the areas of pain medicine, management, and
nationally known center for pain diagnosis, treatment, research, functional restoration; services include credentialing (by
and education; only inpatient pain treatment center in the procedure), educational programs, practice development, quality
Veterans Affairs system accredited by the Commission for the assurance.
Accreditation of Rehabilitation Facilities; referrals for diagnosis
and treatment of veterans with chronic pain accepted from all 50 Pain.com
states, Puerto Rico, and the US Virgin Islands. Dannemiller Memorial Education Foundations
12500 Network Blvd, Ste 101
Doctor’s Guide San Antoinio, TX 78249
www.docguide.com 800/328-2308
At the Pain Management Information and Resources site, links Fax: 210/697-9318
to up-to-date information found on the Internet (eg, articles, E-mail: editor@pain.com
medical news) are collected and kept current. www.pain.com
Experts do in-depth reviews of such subjects as implantable
drug delivery systems, regional blocks, and patient examination;
32
exposition link allows searching for pain products by trade and
generic names; news link collects current articles on various
pain-related topics; library link can be searched by author, title,
or key word; CME credit available.
a
Resources on pain management. Postgrad Med. 1999;106.
References
1 Joint Commission on Accreditation of Healthcare
Organizations, Joint Commission Resources. Pain assessment
and management standards–hospitals. Available at:
www.jcrinc.com/subscribers/perspectives.asp?durki=3243&site
=10&return=2897. Accesssed October 7, 2003.
2 Joint Commission on Accreditation of Healthcare
Organizations, Joint Commission Resources. Pain assessment
and management standards–ambulatory care. Available at:
www.jcrinc.com/subscribers/perspectives.asp?durki=3240&site
=10&return=2897. Accessed October 7, 2003.
3 Yadgood MC, Miller PJ, Mathews PA. Relieving the agony of
the new pain management standards. Am J Hosp Palliat Care.
2000;17:333-341.
4 McCarberg B. Pain assessment, like vital signs, to be checked
on hospital admission. Managed Care Interface. 2001;14(2):31.
5 Wolcott LE, Wheeler PC, Hardwicke HM, Rowley BA.
Accelerated healing of skin ulcers by electrotherapy: preliminary
clinical results. South Med J. 1969:62:795-801.
6 Carey LC, Lepley D Jr. Effect of continuous direct electric
current on healing wounds. Surg Forum. 1962;13:33-35.
7 Carley PJ, Wainapel SF. Electrotherapy for acceleration of
wound healing: low intensity direct current. Arch Phys Med
Rehabil. 1985;66:443-446.
8 Cheng N, Van Hoof H, Bockx E, et al. The effects of electric
currents on ATP generation, protein synthesis, and membrane
transport of rat skin. Clin Orthop. 1982;171:264-272.
9 Kloth LC, Feedar JA. Acceleration of wound healing with high
voltage, monophasic, pulsed current. Phys Ther. 1988;68:503-508.
10 Akers TK, Gabrielson AL. The effect of high voltage galvanic
stimulation on the rate of healing of decubitis ulcers. Biomed Sci
Instrum. 1984;20:99-100.
11 Assimacopoulos D. Wound healing promotion by use of
negative electric current. Am Surg. 1968;34:423-431.
12 Barron JJ, Jacobson WE, Tidd G. Treatment of decubitus
ulcers: a new approach. Minn Med. 1985;68:103-106.
33
13 US Department of Health and Human Services, Centers for
Medicare and Medicaid Services. Decision memo for
electrostimulation for wounds (#CAG-00068N). Available at:
www.cms.hhs.gov/mcd/viewdecisionmemo.asp?id=27.
Accessed October 6, 2003.
14 Gardner SE, Frantz RA, Schmidt FL. Effect of electrical
stimulation on chronic wound healing: a meta-analysis. Wound
Repair Regen. 1999;7:495-503.
15 McCulloch JM. The role of physiotherapy in managing
patients with wounds. J Wound Care. 1998;7:241-244.
16 Melzack R, Wall PD. Pain mechanisms: a new theory. Science.
1965;150:971-979.
17 Carlen PL, Wall PD, Nadvorna H, Steinbach T. Phantom
limbs and related phenomena in recent traumatic amputation.
Neurology. 1978;28:211-217.
18 Winnem MF, Amundsen T. Treatment of phantom limb pain
with TENS. Pain. 1982;12:299-300.
19 Katz J, Melzack R. Auricular transcutaneous electrical nerve
stimulation (TENS) reduces phantom limb pain. J Pain Symptom
Manage. 1991;6:73-83.
20 Katz J, France C, Melzack R. An association between
phantom limb sensations and stump skin conductance during
transcutaneous electrical nerve stimulation (TENS) applied to
the contralateral leg: a case study. Pain. 1989;36:367-377.
21 Kawamura H, Ito K, Yamamoto M, et al. The transcutaneous
electrical nerve stimulator applied to contralateral limbs for
phantom limb pain. Journal of Physical Therapy Science. 1997;9(2):71-
76.
22 Halbert J, Crotty M, Cameron ID. Evidence for the optimal
management of acute and chronic phantom pain: a systematic
review. Clin J Pain. 2002;18:84-92.
23 Wickramasekera I. Electormyographic feedback training and
tension headache: preliminary observations. Am J Clin Hypn.
1972;15:83-85.
24 Melzack R, Casey KL. Sensory, motivational, and central
control determinants of pain. In: Kenshalo DR, ed. The Skin
Senses: Proceedings of the International Symposium on Skin Senses,
1966, Florida State University. Springfield, Ill: Charles C Thomas
Publisher; 1968:423-443.
25 Keefe FJ, Smith SJ, Buffington AL, et al. Recent advances
and future directions in the biopsychosocial assessment and
treatment of arthritis. J Consult Clin Psychol. 2002;70:640-655.
26 Dersh J, Gatchel RJ, Polatin P, Mayer T. Prevalance of
psychiatric disorders in patients with chronic work-related
musculoskeletal pain disability. J Occup Environ Med. 2002;44:459-
468.
27 Turk DC, Okifuji A. Psychological factors in chronic pain:
evolution and revolution. J Consult Clin Psychol. 2002;70:678-690.
28 Eccleston C. Role of psychology in pain management. Br J
Anaesth. 2001;87:144-152.
29 Morley S, Eccleston C, Williams A. Systematic review and
meta-analysis of randomized controlled trials of cognitive
behaviour therapy and behaviour therapy for chronic pain in
adults, excluding headache. Pain. 1999;80:1-13.
30 Guzman J, Esmail R, Karjalainen K, et al. Multidisciplinary
rehabilitation for chronic low pack pain: systematic overview.
BMJ. 2001;322:1511-1516.
31 Nielson WR, Weir R. Biopsychosocial approaches to the
treatment of chronic pain. Clin J Pain. 2001;17(4 suppl):S114-
S127.
32 Karjalainen KA, Malmivaara AO, van Tulder MW, et al.
Biopsychosocial rehabilitation for upper limb repetitive strain
injuries in working age adults. Cochrane Database Syst Rev.
2000;(3):CD002269.
33 Karjalainen KA, Malmivaara AO, van Tulder MW, et al.
Multidisciplinary biopsychosocial rehabilitation for neck and
shoulder pain among working age adults: a systematic review
within the framework of the Cochrane Collaboration Back
Review Group. Spine. 2001;26:174-181.
34 Deepak KK, Behari M. Specific muscle EMG biofeedback
for hand dystonia. Appl Psychophysiol Biofeedback. 1999;24:267-280.
35 Wickramasekra I. How does biofeedback reduce clinical
symptoms and do memories and beliefs have biological
consequences? Toward a model of mind-body healing. Appl
Psychophysiol Biofeedback. 1999;24:91-105.
36 Montgomery GH, DuHamel KN, Redd WH. A meta-analysis
of hypnotically induced analgesia: how effective is hypnosis? Int J
Clin Exp Hypn. 2000;48:138-153.
37 Fordyce WE. Pain viewed as learned behavior. In: Bonica JJ,
ed. International Symposium on Pain, 1973, Issaquah, Washington.
New York, NY: Raven Press; 1974:417. Advances in Neurology; vol
4.
38 Sternbach RA. Pain Patients: Traits and Treatment. New York,
NY: Academic Press Inc; 1974.
39 Waddell G, Main CJ. Illness behavior. In: Waddell G, ed. The
Back Pain Revolution. Edinburgh, United Kingdom: Churchill
Livingstone; 2000:chap 10.
40 Doleys DM, Murray JB, Klapow JC, Coleton ML.
Psychological assessment. In: Ashburn MA, Rice TJ, eds. The
Management of Pain. New York, NY: Churchill Livingstone Inc;
1998:chap 3.
34
41 Spanswick CC, Parker H. Clinical content of interdisciplinary
pain management programmes. In: Main CJ, Spanswick CC, eds.
Pain Management: An Interdisciplinary Approach. New York, NY:
Churchill Livingstone; 2000:chap 13.
42 Brena SF. The Mystery of Pain: Is Pain a Sensation? Management of
Patients With Chronic Pain. Jamaica, NY: Spectrum Publications
Inc; 1983.
43 Wickramasekera I. Biofeedback and behavior modification
for chronic pain. In: Echternach JL, ed. Pain. New York, NY:
Churchill Livingstone; 1987:262-264.
44 Ciccone CD. Pharmacology in Rehabilitation. 3rd
ed. Philadelphia, Pa: FA Davis Co; 2002:chaps 12-17.
45 Evans FJ. The placebo response in pain reduction. Adv
Neurol. 1974;4:289-296.
46 Marchand S, Charest I, Li J, et al. Is TENS purely a placebo
effect? A controlled study on chronic low back pain. Pain.
1993:54:99-106.
47 Turner JA, Deyo RA, Loeser JD, et al. The importance of
placebo effects in pain treatment and research. JAMA.
1994;271:1609-1614.
48 Ernst E, Resch KL. Concept of true and perceived placebo
effects. BMJ. 1995;311:551-563.
49 Hrobjartsson A, Gotzsche PC. Is the placebo powerless? An
analysis of clinical trials comparing placebos with no treatment.
N Engl J Med. 2001;344:1594-1602.
50 Bailar JC 3rd. The powerful placebo and the Wizard of Oz. N
Engl J Med. 2001;344:1630-1632.
51 Fields HL. Pain: Mechanisms and Management. New York, NY:
McGraw-Hill; 1987:150, 251-303, 309, 319-320, 327.
52 Davis KD, Lozano AM, Tasker RR, Dostrovsky JO. Brain
targets for pain control. Stereotact Funct Neurosurg. 1998;71:173-
179.
53 Tasker RR. History of lesioning for pain. Stereotact Funct
Neurosurg. 2001;77:163-165.
54 Wetzel FT, Phillips FM, Aprill CN, et al. Extradural sensory
rhizotomy in the management of chronic lumbar radiculopathy:
a minimum 2-year follow-up study. Spine. 1997;22:2283-2291;
discussion 2291-2292.
55 Kavar B, Rosenfeld JV, Hutchinson A. The efficacy of spinal
cord stimulation for chronic pain. J Clin Neurosci. 2000;7:409-413.
56 Meyerson BA. Neurosurgical approaches to pain treatment.
Acta Anaesthesiol Scand. 2001;45:1108-1113.
57 Kim SH, Tasker RR, Oh MY. Spinal cord stimulation for
nonspecific limb pain versus neuropathic pain and spontaneous
versus evoked pain. Neurosurgery. 2001;48:1056-1064; discussion
1064-1065.
58 Deer TR. Current and future trends in spinal cord stimulation
for chronic pain. Curr Pain Headache Rep. 2001;5:503-509.
59 Kay AD, McIntyre MD, Macrae WA, Varma TR. Spinal cord
stimulation: a long-term evaluation in patients with chronic pain.
Br J Neurosurg. 2001;15:335-341.
60 North RB, Wetzel FT. Spinal cord stimulation for chronic
pain of spinal origin: a valuable long-term solution.
Spine. 2002;27:2584-2591; discussion 2592.
61 Krames E. Implantable devices for pain control: spinal cord
stimulation and intrathecal therapies. Best Pract Res Clin
Anaesthesiol. 2002;16:619-649.
62 Somers DL, Somers MF. Treatment of neuropathic pain in a
patient with diabetic neuropathy usingtranscutaneous electrical
nerve stimulation applied to the skin of the lumbar region. Phys
Ther. 1999;79:767-775.
63 Riddle DL, Rothstein JM, Echternach JL. Application of the
HOAC II: an episode of care for a patient with low back pain.
Phys Ther. 2003;83:471-485.
64 Pittman DM, Belgrade MJ. Complex regional pain syndrome.
Am Fam Physician. 1997;56:2265-2270, 2275-2276.
65 Kirkpatrick AF. Clinical practice guidelines for the diagnosis,
treatment, and management of reflex sympathetic
dystrophy/complex regional pain syndrome (RSD/CRPS). 2nd
ed. Reflex Sympathetic Dystrophy Syndrome Association
of America. Available at: www.rsds.org/cpgeng.htm.
Accessed October 7, 2003.
66 Tahmoush AJ, Malley J, Jennings JR. Skin conductance,
temperature, and blood flow in causalgia. Neurology.
1983;33:1483-1486.
67 Kleinert HE, Norberg H, McDonough JJ. Surgical
sympathectomy: upper and lower extremity. In: Omer GE Jr,
Spinner M, eds. Management of Peripheral Nerve
Problems. Philadelphia, Pa: WB Saunders; 1980:285.
68 Harden RN. A clinical approach to complex regional pain
syndrome. Clin J Pain. 2000;16(2 suppl):S26-S32.
69 Vacariu G. Complex regional pain syndrome. Disabil Reliabil.
2002;24:435-442.
70 Carroll D, Moore RH, McQuay HJ, et al. Transcutaneous
nerve stimulation (TENS) for chronic pain. Cochrane Database Syst
Rev. 2001;(3):CD003222.
35
71 Guzman J, Esmail R, Karjalainen K, et al. Multidisciplinary
bio-psycho-social rehabilitation for chronic back pain. Cochrane
Database Syst Rev. 2002;(1):CD000963.
72 Guide to Physical Therapist Practice. 2nd ed. Phys Ther.
2001;81:9-744.
73 Mannheimer JS, Lampe GN. Clinical Transcutaneous Electrical Nerve
Stimulation. Philadelphia, Pa: FA Davis Co; 1984:190-197, 406.
74 Kaada B. Vasodilation induced by transcutaneous nerve
stimulation in peripheral ischemia (Raynaud’s phenomenon and
diabetic polyneuropathy). Eur Heart J. 1982;3:303-314.
75 Wong RA, Jette DU. Changes in sympathetic tone associated
with different forms of transcutaneous electrical nerve
stimulation in healthy subjects. Phys Ther. 1984;64:478-482.
76 Owens S, Atkinson ER, Lees DE. Thermographic evidence
of reduced sympathetic tone with transcutaneous nerve
stimulation. Anesthesiology. 1979;50:62-65.
77 Headley B. Historical perspective of causalgia: management
of sympathetically maintained pain. Phys Ther. 1987;67:1370-
1374.
78 Frampton VM. Pain control with the aid of transcutaneous
nerve stimulation. Physiotherapy. 1982;66:77-81.
79 Richlin DM, Carron H, Rowlingson JC, et al. Reflex
sympathetic dystrophy: successful treatment by transcutaneous
nerve stimulation. J Pediatr. 1978;93:84-86.
80 Stilz RJ, Carron H, Saunders DB. Reflex sympathetic
dystrophy in a 6-year-old: successful treatment by
transcutaneous nerve stimulation. Anesth Analg. 1977;56:438-443.
81 Leo KC. Use of electrical stimulation at acupuncture points
for the treatment of reflex sympathetic dystrophy in a child: a
case report. Phys Ther. 1983;63:957-959.
82 Crawford F, Atkins D, Edwards J. Intervention for treating
plantar heel pain. Cochrane Database Syst Rev. 2002;(2):CD003584.
83 Brosseau L, Casimiro L, Robinson Y, et al. Therapeutic
ultrasound for treating patellofemoral pain syndrome. Cochrane
Database Syst Rev. 2001;(4):CD003375.
84 Welch V, Brosseau L, Peterson J, et al Therapeutic ultrasound
for osteoarthritis of the knee. Cochrane Database Syst Rev.
2001;(3):CD003132.
85 McQuay HF, Moore A. An Evidence-Based Resource for Pain
Relief. New York, NY: Oxford University Press; 1998;chaps 20,
21, 25.
86 Wetzel FT, Phillips FM, Aprill CN, et al. Extradural
rhizotomy in the management of chronic lumbar radiculopathy:
a minimum 2-year follow-up study. Spine. 1997;22:2283-2291;
discussion 2291-2292.
Fig. 1. The gate control theory of pain modulation.10 SG=substantia gelatinosa, T=transmission cell.

Fig. 2. Gate control theory II. The figure represents a method for understanding how gate control theory accounts for the
activation of higher centers. Modified with permission of Charles C Thomas Publisherfrom Melzack R, Casey KL. Sensory,
motivational, and central control determinants of pain. In: Kenshalo DR, ed. The Skin Senses: Proceedings of the
International Symposium on Skin Senses, 1966, Florida State University. Springfield, Ill: Charles C Thomas Publisher; 1968.

Fig. 3. Gate control theory II (GCT-II). The new model includes excitatory (white circle) and inhibitory (black circle) links
from the substantia gelatinosa (SG) to the transmission (T) cells as well as the descending inhibitory control from brainstem
systems. The round knob at the end of the inhibitory link implies that its actions may be presynaptic, postsynaptic, or both. All
connections are excitatory, except the inhibitory link from SG to T cell. Modified with permission of Penguin Books Ltd from
Melzack R, Wall PD. The Challenge of Pain. London, England: Penguin Books; 1983. Reproduced with permission of Basic
Books.
Fig. 4. Melzack’s neuromatrix theory. Adapted from Melzack R. Pain and stress. In: Gatchel RJ, Tusk DC, eds. Psychosocial
Factors in Pain. New York, NY: Guilford Press; 1999. Reprinted with permission from Guilford Press.

Fig. 5. Pictorial representation of the behavioral characteristics of various types of patients with pain. "Patient A" has pain
behavior directly related to a great degree of tissue destruction. "Patient B" has chronic pain, with behavior that magnifies
minimal tissue destruction. "Patient C" is the "stoic," one whose pain behavior appears minimal compared with the amount of
tissue destruction. "Patient D" is the well-adjusted individual, whose pain behavior is well correlated with the amount of tissue
destruction.

37
Fig. 6. The disease/medical model of the pain experience, in which treatment is directed at modifying a physiological
underlying pathology. (UP=underlying pathology.) Reprinted with permission of Lippincott Williams & Wilkins from Fordyce
WE. Pain viewed as learned behavior. In: Bonica JJ, ed. International Symposium on Pain, 1973, Issaquah, Washington. New
York, NY: Raven Press; 1974:415. Advances in Neurology; vol 4.

Fig. 7. The learning model of the pain experience, in which treatment is directed at the symptoms or pain behaviors because
the underlying pathology is no longer present or defies treatment. Reprinted with permission of Lippincott Williams & Wilkins
from Fordyce WE. Pain viewed as learned behavior. In: Bonica JJ, ed. International Symposium on Pain, 1973, Issaquah,
Washington. New York, NY: Raven Press; 1974: 417. Advances in Neurology; vol 4.

Fig. 8. Reinforcement of pain behavior. (Top) Noxious stimulus elicits a pain behavior (eg, rest). (Middle) Noxious stimulus
elicits a pain behavior that is reinforced in two wasy: First, it reduces the pain; second, in the case or rest, it allows the patient
to avoid unpleasant jobs or situations. To the extent that it occurs because of reinforcement rather than the continued
presence of a noxious stimulus, rest is a learned pain behavior. (Bottom) No noxious stimulus. The pain behavior is sustained
solely by avoidance of unpleasant jobs or situations. Reprinted with permission of McGraw-Hill from Fields HL. Pain:
Mechanisms and Management. New York, NY: McGraw-Hill Inc; 1987.

38
Fig. 9. Samples of simple descriptive scales (verbal pain reports). Reprinted from Echternach JL. Pain. New York, NY:
Churchill Livingstone Inc; 1987:44, with permission of Elsevier Science.

Fig. 10. Samples of numerical rating scales. The resemble visual analog scales, but have numbers, as well as words, in place.
Reprinted with permission from Echternach JL. Pain. New York, NY: Churchill Livingstone Inc; 1987:45, with permission of
Elsevier Science.

39
Fig. 11. Samples of the visual analog scale. Notice that the scale may be oriented vertically or horizontally. Reprinted from
Scott J, Huskisson EC. Graphic representation of pain. Pain. 1976;2:175, with permission from the International Society for
the Study of Pain.

40
Fig. 12. A sample of the semantic differential word list from the McGill Pain Questionnaire. Words in each of the 20 groups
are rank-ordered by intensity, Words in each group represent qualities associated with the sensory, affective, or evaluative
aspects of pain. Reprinted from Melzack R. The McGill Pain Questionnaire: major properties and scoring methods. Pain.
1975;1:277-299, with permission from the International Society for the Study of Pain.

Fig. 13. (A, B) Body diagrams on which the patient may indicated the location and quality of pain. Reprinted with permission
of FA Davis Co from Mannheimer JS, Lampe GN. Clinical Transcutaneous Electrical Nerve Stimulation. Philadelphia, Pa: FA
Davis Co; 1984:192.

41