Download PRESIDENT`S MESSAGE Psychogenic Pain—What It Means, Why It

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts
no text concepts found
Transcript
PAIN MEDICINE
Volume 1 • Number 4 • 2000
PRESIDENT’S MESSAGE
Psychogenic Pain—What It Means, Why It Does Not Exist, and How
to Diagnose It
The concept of psychogenic pain has stimulated controversy in the field of pain medicine, not only regarding its prevalence, but indeed its very existence.
Some would even hold that the term is fundamentally meaningless. Whether meaningless or not, it is
often hated—by physicians in pain medicine whose
patients have been harmed by not having been taken
seriously, and by patients who experience the unspoken judgment that, “since there’s nothing wrong
with your body, there must be something wrong
with you.”
Although this appears to be a question of fact,
our recent presidential election demonstrates that
interpretations of events are subject to distortion by
biases, and there is a surfeit of bias surrounding the
question of psychogenic pain.
The IASP defines pain as an experience, and it
could be concluded that, since all experiences are
psychological phenomena, the term psychogenic pain
is a meaningless tautology, much like psychogenic
joy. Pain has even been called “a localized form of
sorrow” by Spinoza. The acknowledged duality of
pain—the fact that it is both sensation and emotion—is reflected in anatomy and physiology. Its
affective components may transit the spinoreticular
tracts en route to the anterior cingulate cortex, while
its algosity, to borrow a term [1], may traverse the
spinothalamic tracts toward the sensory cortex. Yet
this emotional part of pain does not resolve the
question. One could argue that every thought, emotion, and fantasy is at some level a neurochemical
event, so that everything is ultimately “organic,”
i.e., not psychogenic. Nevertheless, it may be useful
to explore the concept to determine whether it has
value.
Perhaps the biases should be addressed first,
since they affect perception. You have to believe it
to see it, as it were.
Disincentives to Recognition
The imperative that physicians work on behalf of
their patients leads naturally to a desire to protect
them from stigmatization, which is integral (in our
culture) to a diagnosis of psychopathology. It is unclear whether the evolution of nomenclature (hys© Blackwell Science, Inc. 1526-2375/00/$15.00/287 287–294
teria, conversion, psychogenic pain, somatoform pain
disorder, pain disorder) was primarily a search for
better science or a search for a euphemism. Unfortunately, euphemisms become terms of opprobrium
so long as the concepts with which they are linked
are disparaged. Certainly the diagnosis is sufficiently
hated that we might refer to it as “the P word.”
Even more troubling to patients than the suggestion of psychological illness may be the threat of
loss of validation. All pain physicians are aware of
the struggle of patients in pain for validation of their
invisible illness, and we have all heard them wish
aloud that they could bleed so that others would
know that their pain was genuine. Given the belief
that what is psychogenic is somehow unreal or illusory, such a diagnosis is a great fear. Psychiatric/
psychological referral of pain patients has been understandably referred to as adding insult to injury.
Physicians and patients alike may see a psychogenic diagnosis not as dismissive of serious occult
pathology, but as dismissive of the patient and his/
her suffering, and therefore to be avoided.
There may also be less noble reasons for dismissing psychogenic pain as an entity. Those who advocate for plaintiffs gain from emphasizing the “organic” nature of the complaint, as do those who
manufacture and prescribe analgesics, adjuvant drugs,
and implantable technology.
An additional source of skepticism is the diminished credibility of the attribution to psychic causes
of things not understood. The situation resembles
that of the ancient gods, who were invoked to explain whatever couldn’t be explained with current
knowledge. Their purview waned as more prosaic
causes of such events as eclipses and thunder were
identified. Similarly, the hypersensitive left knee after an injury to the right one strains credulity until
it is demonstrated in the rodent. This, of course, is
only one of many instances of pain in “perfectly
healthy” body parts that could have been deemed
not to be “organic,” along with even more instances
of conditions that “couldn’t hurt that bad.” Thus,
there is egg on the face of those who have equated
unexplainable with psychogenic. The concept of
psychogenic pain was further weakened by the fact
that its diagnostic signs have been challenged [2].
287
288
While some are benefited by skepticism regarding the diagnosis of psychogenic pain, others are
benefited by its acceptance. This is particularly true
in those who must pay compensation or disability
income, those who plead for defendants, and those
who pay for health care. Perhaps even the chagrin
of physicians may be assuaged by concluding that
surgery corrected the real problems and the residual complaints are psychological (and presumably
therefore the patient’s fault).
What Does Psychogenic Pain Mean?
Is it meaningful to aver that pain is caused by the
psyche? Webster’s defines psyche thus: (1) Class. Myth.
A personification of the soul, which in the form of a
beautiful girl was loved by Eros; (2) the human soul,
spirit, or mind; (3) the mental or psychological structure of a person, especially as a motive force.
The psyche seems an object of great ambivalence. It is that which the androids of science fiction all wish they had, and that which pain patients
seem to wish they hadn’t. It may be the human facility of which we’re most proud, yet most ashamed.
It makes us CEOs and bums, heroes and villains,
yet we minimize its significance.
Webster’s also defines mental as pertaining to the
mind, while it defines mind as psychic or spiritual
being, as opposed to matter; the part that reasons,
thinks, feels, wills, perceives, judges, etc.; the totality of the conscious and unconscious mental processes and activities of the organism. These definitions have a circularity about them, which reflects
the ineffable nature of the concept.
I will use psychological to encompass the functions of beliefs, thoughts, feelings, and behaviors.
Further, I will attempt to distinguish the experience
of pain from pain behavior, despite the difficulty of
demonstrating pain in organisms other than through
pain-associated behaviors.
Potential Psyche—Pain Relationships
Psychic Consequences of Pain
There seems no dispute, either of the affective component of pain, or of the depression, anxiety, demoralization, and irritability that often follow it. People
vary as to whether the dysphoria is more a reaction
to the pain or to the losses of life style and autonomy that it may entail, but that is another subject.
Psychic Causes of Pain
Unlike psychogenic pain, other psychogenic symptoms can be confirmed. Conversion blindness pre-
Covington
serves the opticokinetic reflex; psychogenic seizures
occur during a normal EEG recording; conversion
anesthesia does not diminish the sensory evoked
potential; and psychogenically paralyzed extremities move during sleep or with distraction. Such
confirmation is unavailable in the case of pain.
Most demonstrations of psychogenic pain involve
acute pain created in the laboratory, so their relevance to clinical chronic pain is undetermined. Placebo arms of new drug trials invariably document
headache, abdominal pain, or other symptoms [3].
When treated with a functionless machine, 5 of 58
chronic pain patients dropped out because it worsened their pain. Sham magnetic therapy significantly
increased pain in 11% of trials [4]. More than twothirds of a sample of college students reported mild
headaches when told that a (nonexistent) electric current was passing through their heads [5]. Perhaps
the strongest demonstration of psychogenic clinical
pain is failure of dense sensory-motor blockade to
relieve persistent extremity pain. Whether from conditioning or such factors as beliefs, expectations of
pain do seem to produce pain despite the absence
of noxious perceptual stimulus, and such perception is reflected in functional MRI changes in the
expected regions of the brain [6]. Primates presented
with tasks requiring attention to painful stimuli show
activation of medullary “on-cells” that facilitate pain
transmission—prior to the presentation of the actual pain [7]. Clinically, this suggests that patients
who have come to expect that particular activities
produce pain will find that they do produce pain,
which promotes the inactivity and deconditioning
so detrimental in chronic pain.
The provocation of chest and abdominal pain by
panic attacks is so well known that it is joked in some
institutions that panic disorder cannot be treated
until the patient has first undergone coronary angiography and esophagogastroduodenoscopy.
An old literature demonstrates that most patients
with severe depressive illness also have pain [8–11].
It is probably not possible at present to say whether
the depression is experienced as pain, or whether
the perceived affective and physical suffering are different manifestations of the same neurochemical
pathology.
Provocative studies that are only indirectly related
to the question confirm that emotional states induced
by fantasy or films are associated with PET scanconfirmed cortical changes [12,13]. These changes
are “real,” which suggests that pain produced by
beliefs and fears will be equally so. Some quirk seems
to have resulted in derision of things psychological,
as though they were somehow trivial. It is a word
President’s Message
often preceded by “only.” Perhaps it is worth recalling that voodoo death seems to be a nocebo effect and that an orgasm is no less real for having
been produced by a dream.
It is not clear how somatization should be understood. Somatization disorder seems typically to
result from extreme trauma, usually in childhood
[14–17], but also after later life adult disasters [18].
It is characterized by a plethora of symptoms without organic explanation, some of which include pain.
Absent evidence to the contrary, it seems reasonable to acknowledge the legitimacy of the suffering
these symptoms entail without supporting beliefs in
medical illness or needs for interventions.
Psychological Modulation of Pain
The evidence that psychic factors can reduce pain is
compelling, and stories of athletes and soldiers who
were oblivious to injury during periods of intense
stimulation are well known. Distraction is one of
the more obvious pain mitigating factors, and it was
recently demonstrated with PET scanning that cortical activation from induced pain is reduced by a
distracting cognitive task [19]. Descending inhibitory tracts may be subject to psychological influence.
Hypnosis is certainly a psychological process,
and, in a fascinating study, was found to be capable
of selectively attenuating the anterior cingulate
cortex without reducing somatosensory activation
in response to suggestions that targeted only the
“unpleasantness” of pain and not its intensity [20].
[xviii] Hypnosis also appears able to reduce sensory
components of pain as well [21].
There is also evidence that pain can be augmented by such psychological factors as negative
beliefs (or bewilderment) concerning the cause of
pain, and negative beliefs regarding the person’s capacity to cope.
In addition to descending pain inhibitory tracts,
there is also a descending pain facilitatory tract located in the dorsolateral funiculus. Significantly,
these tracts are activated by electrical or glutamate
stimulation of the anterior cingulate cortex, a region considered important in affective responses.
Psychological Modulation of Communication and
Other Pain Behavior
Conceptually, we can consider the expression of
pain separately from the experience of pain, and a
number of factors extrinsic to the organism demonstrably modify it—a child’s stomachache before the
circus is likely to be expressed differently than one
289
before church. Such behaviors as physical function
and complaints serve as markers by which pain is
judged; however, voluminous literature demonstrates that these markers reflect social and environmental factors as much as they reflect pain. It
has been shown, for example, that patient ratings of
pain severity diminish when “well talk” is reinforced. With repeated identical pain stimuli, intensity reports vary with feedback. Verbal reinforcement increases performance in back pain patients.
Spouse solicitousness is correlated with pain behavior [22]. Pain complaints are quite likely to be exaggerated by any person who feels that strong emphasis is required in order to be taken seriously. We
commonly think of factors that increase pain behavior, because these are the patients who come to
pain physicians; however, minimization of pain would
be expected in situations that provide powerful incentives for appearing healthy.
Prospective studies show that onset of disabling
pain is highly associated with job dissatisfaction,
lack of support at work, stress, and perceived inadequacy of income [23–26]. Once initiated, the progression of pain to chronicity is contingent on similar factors [27,28]. Financial compensation, receipt
of sickness payments, and compensation-related litigation are also associated with chronicity, as are
poor education, language problems, and low income. Chronicity is also favored by such personality factors as tendencies to catastrophizing and somatization [27,29]. Even in patients with clear-cut
radicular pain with disc prolapse/protrusion, application for retirement at 6 months was best predicted by depression and daily hassles at work [30].
In the case of injured workers, performance on
functional capacity evaluation is reduced if the
worker is informed that the test results will be used
to determine work classification [31]. Industrial injuries and compensation situations appear to provide a disproportionate number of patients with
such issues [32–35].
Litigation may adversely affect recovery from
trauma, perhaps especially when the pathology is
ambiguous. This is indirectly supported by the rarity of whiplash in situations where litigation is uncommon, compared with the US, where whiplash/
neck sprains make up two thirds of all bodily injury
claims [36]. It may be significant that the rate of
compensated whiplash in Saskatchewan, which has
a tort system, is 10 times that of Quebec, which has
a no-fault system [37] and that eliminating compensation for pain and suffering seems to have had
the effect of reducing whiplash-related morbidity
[38]. Long [39] studied more than 2000 LBP patients
290
with no more than 1 previous operation and noted
that all those working at the time of initial visit returned to work, with the exception of those in litigation, of whom not one returned to work. This
vocational failure was despite success on other outcome variables equal to those not litigating. Blake
and Garrett found that litigating patients improved
as much as others in a multidisciplinary pain management program, with the exception of the quality
of life score, in which they showed no significant
improvement [40].
It seems clear that pain complaints and reports
of inability to function increase when there are positive incentives for illness. They also increase when
work is an adverse experience, whether due to a
hostile work environment or to limitations on the
part of the worker. What is less clear is the extent
to which these factors modify the pain experience.
The illness behavior does produce other forms of
suffering, as the person regresses physically and
emotionally, withdraws from life, and becomes debilitated.
Counterfeit Pain
Factitious illness and malingering should not be
considered psychogenic pain but rather simulated
pain. The urban legends of pedestrians’ having to
be restrained from entering rear-ended city buses
so that they could claim whiplash injury are about
avarice, not pain. Malingering, the use of willful deception for a covert purpose, is declared to be quite
uncommon by most authorities, though supporting
data is rarely offered regarding its frequency. Fishbain et al. reviewed literature suggesting that malingering is present in 1.25–10.4% of chronic pain
patients, but concluded that serious methodological
flaws precluded conclusions from the data [41].
Data from other fields provide some hints as to
the prevalence of malingering. In patients with unexplained intractable diarrhea, 14% had positive
stool examinations for laxatives, though all had denied their use [42]. Among 333 people who claimed
compensation for noise induced hearing loss, the
incidence of exaggeration on hearing tests (as determined by cortical evoked response audiometry)
was 17.7% [43]. Weintraub cites studies showing
that 20–46% of people considered purposeful misrepresentation of compensation claims to be acceptable [44]. These studies suggest that factitious
illness and malingering may not be rare, but do not
provide information as to how often they simulate
pain. They do suggest keeping an open mind as to
the possibility of these phenomena, which are prob-
Covington
ably less common in those seeking treatment than
in those seeking compensation.
Mixed, Interactive Components
There is no reason to suspect that these mechanisms
are in any way mutually exclusive. They would, in
fact, be expected to occur concurrently and in concert with nociceptive pain. Addiction, for example,
is common in abuse victims, as is somatization disorder. Addiction would create powerful incentives
for exaggerating pain, while trough levels of some
substances (opioids, benzodiazepines) are associated
with hyperalgesia. Thus a tangled web of interacting factors is presented to the clinician. If deactivation reduces pain threshold, then inactivity that began as a form of exaggerated pain behavior could
become generative of pain.
Diagnosing Psychogenic Pain
Is It Best Not to See It?
Perhaps the first question regarding this diagnosis
is whether it is best not made. We know that it is a
false kindness if we “overlook” a diagnosis of addictive disorder while a person develops cirrhosis, peripheral neuropathy, and cerebellar degeneration,
but we should consider whether patients are better
off if we simply take their pain complaints as prima
facie evidence of activity in the neural structures that
subserve pain. The question is not absurd. Publications decry the misdiagnosis of “real” illnesses as
psychogenic, and every clinician has a fear of missing
organic illness in this fashion; yet concerns about
the opposite error seem few. This is a puzzling phenomenon.
One of the early diagnostic criteria that students
were taught to recognize “hysteria” was the presence
of the “battlefield abdomen”—the patients had undergone so many laparotomies that their abdomen
looked as though combat had occurred there. The
patients did not inflict the wounds that left these
scars, rather they were inflicted by compassionate
physicians who took their complaints literally. We
continue to damage patients when we ignore psychogenic pain. Avascular necrosis from unnecessary
steroids, complications of implantable technologies,
failed back surgeries, adverse drug effects, and unwarranted disability are all complications of applying chemical and mechanical remedies for problems
that are largely psychologically determined. The expense of repeated futile interventions goes without
saying. It amounts to repairing hardware when the
problem is with the programming. Thus, it is not a
virtue to look the other way.
President’s Message
Diagnostic Clues
Our official diagnostic guides do not tell us how to
determine that psychological factors contribute to a
serious pain problem, which is a reflection of the
difficulty of this issue. The following suggestions
are offered as largely unsubstantiated aids.
In chronic pain, where signs of illness and injury
are often healed, our principle tool for diagnosing
pain is the patient’s behavior, which includes verbal
communication. It is therefore important to assess the
reliability of this tool. A primary step in radiographic
interpretation is assessment of image quality. Incorrect exposure, motion artifact and other technical deficiencies may weaken the conclusions that can be
drawn. Inappropriate pain behavior, embellishment,
and symptom magnification are not uncommon, particularly in medico-legal circumstances and entitlement programs, and, when present, they weaken
medical conclusions that can be drawn from behavior.
Several observations can help assess the reliability of
pain behavior as a guide to the patient’s experience.
Congruence with Known Conditions. In phantom pain the patient describes pain in an absent extremity. This does not evoke incredulity because
the condition has been well known since long before its pathophysiology was understood. Similarly,
a person with complex regional pain syndrome may
describe exquisite pain on light touch of a healthyappearing extremity following a trivial injury. A constellation of associated signs and symptoms helps to
confirm that the complaint is consistent with a known
syndrome. Intolerance of light touch over a region
of the lower back in patients with mechanical back
pain is not consistent with a defined disease process
and fails to meet this criterion.
Most known conditions have such expected concomitants. Typically a patient would not watch television or read while waiting for a migraine to abate,
and there would be an expected response to ergots,
triptans, or other anti-migraine preparations. A patient with neuropathic pain would likely, but not always, show some response to certain antiepileptic
drugs (e.g., gabapentin, carbamazepine) or antidepressants (e.g., tricyclics). A person with persistent
pain of pancreatitis is unlikely to gain weight.
Consistency Over Time and Situation. Patients
are seen who can tolerate only 10⬚ forward flexions
while standing, yet while sitting with legs outstretched
can touch their toes. Others demonstrate collapsing
with pain on manual testing of plantar flexion, yet
can tiptoe. A patient may limp on one leg walking
forward, the other walking backward, and not at
all on a treadmill. Grip strength may be measured
291
repeatedly and coefficients of variation calculated,
though these methods have been criticized [45,46].
Rapid exchange grip strength testing may provide
similar information [47]. Isokinetic strength testing
may discriminate between maximal and submaximal effort. Complaints and dysfunction should be
relatively independent of the observers present and
should generally persist despite distraction. Gait
disturbances and other pain behaviors that change
dramatically in the presence or absence of certain
persons are not likely to be of organic origin.
Consistency With Anatomy, Physiology. Waddell’s signs are perhaps the best known clues that
pain behaviors may reflect more than organic pathology [48,49]. One example is that of axial rotation,
in which the standing patient’s hips are rotated in
each direction by the examiner. This essentially effects only the hips and ankles, leaving the pelvis and
all above it to move as a unit. Exacerbation of back
pain by this maneuver is considered abnormal. Pain
drawings may also provide suggestions of symptoms that are incongruent with our understanding
of disease processes and pain mechanisms.
Confirmatory Information. Collateral information
from other evaluating professionals and relatives is
of critical value in determining the consistency of
patient behaviors, which helps to confirm that their
relationship is to perceived pain and varies little
with changes in observers.
The confirmation of malingering is extremely difficult and generally depends on intentional or inadvertent “surveillance.” Anecdotes abound of providers encountering wheelchair-bound patients strolling
about a mall, or seeing a patient walking normally
through a parking lot with their cane in the air. At
times there are clinical signs of factitious illness, such
as ligature signs in faux complex regional pain syndrome or phenolphthalein tests in laxative abuse.
Excessive Illness Behavior. It may be difficult to
judge whether behavior is compatible with perceived pain. For example, since one cannot know
how much leg pain a patient experiences on walking, it is hard to know whether an antalgic gait is
exaggerated. Inappropriate illness behavior is suggested, however, by dysfunction in unrelated domains. For example, except in extreme situations, a
patient with back pain should not require that the
spouse complete a patient’s questionnaire—or his
sentences. Chronic pain does not often preclude
making one’s own phone calls to the doctor, paying
bills, etc. When a person has delegated these functions to others, abnormal illness behavior is likely.
292
Cautions. While no one would conclude that because an x-ray was of poor quality there was unlikely to be pathology of concern, this non sequitur
frequently occurs in the case of aberrant pain behaviors. Such behaviors should cause the physician
to be uncertain, but not dismissive. Behavior is affected by many factors. The appearance of symptom exaggeration can be created by fear, or by having learned that certain actions or positions provoke
pain. “Non-physiologic” signs may occur in dementia. Excessive or exaggerated pain behaviors can be
a response to feeling discounted or mistrusted, so
that one must emphasize symptoms to persuade the
physician of their reality. Anyone might dramatize
a problem in an effort to have it taken seriously.
Thus, symptom magnification can be an iatrogenic
phenomenon that occurs when patients feel mistrusted or poorly cared for.
Pain As Problem, Pain As Solution
What are we to make of the too happy pain patient
who reports an extreme level of pain (often ⬎ 10/10)
and whose scores on depression indices are several
times the threshold for severe depression, yet who
is frequently seen in animated and jocular conversation with peers, sleeps well, and appears comfortable? Clearly, there is a continuum of severity of
pain experience and suffering. There is also a continuum of gains and losses associated with illness. It
seems that if the experience of pain is minimal, and
the gains of illness far outweigh the losses, then the
person has little reason for unhappiness, but considerable reason to report high levels of symptomatology. For such individuals, pain is more of a solution than a problem.
Terminology
While the terms hysteria, conversion, psychogenic
pain, and somatoform pain disorder have been criticized as stigmatizing to patients, they (along with
“central pain”), have also been used to de-stigmatize malingerers and exaggerators. Perhaps it would
be clearer to use the term psychologically augmented
pain for those whose suffering is thought to be in
part derived from emotional factors, and to use the
term excessive illness behavior for conscious or unconscious exaggeration.
Management
The person suffering a great deal of pain that is
psychologically induced evokes sympathy and a de-
Covington
sire to help. Unfortunately, the treatment may miss
the target if the diagnosis is missed. In these situations, our motto “pain is the disease” is incorrect,
and treatment should be directed toward the genesis of the suffering.
The person who complains of great pain, yet has
obvious inconsistencies and spurious findings on
examination may evoke suspicion, especially if in
litigation or seeking a disability entitlement. They
may also provoke anger in caregivers who find their
repeated efforts to help thwarted. Perhaps this explains such epithets as “turkeys” and “crocks.”
A key issue in the management of such patients
may be to address the negative attitudes that trainees and staff have toward them. The following may
be useful.
Evolution would seem to mandate that organisms have at least a propensity to act in their perceived best interests. If opossums can play dead to
escape a predator, it shouldn’t surprise us that humans can play sick. The person who suffers from a
bad back, a job that is tenuous, and a lack of marketable skills may have no assurance of income and
health care for his family except through his disability. It is understandable that such a person
might exaggerate symptoms of illness.
The needs that seem to motivate inordinate illness behavior are rarely a desire to strike it rich.
Rather, patients seem to be reinforced by needs for
security, to feel loved, to avoid intolerable situations, or, in the case of those with addictive disorder, to obtain substances. When staff deprecate the
patient who is “just looking for a free ride,” they
may be asked to consider whether they’d willingly
trade places with the patient. It is easy to be contemptuous if the sought-after gain is a big settlement, harder if it is to escape a painful, hazardous,
or abusive workplace in which one is trapped by
training, language, or other handicaps. An understanding of the exigencies of these patients’ lives
will often help care givers form a non-judgmental
alliance with the patients in order to help them find
more adaptive solutions to their problems than the
adoption of the sick role.
Conclusions
There is good reason to believe that psychological
factors can generate pain, and that the experience is
as genuine as that produced by the known pain
transmission pathways. We accept that the pain of
aortic aneurysm radiates to the back, but may not
the pain of despair also radiate to the back? Pain exaggeration is a different thing, though it is likely
293
President’s Message
that behaving as a pain patient for a long period of
time can become painful. Orthopedists learned long
ago that they are unable to correct this with surgery,
and we are finding that we cannot correct it with
opioids, stimulators, facet denervations, or IDET.
We may face a dilemma in the person who has
mixed organic and psychogenic pain, that being the
choice between withholding treatment from someone because they have a psychological problem versus providing expensive and potentially harmful
treatment to someone with little likelihood of benefiting.
The specialty of pain medicine has struggled for
credibility, and part of the struggle has been to
demonstrate the reality of the invisible condition
we treat. Our laudable desire to do this may blind
us to the fact that not all pain originates in sensory
structures, and not all pain behavior reflects pain.
The concepts of psychogenic pain and of pain
exaggeration should not alter our position vis-à-vis
patients. Our mission is to reduce their suffering and
improve the quality of their lives. The admonition
that “pain is exactly what the patient says it is” is an
excellent basis for management of acute and malignant pain, though psychogenic factors can play a role
here also. With chronic non-malignant pain, reports
should be presumed to be accurate absent evidence
to the contrary, especially when the patient is seeking treatment rather than compensation. “Trust but
verify” is a useful stance when there are symptoms
that appear nonphysiologic.
We are challenged to respect the dignity of our
patients and to validate them as persons without
necessarily accepting their understanding of their
conditions. With all of us, pain is not simply an analog gauge of sensory input or even of nociceptive
transmission to the cortex, but is a product of the
interplay of these factors with ourselves as human
beings. That is not difficult to accept or to respect.
Edward C. Covington, MD
References
1 Fields HL. Pain: an unpleasant topic. Pain 1999;
83(Suppl 6):S61–9.
2 Gould R, Miller BL, Goldberg MA, Benson DF.
The validity of hysterical signs and symptoms. J
Nerv Ment Dis 1986;174:593–7.
3 Rosenzweig P, Brohier S, Zipfel A. The placebo effect in healthy volunteers: influence of experimental
conditions on the adverse events profile during phase
I studies. Clinical Pharmacology & Therapeutics
1993;54:578–83.
4 Long DM, Uematsu S, Kouba RB. Placebo re-
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
sponses to medical device therapy for pain. Stereotactic & Functional Neurosurgery 1989;53:149–56.
Schweiger A, Parducci A. Nocebo: the psychologic
induction of pain. Pavlovian Journal of Biological
Science 1981;16:140–3.
Sawamoto N, Honda M, Okada T, et al. Expectation
of pain enhances responses to nonpainful somatosensory stimulation in the anterior cingulate cortex and
parietal operculum/posterior insula: an event-related
functional magnetic resonance imaging study. J
Neurosci 2000,20:7438–45.
Duncan GH, Bushnell MC, Bates R, Dubner R.
Task-related responses of monkey medullary dorsal
horn neurons. Journal of Neurophysiology 1987;57:
289–310.
France RD, Krishnan RKK. Pain in psychiatric disorders. In: France RD, Krishnan RKK, eds. Chronic
Pain. Washington: American Psychiatric Press; 1988:
116-141.
Von Knorring L, Perris C, Eisemann L, et al. Pain as
a symptom in depressive disorders; I. Relationship to
diagnostic subgroup and depressive symptomatology. Pain 1983;15:19–26.
Lindsay P, Wyckoff M. The depression-pain syndrome and its response to antidepressants. Psychosomatics 1981;22:511–77.
Ward NG, Bloom VL, Friedel RO. The effectiveness of tricyclic antidepressants in the treatment of
coexisting pain and depression. Pain 1979;7:331–41.
Damasio AR, Grabowski TJ, Bechara A, et al. Subcortical and cortical brain activity during the feeling
of self-generated emotions. Nat Neurosci 2000;3:
1049–56.
Reiman EM. The application of positron emission
tomography to the study of normal and pathologic
emotions. J Clin Psychiatry 1997;16(Suppl 58):4–12.
van der Kolk BA, Pelcovitz D, Roth S, et al. Dissociation, somatization, and affect dysregulation: the
complexity of adaptation to trauma. Am J Psychiatry
1996;153:7(Suppl)83–93.
McCauley J, Kern DE, Kolodner K, et al. Clinical
characteristics of women with a history of childhood
abuse: unhealed wounds. JAMA 1997;277:1362–8.
Bendixen M, Muus KM, Schei B. The impact of
child sexual abuse—a study of a random sample of
Norwegian students. Child Abuse & Neglect 1994;
18:837–47.
Nijenhuis ER, Spinhoven P, van Dyck R, van der
Hart O, Vanderlinden J. Degree of somatoform and
psychological dissociation in dissociative disorder is
correlated with reported trauma. J Trauma Stress
1998;11:711–30.
Pavlovic S, Sinanovic O. (Somatization in post-traumatic stress disorders in soldiers during the war in
Bosnia-Herzegovina). Med Arh 1999;53:145–9.
Petrovic P, Petersson KM, Ghatan PH, StoneElander S, Ingvar M. Pain-related cerebral activation
is altered by a distracting cognitive task. Pain 2000;
85:19–30.
294
20 Rainville P. Pain affect encoded in human anterior
cingulate but not somatosensory cortex. Science
1997;277:968–71.
21 Kiernan BD, Dane JR, Phillips LH, Price DD. Hypnotic analgesia reduces R-III nociceptive reflex: further evidence concerning the multifactorial nature of
hypnotic analgesia. Pain 1995;60:39–47.
22 Fishbain DA, Rosomoff HL, Cutler RB, Rosomoff
RS. Secondary gain concept: a review of the scientific
evidence. Clin J Pain 1995;11:6–21.
23 Bigos SJ, Battie MC, Spengler DM, et al. A prospective study of work perceptions and psychosocial factors affecting the report of back injury. Spine 1991;
16:1–6.
24 Krause N, Ragland DR, Fisher JM, Syme SL. Psychosocial job factors, physical workload, and incidence of work-related spinal injury: a 5-year prospective study of urban transit operators. Spine 1998;
23:2507–16.
25 Papageorgiou AC, Macfarlane GJ, Thomas E, et al.
Psychosocial factors in the workplace—do they predict new episodes of low back pain? Evidence from
the South Manchester Back Pain Study. Spine 1997;
22:1137–42.
26 van Poppel MNM, Koes BW, Devillé W, Smid T,
Bouter LM. Risk factors for back pain incidence in
industry: a prospective study. Pain 1998;77:81–6.
27 Valat JP, Goupille P, Vedere V. Low back pain: risk
factors for chronicity. Rev Rhum Engl Ed 1997; 64:
189–94.
28 Williams RA, Pruitt SD, Doctor JN, et al. The contribution of job satisfaction to the transition from
acute to chronic low back pain. Arch Phys Med Rehabil 1998;79:366–74.
29 Gatchel RJ, Polatin PB, Mayer TG. The dominant
role of psychosocial risk factors in the development
of chronic low back pain disability. Spine 1995;20:
2702–9.
30 Hasenbring M, Marienfeld G, Kuhlendahl D, Soyka
D. Risk factors of chronicity in lumbar disc patients.
A prospective investigation of biologic, psychologic,
and social predictors of therapy outcome. Spine
1994;19:2759–65.
31 Scheman J, Covington EC, Blosser T, Green K. Effects of Instructions on Physical Capacities Outcome
in a Workers’ Compensation Setting. Pain Medicine
2000;1:116–22.
32 Greenough CG, Fraser RD. The effects of compensation on recovery from low-back injury. Spine 1989;
14:947–55.
33 Greenough CG, Taylor LJ, Fraser RD. Anterior
lumbar fusion. A comparison of noncompensation
patients with compensation patients. Clin Orthop
1994;300:30–7.
Covington
34 Penta M, Fraser RD. Anterior lumbar interbody fusion. A minimum 10-year follow-up. Spine 1997;22:
2429–34.
35 Rainville J, Sobel JB, Hartigan C, Wright A. The effect of compensation involvement on the reporting
of pain and disability by patients referred for rehabilitation of chronic low back pain. Spine 1997;22:
2016–24.
36 Schrader H, Obelieniene D, Bovim G, et al. Natural
evolution of late whiplash syndrome outside the
medicolegal context. Lancet 1996;347:1207–11
37 Spitzer WO, Skovron ML, Salmi LR, et al. Scientific
Monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining “whiplash”
and its management. Spine 1995;20:3S–73S.
38 Cassidy JD, Carroll LJ, Cote P, et al. Effect of eliminating compensation for pain and suffering on the
outcome of insurance claims for whiplash injury. New
England Journal of Medicine 2000;342:1179–86.
39 Long DM. Effectiveness of therapies currently employed for persistent low back and leg pain. Pain Forum 1995;4:122–5.
40 Blake C, Garrett M. Impact of litigation on quality of
life outcomes in patients with chronic low back pain.
Ir J Med Sci 1997;166:124–6.
41 Fishbain DA, Cutler R, Rosomoff HL, Rosomoff
RS. Chronic pain disability exaggeration/malingering and submaximal effort research. Clin J Pain
1999;15:244–74.
42 Bytzer P, Stokholm M, Andersen I, et al. Prevalence
of surreptitious laxative abuxe in patients with diarrhea of uncertain origin: a cost benefit analysis of a
screening procedure. Gut 1989;30:1379–84.
43 Rickards FW, De Vidi S. Exaggerated hearing loss in
noise induced hearing loss compensation claims in
Victoria. Med J Aust 1995;163:360–3.
44 Weintraub MI. Chronic pain in litigation: what is
the relationship? Neurologic Clinics 1995;13:341–9.
45 Shechtman O. Using the coefficient of variation to
detect sincerity of effort of grip strength: a literature
review. J Hand Ther 2000;13:25–32.
46 Lechner DE, Bradbury SF, Bradley LA. Detecting
sincerity of effort: a summary of methods and approaches. Phys Ther 1998;79:867–88.
47 Hildreth DH, Breidenbach WC, Lister GD, Hodges
AD. Detection of submaximal effort by use of the
rapid exchange grip. J Hand Surg 1989;14A:742–5.
48 Waddell G, McCulloch J, Kummel E, Venner RM.
Non-organic physical signs in low-back pain. Spine
1980;5:117–25.
49 Gaines WG Jr, Hegmann KT. Effectiveness of
Waddell’s nonorganic signs in predicting a delayed
return to regular work in patients experiencing acute
occupational low back pain. Spine 1999;24:396–400.