Managing Chronic Pain Biopsychosocial

670_Chronic Pain.
prelims 19/02/2002 9 27 am Page i
Managing Chronic Pain:

A Biopsychosocial Approach
670_Chronic Pain.prelims 19/02/2002 9 27 am Page iii
Managing Chronic Pain:

A Biopsychosocial
Approach
SAXBY PRIDMORE, MB, BS, BMEDSC, DPHYSIO, MD
FRANZCP, FAFPHM
CLINICAL PROFESSOR OF PSYCHIATRY
UNIVERSITY OF TASMANIA
AND
DIRECTOR OF PSYCHOLOGICAL MEDICINE
ROYAL HOBART HOSPITAL
TASMANIA, AUSTRALIA
MARTIN DUNITZ
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742
© 2002 by Taylor & Francis Group, LLC

CRC Press is an imprint of Taylor & Francis Group, an Informa business
No claim to original U.S. Government works

Version Date: 20130325
International Standard Book Number-13: 978-1-4822-0752-1 (eBook - PDF)
This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts
have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any
legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that
any views or opinions expressed in this book by individual editors, authors or contributors are personal to them
and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this
book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement
to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant
manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical
science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader
is strongly urged to consult the drug companies’ printed instructions, and their websites, before administering any
of the drugs recommended in this book. This book does not indicate whether a particular treatment is appropriate
or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his
or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers
have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to
copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been
acknowledged please write and let us know so we may rectify in any future reprint.
Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted,
or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, includ-
ing photocopying, microfilming, and recording, or in any information storage or retrieval system, without written
permission from the publishers.
For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://
www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA
01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of
users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has
been arranged.
Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for
identification and explanation without intent to infringe.
Visit the Taylor & Francis Web site at

http://www.taylorandfrancis.com
and the CRC Press Web site at

http://www.crcpress.com
670_Chronic Pain.prelims 19/02/2002 9 27 am Page v
Contents
1. Introduction 1
2. A reasonable approach to chronic pain
reduction 5
3. Anatomy and physiology 9
4. Plasticity and neuropathic pain 17
5. The biopsychosocial model in
chronic pain 27
6. Biopsychosocial pain and diagnostic
systems 37
7. Pain and psychiatric comorbidity 43
8. Pain and somatization 49
9. Fear of movement and pain 59
10. Relaxation, hypnosis and meditation 63
11. Psychotherapy in chronic pain 81
12. Fibromyalgia 91
13. Headache 105
14. Low back pain and sciatica 119
15. Pharmacotherapy 129
Index 159
670_Chronic Pain.prelims 19/02/2002 9 27 am Page vi
Said a faith-healer from Brazil

‘I know that pain isn’t real
but when I sit on a pin
and it pricks my skin
I dislike what I fancy I feel.’
Anonymous
670_Chronic Pain.ch.01 19/02/2002 9 28 am Page 1
Introduction
1 ‘To help the patient to cope the psychiatrist must be a teacher,

doctor, soothsayer, and wise friend with the right mixture of
palliative care, hope, denial, catharsis, family counseling,
relaxation, exercise, physical rehabilitation, pharmacotherapy,
and sensitivity to the unconscious.’
Anthony Bouckoms, 1996
Pain is a common human experience, but difficult to describe.

The most influential definition (Merskey, 1979) states that
pain is an unpleasant sensory and emotional experience that is
associated with actual tissue damage or is described in terms of
such damage. Immediately, unexpected elements are
introduced by this definition: pain involves an emotional
experience; and it may be experienced in the absence of
‘actual’ tissue damage.
Acute pain is a component of the warning system that
helps to preserve the individual and the species. Nociceptors
are specific primary afferent nerves that respond to potentially
tissue-damaging stimuli. Nociception is the activity in the
nervous system that occurs as a consequence of nociceptor
stimulation. A physiological view is that pain is the perception
of nociception. However, it is more than sensory system
2 Managing Chronic Pain: A Biopsychosocial Approach
activity. Nociception, through identified hard- symptom (rheumatologists, oncologists)

wired circuits, triggers emotional and provide direction. The neuropathic and
motivational-affective responses (which can be psychogenic chronic pain syndromes are less
called the pain experience). The well understood and managed. Other
environmental circumstances that give rise to important chronic pain syndromes include
the nociception, along with the acute pain fibromyalgia and the various headaches, which
experience, are stored in memory. Thus, not may involve complicated mixtures of physical
only can the circumstances that lead to danger and psychological contributions.
be avoided in the future (providing survival Chronic pain lacks a useful function. It has
advantage), but the pain experience can be been defined as pain lasting more than six
remembered in the future, providing at least a weeks (Bouckoms, 1996) and as pain lasting
partial basis for chronic pain. more than six months (Russo & Brose, 1998).
In addition to the acute–chronic division, Others (Loeser and Melzack,1999) have
pain can be classified according to current argued for a conceptual rather than a
pathophysiologic knowledge. This introduces quantitative definition: ‘It is not the duration
nociceptive, neuropathic and psychogenic of pain that distinguishes acute from chronic
pain. Nociceptive pain occurs when the pain but, more importantly, the inability of
nervous system is intact and the symptoms are the body to restore its physiological functions
consistent with known or suspected somatic to normal homeostatic levels.’
or visceral damage. Neuropathic pain is the Chronic pain is a common disorder that
result of an abnormality of the nervous causes great individual suffering. It is costly in
system. A range of pathophysiological fiscal as well as human terms. It is often
mechanisms may be present in the peripheral, associated with increasing dependence,
central or sympathetic systems. The term irritability, somatic concern, social
‘psychogenic pain’ has been applied when withdrawal, physical and occupational
psychological factors appear to be of primary disability, and a higher than normal
aetiological importance (Roth, 2000). prevalence of psychiatric disorders such as
Often the tissues producing nociceptive anxiety and depression.
pain (a calf muscle injury, for example) heal in Non-invasive techniques such as provision
a matter of weeks and the pain resolves. of information, goal setting,
Where this does not happen there is usually pharmacotherapy, relaxation, logical thinking,
an ongoing process, such as an inflammatory and exploration of psychological issues are
or a neoplastic process, and specialists important in chronic pain reduction. In many
experienced in the management of this cases they constitute the most appropriate
Introduction 3
approach. In other cases they are an chronic pain. A particular aim is to provide
alternative to the invasive therapeutic material that will be useful to Psychiatrists and
techniques. When the invasive therapeutic General Practitioners.
techniques are the treatment of choice, the
addition of complementary non-invasive
References
techniques ensures comprehensive care.
Invasive techniques in chronic pain Bouckoms A. Chronic pain:
neuropsychopharmacology and adjunctive
comprise an array of diagnostic and psychiatric treatment. In: Rundell J, Wise M
therapeutic manoeuvres that rest on an (eds) Textbook of Consultation-Liaison Psychiatry.
extensive scientific base. It is unreasonable to American Psychiatric Press, Washington, DC,
1996; 1007–36.
expect invasive therapeutic techniques to
Cheville A, Caaceni A, Portney R. Pain: definition
bring relief if the evidence for a treatable
and assessment. In: Massie MJ (ed) Pain: What
organic pathology is doubtful or when similar Psychiatrists Need to Know. (Review of
past treatments have brought little lasting Psychiatry Series, Vol. 19, No 2; Oldham J and
relief. Riba M, series eds). American Psychiatric Press,
Washington, DC, 2000; 1–22.
The biopsychosocial model of illness,
Loeser J, Melzack R. Pain: an overview. Lancet
which emphasizes the contribution of 1999; 353: 1607–9.
biological/medical, psychological/psychiatric Merskey H. Pain terms: a list with definitions and a
and social/environmental factors in aetiology note on usage. Recommended by the
and management, has been a guiding concept International Association for the Study of Pain
(IASP) Subcommittee on Taxonomy. Pain
in psychiatry and comprehensive family
1979; 6: 249–52.
medicine for more than two decades. It is the
Roth R. Psychogenic models of chronic pain: a
ideal recommended approach in all forms of selective review and critique. In: Massie MJ
pain (Cheville et al, 2000). The (ed) Pain: What Psychiatrists Need to Know.
social/environmental component should be (Review of Psychiatry Series, Vol. 19, No 2;
Oldham J and Riba M, series eds). American
expanded to include cultural factors. Different Psychiatric Press, Washington, DC, 2000;
ethnic groups demonstrate different responses 89–131.
to the experience of pain (Zborowski, 1969), Russo C, Brose W. Chronic pain. Annual Review of
and it is argued that ‘pain and suffering in Medicine 1998; 49: 123–33.
society are manifested in pain and suffering in Ware N, Kleinman A. Culture and somatic
experience: the social course of illness in
the body’ (Ware and Kleinman, 1992).
neurasthenia and chronic fatigue syndrome.
This book contains theoretical and Psychosomatic Medicine 1992; 54: 546–60.
practical information that will assist a range of Zborowski M. People in Pain. Jossey-Bass, San
professionals in their work with patients with Francisco, 1969.
A reasonable approach to
chronic pain reduction
2 ‘Doctors think a lot of patients are cured who have simply

quit in disgust.’
Don Herold
Woven together, the following points form a useful approach

to chronic pain.
1. The fundamental Hippocratic principle of ‘first do no

harm’ applies throughout medical practice. In chronic
pain management, the non-invasive techniques carry a low
risk of causing harm. There is a need to prescribe
medication cautiously and to make every effort to avoid
medication abuse and addiction.
2. Comprehensive examination and investigation is
mandatory. Once this process is complete the most likely
diagnosis should be decided and the most appropriate
treatment commenced. It is not necessary for the pain
therapists to re-investigate the case, if suitable investigations
have already been conducted by a capable clinician. Further
investigations should be kept to a minimum and should be
conducted only when there is good reason to expect that the
result will be different from those obtained previously.
3. The health professionals working in relative or friend. Such an individual can

chronic pain should communicate that give important information regarding the
they accept that the patient’s pain is patient’s level of function in daily life and
‘real’. This is the case in all except encourage the patient to comply with
malingerers. Research has revealed a professional suggestions when at home or
range of mechanisms by which firing in social settings.
thresholds of sensory processing 7. It is most important to provide the
neurones may be lowered, allowing for patient with good information, from the
stronger pain than might have been first and at every subsequent meeting.
expected in particular clinical situations. 8. Realistic expectations should be
Pain that is predominantly of encouraged. Chronic pain has by
psychological origin is no less real to the definition persisted well beyond the
patient than that which is predominantly normal healing time. It is realistic to
of physical origin. expect that treatment will reduce pain
4. A supportive patient–therapist and make a fuller life possible (albeit
relationship is encouraged. The with residual pain). While it is healthy to
characteristics of this relationship differ hope and work toward complete
slightly, depending on the theoretical cessation of pain, it is also healthy for the
and clinical training of the therapist. patient to understand and accept that
Universal characteristics are respect for this may be unlikely given present
the patient and the belief that patient medical knowledge and technology.
choices are possible and change is Accordingly, in most cases it is
necessary. unhealthy, in so far as it will delay
5. Pain is best conceptualized using the adjustment and risk iatrogenic
biopsychosocial model. Thus, both complications, for patients to persist in
biological/physical, the search for the total medical cure to
psychological/psychiatric and chronic pain.
social/environmental factors should be 9. Patients need to be prepared for setbacks.
considered in both aetiology and Fluctuations in clinical state are a feature
treatment. of all chronic conditions. These are
6. Whenever possible, a person from the particularly common when activity is
patient’s family or social life should be increased. Patients who are increasing
involved in the examination and their activity after a period of relative
treatment process. This may be a partner, inactivity need to expect such
A reasonable approach to chronic pain reduction 7
fluctuations and to continue (rather than pattern of behaviour. It is also an

abandon) the pain reduction process. experience. Nevertheless, it makes sense
10. Hurting does not indicate harm. In to encourage behaviour that does not
chronic pain there has been time for the typify the patient as an invalid.
healing of any damaged structures. 13. Operant formulations that pain
Unstable joints will have been stabilized, behaviour is performed as a means of
entrapped structures will have been attracting rewards lead to scepticism and
released and any other necessary suspicion of malingering. It may result in
procedures will have been performed. unfair withholding of support. The
Thus, pain associated with activity does apparent increase in pain behaviour
not indicate further damage to the body. when a patient is in the presence of
It is most important for the patient to supportive individuals is given a different
understand and accept this point. and more positive interpretation by
11. Return to normal or near-normal activity evolutionary psychology. The patient is
is desirable. Pain fosters inactivity. This viewed as suppressing or hiding pain
results in loss of motor power and joint behaviour when in the company of
stiffness. As muscles atrophy they lose unsupportive individuals ‘in the field’;
the capacity to perform their ‘bracing’ or however, in supportive environments,
supporting function. Thus pain and this suppression is released and pain
inactivity can lead to the downward behaviour, vulnerability and care-
spiral of ever more pain and inactivity. eliciting are revealed.
Inactivity has the additional unhelpful 14. Pacing behaviour is encouraged. Clinical
consequence of loss of social role and wisdom is that when patients with
self-esteem. Retaining or returning to chronic pain have relatively pain-free
near-normal activity minimizes pain and periods, they tend to be overactive,
provides a range of benefits. which then causes temporary increases in
12. Operant conditioning-based therapy pain. These ‘flare ups’ result in a return
states that the rewarding of positive to periods of inactivity. Instead, patients
efforts with encouragement and the non- are encouraged to ‘pace’ themselves: to
rewarding of (withholding of approval be active regularly, but to limit the
from) pain behaviour may encourage amount of activity so that ‘flare ups’ do
return to normal behaviour. The not occur. Specific studies to support
weakness of behaviourism in this clinical ‘pacing’ have not been reported, but the
setting is that pain is not simply a concept has face validity.
15. Logical thinking is more helpful than also be indicated where physically based
illogical thinking. Thoughts influence pain necessitates difficult psychological
the way one feels. This is the basis of the adjustments.
original cognitive behaviour therapy. 18. Medication is indicated, almost without
Thoughts such as ‘I cannot pick my exception. Excessive or inappropriate
children up so I am a failure as a parent’ medication, however, is to be avoided.
result in demoralization and depression, This is particularly the case with the
and must be challenged and corrected for short-acting opioids and certain
the patient to achieve the best possible benzodiazepines. Such medications have
result. limited beneficial effects in chronic pain
16. Relaxation training, self-hypnosis and and carry the risk of addiction.
medication have all been shown to 19. Excessive health-care utilization is
relieve chronic pain. The patient should discouraged. It not only wastes the
be taught and encouraged to practise at patient’s resources and delays recovery,
least one such technique. but is also wasteful of community
17. Psychotherapy has a place when there is a resources. It usually arises from excessive
need for the patient to adjust human patient concern about the pain.
relationships, sense of self or goals. It is Reducing undue utilization is not an easy
particularly indicated where task and may, after clear and repeated
psychological factors are important in the reassurance and a period of support, call
aetiology or maintenance of pain. It may for limit-setting.
Anatomy and physiology
3 ‘Symptoms, then, are in reality nothing but the cry from

suffering organs.’
Jean-Martin Charcot
The anatomic and physiologic basis of pain is a highly

sophisticated and emerging field. The interested reader should
consult encyclopaedic textbooks such as Bonica (1990a), Wall
and Melzack (1999) and Haines (1997).
Most clinicians do not require the details of latest animal
laboratory studies. Instead, a brief account is presented that
brings some preclinical and clinical matters together.
Local response to trauma/inflammation

Initial traumatic events depolarize pain neurones and cause
initial pain. Subsequent physiologic changes make these
neurones more sensitive than normal to noxious stimuli
(hyperalgesia).
The macroscopic hallmarks of trauma/inflammation are
redness, swelling, heat and loss of function (which encourages
repair). The microscopic hallmark is the accumulation of fluid
and cells at the site. Mast cells are important activators,
releasing histamine from preformed a range of stimuli. They transmit slowly

cytoplasmic granules and synthesizing other (1 m/s) and provide the ‘slow pain’, which is
mediators, including prostaglandins. felt 1–2 s after the application of a noxious
Serotonin is produced by platelets. Bradykinin stimulus.
is synthesized in the plasma. Substance P (sP)
is released from stimulated nerve endings.
Terminals of the primary
Catecholamines are released from sympathetic
endings into the traumatized region.
afferents
Histamine, prostaglandins, serotonin, There is some individual variation in the
bradykinin, sP and catecholamines, among arrangement of the neural structures
other agents, are believed to increase the subserving pain. Thus, predictions of
permeability of capillaries, resulting in the aetiology and response to procedures should
local swelling. Also, they excite pain neurones be attempted with caution. The following is
and are responsible for the hyperalgesia. the most common arrangement (see Figure
3.1):
Sensory neurones have cell bodies in the
Primary sensory neurones
dorsal root ganglion and enter the spinal cord
There are two broad groups of sensory via the dorsal root. They divide into ascending
neurones: (1) myelinated A fibres, and (2) and descending branches and travel short
smaller diameter, unmyelinated C fibres. distances in the dorsolateral tract before
A-beta fibres have a low threshold and terminating in the dorsal horn. The dorsal
transmit non-noxious tactile and mechanical horn is arranged in a series of laminae (Brose
information. and Spiegel, 1992).
Thinly myelinated A-delta fibres and C Lamina I is superficial and posteriorly
fibres have a higher threshold and are located. The second-order neurones with cell
nociceptors: specific primary sensory neurones bodies in this lamina receive input from
that signal noxious stimulation. They are nociceptors A-delta and C fibres.
activated by energy (mechanical, thermal or Lamina II is deep to lamina I and is
chemical), which can, in the extreme, cause known as substantia gelatinosa, on the basis of
tissue damage. its appearance. The second-order neurones in
A-delta fibres detect mechanical and this lamina receive input exclusively from C
thermal stimuli. They transmit impulses fibres (Woolf and Mannion, 1999). In
rapidly (12–30 m/s) and provide the ‘first addition, lamina II is densely packed with
pain’. C fibres are ‘polymodal’, responding to small cells that synapse both internally and in
Anatomy and physiology 11
A beta
Dorsolateral
Tract
C
I
II
III
IV
V
Figure 3.1
Termination of peripheral sensory neurones in the laminae of the dorsal horn (much simplified). Touch (A
beta) fibres terminate in lamina III, IV or V. Pain (C) fibres terminate predominantly in lamina II. The
dorsolateral tract is superficial to laminae I and II.
other laminae. They are important in the Ascending sensory pathways

inhibition of second-order cells.
Laminae III and IV contain the cell bodies The axons of the second-order cells of the
of neurones that receive the terminal dorsal horn usually cross the cord and pass
projections of A-beta neurones, which are upward as the spinothalamic or spinoreticular
responsive to non-noxious stimulation, systems (see Figures 3.2 and 3.3), within the
including touch. contralateral anterolateral funiculus (Price,
2000). The spinothalamic system is composed
of neospinothalamic and palaeospinothalamic
divisions.
CORTEX
limbic
forebrain medial/ ventroposterolateral
structures intralaminar nucleus and medial
thalamic nuclei part of the posterior
thalamus
hypothalamus palaeospinothalamic
tract
neospinothalamic
tract
periaqueductal reticular
grey formation
to dorsal horn cells spinothalamic

tract
Figure 3.2
Projection of spinothalamic tract. The spinothalamic tract (composed of palaeospinothalamic and
neospinothalamic fibres) is passing upward at the bottom right.
The fibres which are to become the palaeospinothalamic tract relay at the reticular formation. Projections
then proceed to the hypothalamus and thalamus, and subsequently, the limbic system and cortex. This
arrangement may provide the anatomical substrate for the emotional and motivational aspects of pain. The
neospinothalamic tract bypasses the reticular formation and relays at the thalamus before reaching the
cortex. It is believed to provide an anatomical substrate for the informational aspects of pain. Projections
from the reticular formation to the periaqueductal grey matter are part of a feedback pathway to the dorsal
horn cells.
CORTEX
limbic forebrain
structures
medial/intralaminar
thalamic nuclei
reticular
hypothalamus formation
periaqueductal
grey
to dorsal horn cells

spinoreticular
tract
Figure 3.3
Projections of spinoreticular tract. The spinoreticular tract is passing upward at the bottom right. It ends at
the reticular formation. Output from the reticular formation goes to the hypothalamus, thalamus and the
limbic system. Projections then reach the cortex. This arrangement may provide the anatomical substrate for
the emotional and motivational aspects of pain in the human.
As with the spinothalamic tract, output from the reticular formation goes to the periaqueductal grey
matter which projects to the dorsal horn cells, thus providing a mechanism for the reduction of nociceptive
input.
Other ascending nociceptive pathways are Thalamus

found in the spinomesencephalic tract, dorsal
column system, spinocervical tract and The thalamus is a complex of many nuclei,
multisynaptic ascending system (Bonica, differently named by different authors. For
1990b). These are listed only and will not be present purposes, we can focus on two parts:
discussed further. (1) the posterior thalamus (precisely, the
ventroposterolateral thalamic nucleus, and the
medial part of the posterior thalamus); and (2)
Brain-stem relays the medial/intralaminar thalamic nuclei.
The brain stem contains a complex The posterior thalamus receives input
arrangement of grey matter nuclei. Most from the neospinothalamic tract, which
pathways, passing in both directions (cephalad bypasses the reticular formation. It projects to
and caudad), synapse in the brain stem and the cortex.
can be modified at these relay stations. (The The medial/intralaminar thalamic nuclei
neospinothalamic tract bypasses these nuclei, receive pathways from the reticular formation,
and is thus an exception.) which is a relay station of the
The reticular formation extends from the palaeospinothalamic and the spinoreticular
mesencephalon through the pons to the tracts.
medulla. It is described as a collection of The medial/intralaminar thalamic nuclei
nineteen separate nuclei (Bonica, 1990b); but nociceptive outflows go to the hypothalamus,
for simplicity, it can be considered here as a limbic forebrain structures and the cerebral
single entity. In this view the important locus cortex. The connections with the limbic
coeruleus is an integral part of the reticular system are believed to provide the mechanism
formation. The reticular formation projects for the emotional and motivational aspects of
fibres to the thalamus, hypothalamus and pain.
limbic structures.
The periaqueductal grey matter is situated
The cortex
in the midbrain. Along with the locus
coeruleus and other reticular formation nuclei, The posterior thalamus (which receives input
it has an important role in modifying from the neospinothalamic tract) projects to
descending information, both locally and via the primary somatosensory (SI) cortex, which
projections that descend in the dorsal columns is bordered anteriorly by the central sulcus.
to the dorsal horn cells at segmental levels. This arrangement is believed to provide the
mechanism for the localization of pain.
The medial/intralaminar thalamic regulation mechanism that allows us to ignore

projections (after passage through limbic certain stimuli.
structures) extend to the second The ability of supraspinal components to
somatosensory cortex (SII), which lies on the reduce the experience of pain is consistent
inner face of the upper bank of the lateral with the finding that relaxation and hypnosis
sulcus (Treede et al, 2000). The role of SII is (strong methods of focusing of attention) have
not well established, but may include the well-established analgesic actions.
emotional and motivational aspects and the The physiologic ‘gate’ can also be closed at
memory of pain. the segmental level, by activation of large
neurones in the skin. This principle is well
known to anyone who has grazed and rubbed
Descending Pathways
their knee, and has found clinical utility in the
People may not experience immediate pain, application of heat and electrical currents to
even though they are seriously injured. reduce pain.
Physiologic mechanisms are involved,
consistent with the closing of a physiologic
‘gate’ (Melzack and Wall, 1965). Neurones References
with cell bodies in periaqueductal grey matter Bonica J. The Management of Pain, 2nd edn. Lea &
and fibres in the dorsal column can inhibit the Febiger, Philadelphia, 1990a.
discharge of dorsal horn cells, thereby Bonica J. Anatomic and physiologic basis of
reducing nociceptive input. A feedback loop is nociception and pain. In: Bonica J (ed) The
formed, with input from the spinoreticular Management of Pain, 2nd edn. Lea & Febiger,
Philadelphia, 1990b.
and palaeospinothalamic tracts, the reticular
Brose W, Spiegel D. Neuropsychiatric aspects of
formation and the periaqueductal grey
pain management. In: Yudofsky S and Hales R
matter. (eds) The American Psychiatric Textbook of
As pain is a warning system, it is uncertain Neuropsychiatry, 2nd edn. American
why a mechanism for reducing nociception Psychiatric Press, Washington, DC, 1992:
245–75.
should exist. However, if you come across a
Haines D. Fundamental Neuroscience. Churchill
sleeping lion in the jungle and step on a thorn
Livingstone, New York, 1997.
as you back away, it is better that you
Melzack R, Wall P. Pain mechanisms: a new theory.
continue to focus your attention on the lion, Science 1965; 150: 971–9.
rather than scream and leap in the air. The
Price D. Psychological and neural mechanisms of
pain-suppression pathway appears to be a the affective dimensions of pain. Science 2000;
component of a general sensory input 228: 1769–72.
Treede R, Apkarian A, Bromm B. Cortical Woolf C, Mannion R. Neuropathic pain: aetiology,

representation of pain: functional symptoms, mechanisms, and management.
characterization of nociceptive areas near the Lancet 1999; 353: 1959–64.
lateral sulcus. Pain 2000; 87: 113–17.
Wall P, Melzack R. Textbook of Pain. Churchill
Livingstone, Edinburgh, 1999.
Plasticity and neuropathic pain
4 ‘To every human problem there is a neat and easy solution –

and it’s wrong’
H L Mencken
Acute pain is a warning signal that serves a necessary survival

function. Two types of acute pain can be recognized:
physiologic/normal pain and clinical (see Figure 4.1). In
physiologic/normal pain there is minimal or no tissue damage,
such as when one picks up, and quickly puts down, an
unexpectedly hot dinner plate (Woolf and Salter, 2000).
Clinical pain, on the other hand, is associated with severe
noxious insult and tissue damage. Two types can be
recognized: acute and chronic. Unlike acute pain, chronic
pain performs no useful function, representing instead a tragic
human burden. Three types of chronic pain can be
recognized: psychogenic, inflammatory and neuropathic.
Inflammation is a fundamental pathologic process, a
dynamic complex of cytologic and histologic reactions that
occur in affected blood vessels and adjacent tissues, in
response to an injury or abnormal stimulation, caused by a
physical, chemical or biologic agent. For present purposes,
inflammatory pain is most frequently associated with trauma
Pain
Physiological/ Clinical
normal pain pain
Acute Chronic
Nociceptive Neuropathic Psychogenic
Figure 4.1
The pain tree, Physiological/normal pain is a distant relative of neuropathic pain and the other forms of
chronic pain. There is, at most, a slight family resemblance.
and the ‘inflammatory diseases’. An important on change in gene expression and phenotype
recent finding is that neuropathic changes (Hunt and Mantyh, 2001). For example, the
may be associated not only with direct trauma biology of sensory neurones is maintained by
to neural tissue, but also with continuous or growth factors for the innervated tissues, and
severe nociceptive input from inflammatory following inflammation, changes in
lesions (Terayama et al, 2000). phenotype are triggered by changes in the
Neuropathic pain is defined as ‘pain factors released at the injury site.
initiated or caused by a primary lesion or The symptoms that suggest neuropathic
dysfunction in the nervous system’ (Mersky pain include spontaneous pain, hyperalgesia
and Bogduk, 1994). It may manifest very and allodynia. The spontaneous pain is
severe symptoms; it is usually chronic, always characteristically burning or shooting in
difficult to treat. It is poorly understood, and nature. Hyperalgesia is an increased pain
deserves special consideration. Neuropathic response to a suprathreshold noxious stimulus
pain depends on neuroplasticity, that is, (that is, a painful stimulus hurts more than it
change in the function, chemistry and should). Allodynia is the sensation of pain
structure of neurones. Accordingly, it depends elicited by a non-noxious stimulus, such as the
Plasticity and neuropathic pain 19
gentle touch of clothes or the bending of a mechanisms is helpful to the clinician. It gives
cutaneous hair by a puff of wind. Spontaneous a better understanding of the mode of action
pain may be conceptualized as ‘stimulus- of some of our rudimentary interventions. For
independent’ and hyperalgesia and allodynia example, in neuropathic pain the tricyclic
as ‘stimulus-dependent’ pain. antidepressants function not only on
Focusing on symptoms and aetiology has neurotransmitters but also as sodium channel
not provided a productive model for blockers, thus reducing ectopic discharges (see
understanding or intervention. It has become below). Importantly, these mechanisms give a
clear that neuropathic pain does not have a more complete understanding of the
single underlying mechanism. In fact an neuropathic pain patient. They give
extensive range of mechanisms has been legitimacy to a range of claimed symptoms
discovered. No particular injury or disease that have often been doubted by clinicians.
process is associated with a unique pain They explain how pain can be felt when there
mechanism, and many different mechanisms is no activity and how activity may make pain
may produce the same symptom. In any given worse. They explain how pain can be triggered
patient suffering neuropathic pain, a number by the slightest touch, how pain can spread
of mechanisms are usually operating at the beyond the site of trauma and, with the
same time, and they usually change over time. change of mechanisms over time, how one
The newly described neuropathic agent may be useful at one time but become
mechanisms operate at the peripheral, spinal frustratingly useless later on.
cord and supraspinal levels (Taylor, 2001).
We currently lack reliable methods of
Predisposition
preventing the development of these
mechanisms. We are unable to determine Trauma and inflammatory conditions are of
reliably, in the clinical setting, which aetiological importance, leading to local
particular mechanism/s is/are operating in a changes and subsequent phenotypic
given patient. Finally, we lack a specific and modification (Hunt and Mantyh, 2001).
effective therapeutic intervention for each However, by no means all of those people
mechanism. Understanding of these exposed to trauma and inflammatory
mechanisms, however, is growing, new conditions develop neuropathic pain. There is
interventions are being developed, and there is now evidence of an inherited predisposition to
promise for the future. There is a basis for chronic pain (Mogil et al, 1999).
progress. There is evidence that a disturbed early life
Even at this early stage, knowledge of the may result in brain changes and a
predisposition to depression. Depression is directions, and such agents are released by

common in chronic pain, and chronic pain is antidromic potentials, which proceed from
more common among the socially ectopic discharges (Woolf and Mannion, 1999).
disadvantaged. Such threads have led to
speculation that a disturbed early life may also
Cross-excitation
predispose to chronic pain (Rome and Rome,
2000). Injury may lead to disruption of glial sheaths.
Adjacent denuded axons may make electrical
or chemical contact, resulting in cross-
The mechanisms excitation. Undamaged neurones may also
Ectopic discharge become involved (Amir and Devor, 2000).
When A-beta fibres activate C fibres, non-
Spontaneous activity in normal primary noxious stimuli may produce pain.
sensory neurones is low. After injury,
however, spontaneous ectopic discharges are
observed in skeletal muscle afferents Neurotransmitter change
(Michaelis et al, 2000). These are the result of After injury, phenotypic change in the
phenotypic changes in the nature of and production of neurotransmitters of peripheral
distribution of sodium and calcium channels, nerves may result in pain. A-beta fibres, which
which occur throughout the damaged normally transmit non-noxious tactile
neurone, including the dorsal root ganglion messages, may begin to release pro-nociceptive
(DRG). These changes may not only result in transmitters, such as substance P, at the spinal
spontaneous pain, but contribute to central cord (Noguchi et al, 1995). Thus, touch may
sensitization (to be discussed below). cause pain.
Interestingly, after insult to a region, some
uninjured neurones may also demonstrate
ectopic discharge (Bridges et al, 2001). Coupling between the sympathetic
and sensory nervous systems
In normal physiologic conditions, the
Sensitization of sensory terminals
sympathetic nervous system cannot cause
Nociceptor peripheral terminals of injured and pain. Uninjured primary sensory nerve
uninjured neurones are sensitized by substance endings are not sensitive to catecholamines
P, released from the terminals of local damaged and are functionally distinct from the efferent
neurones. Axons transmit potentials in both sympathetic nervous system.
After injury, however, there are at least two of C fibres in lamina II. There may be
mechanisms by which coupling between the numbness. The central projections of
sympathetic and sensory motor systems may surviving A-beta fibres in laminas III and IV
be established, providing mechanisms for may sprout into the territory vacated by the
neuropathic pain. First, both injured and C-fibre terminals in lamina II and make
uninjured neurones develop alpha- contact with second-order pain transmission
adrenoreceptors, which makes them neurones (Woolf et al, 1995). Thus non-
responsive to noradrenaline from sympathetic noxious information, such as proprioceptive
nerve terminals. (Injured neurones are also information or touch, may be interpreted as
believed to be responsive to circulating being of noxious origin. This is a
adrenaline and noradrenaline.) Second, pathophysiological explanation for pain from
sprouting of sympathetic axons into the movement and allodynia (Kohama et al,
DRGs forms baskets around the cell bodies of 2000).
sensory neurones and appears to be capable of
causing depolarization (Woolf and Mannion,
Spinal cord increased excitability
1999).
In spite of these potential mechanisms, the Any prolonged or excessive sensory input
actual proportion of cases of neuropathic pain from persistent inflammation or nerve injury
in which there is significant contribution from may result in increased excitability in the
the sympathetic nervous system is probably spinal cord (Woolf and Wall, 1986). This has
small. Current treatments of neuropathic pain been called ‘central sensitization’. Several
that are aimed at the sympathetic system have mechanisms have been described. Nociceptor
produced equivocal results (Kingery, 1997). input may lead directly to sensitization of
secondary dorsal horn neurones. Peripheral
nerve injury may lead to elevated spinal
Spinal cord reorganization
dynorphin (endogenous opioid), which may
The normal arrangement is that primary sensitize the second-order neurones in the
afferent neurones terminate in particular cord. Such elevation may be ‘multisegmental’,
layers of the dorsal horn of the spinal cord, occurring at levels distant from the segment of
synapsing with particular, predetermined the injured nerve, causing ‘extraterritorial’
second-order neurones. Lamina II receives neuropathic pain, or pain in a region not
nociceptor C-fibres exclusively. After nerve supplied by the damaged nerve (Malan et al,
injury, however, there may be substantial 2000).
degeneration and loss of the central terminals With healing, central sensitization may
subside. However, through ectopic activity in The above findings are largely from single-
A-beta neurones, it may be sustained cell neurophysiology studies of experimental
indefinitely. animals. These techniques are not at present
available in clinical practice. Valuable human
information, however, can be derived from
Spinal cord decreased inhibition
imaging and related studies.
Nerve injury may result in death of inhibitory The thalamus is believed to experience
dorsal horn interneurones, which leads to pain-related plastic change (Lenz et al, 2000).
disinhibition and the increased likelihood of Quantitative sensory testing and
dorsal horn neurones firing spontaneously or neurophysiological and psychological
in an exaggerated manner (Woolf and examination of patients with complex regional
Mannion, 1999). Decreased spinal cord pain syndrome suggest thalamic plasticity in
gamma amino butyric acid (GABA) chronic pain (Rommel et al, 2001). Regional
concentration and GABA receptor binding blood flow changes have been observed in the
sites have been reported (Castro-Lopes et al, basal ganglia of patients with chronic pain
1993). Thus the ‘gate’ can no longer be closed (Mountz et al, 1998). Altered facilitation and
by stimulating intact peripheral A-beta fibres inhibition of the motor cortex using
or via descending impulses from higher transcranial magnetic stimulation in two
centres. groups of patients with two painful disorders,
fibromyalgia and rheumatoid arthritis, have
been demonstrated by Salerno et al (2000).
Supraspinal influences
They hypothesized these findings were
The ability of descending fibres to inhibit secondary to pain-induced changes in the
nociception is well established. More recently, basal ganglia.
descending fibres with an ability to facilitate Chronic back pain (Flor et al, 1997) and
nociception have been reported. Evidence amputation (Wiech et al, 2000) are associated
indicates that injury and persistent noxious with spatial reorganization of somatosensory
input associated with inflammatory pain cortical mapping. Birbaumer et al (1995) have
causes long-term changes in the activity of described ‘corticalization’ of chronic pain.
brain stem neurones that enhance facilitation Such changes have yet to be thoroughly
and contribute to neuropathic pain (Ossipov investigated; however, it is probable that
et al, 2000). This facilitation appears to be plastic brain changes secondary to pain are
driven by brain-stem cholecystokinin important in causing and maintaining
(Kovelowski et al, 2000). neuropathic pain.
Treatment implications an established role in trigeminal neuralgia,

and, along with sodium valproate, appears to
Neuropathic pain is difficult to treat. We are have more general application in neuropathic
waiting for the new understanding of the pain. Gabapentin appears to have a place in
pathophysiologic mechanisms to lead the way. the management of post-herpetic neuralgia
Clinical tests are required to identify which and other neuropathies (Backonja et al, 1998).
mechanisms are present, and new therapeutic Lamotrigine and topiramate may prove to be
options are also necessary to address each. useful.
Research is currently being conducted on In general, in chronic pain, it is important
many potentially useful pharmacological to recognize and treat concurrent depression
agents, including unique sodium channel and anxiety. This enables people to ‘cope’
blocker and nerve growth factors. with their pain and associated difficulties.
From the existing pain treatments, the Insomnia is common, can lead to dysphoria,
non-steroidal anti-inflammatory drugs have and is usually responsive to tricyclics.
little effect, and the use of opiates in Psychotherapy that focuses on cognitive
neuropathic pain is a matter of debate behaviour may be of benefit. Patients are
(Rowbotham et al, 1998). Dorsal column encouraged to take a logical and practical
stimulation and chronic epidural approach to their condition and life situation.
administration of a range of drugs using They are encouraged to measure their self-
implanted devices are available at special worth using philosophical rather than physical
centres. Woolf and Mannion (1999) described productivity criteria. Meditation of various
the former as controversial and the latter as forms has a beneficial role, reducing anxiety
not having been adequately assessed. Various and improving pain status (Kabat-Zinn et al,
anaesthetic blocks may provide temporary 1987). Compliance can be a problem, but this
relief. approach has high patient acceptance and has
The tricyclic antidepressants and the advantage of being side-effect free, and
anticonvulsants have been the most useful strongly involves patients in their own care.
agents over a number of decades. It has long Activity and independence is encouraged.
been thought that the beneficial action of the While regular opioids are better avoided if
tricyclics was related to increases in possible, it is important not to leave patients
noradrenaline and serotonin in the dorsal with only psychological techniques when pain
horn. Recent evidence indicates that they does crescendo. Tramadol or another suitable
reduce ectopic depolarization by a sodium agent has a place as an ‘as needed rescue
channel blocking action. Carbamazepine has package’ when the activity recommended by
the physician leads to an exacerbation of trials for peripheral neuropathic pain and
symptoms. complex regional pain syndromes. Pain 1997;
73: 123–39.
Kohama I, Ishikawa K, Kocsis J. Synaptic
References reorganization in substantia gelatinosa after
peripheral nerve neuroma fomation: aberrant
Amir R, Devor M. Functional cross-excitation
innervation of lamina interneurons by A-beta
between afferent A- and C-neurons in dorsal
afferents. Journal of Neuroscience 2000; 20:
root ganglia. Neuroscience 2000; 95: 189–95.
1538–49.
Backonja M, Beydoun A, Edwards K, et al. Kovelowski C, Ossipov M, Sun H, Lai J, Malan T,
Gabapentin for the symptomatic treatment of Porreca F. Supraspinal cholecystokinin may
painful neuropathy in patients with diabetes drive tonic facilitation mechanisms to maintain
mellitus: a randomized controlled trial. Journal neuropathic pain in the rat. Pain 2000; 87:
of the American Medical Association 1998; 280: 265–73.
1831–6.
Lenz F, Lee J, Garonzik I, Rowland L, Dougherty
Birbaumer N, Flor H, Lutzenberger W, Elbert T. P, Hua S. Plasticity of pain-related neuronal
Corticalization of chronic pain. In: Bromm B activity in the human thalamus. Progress in
and Desmedt J (eds) Pain and the Brain: From Brain Research 2000; 129: 259–73.
Nociception to Cognition. Advances in Pain
Research and Therapy Vol. 22. Raven Press, New Malan T, Ossipov M, Gardell L, Ibrahim M, Bian
York, 1995; 331–43. D, Lai J, Porreca F. Extraterritorial neuropathic
pain correlates with multisegmental elevation of
Bridges D, Thompson S, Rice A. Mechanisms of spinal dynorphin in nerve-injured rats. Pain
neuropathic pain. British Journal of Anaesthesia 2000; 86: 185–94.
2001; 87: 12–26.
Mersky H, Bogduk N. Classification of Chronic
Castro-Lopes J, Tavares I, Coimbra A. GABA Pain, 2nd edn. IASP Press, Seattle, 1994; 394.
decreases in the spinal cord dorsal horn after
peripheral neurectomy. Brain Research 1993; Michaelis M, Liu X, Janig W. Axotomized and
620: 287–91. intact muscle afferents but not skin afferents
develop ongoing discharges of dorsal root
Flor H, Christoph B, Elbert T, Birbaumer N. ganglion origin after peripheral nerve lesion.
Extensive reorganization of primary Journal of Neuroscience 2000; 20: 2742–8.
somatosensory cortex in chronic back pain
patients. Neuroscience Letters 1997; 224: 5–8. Mogil J, Wilson S, Bon K. Heritability of
nociception II. ‘Types’ of nociception revealed
Hunt S. Mantyh P. The molecular dynamics of by genetic correlation analysis. Pain 1999; 80:
pain control. Neuroscience 2001; 2: 83–91. 83–93.
Kabat-Zinn J, Lipworth L, Burney R, Sellers W. Mountz J, Bradley L, Alarcon G. Abnormal
Four-year follow-up of a meditation-based functional activity of the central nervous system
program for the self-regulation of chronic pain: in fibromyalgia syndrome. American Journal of
treatment outcome and compliance. Clinical Medical Science 1998; 315: 385–96.
Journal of Pain 1987; 2: 159–73.
Noguchi K, Kawai Y, Fukuoka T. Substance P
Kingery W. A critical review of controlled clinical induced by peripheral nerve injury in primary
afferent sensory neurons and its effect on dorsal Taylor B. Pathophysiologic mechanisms of
column nucleus neurons. Journal of Neuroscience neuropathic pain. Current Pain and Headache
1995; 15: 7633–43. Reports 2001; 5: 151–61.
Ossipov M, Lai J, Malan T, Porreca F. Spinal and Terayama R, Guan Y, Dubner R, Ren K. Activity-
supraspinal mechanisms of neuropathic pain. induced plasticity in brain stem pain
Annals of New York Academy of Science 2000; modulatory circuits after inflammation.
909: 12–24. Neuroreport 2000; 11: 1915–19.
Price D. Psychological and neural mechanisms of Wiech K, Preissl H, Birbaumer N. Neuroimaging of
the affective dimension of pain. Science 2000; chronic pain: phantom limb and
288: 1769–72. musculoskeletal pain. Scandinavian Journal of
Rheumatology 2000; 29: 13–18.
Rome H, Rome J. Limbically augmented pain
syndrome (LAPS): kindling, corticolimbic Woolf C, Wall P. Relative effectiveness of C
sensitization, and the convergence of affective primary afferent fibers of different origins in
and sensory symptoms in chronic pain disorder. evoking a prolonged facilitation of the flexor
Pain Medicine 2000; 1: 7–23. reflex in the rat. Journal of Neuroscience 1986; 6:
1433–42.
Rommel O, Malin J, Zenz M, Janig W.
Quantitative sensory testing, neurophysiological Woolf C, Shortland P, Reynolds M, Riding J,
and psychological examination in patients with Doubell T, Coggeshall R. Reorganization of
complex regional pain syndrome and central terminals of myelinated primary
hemisensory deficits. Pain 2001; 93: 279–93. afferents in the rat dorsal horn following
peripheral axotomy. Journal of Comparative
Rowbotham M, Kalso E, McQuay H, Wiesenfeld-
Neurology 1995; 360: 121–34.
Hallin Z (eds) The Debate over Opioids and
Neuropathic Pain. Opioid Sensitivity of Chronic Woolf C, Mannion R. Neuropathic pain: aetiology,
Non-cancer Pain. IASP Press, Seattle, 1998; symptoms, mechanisms, and management.
218: 307–17. Lancet 1999; 353: 1959–64.
Salerno A, Thomas E, Olive P, Blotman F, Picot M, Woolf C, Salter M. Neuronal plasticity: increasing
Georgesco M. Motor cortical dysfunction the gain in pain. Science 2000; 288: 1765–8.
disclosed by single and double magnetic
stimulation in patients with fibromyalgia.
Clinical Neurophysiology 2000; 111: 994–1001.
The biopsychosocial model in

chronic pain
5 ‘A biopsychosocial model . . . includes the patient as well as the

illness . . .’
George L Engel 1977
Before focusing on the biopsychosocial model, it is worth

considering two less satisfactory models.
Biomedical model
The biomedical model conceptualizes disorders as arising
from physical causes. It looks to eradicate such causes with the
expectation that the resolution of the disorders and a return to
normal function will automatically follow.
This model is well suited to the treatment of certain
infections and fractures. It is less well suited to the
management of mental illness.
The biomedical model is suited to the management of
acute pain where a close relationship usually exists between
the symptom and the degree of tissue injury. Narrow focus,
however, renders the biomedical model unsatisfactory in
chronic pain. Slavish devotion to the biomedical model in
chronic pain, with progression to repeated invasive
techniques, is unlikely to be beneficial and but that this was not the case with chronic
may end in iatrogenic complications. pain behaviour, as some environmental figures
provided support while others withdrew from
the patient. Jaynes (1985) pointed out that
Operant model
the reinforcer/rewards should have the same
This model of chronic pain has roots in effect on every patient, but that does not hold
learning theory (Fordyce, 1976). For a critical in the chronic pain scenario either, as some
review see Roth (2000). The observations patients find money positively rewarding,
were made that pain is communicated by while others are relatively indifferent. Roth
‘pain behaviours’ and that chronic pain (2000) points out that some losses that are
persists beyond the expected healing time. generally regarded as among the unwanted
This led to the theory that while acute pain consequences of chronic pain, such as the loss
was associated with appropriate acute pain of work status, are regarded as gains in
behaviour, chronic pain behaviour was operant pain theory.
reinforced or maintained by environmental While some pain behaviours communicate
factors. In operant theory, chronic pain that the patient is experiencing pain, this does
behaviours are maintained by financial not necessarily imply that such behaviour is
rewards, the attention of others and the under conscious control. There is strong
avoidance of duty. Pain behaviour rather than evidence that facial pain behaviour has an
pain experience became the focus of clinical evolutionary (survival) basis and that much of
attention. It is unclear whether proponents it is involuntary in origin (Williams,
believe that chronic patients are suffering pain unpublished). It is possible to exert some
and whether or not changing behaviour control over the pain behaviour of facial
reduces any such suffering. expression, but it cannot be completely
The operant pain model was hidden and is detectable by observers (Poole
enthusiastically embraced. It became and and Craig, 1992). There is evidence that
remains, a central plank of some intensive patients may openly demonstrate pain
multidisciplinary treatment programmes, behaviour when in the presence of supportive
supported by cognitive therapy, occupational and caring people (Block et al, 1980). But this
therapy, physiotherapy and medication may be interpreted in many ways. Williams
reduction. (unpublished) offers a credible interpretation,
However, theoretical objections have been proposing that when suffering patients are in
raised. Lacy (1985) pointed out that operant the presence of supportive people they are able
behaviours should result in predictable results, to release the control they have been exerting
The biopsychosocial model in chronic pain 29
over their pain behaviour, which may lead to that predispose the individual to depression in
an apparent but not an actual exaggeration. adult life. They speculate that these changes
An analogy is drawn with grieving: the ‘brave’ also predispose the individual to chronic pain,
individual is able to remain composed until a as sensitization of similar corticolimbic
supportive or ‘safe’ individual expresses structures could be involved. This theory
sympathy. might help to explain the high prevalence of
While some chronic pain patients are comorbidity of chronic pain and psychiatric
undoubtedly motivated by secondary gains, disorders and the pain-prone disorders that
operant pain theory cannot be accepted as a are discussed below.
generalized explanation of chronic pain
(Schmidt, 1987).
The biological/medical component
The biological/medical or physical basis of pain
Biopsychosocial model
is not contested. The chapters on Anatomy and
The biopsychosocial model of illness (Engel, physiology, Plasticity and neuropathic pain,
1977) highlights the importance of and Pharmacotherapy give relevant information
biological/medical, psychological/psychiatric on aetiology and therapy.
and social/environmental contributions to Other physical/medical forms of pain
aetiology and therapy. It is a guiding concept therapy include trigger point injection,
in psychiatry and comprehensive family temporary neural blockade, chemical and
medicine. radiofrequency neurolysis, cordotomy,
The biopsychosocial model is a useful massage, acupuncture, intraspinal drug
concept in pain medicine and is consistent administration, transcutaneous electrical nerve
with the International Association for the stimulation (TENS), dorsal column
Study of Pain definition: ‘Pain is an stimulation and deep brain stimulation.
unpleasant sensory and emotional experience
associated with actual or potential tissue
damage, or described in terms of such
The psychological/psychiatric
component
damage’ (Merskey, 1979).
Rome and Rome (2000) have proposed a The contention of the International
structural process for the biopsychosocial Association for the Study of Pain that pain
model of chronic pain. They reviewed involves ‘emotional experience’ raises the
information suggesting that disturbing early question of mechanism. In exploring this issue
life experiences lead to plastic brain changes some material is presented here that could
also have been listed under the above heading Neurones from the medullary region of
of ‘The biological/medical component’ – this the reticular formation form the ventral
testifies to the unity of mind and body. noradrenergic bundle (VNB), which also
Darwin (1872) conceptualized emotion as passes upwards in the MFB, projects to the
having evolutionary significance, as being a hypothalamus, and provides the
mechanism that facilitates communication neurophysiological link between tissue injury
and behaviour, and thereby, survival of the and the endocrine system. Hypothalamic
individual and the species. Later, Papez activity releases cortisol, which has wide-
(1937) described the limbic brain as ‘the ranging effects on the brain, including
hypothalamus, the anterior thalamic nuclei, modification of the firing rate of the limbic
the gyrus cinguli, the hippocampus and their forebrain. Also, the hypothalamus has neural
connections’ and proposed it as ‘a harmonious links with the limbic brain and the autonomic
mechanism which may elaborate the functions nervous system.
of central emotion’. These observations were Melzack (1999) has emphasized the
elaborated by MacLean (1952, 1990) who importance of the interconnections between
emphasized the importance of the limbic the endocrine, autonomic and limbic systems,
system and its functions to evolution. which, in addition to the neural and
Communication between the periphery endocrine factors, include the endogenous
and the brain was reviewed by Chapman opioids.
(1995). He found that, in the nervous system, The immune system is another mechanism
the differentiation between sensory and by which tissue damage results in limbic brain
emotional processing begins at the dorsal horn activation. Within seconds of tissue damage,
of the spinal cord. Information serving the cytokines are released from blood cells. They
sensory experience proceeds via the immediately cross the blood–brain barrier and
spinothalamic pathways and that serving the stimulate the hypothalamus, and thus the
emotional experience proceeds via the adrenal medulla and the limbic system. The
spinoreticular pathways. With respect to cytokine interleukin-1 stimulates the
emotion, important among the reticular hypothalamus to produce fever. Dantzer and
formation projections is the dorsal Kelley (1989) report that increased cytokine
noradrenergic bundle (DNB), which release results in malaise, fatigue, sleepiness,
originates in the pontine locus coeruleus (LC) anorexia, apathy and irritability. Experimental
and passes upward in the median forebrain immune activation using an endotoxin
bundle (MFB) to project throughout the produced negative emotional states and
limbic brain and the neocortex. decreased performance in memory function
tests (Reichenberg et al, 2001). These effects ‘splinting’ or tightening of muscles occurs to
were considered to be due to cytokine release, reduce the movement of painful structures.
and this study has relevance to a range of Thus, positive feedback loops develop, in
clinical conditions, including infectious and which pain leads to emotional tension or
autoimmune diseases (including multiple splinting, which lead to further pain.
sclerosis), cardiac disease, brain trauma and It is also a common experience that pain is
neuro-degenerative diseases. experienced as more intense at night. While a
circadian explanation could be involved, an
important feature is the reduction of stimuli.
Psychological factors in aetiology
Other people are asleep and unavailable, and
Common sense and clinical experience both the television offers little of interest. There is
suggest that the mental state can impact on thus no distraction, and pain that prevents
pain. Most forms of mental distress result in sleep becomes the focus of attention.
increased muscle tension, which leads to ‘Worry’ or apprehension, concern and
increased pain. (Mental distress, here, includes anticipation of future adverse events or
normal emotional arousal as well as the misfortunes are a very common human
diagnosable conditions of anxiety and problem. They form a feature of generalized
depression. It also includes other mental anxiety disorder, but are also present to a
disorders in which emotional arousal may be a lesser extent in a much broader section of the
feature, such as schizophrenia.) population. Such worries may focus on
The physiology of increased muscle external possibilities, such as floods or loss of
tension leading to increased pain has not been spouse or job, or on internal events such as
definitively elucidated. Contributing factors, loss of beauty or virility or onset of disease.
however, include an increased Worry is unpleasant, and often
mechanoreceptor inflow, increased mechanical uncontrollable. A frequent accompanying
forces applied to nociceptor endings and feature is muscle tension. Thus what can be
increased local metabolites with the potential called ‘normal’ worrying may accentuate
to sensitize nociceptor endings. muscle tension and pain. Worry is even more
Pain also leads to increased muscle tension likely and potent when there is ‘something to
by various mechanisms. It triggers the worry about’, that is, when disease or injury
autonomic fight or flight reaction, in which has brought loss or potential loss of income or
increased muscle tension prepares the family, or the prospect of long-term health
organism to respond to threat with quick problems. Finally, particular difficulties can be
strong movements. Also, an automatic anticipated when the worrying of the past has
focused on concerns about disease or strain injury’ because they imply a single
disability. uniform aetiology and neglect major
Various formal psychological theories have psychosocial contributions.
been offered as explanation for medically There is a high prevalence of psychiatric
inexplicable pain. Freud (1953 [1893]) disorder among those with chronic pain
described hysteria as the transformation of disorder (see the chapter on Pain and
unacceptable unconscious conflicts into bodily psychiatric comorbidity). One disorder may
pain as a means of preventing conscious exacerbate the other: hence psychiatric
awareness. In his seminal and sensitive paper, disorders need to be considered in the
‘Psychogenic pain and the pain-prone aetiology and treatment of chronic pain.
patient’, Engel (1959) emphasized the
importance of guilt in the generation of
Psychological factors in
chronic pain. Blumer and Heilbronn (1982)
treatments
argued that chronic pain is a variant of
depressive disorder or ‘masked depression’. The psychological support provided by
They introduced the term ‘pain-prone clinical staff and family and friends is
disorder’ in which hard-working people with important in maintaining a positive attitude
limited capacity to express emotions and encouraging efforts to regain function.
(alexithymia), after loss or disappointment, Where psychological contributions are
with or without painful injury or ailment, particularly important, psychological
become dependent and anergic and suffer treatments such as dynamic psychotherapy or
continuous pain. All these psychological cognitive behaviour therapy have an
explanations probably explain the symptoms important place. Psychotherapy also has a
of occasional chronic pain patients, but not place where biological contributions are of
the majority. primary importance, but adjustment to
In a large prospective study of the onset of changed circumstances is proving difficult.
forearm pain (Macfarlane et al, 2000), The pain-management ‘system’ and the
mechanical and psychological factors were less than optimal current treatments are a
identified. The important mechanical factors cause of great frustration and anger (Walker et
were repetitive movements of the hand and al, 1999). While these emotions may not have
wrist. The most important psychological initiated the pain, they play an important role
factor was dissatisfaction with support from in perpetuating distress. It is important to
colleagues or supervisors. The authors treat patients with respect and without
cautioned against terms such as ‘repetitive unnecessary delay. It is best to keep them
informed and involved as a means of helping Cultural factors are also important in the
them to deal with demoralization and anger. expression of illness and the granting of the
sick role. Considerable ethnic differences can
be found between groups living in the same
Social/environmental/cultural
country. Zborowski (1969) looked at whites
component
living in the USA. Italo-Americans were very
• Disease: biological or pathological changes ‘present-orientated’ about pain and were
that one ‘has’. primarily concerned about obtaining
• Illness: psychological or the way one ‘feels’ immediate relief. Jews were more ‘future-
when diseased. orientated’ and more concerned about the
• Sick: one acts or behaves the role ‘given’ by long-term meaning of pain. Anglo-Saxons
society. complained less and took a more detached,
‘unemotional’ view of symptoms.
In sociological terms there are distinctions Asians living in Britain are twice as likely,
between illness, disease and sickness. Illness is in comparison to Europeans, to consult their
the subjective sense that one is not well. Disease general practitioner (Balarajan et al, 1989),
is an objective pathology of the body such as and musculoskeletal pain is one of the most
cancer. Sickness is the condition of those who common reasons for consultation (OPCS,
are socially recognized as unwell. To put this in 1995). Non-specific musculoskeletal pain, low
another way, illness is a ‘psychological’ back pain and soft-tissue conditions are more
phenomenon in that one ‘feels’ ill, disease is a common in Pakistanis living in England than
‘biological’ phenomenon in that one ‘has’ a in those living in Pakistan (Hameed and
disease and sickness is a ‘social’ phenomenon in Gibson, 1997). However, Pakistanis required
that one ‘acts or behaves’ in the manner of a sick less postoperative analgesia than European
person (Twaddle and Hessler, 1986). patients, although pain scores were observed
Difficulties may arise when an individual has to be similar (Houghton et al, 1992).
one or two of these without the third. An Research indicates that Asians living in Britain
individual with cancer and obvious signs of the are significantly disadvantaged, and this may
disease may refuse to accept the sick role, be reflected in the difference in pain
including consulting a doctor. A more common complaints.
disjunction is when an individual claims the sick Cultural values and the potency of stigma
role but others do not accept that there is influence whether the distress is perceived and
disease. The term ‘abnormal illness behaviour’ reported in psychological or in somatic terms
can be applied in both of these examples. (Raguram et al, 1996). Depressed Chinese
patients most commonly present to general stop hiding, their pain behaviour. There is
practitioners with complaints of somatic evidence that pain behaviour has evolutionary
symptoms, including pain (Cheung et al, origins and that animals are ‘hard-wired’ to
1981). Ware and Kleinman (1992) compared elicit care that may promote survival.
Chinese suffering neurasthenia and North Nevertheless, common sense and clinical
Americans suffering chronic fatigue syndrome. experience suggest that a patient whose pain
They argued that ‘pain and suffering in behaviour elicits excessive attention and
society are manifested in pain and suffering in protection from the social environment will
the body’. They supported the claim that often be slower to move out of this role than a
somatic symptoms form part of a ‘hidden patient whose social environment is less
transcript’, a covert unofficial discourse that attentive and protective. Optimally, a balance
takes place out of sight of the wielders of is found when the patient feels valued and
power, and a way of addressing the desire for supported but also encouraged to strive for
change in social life. independence.
The operant model of pain has been Group activities as well as group therapy
described above under a dedicated heading. It have a place, providing for ventilation and
is built on learning theory, and could be listed inspiration through association with similarly
with psychological contributions; however, afflicted peers.
the purported rewards are derived from the
social environment, and include the promise
of money, the attention of others and the References
avoidance of duty. These so-called rewards Balarajan R, Yuen P, Soni Raleigh V. Ethnic
cannot be universally applied, however: for differences in general practitioner consultations.
British Journal of Medicine 1989; 299: 958–60.
example, while some may find the avoidance
of duty to be a positive, just as many others Block A, Kremer E, Gaylor M. Behavioral treatment
of chronic pain: the spouse as a discriminative
find loss of social role to be a strong negative cue for pain behavior. Pain 1980; 9: 243–52.
aspect of chronic pain. An alternative
Blumer D, Heilbronn M. Chronic pain as a variant
explanation has been offered for the apparent of depressive disease. The pain prone disorder.
exaggeration of pain behaviour when patients Journal of Nervous and Mental Disorders 1982;
suffering chronic pain are in the company of 170: 381–406.
supportive people. Williams (unpublished) Chapman C. The affective dimension of pain: a

model. In: Bromm B, Desmedt J (eds) Pain and
has proposed that in the company of
the Brain: From Nociception to Cognition,
supportive people, patients suffering chronic Advances in Pain Research and Therapy Vol. 22.
pain are able to release their suppression of, or Raven Press Ltd, New York, 1995; 283–301.
Cheung F, Lau B, Waldmann E. Somatization Lacy H. Pain behavior: how to define this operant.
among Chinese depressives in general practice. Behavior and Brain Science 1985; 8: 64–5.
International Journal of Psychiatry Medicine
Macfarlane G, Hunt I, Silman A. Role of mechanical
1981; 10: 361–74.
and psychosocial factors in the onset of forearm
Dantzer R, Kelley K. Stress and immunity: an pain: prospective population base study. British
integrated view of relationships between the Medical Journal 2000; 321: 676–9.
brain and the immune system. Life Sciences MacLean P. Some psychiatric implications of
1989; 44: 1995–2008. physiological studies on frontotemporal
Darwin C. The Expression of the Emotions in Man portions of the limbic system (visceral brain).
and Animals. John Murray, London, 1872. Electroencephalography and Clinical
Neurophysiology 1952; 4: 407–18.
Engel G. ‘Psychogenic’ pain and the pain-prone
MacLean P. The Triune Brain in Evolution: Role in
patient. American Journal of Medicine 1959; 26:
Paleocerebral Functions. Plenum Press, New
899–918.
York, 1990.
Engel G. The need for a new medical model: a Melzack R. Pain and stress: a new perspective. In:
challenge for biomedicine. Science 1977; 196: Gatchel R, Turk D (eds) Psychosocial Factors in
129–36. Pain. The Guilford Press, New York, 1999;
Fordyce W. Behavioral Methods for Chronic Pain 89–106.
and Illness. Mosby, St Louis, MO, 1976. Merskey H. Pain terms: a list with definitions and
Freud S. On the psychical mechanisms of hysterical notes on usage. Recommended by the
phenomena. The Standard Edition of the International Association for the Study of Pain
Complete Psychological Works of Sigmund Freud, (IASP) Subcommittee on Taxonomy. Pain
Volume 3 (1893) Edited and translated by 1979; 6: 249–52.
James Strachey. Hogarth Press, London, 1953; OPCS (Office of Population Census and Surveys),
25–42. The Royal College of General Practitioners,
Department of Health and Social Security.
Hameed K, Gibson T. A comparison of the
Morbidity Statistics from General Practice: Fourth
prevalence of rheumatoid arthritis and other
National Study 1991–1992. HMSO, London,
rheumatic diseases amongst Pakistanis living in
1995.
England and Pakistan. British Journal of
Rheumatology 1997; 36: 781–5. Papez J. A proposed mechanism of emotion.
Archives of Neurology and Psychiatry 1937; 38:
Houghton I, Aun C, Lau J. Inter-ethnic differences 723–43.
in postoperative pethidine requirements.
Anaesthesia and Intensive Care 1992; 20: 52–5. Poole G, Craig K. Judgements of genuine,
suppressed and faked facial expressions of pain.
Jaynes J. Sensory pain and conscious pain. Behavior Journal of Personality and Social Psychology 1992;
and Brain Science 1985; 8: 61–3 63: 797–805.
Kleinman A. Culture and somatic experience: the Raguram R, Weiss M, Channabasavanna S, Devins
social course of illness in neurasthenia and G. Stigma, depression and somatization in
chronic fatigue syndrome. Psychosomatic South India. American Journal of Psychiatry
Medicine 1992; 54: 546–60. 1996; 15: 1043–9.
Reichenberg A, Yirmiya R, Schuld A, Kraus T, Twaddle A, Hessler R. A Sociology of Health, 2nd

Haack M, Morag A, Pollmacher T. Cytokine- edn. Macmillan, New York, 1986.
associated emotional and cognitive disturbances
Walker J, Holloway I, Sofaer B. In the system: the
in humans. Archives of General Psychiatry 2001;
lived experience of chronic back pain from the
58: 445–52.
perspectives of those seeking help from pain
Rome H, Rome J. Limbically augmented pain clinics. Pain 1999; 80: 621–8.
syndrome (LAPS): kindling, corticolimbic
Ware N, Kleinman A. Culture and somatic
sensitization, and the convergence of affective
experience: the social course of illness in
and sensory symptoms in chronic pain disorder.
neurasthenia and chronic fatigue syndrome.
Pain Medicine 2000; 1: 7–23.
Psychosomatic Medicine 1992; 54: 546–60.
Roth R. Psychogenic models of chronic pain: a
Williams A. Facial expression of pain: an
selective review and critique. In: Massie MJ (ed)
evolutionary account (unpublished manuscript).
Pain: What Psychiatrists Need to Know. (Review
of Psychiatry Series, Vol. 19, No 2, Zborowski M. People in Pain. Jossey-Bass, San
Washington, DC, Oldham J and Riba M, series Francisco, 1969.
eds). American Psychiatric Press, 2000; 89–131.
Schmidt A. The behavioral management of pain: a
criticism of a response. Pain 1987; 30: 285–91.
Biopsychosocial pain and

diagnostic systems
6 ‘The task of the real intellectual consists of analyzing illusions

in order to discover their causes.’
Arthur Miller
The biopsychosocial model draws attention to the

biological/physical, psychological/psychiatric and
social/environmental contributions to disorders, diseases and
conditions. It was described over two decades ago and is well
regarded. It is a useful model when considering chronic pain.
This chapter examines the major diagnostic systems for
evidence of elements of the biopsychosocial model.
Current taxonomy has been criticized for failing to
identify the multifactorial nature of pain, and an alternative,
sign–symptom-based approach is recommended (Nicholson,
2000). Any such approach would be enriched by including
psychosocial signs and symptoms.
Classification of Chronic Pain

Classification of Chronic Pain (Merskey and Bogduk, 1994) is
the work of the Task Force on Taxonomy of the International
Association for the Study of Pain. It was developed because
pain was not comprehensively classified by the symptom of an anxiety disorder. The other is
other taxonomies. This system incorporates all called ‘psychological origin’, and examples
forms of chronic pain and codes according to include ‘conversion hysteria’ and ‘depressive
five axes. hallucinations’.
Axis I records the site of the pain. This is Classification of Chronic Pain is a valuable
relatively straightforward. Example categories contribution to the field of pain medicine.
are head, face and mouth, cervical region and The psychological/psychiatric and
upper shoulders and upper limbs. social/environmental contributions receive
Axis II records the system that is involved. some attention. Axis II is designed to code the
Systems such as the gastrointestinal and relevant system, and has two categories for the
genitourinary systems have a single category nervous system, depending on whether there
each. The nervous system has two categories, is a physical disturbance or dysfunction, or a
one for the presence of a physical disturbance psychological, psychiatric or social problem.
or dysfunction and the other for Thus this axis, which deals with systems, is in
psychological, psychiatric and social danger of being confounded by aetiological
conditions. factors. Further, Axis V, which is designed to
Axis III records the temporal code for aetiology, has a category called
characteristics and the pattern of occurrence ‘dysfunctional’ that may have an anxiety
of the pain. Examples of options include disorder as a root cause, and another category
single episode, recurring regularly and called ‘psychological origin’ that may have
recurring irregularly. ‘conversion hysteria’ as a root cause (a
Axis IV records the patient statement of condition that may result from an anxiety-
intensity and the time since onset. The provoking situation such as warfare). Thus
intensity is recorded as mild, moderate or pain with similar psychological/psychiatric
severe. The duration options are less than one contributions may be placed in different
month, one month to six months and greater aetiological categories. Finally, in the
than six months. ‘psychological origin’ category, of the two
Axis V records aetiology. There are examples given, one is a psychiatric disorder
relatively straightforward categories such as (conversion hysteria) and the other is a
neoplasm. There are two categories that psychiatric symptom (depressive
involve psychological issues. One, called hallucination). Thus, the
‘dysfunctional’, includes pains with a psychological/psychiatric and social/cultural
psychophysiological basis. Examples include contributions are superficially and confusingly
tension headache, which may or may not be a presented.
Biopsychosocial pain and diagnostic systems 39
Classification of Chronic pain elegantly the system, based on physical/medical criteria.

and comprehensively classifies chronic pain Tension headache is an example. Mental
from the biological/medical perspective. The tension may lead to muscular tension that in
International Association for the Study of turn leads to headache. If the diagnostic
Pain appears to be sympathetic to the criteria for a mental disorder are satisfied, that
biopsychosocial model. The fact that the diagnosis is also recorded.
psychological/psychiatric and Persistent somatoform pain disorder is
social/environmental contributions to chronic described as ‘severe, and distressing pain,
pain are not more clearly reflected in which cannot be explained fully by a
Classification of Chronic Pain is testimony to physiological process or a physiological
the difficulty of this task. disorder. Pain occurs in association with
emotional conflict or psychological problems
that are sufficient to allow the conclusion that
International Classification of
they are the main causative influences.’ In
Disease – Version 10 (ICD-10) practice it is often difficult to elaborate fully
ICD-10 (World Health Organization, 1992) the predicted ‘emotional conflict or
is a comprehensive system that deals with the psychological problems’. Patients may not
full spectrum of human diseases and extends have full insight into such issues, and may
over many volumes. It relies heavily on the angrily deny the possibility of important
biological/medical contributions, using psychological factors. Older classifications of
combinations of system and aetiology in the ‘hysteria’ (Freud, 1953 [1893]) and the more
classificatory process. It provides for recent dynamically orientated ‘pain-prone
psychological contributions to pain in the personality disorder’ (Engel, 1959) would be
following ways. here incorporated.
‘Histrionic elaboration of organically Pain can be experienced during the course
caused pain’ is mentioned. Such behaviour is of depressive disorder, being placed under the
recognized in clinical practice. (Contrary to heading of ‘other depressive episodes’, which
the thinking of some, statements to this effect incorporates the older diagnoses of atypical
can be made while fully respecting the dignity and masked depression. This is consistent
of the patient.) with the work of Blumer and Heilbronn
‘Psychological and behavioural factors (1982). Theoretically, pain could present as a
associated with disorders or diseases classified hallucination or delusion in psychotic
elsewhere’ is a useful category. ‘Classified depression; but in practice this is extremely
elsewhere’ refers to classification elsewhere in rare.
Pain can be experienced as a hallucinatory Axis I records the main mental diagnoses
phenomenon during the course of (one or more), except Personality Disorder
schizophrenia. However, in such cases other and Mental Retardation.
symptoms will be present on examination and Axis II records Personality Disorders and
the diagnosis should not be difficult. Mental Retardation. It may also be used to list
The ICD-10 alerts to the possibility that maladaptive personality features and defensive
reports of pain may be exaggerated (histrionic mechanisms. The listing of Personality
elaboration) and recognizes that psychological Disorder and Mental Retardation on a
factors may exacerbate organically caused pain separate axis ensures that these important
to cause what has been classified as a painful aspects receive attention.
organic disorder (‘psychological and Axis III records any General Medical
behavioural factors associated with disorders Conditions. These are coded according to
or diseases elsewhere classified’). It also ICD-9CM.
describes pain arising from psychiatric Axis IV reports Psychosocial and
disorders (persistent somatoform pain Environmental Problems that may affect the
disorder, depression and schizophrenia). diagnosis, treatment and prognosis. Included
The ICD-10 is predominantly a here are negative life events, familial or other
biological/medical classificatory system. As has interpersonal stresses, and inadequacy of social
been detailed in the above paragraph, there is support.
some effort to credit the importance of Axis V is the patient’s Global Assessment
psychological contributions. There is mention of Functioning. It is useful in determining the
of the use of ‘a culturally acceptable impact of the condition, in planning
explanation’ under the heading of treatment and in predicting outcome.
‘somatoform disorders’, but this is An Axis I diagnosis of Pain Disorder
exceptional. While a most useful diagnostic requires the satisfaction of five criteria.
system, the ICD-10 does not fully incorporate Important features are that pain is the
the biopsychosocial model. predominant focus of clinical attention, that it
causes significant distress and impairment and
that psychological factors are judged to have
Diagnostic and Statistical
an important role in the onset, severity,
Manual, 4th Edition (DSM-IV) exacerbation, or maintenance of the pain.
The DSM-IV (American Psychiatric Two subtypes are available: (1) Pain
Association, 1994) is concerned with mental Disorder Associated With Psychological
disorders. It is a multiaxial (five axes) system. Factors (here psychological factors are judged
Biopsychosocial pain and diagnostic systems 41
to have a major role) and (2) Pain Disorder References

Associated With Both Psychological Factors
American Psychiatric Association. Diagnostic and
and General Medical Condition. Statistical Manual of Mental Disorders, 4th edn.
Pain disorder associated with a general American Psychiatric Association, Washington,
medical condition is not considered to be a DC, 1994.
mental disorder and is placed on Axis III. Blumer D, Heilbronn M. Chronic pain as a variant
of depressive disease: the pain prone disorder.
The DSM-IV, through the multiaxial
Journal of Nervous and Mental Disease 1982;
arrangement, approximates to the 170: 381–406.
biopsychosocial model. Axis I records whether
psychological factors play the major or an patient. American Journal of Medicine 1959; 26:
ancillary role. Axis II also calls for attention to 899–918.
be paid to psychological factors. Axis III Freud S. On the psychical mechanisms of hysterical
records potentially contributing biological phenomena. In: The Standard Edition of the
Complete Psychological Works of Sigmund Freud,
factors. Axis IV takes special account of the
Vol 3. Edited and translated by James Strachey.
psychosocial and environmental problems, Hogarth Press, London, 1953 [1893]; 25–42.
while Axis V takes account of the impact on Merskey H, Bogduk N. Classification of Chronic
the ability to function, which will determine Pain. 2nd edn. IASP Press, Seattle, 1994.
the response of the environment. Nicholson B. Taxonomy of pain. Clinical Journal of
Pain 2000; 16: S114-17.
World Health Organization. The ICD-10
Summary Classification of Mental and Behavioural
Elements of the biopsychosocial model have Disorders Clinical Descriptions and Diagnostic
Guidelines. World Health Organization,
been incorporated into Classification of Geneva, 1992.
Chronic Pain, ICD-10 and DSM-IV. The last
of these systems appears to contain more such
features than the other two systems.
Pain and psychiatric

comorbidity
7 ‘It has been proven that cigarettes are a major cause of

statistics.’
Anonymous
It is important to emphasize the high prevalence of psychiatric

disorder among patients with chronic pain. Evidence suggests
that, in some cases, chronic pain leads to psychiatric disorder
(Fishbain et al, 1997), while in other cases, psychiatric disorder
leads to pain (Blumer and Heilbronn, 1982). Each of these
pathways is right for different patients (Dworkin and Gitlin,
1991). In some cases this concurrence must be coincidental.
In a wide range of disorders, from diabetes to cancer, the
treatment of concomitant psychiatric disorders contributes to
a better clinical outcome. While randomized double blind
trials have not been conducted to test the practice, common
sense and clinical wisdom support the treatment of psychiatric
disorders when they coexist with chronic pain (Atkinson et al,
1986; Dworkin and Gitlin, 1991; Sullivan et al, 1992;
Fishbain, 1999), irrespective of the supposed precedence. At
best, concomitant psychiatric disorders will delay recovery and
increase suffering; at worst, they will contribute to death by
suicide.
Psychiatric disorders overall They found 10% suffered an unequivocal

depressive syndrome (endogenous-psychotic
• Depression – probably 30% depression or reactive-neurotic depression).
• Anxiety – probably 40% This finding was less than half that for the
• Personality disorder – probably 50%. next lowest assessment. The Levine–Pilowsky
Depression Questionnaire has not been used
Atkinson et al (1986) used Research in subsequent studies of pain populations, and
Diagnostic Criteria in their study of 52 may not be suited to the task.
patients admitted to a neurosurgery unit for Blumer and Heilbronn (1982) coined the
the treatment of pain, and found 78.4% to be term ‘pain-prone disorder’ and conceptualize
suffering from a mental disorder. Merskey et chronic pain as a variant of depression and
al (1987) used self-assessment questionnaires thus, by definition, considered all those
in their study of 378 patients from four suffering chronic pain to be suffering
different pain services. Using the General depression. While this work drew attention
Health Questionnaire, they found possible back to the importance of psychological
mental illness in 65.3% and probable mental factors in chronic pain, the hypothesis that all
illness in 41% of patients. These are different chronic pain resulted from depression in
studies, as Atkinson et al (1986) considered individuals with psychodynamic vulnerability
inpatients and Merskey et al (1987) was not accepted (Turk and Flor, 1984).
considered outpatients. However, even if the Davidson et al (1985) examined 57
lower figures of Merskey et al (1987) are patients with chronic pain using the Research
accepted, the concurrence is high, making Diagnostic Criteria and found major
psychiatric assessment and treatment in depression in 42% and minor depression in
chronic pain an important contribution. 37%, for a total with depressive disorder of
79%. Atkinson et al (1986) examined 52
patients with chronic pain using the Research
Depression
Diagnostic Criteria and found major
Depression is the psychiatric disorder that has depression in 21.6% and minor depression in
received the most attention, and is present in 44.2%, for a total with depressive disorder of
those with chronic pain in the range 65.8%.
10%–100%. Sullivan et al (1992) reviewed the studies
Pilowsky et al (1977) examined 100 of depression in chronic low back pain and
patients attending a pain clinic using the concluded that the levels of depression were
Levine–Pilowsky Depression Questionnaire. approximately four times greater than that
Pain and psychiatric comorbidity 45
reported in the general population. Probably, unrecognized in chronic pain, because the
one-third of those with a range of chronic symptoms are attributed to the pain condition
pain suffer major depression Roth (2000). or to minor depression. Atkinson et al (1986)
found no cases of anxiety disorders in 52
chronic pain patients. In an extensive review
Anxiety
of chronic back pain Fishbain (1999) found a
Fear is akin to anxiety, and differentiation is prevalence of anxiety disorders higher than
often difficult. Fear/anxiety is a response to expected for the general population.
threat and is ubiquitous in acute pain. In
chronic pain it is less common, but
nevertheless frequently present. Wise and
Personality disorder
Taylor (1990) confirm that anxiety is Merskey (1992) described the selection
commonly associated with most chronic process preceding presentation at the pain
medical conditions. As has been mentioned, clinic. Faced with chronic non-terminal pain,
depression is frequently present and anxiety many individuals will tolerate the condition
symptoms are common in depression. and get on with their normal activities as best
By contrast with depression, no theory has as they can. Some will take over-the-counter
been advanced that chronic pain is a variant of medicines. Only a proportion will consult
anxiety. Certain conditions have been their general practitioner, and a small number
identified, however, such as tension headache, of these will keep returning to the doctor after
for which a significant aetiological initial examination, reassurance and
contribution from anxiety has been generally conservative treatment. Those who reach the
accepted. pain clinic are a tiny, highly filtered and
Fear avoidance leading to disability has selected population. For those patients who
begun to receive attention in the literature. reach the chronic pain clinic with similar
Such constructions are consistent with the physical pathology to those who do not, other
clinical observations of the present author, factors, including personality features, may
and are considered in greater detail in drive the presentation.
Chapter 9. Friedman et al (1963) described a
Merskey et al (1987), using the ‘demanding, hypochondrical’ form of
Irritability/Depression and Anxiety depression. In most instances, this reflects
Questionnaire, found that 37% of 387 depression in an individual with demanding
chronic pain patients were pathologically and hypochondrical personality features.
anxious. Perhaps anxiety is frequently Pilowsky et al (1977) compared pain clinic
patients to family medicine clinic patients looking for and treating concurrent
using the Illness Behavior Questionnaire and psychiatric disorders whenever they are
found that pain patients demonstrated detected.
significantly more ‘disease conviction’ and
‘somatic preoccupation’ and were significantly References
more likely to ‘deny life problems unrelated to
Atkinson J, Ingram R, Kremer E, Saccuzzo D.
their physical problem’. These features set the MMPI subgroups and affective disorder in
scene for a patient–doctor relationship that is chronic pain patients. Journal of Nervous and
unsatisfactory to both participants. Mental Disease 1986; 174: 408–13.
Somatizing and chronic pain patients are Barsky A, Wyshak G, Latham K, Klerman G.
Hypochondrical patients, their physicians, and
described as critical and unrewarding patients
their medical care. Journal of Internal Medicine
to manage, and unpopular with many 1991; 6: 413–19.
clinicians (Barsky et al, 1991). They have been Blumer D, Heilbronn M. Chronic pain as a variant
characterized as querulous, self-preoccupied, of depressive disease. The pain-prone disorder.
demanding and irritable (Engel, 1959). Journal of Nervous and Mental Disorders 1982;
170: 381–406.
Fishbain et al (1986) examined 283
Davidson J, Krishhnan R, France R, Pelton S.
patients using the DSM-III and found 62.3% Neurovegetative symptoms in chronic pain and
of men and 55.1% of women merited a depression. Journal of Affective Disorders 1985;
diagnosis of personality disorder. In a recent 9: 213–18.
review of the field, Weisberg (2000) found Dworkin R, Gitlin M. Clinical aspects of depression
in chronic pain patients. Clinical Journal of Pain
that personality disorders are significantly
1991; 7: 79–94.
greater in the pain population than in the
general population or in medical or patient. American Journal of Medicine 1959; 26:
psychiatric populations. 899–918.
Fishbain D. Approaches to treatment decisions for
psychiatric comorbidity in management of the
Conclusion chronic pain patient. Medical Clinics of North
America 1999; 83: 737–60.
Chronic pain is rarely cured. The reasonable
Fishbain D, Goldberg M, Meager B, Rosomoff H.
aim is to relieve symptoms as much as Male and female chronic pain patients
possible. It is not clear that chronic pain is categorized by DSM-III criteria. Pain 1986; 26:
frequently accompanied by psychiatric 181–97.
disorder. Given our limited ability to assist Fishbain D, Cutler R, Rosomoff H. Chronic pain
associated depression: antecedent or
those with chronic pain we should take every
consequence of chronic pain? A review. Clinical
opportunity to relieve distress, this includes Journal of Pain 1997; 13: 79–87.
Pain and psychiatric comorbidity 47
Friedman A, Cowitz B, Cowen H, Gramick S. Pain: What Psychiatrists Need to Know. (Review
Syndromes and themes of psychiatric of Psychiatry Series, Vol. 19, No 2, Oldham J
depression. Archives of General Psychiatry 1963; and Riba M, series eds). American Psychiatric
9: 504–9. Press, Washington, DC, 2000;
89–131.
Merskey H. Chronic pain problems and psychiatry.
In: Tyrer S (ed) Psychology, Psychiatry and Sullivan M, Reesor K, Mikail S, Fisher R. The
Chronic Pain. Butterworth Heinemann, Oxford, treatment of depression in chronic low back
1992; 45–56. pain: review and recommendations. Pain 1992;
50: 5–13.
Merskey H, Lau C, Russell E, Brooke R, James M,
Lappano S, Neilsoen J, Tilsworth R. Screening Turk D, Flor H. Etiological theories and treatments
for psychiatric morbidity. The pattern of for chronic back pain. II Psychological models
psychological illness and premorbid and interventions. Pain 1984; 19: 209–33.
characteristics in four chronic pain populations.
Weisberg J. Personality and personality disorders in
Pain 1987; 30: 141–57.
chronic pain. Current Review of Pain 2000; 4:
Pilowsky I, Chapman C, Bonica J. Pain depression 60–70.
and illness behavior in a pain clinic population.
Wise M, Taylor S. Anxiety and mood disorders in
Pain 1977; 4: 183–92.
medically ill patients. Journal of Clinical
Roth R. Psychogenic models of chronic pain: a Psychiatry 1990; 51: 27–32.
selective review and critique. In: Massie MJ (ed)
Pain and somatization
8 ‘Our doctor would never really operate unless it was necessary.

If he didn’t need the money, he wouldn’t lay a hand on you’
Herb Shriner
One of the great challenges faced by medical practitioners is

the care of people who complain of physical symptoms for
which no physical cause, or only insufficient physical cause,
can be found. This problem has a long history. When
observed in the women of ancient Greece it was believed that
the womb (hystera) of the patient was roaming within her
body, and the condition was called ‘hysteria’. When a person
believed that he or she had an illness for which there was no
evidence the term ‘hypochondria’ was employed, which
indicated that the problem was under the cartilage
(chondrium) of the front of the chest.
Overlapping conditions
Somatization
Somatization is defined (Lipowski, 1988) as the propensity to
experience and report somatic symptoms that have no
pathophysiological explanation, to misattribute them to
disease, and to seek medical attention for Alexithymia, which means being ‘without
them. The elements of this definition deserve words to describe emotions’, has also been
individual examination. There is a reported to be an important factor (Sifneos,
‘propensity’: thus particular personality traits 1996). It is proposed that, in the absence of
or beliefs are present and repetition of the the ability to describe emotions, individuals
behaviour can be expected. The symptoms are respond to life situations in maladaptive ways.
‘experienced’, not just reported. Thus, Alexithymic individuals focus on facts, details
somatizing patients are not feigning and external events, and tend to have a limited
symptoms, and somatization is distinct from fantasy life.
factitious disorder and malingering. There is Many individuals who do not satisfy strict
no ‘pathophysiological explanation’ to be diagnostic criteria for alexithymia nevertheless
found in the organ or region in which such a have an impoverished ability to express their
finding could be expected; however, comorbid emotions in words or by other adaptive
psychiatric symptoms may exist. The means. Important factors include intelligence,
misattribution of symptoms to disease may education and culture/sub-culture (e.g.
result in, or in cases of longer standing, arise ‘macho’ males). Somatization is more frequent
out of, the belief that disease is present. There in the lower socioeconomic classes, where
is ample opportunity for misattribution, as opportunities are limited (Gentry et al, 1974).
population-based surveys reveal that healthy Also important, once the patient has
adults experience more than one somatic presented, is the ability of the patient and the
symptom each week (Egan and Beaton, doctor to communicate effectively. Here,
1987). Medical attention is sought and sought much responsibility rests with the doctor, who
frequently; however, this may be insignificant must attend and work to understand the
in comparison to the attention sought from patient’s ‘physical’ language.
relatives, friends, pharmacist and alternative
therapists.
Somatization disorder
This is a descriptive account, free of
aetiological speculation. Others (Shapiro, Somatization disorder as defined in DSM-IV
1965; Schalling et al, 1973), using (APA, 1994) remains a controversial
neuropsychological testing, have shown that diagnosis. Somatization (the process) as
somatization is associated with information- described by Lipowski does occur in
processing deficits. A current review has somatization disorder; but the presence of the
confirmed that such patients manifest specific process is not sufficient to justify the
cognitive features (Rief and Nanke, 1999). diagnosis. For somatization disorder there
Pain and somatization 51
must be a lifetime history of pain in at least In the earlier diagnostic systems that did
four different parts of the body and at least allow hypochondriasis as a discrete entity,
one conversion or dissociative symptom. hypochondrical thoughts could be held with
In hysteria, an earlier designation for this delusional intensity. Using the DSM-IV
disorder, using neuropsychological testing, system, when delusions are present it is
information-processing deficits were necessary to make the diagnosis of delusional
demonstrated. These were characterized by disorder.
distractibility and difficulty in distinguishing
target stimuli (Ludwig, 1972; Flor-Henry et
Pain disorder
al, 1981).
Pain disorder associated with psychological
factors or with both psychological factors and
Hypochondriasis
a general medical condition is distinct from
Hypochondriasis (DSM-IV) involves somatization disorder in the DSM-IV system.
preoccupation with an unrealistic fear or belief However, some (Katon et al, 1984; Aigner
of having a serious disease, despite negative and Bach, 1999) regard chronic pain as the
investigation and assurance that no relevant most common form of somatization. The
pathophysiology is present. Fear or belief of diagnosis of pain disorder is particularly
having a serious disease, however, is common difficult when there has been physical disease
to all somatoform disorders. There are doubts or injury due to incompletely understood
as to whether hypochondriasis is a discrete phenomena, including sympathetically
disease entity (Rief et al, 1998). The diagnosis maintained pain (Walker and Cousins, 1997)
is frequently made in the primary care setting. and the painful joint stiffness and muscular
Management is notoriously difficult. weakness associated with disuse.
The DSM-IV can be criticized for giving a There is evidence that prior experience of
new definition to an old problem. Many older pain can influence the response to stimuli
textbooks (Curran and Partridge, 1969) did (Bayer et al, 1998). Learning appears to be
not list hypochondriasis as a discrete entity, aetiologically important in pain disorder, as
instead, indexing it ‘in endogenous depression, secondary gains reinforce pain-related
in GPI, in involutional melancholia, in behaviour; and prior social models, especially
schizophrenia, in senescence’. Kenyon (1976) sick and suffering parents, predispose to the
has strongly argued that hypochondriasis is development of the condition (Apley, 1975).
always a secondary part of another syndrome, The factors that sustain chronic pain
usually a depressive disorder. (particularly low back pain) probably include
fear of movement and pain, which can lead to about disease and discomfort, and is
the disuse syndrome and a self-perpetuating consequently culturally constructed (Wexler,
cycle (Vlaeyen and Linton, 2000). 1974). It may be construed as the patient’s
view of clinical reality (patient’s view). Some
Conceptual underpinning (Stimson, 1974) claim that medical doctors
treat illness poorly, while traditional and
Attribution theory alternative therapists, who listen and give
What individuals believe about their culturally relevant explanations, treat illness
symptoms greatly influences whom they well.
consult and how they manage those symptoms Disease may be defined as ‘abnormalities
(King, 1983). Individuals have enduring in the structure and function of body organs
attributional styles (Garcia-Campayo et al, and systems’. It may be construed at the
1997), such that when a symptom is medical view of clinical reality (medical view).
experienced, it is likely to be attributed to a One criticism of modern medicine is that it
physical, psychological or focuses on the treatment of disease and
environmental/normalizing explanation ignores the treatment of illness (Engel, 1977).
(Robins and Kirmayer, 1991). Not Common sense suggests a better outcome
surprisingly, general practice attenders with will be achieved if both illness and disease are
hypochondrical tendencies have more physical treated. Toward this end, the doctor should
attributions than those with anxiety disorders seek to understand the patient’s view fully, to
(MacLeod et al, 1998). Educational explain the medical view and to negotiate a
programmes designed to modify attribution shared view (Von Korff et al, 1997).
style are useful in the management of chronic
pain and somatization. Abnormal illness behaviour
Abnormal illness behaviour (AIB) provides an
Medical anthropology
intellectual framework for a comprehensive
Illness may be defined, anthropologically, as range of human behaviours (Pilowsky, 1969).
‘the human experience of sickness’. The It depends on two sociological concepts:
process begins with personal awareness of a illness behaviour and the sick role. Illness
change in body feeling and continues with the behaviour is defined as ‘the ways in which
labelling of the sufferer by self and family as individuals experience, perceive, evaluate and
‘ill’ (Kleinman et al, 1978). Illness is greatly respond to their own health status’
dependent on family and cultural beliefs (Mechanic, 1968). The sick role is
conceptualized as bringing obligations and basis for illness-related behaviour, including

privileges (Parsons, 1964). The obligations are but extending beyond the somatoform
that the person seeking the role: (1) accepts disorders to factitious disorder and
that the role is undesirable; (2) co-operates malingering, and, in another direction, to the
with others to achieve health; and (3) utilizes denial of illness. It casts the individual who
the services of those regarded by society as denies illness and stays at work under the
competent in healing. If these obligations are same umbrella as the individual who pretends
fulfilled, the individual is granted the illness and goes to the football – with the vast
following privileges: (1) to be regarded as not majority of illness behaviours lying somewhere
being responsible for his/her condition; (2) to between these two extremes.
be accepted as someone requiring care; and In addition, AIB supplies the context for
(3) exempted from normal obligations (such the responsibility of the doctor as the socially
as work). designated controller of sick role privileges, a
On these foundations, Pilowsky (1997) frequently onerous and unwelcome duty.
defined AIB as ‘an inappropriate or
maladaptive mode of experiencing, evaluating
Medicalization
or acting in relation to one’s own state of
health, which persists, despite the fact that a Medicalization describes the tendency of
doctor (or other recognized social agent) contemporary society to focus attention on
offered accurate and reasonably lucid the medical aspects of everyday life. It shares
information concerning the person’s health roots with the principle of social justice, in an
status and the appropriate course of increasingly humane society. In general it
management (if any), with provision of places increased responsibilities with health
adequate opportunity for discussion, professionals, health authorities and health
clarification and negotiation, based on a insurers. This process is a feature of society,
thorough examination of all parameters of not of the individual. However, the constructs
functioning (physical, psychological and of society influence the course of action and
social) taking into account the individual’s options that will be chosen by the individual.
age, educational and sociocultural An example of one form of medicalization
background’. is the presentation at the general hospital of
AIB is a multifaceted thesis of great people with social problems. Marital disputes
theoretical importance. It highlights the frequently result in one party’s achieving
connection between social influences and admission to hospital, wrongly diagnosed as
health and provides a unifying conceptual suffering a psychiatric disorder. Another form
is an accompaniment of very sensible, well- enduring pathology has been demonstrated

intentioned public health endeavours such as using current medical technology. Important
those that urge people to take chest pain psychosocial determinants are observed in
seriously and to be alert for the early signs of cultures that provide ‘overwhelming
diabetes/cancer. In all probability these save information’ regarding the potential for
lives. Just as probably, they encourage the chronic pain following whiplash injury,
public to regard every ache and pain as a medical systems that encourage inactivity and
warning sign of disease and an indication for caution, and litigation processes that involve
medical examination. protracted battles with insurance companies.
Patients are led to expect, amplify and
attribute symptoms in a chronic fashion.
The biopsychosocial model
The biopsychosocial model aims to take
Synthesis/summary
account of the broad range of influences
(biological, psychological and social – cultural Lipowski’s view that some individuals have a
can also be included) that may coalesce in the propensity to experience and report somatic
formation of a disorder. symptoms that have no pathophysiological
An example is provided by the explanation, to misattribute them to disease,
consideration of chronic pain resulting from and to seek medical attention has not been
whiplash injury following rear-end collisions disputed in the literature and can be accepted.
(Ferrari and Russell, 1999). The late whiplash Somatoform disorder, hypochondriasis and
syndrome is culturally constructed, being non- pain disorder remain contentious, in so far as
existent or almost non-existent in Singapore, they may not represent discrete disease
Lithuania, Germany and Greece, and among entities. However, they all have elements of
laboratory volunteers and fairground bumper somatization and currently emerge in a setting
car revellers, but common in the USA and of medicalization. Evidence suggests that
Australia. Evidence suggests that in England, cognitive processes may be aetiologically
whiplash replaced ‘railway spine’ (Trimble, important. Both somatization and
1981). The claimants are neither malingering somatoform disorder are reported to be
nor suffering a psychiatric disorder. associated with information-processing
In this example, the biological dimension deficits. In pain disorder learning appears to
is most probably an acute sprain, which be an aetiological factor; there is evidence
resolves/heals without any significant residual supporting the influence of secondary gains
structural damage. At least, no convincing, and social models. Fear of pain and movement
may be important in the maintenance of some respective belief systems and come to a
chronic pain. shared view of clinical reality. Others
Other support for the importance of have made similar observations. This
cognition in somatization and somatization approach is recommended.
disorder is available. Attributional theory is 2. The evidence for information-processing
not yet firmly established, but advances the deficits in these clinical presentations
reasonable proposition that ambiguous suggests that information should be
symptoms will be interpreted in accordance presented in an understandable form and
with personal beliefs and experience. Medical repeated frequently. The presence of
anthropology emphasizes the importance of information-processing deficits is one
the beliefs of the individual and the culture. reason why such patients may not
The sociological concepts mentioned here respond to the advice and information in
impact on classification rather than aetiology. the same manner as might other patients.
AIB forms an alternative envelope for certain This knowledge may reduce the burden
DSM-IV disorders, and does not obstruct the of their care.
proposal that cognitive factors are of 3. Present at all times as caring, confident,
aetiological importance. Whiplash disorder is firm and approachable (within agreed
an example of a chronic, painful, limits).
incapacitating syndrome that is secondary to 4. After appropriate investigation, inform
the cognitions of the patient, plus those of the the patient that no further investigations
society and culture in general, and the medical are indicated, at this time. Investigations
and legal professions in particular. (With are expensive, dangerous and usually
respect to chronic pain, fear of movement and unhelpful. Reassure that investigations
pain may serve to perpetuate this condition will be conducted, in the future, as
via the disuse syndrome.) indicated.
5. Limit the number of invasive treatments.
6. Limit the number of doctors the patient
Management
consults. The limitation of investigations
recommendations and invasive treatments is only possible
1. The anthropologists inform us that there when there is a limit on the number of
are at least two views of clinical reality doctors involved in the case. Continue to
(the patient’s and the medical view) and be involved on condition that the patient
that the best outcome is achieved when does not go outside the agreed team. An
the patient and doctor can discuss their interested general practitioner is
essential. In the case of somatization, individuals or where psychosis is

somatization disorder and observed or suspected.
hypochondriasis, a combination of an 10. Analgesics should be taken on a regular
interested general practitioner and a basis. The taking of medication ‘as
consulting psychiatrist, who are able to required’ reinforces pain behaviour by
communicate as necessary, is providing sudden rewarding pain relief,
recommended. In the case of pain and in the worst case scenario, a ‘rush’,
disorder, a combination of an interested in response to the taking of a pill. This is
general practitioner and a consulting not to prohibit the patient on long-
psychiatrist or pain medicine specialist, acting medication from taking small
who are able to communicate as additional amounts for ‘breakthrough’
necessary, is recommended. pain.
7. Limit the time spent with the patient. 11. Diagnose and adequately treat comorbid
Do not present this as a punitive issue. psychiatric disorders.
Rather, discuss the fact that the patient’s 12. Provide some emotional support.
needs can best be met by regularly Chronic pain patients suffer emotionally
scheduled time-defined appointments. as well as physically.
Point out that you are prepared to help, 13. Encourage return to normal activities.
but that this is only possible if meetings This is the best way to combat pain-
are regularized. Negotiate a sensible related fear that leads to the disuse
protocol to be followed in the case of syndrome and cyclical pain. Encourage
crises. hobbies, exercise, education and cultural
8. The patient has the right to care. pursuits – these will distract the patient
Attention may be according to a time from his/her body, stretch and
schedule, but should not be contingent strengthen the body and assist the return
on the patient’s suppressing or hiding to normal function. Reward attempts at
pain behaviour. activities with praise.
9. Limit the amount of medication. (The joints and muscles stiffen during
Benzodiazepines, stimulants and prolonged inactivity. The return to
analgesics should be strenuously limited. activity must be graded and gradual, but
These patients do experience distress, relentless. The active patient should take
and the use of antidepressants and mood frequent rests. Activity that is overzealous
stabilizers has a role. Antipsychotic may result in the exacerbation of
medication has a place in highly aroused symptoms. This in turn may lead to
further patient-imposed bed rest and the Schopflocher D. A neuropsychological study of

avoidance of activity. In chronic painful the stable syndrome of hysteria. Biological
Psychiatry 1981; 16: 601–627.
conditions, pain usually does not
Garcia-Campayo J, Larrubia J, Lobo A, Perez-
indicate further damage.)
Echeverria M, Campos R. Attribution in
14. Educate and involve the family in somatizers: stability and relationship to outcome
management. at 1-year follow-up. Acta Psychiatrica
15. Understand the need to repeat the Scandinavica 1997; 95: 433–8.
reassurance, encouragement of activities Gentry W, Shows W, Thomas M. Chronic low

back pain: a psychological profile. Psychosomatics
and conditions of care (the limits).
1974; 15: 174–7.
Katon W, Ries R, Kleinman A. The prevalence of
References somatization in primary care. Comprehensive
Psychiatry 1984; 25: 208–15.
Aigner M, Bach M. Clinical utility of DSM-IV pain
disorder. Comprehensive Psychiatry 1999; 40: Kenyon F. Hypochondrical states. British Journal of
353–7. Psychiatry 1976; 129: 1–14.
APA (American Psychiatric Association). Diagnostic King F. Attribution theory and the health belief
and Statistical Manual of Mental Disorders, 4th model. In: Hewstone M (ed) Attribution Theory:
edn. American Psychiatric Association, Social and Functional Extensions. Basil Blackwell,
Washington, DC, 1994. Oxford, 1983; 170–86.
Apley J. The Child With Abnormal Pains. Blackwell, Kleinman A, Eisenberg L, Good B. Clinical lessons
Oxford, 1975. from anthropologic and cross-cultural research.
Annals of Internal Medicine 1978; 88: 251–8.
Bayer T, Coverdale J, Chiang E, Bangs M. The role
of prior pain experience and expectancy in Lipowski Z. Somatization: the concept and its
psychologically and physically induced pain. clinical applications. American Journal of
Pain 1998; 74: 327–31. Psychiatry 1988; 145: 1358–68.
Curran D, Partridge M. Psychological Medicine, 6th Ludwig A. Hysteria: a neurobiological theory.
edn. E & S Livingstone, Edinburgh, 1969. Archives of General Psychiatry 1972; 27: 771–86.
Egan K, Beaton R. Response to symptoms in health MacLeod A, Haynes C, Sensky T. Attributions
low utilisers of the health care system. Journal of about common body sensations: their
Psychosomatic Research 1987, 31, 11–21. associations with hypochondriasis and anxiety.
Psychological Medicine 1998; 28: 225–8.
Engel G. The need for a new medical model: a
challenge for biomedicine. Science 1977; 196: Mechanic D. Medical Sociology. Free Press, New
129–36. York, 1968.
Ferrari R and Russell A. Epidemiology of whiplash: Parsons T. Social Structure and Personality. Collier-
an international dilemma. Annals of the Macmillan, London, 1964.
Rheumatic Diseases 1999; 58: 1–5.
Pilowsky I. Abnormal illness behaviour. British
Flor-Henry P, Fromm-Auch D, Tapper M, Journal of Medical Psychology 1969; 42: 347–51.
Pilowsky I. Abnormal Illness Behaviour. John Wiley Stimson G. Obeying the doctor’s orders: a view
& Sons Ltd, Chichester, 1997. from the other side. Social Science Medicine
1974, 8, 97–104.
Rief W, Nanke A. Somatization disorder from a
cognitive-psychobiological perspective. Current Trimble M. Post-traumatic Neurosis: From Railway
Opinion in Psychiatry 1999; 12: 733–8. Spine to the Whiplash. Wiley, Chichester, 1981.
Rief W, Hiller W, Margraf J. Cognitive aspects of Vlaeyen J, Linton S. Fear-avoidance and its
hypochondriasis and the somatization consequences in chronic musculoskeletal pain: a
syndrome. Journal of Abnormal Psychology 1998; state of the art. Pain 2000; 85: 317–32.
107: 587–95.
Von Korff M, Gruman J, Schaefer J, Curray S,
Robins J, Kirmayer L. Attributions of common Wagner E. Collaborative management of
somatic symptoms. Psychological Medicine 1991; chronic illness. Annals of Internal Medicine
21: 1029–45. 1997; 127: 1097–102.
Schalling D, Cronholm B, Asberg M, Espmark S. Walker S, Cousins M. Complex regional pain
Rating of psychiatric and somatic anxiety syndromes: including ‘reflex sympathetic
incidents – interrater reliability and relations to dystrophy’ and ‘causalgia’. Anaesthesia and
personality variables. Acta Psychiatrica Intensive Care 1997; 25: 113–25.
Scandinavica 1973; 49: 353–68.
Wexler N. Culture and mental illness: a social
Shapiro D. Neurotic Styles. Basic Books, New York, labelling perspective. Journal of Nervous and
1965. Mental Diseases 1974; 159: 379–95.
Sifneos P. Alexithymia: past and present. American
Journal of Psychiatry 1996; 153 (7 Suppl):
137–42.
Fear of movement and pain
9 ‘No passion so effectively robs the mind of all its powers of

acting and reasoning as fear.’
Edmund Burke 1729–1797
Fear of movement and pain (pain-related fear), leading to

avoidance, inactivity and disability, appears to be a factor in
the aetiology of some cases of chronic pain. The theory is
consistent with clinical experience and is supported by an
impressive body of research. The ‘fear-avoidance model’ of
chronic pain was first described by Lethem et al in 1983.
Recent reviews of the field are available (Asmundson et al,
1999; Crombez et al, 1999). The research has been mainly
concerned with low back pain; but in clinical practice pain-
related fear and consequent avoidance of activity is observed
with other chronic pain conditions.
Pain is the most aversive stimulus known to man.
It is reasonable to expect that patients who were
premorbidly anxious about health matters will be especially
susceptible to developing pain-related fear.
Fear of movement The disuse syndrome

Fear of activity may develop when pain has A consequence of the avoidance of movement
been experienced acutely, during activity. is the disuse syndrome (Kottke, 1996). This
Warnings from doctors and other authorities includes the loss of muscle strength, increasing
to avoid activity or the witnessing of pain joint stiffness, lowering of the pain threshold
experienced by others while performing tasks and the impairment of muscle coordination.
may have similar effects. Both classical and In clinical practice the impairment of muscle
operant learning may be involved (Vlaeyen coordination takes the form of ‘guarding’ or
and Linton, 2000). In so far as these patients prevention, by muscle contraction, of
cease normal functions, they are disabled. particular movements. The scene is thus set
for a destructive cycle in which pain-related
fear leads to further pain and so forth.
Fear of pain
Theoretically, at least, the process persists
The fear of pain model is similar to the fear of because extinction is delayed. As there is little
movement model, but is more elaborate and is movement there is little opportunity to learn
more concerned with cognitive processes that movement does not lead to unendurable
(Waddell et al, 1993). In this model the pain.
patient has an inaccurate understanding of the
pain and its consequences. When the patient
believes that pain indicates damage, pain is Fear and cognitive functions
feared and movements that cause pain are
Fear increases vigilance. Once a patient has
avoided. The patient needs to learn that, in
experienced pain-related fear, he/she is more
acute pain situations, pain does indicate
likely to notice and place importance on
damage and activities that extend the pain
minor pains and sensations and overestimate
may extend the damage. However, the chronic
the importance of them.
pain situation is different. Healing has taken
Fear distracts and impairs concentration
place and the structure of the body is stable.
and thereby interferes with cognition. There is
In this situation pain does not indicate
speculation that pain-related fear may
ongoing damage; in fact, the fear of pain and
interfere with the patient’s ability fully to
the avoidance of activity will delay the
comprehend and accept information provided
optimization of outcome.
by health professionals, and to utilize
information to change thinking and behaviour
patterns. In particular, the effect of pain-
Fear of movement and pain 61
related fear may be to impair the ability to Educational efforts can be focused on
accept that, in the chronic situation, pain does misunderstandings. Theoretically, correction
not mean further injury. of illogical thinking or catastrophizing could
prevent or reduce pain-related fear, avoidance
and disability.
Clinical implications
The term ‘cognitive behaviour therapy’ has
Many aspects of pain-related fear have been been applied to such patient–clinician
confirmed, and formal screening of patients interactions. This may discourage clinicians
may become routine clinical practice. who lack such training. However, clear
At present, screening may be achieved communication, accurate information and
using clinical skills. It is common for fearful encouragement are central, and are skills
patients to deny fear on initial, direct possessed by all experienced clinicians.
questioning. Matters become clearer if Graded physical activity may be the most
patients are asked to give an account of their effective method of preventing and
understanding of the nature of their problem rehabilitating pain-related fear and disability
and the consequences of movement. It is (Vlaeyen et al, 2001). A recent advance in the
important to know if patients anticipate management of acute back pain was the
immediate or delayed pain, or further injury. change from extended bed rest to early return
A number of questionnaires may be useful to normal activities.
in the identification process. Fear of pain has Graded physical activity makes particular
been measured using Pain And Impairment sense where there is a phobia about pain and
Relationship Scale (PAIRS: Riley et al, 1988) movement (McQuade et al, 1988). Also, there
and the Pain Anxiety Symptoms Scale (PASS: are people who are impervious to persuasion
McCracken et al, 1992). Fear of movement’s and who need to ‘see things with their own
causing further damage has been measured eyes’. Finally, after a period of inactivity, those
using the Survey Of Pain Attitudes (SOPA: with chronic pain are likely to experience
Jensen et al, 1987) and the Tampa Scale for increased pain during the recommencement of
Kinesiophobia (TSK: Kori et al, 1990). Fear activity. There may or may not be an eventual
of work-related activities has been measured diminution of pain. What will be achieved in
using the Fear Avoidance Beliefs the vast majority of cases, however, is a decrease
Questionnaire (FABQ: Waddell et al, 1993). in disability. This is a frightening, worrying
These may provide a screening role, but cut- time, and the presence of an informed clinician
off points indicating clinical significance have who acknowledges that the task is difficult, but
yet to be published. encourages perseverance, is a great advantage.
The best results can be expected when McCracken L, Zayfert C, Gross R. The pain anxiety
cognitive and physical approaches are symptom scale: development and validation of a
scale to measure the fear of pain. Pain 1992; 50:
combined in a supportive environment. 63–7.
McQuade K, Turner J, Buchner D. Physical fitness
References and chronic low back pain. Clinical
Orthopaedics Related Research 1988; 198–204.
Asmundson G, Norton P, Norton G. Beyond pain:
Riley J, Ahern D, Follick M. Chronic pain and
the role of fear and avoidance in chronicity.
functional impairment: assessing beliefs about
Clinical Psychology Review 1999; 19: 97–119.
their relationship. Archives of Physical Medicine
Crombez G, Vlaeyen J, Heuts P, Lysens R. Pain- and Rehabilitation 1988; 69: 579–82.
related fear is more disabling than pain itself.
Vlaeyen J, Linton S. Fear-avoidance and its
Evidence of the role of pain-related fear in
consequences in chronic musculoskeletal pain: a
chronic back pain disability. Pain 1999; 80:
state of the art. Pain 2000; 85: 317–32.
329–40.
Vlaeyen J, de Jong J, Geilen M, Heuts P, van
Jensen M, Karoly P, Huger R. The development
Breukelen G. Graded exposure in vivo in the
and preliminary validation of an instrument to
treatment of pain-related fear: a replicated
assess patients’ attitudes toward pain. Journal of
single-case experimental design in four patients
Psychosomatic Research 1987; 31: 393–400.
with chronic low back pain. Behavior Research
Kori S, Miller R, Todd D. Kinisophobia: a new Therapy 2001; 39: 151–66.
view of chronic pain behavior. Pain
Waddell G, Newton M, Henderson I, Somerville
Management 1990; Jan/Feb: 35–43.
D, Main C. A Fear-Avoidance Beliefs
Kottke F. The effects of limitation of activity upon Questionnaire (FABQ) and the role of fear-
the human body. Journal of the American avoidance beliefs in chronic low back pain and
Medical Association 1996; 196: 117–22. disability. Pain 1993; 52: 157–68.
Lethem J, Slade P, Troup J, Bentley G. Outline of
fear-avoidance model of exaggerated pain
perceptions. Behavior Research Therapy 1983;
21: 401–8.
Relaxation, hypnosis and

meditation
10 ‘The highest possible stage in moral culture is when we

recognize that we ought to control our thoughts.’
Charles Darwin 1871
It is possible to gain some relief from the separate entities of

anxiety and physical pain through the use of relaxation,
hypnosis and meditation techniques. Physical pain is usually
accompanied, and is always heightened, by anxiety or similar
mental distress. Faced with the dilemma of chronic pain, these
techniques should be exploited.
Overview of techniques
Relaxation is infrequently defined. It has been described as the
absence of tension, stress, discomfort, anxiety and distress. It
is a psychophysiological state (it has mental and physical
components). The key features include increased slow brain
wave activity, lowered respiration and heart rate, lowered
adrenal outflow, and a lowering of mental activity other than
effortless attention. A definition from scholars interested in
response to stimuli reads ‘A generalized psychophysiological,
wakeful state of minimal activity or preparation for response
to any demand placed upon the body and the risk of strong transference (Freud is said to
mind’ (Wentworth-Rohr, 1988). Both have been unexpectedly kissed by a patient
components, mental and physical, must be when she woke from a trance). There is also
targeted in the pursuit of the relaxed state. the risk of the hypnotist developing the
Hypnosis also lacks a straightforward ‘Messiah Complex’ (Scott, 1974).
definition. It is swathed in mystique. It is These difficulties represent no challenge
known as a method by which deep trance for the thoroughly trained hypnotherapist.
states can be induced and potent post- For those without such training, however,
hypnotic suggestions implanted. Importantly, they represent significant obstacles. The
to the present time, it lacks a physiological present account will borrow elements from
profile to distinguish it from relaxation. One hypnosis, but does not attempt a
definition of hypnosis is ‘a consent state of comprehensive coverage of that field.
physiological relaxation in which the critical Relaxation, hypnosis and meditation all
faculty of the conscious mind is by-passed to have the potential to narrow concentration,
some degree’ (Scott, 1974). This purported focus attention and increase receptivity to
distinguishing feature of hypnosis, the suggestion. The common denominator is the
potential for by-passing ‘the critical faculty of reduction of physiological arousal and the
the conscious mind’, may not be unique, removal of distressing thoughts.
however, as proponents of relaxation and
meditation also claim to achieve increased
Benefits persist
receptivity to suggestion (Meares, 1968).
The difficulties of hypnosis include the The relaxation, hypnosis and meditation
stigma of charlatanism (the legacy of stage treatments of anxiety and pain have not been
hypnotists) and the suspicion of malevolent extensively studied with the randomized,
mind control that pervade the public view. double blind, placebo-controlled trials that
There is the difficulty of deciding whether or characterize medication treatment research.
not a patient is a good hypnotic subject. Nevertheless, various relaxation procedures
There may be difficulty in inducing hypnosis; have earned a place as effective treatments of
even patients who appear to be good these conditions.
candidates and have received adequate When a patient is physically and mentally
preparation may resist induction. Patients may relaxed, there can be little anxiety and mental
claim that they were ‘not really’ hypnotized distress. Proponents of relaxation, hypnosis
and were ‘just pretending’, a situation that and meditation tell us that with daily practice
calls for time-consuming exploration. There is the benefits experienced during active
Relaxation, hypnosis and meditation 65
treatment sessions begin to persist after the indicates that appropriate processes have been
sessions have ceased. Over time these benefits initiated. With each initiation, ability
last for longer and longer periods, until they increases. In the maintenance stage (after the
remain throughout the entire day. first month) the technique should be practised
every day. Some would say twice a day, but
that may be unrealistic. A minimum of 20
General technical details
minutes per day (total) should be so
The therapist should learn by undergoing dedicated. With practice, ability to initiate
instruction or attending classes whenever relaxation increases and the total time
available. However, it is possible to learn necessary for good effect may be reduced.
sufficiently from books and personal In general, it is better for the patient to sit
experimentation to be able to offer patients on a dining-style chair without arms or head
some simple techniques. rest, with feet flat on the floor and hands
It is better to avoid the use of the term resting on the thighs. The relaxation sought is
‘hypnosis’, which generates fear in some not like that which precedes sleep, and
patients and may cause others to twist therapy patients do not fall off their chairs. There are
into a contest of wills. Do not hesitate to advantages to providing less than full body
involve a chaperon or friend/relative of the support; when sitting as described, it is
patient. Exercises for the body are an accepted necessary to work hard at achieving relaxation.
feature of modern society. Relaxation, Some authorities recommend a head rest; and
hypnosis and meditation are exercises for the it is possible to achieve relaxation in the
mind and should be conduced in a similar, supine position.
open (but confidential) matter-of-fact The patient usually sits with eyes lightly
manner. closed. This is not essential, as it is possible to
In the skill-acquisition stage (the first achieve relaxation with the eyes open. When
month) a technique should be practised as deep relaxation is achieved, the eyes may
often as possible. This may be five or six times partially open. In the early skill-acquisition
per day. The actual number of times this stage the patient may be troubled by
happens depends on enthusiasm and trembling eyelids, but this passes within a
opportunity. Each practice session can be week or so.
short: perhaps three to five minutes. It is The therapist should speak in a quiet flat
better to persist until a noticeable change voice, similar to that used to deliver a sermon.
occurs, such as a change in rate of pulse or Speaking slowly gives the patient time to
breathing or a sense of emotional peace. This perform the indicated tasks and the therapist
time to decide on the next instruction. The in motivation following the early honeymoon
therapist should repeat instructions for the phase. Brief periods of even a few seconds of
same reasons. heaviness of limbs or drifting free of everyday
Permissive phraseology should be thoughts during relaxation sessions are
employed. Use of commands (‘You must relax evidence that a favourable result can be
your legs’) will discourage co-operation and achieved. Patients should be informed that,
will usually result in failure of therapy. Some from this point, abilities and rewards rapidly
confident hypnotherapists use predictions become apparent.
(‘Your finger will lift’) to good effect. These Whether relaxation, hypnosis or
predictions may be relying on little-known meditation is achieved depends on the quality
normal human physiology – for example, of the instructions of the therapist and the
relaxed fingers do twitch from time to time – abilities of the patient. It is a given that
or on the power of suggestion, which may be treatment sessions are only attempted in safe,
facilitated by charisma, training and a good warm, suitably lit environments. The
sense of timing. The term ‘maybe’ lacks information made available by the therapist is
confidence and is unlikely to be successful. standard information. From the outset it must
The word ‘can’ (‘See if you can slow your be made clear that whether the desired
breathing still further’) places the task with endpoint is reached depends not on the
the patient. abilities of the therapist, but on the abilities of
Certain words, such as ‘calm’, ‘drift’, the patient to follow and apply that
‘peace’, ‘sink’, ‘ease’ and ‘heavy’, are favoured, information. This relieves the therapist of
as they not only impart information, but also responsibility, and leaves it with the patient.
strike a psychological cord that helps in In handing this responsibility to the
triggering the desired response. New therapists patient, the therapist should remember that a
develop their own lexicons and scripts with minority of people lack the ability to perform
which they have success. these activities and that these people must be
Patients should be informed of the need protected from a sense of failure. Thus from
for regular practice. Relaxation sessions will be the outset it is necessary to affirm that some
followed by periods of tranquillity, and the people are good at some things and other
length of these periods will increase with people are good at other things. Some people
practice. Sleep should also improve after a few are good at arithmetic, some are good at
days. Benefit during the day may be apparent dancing and others are good at relaxation in
at one week and will increase indefinitely. therapists’ offices. No one is good at
Patients need to be warned of the risk of a dip everything, and some people are not
particularly good at this form of relaxation. off the task and unbidden thoughts enter, they
These people may be able to find relief in are not pushed away, but they are not
activities such as swimming or playing attended and are allowed to pass through and
computer games. The point can be made that away. The patient maintains a passive mental
a mantra is (usually) a meaningless utterance attitude, the only mental activity being the
that is useful because it allows participants to effortless focusing and refocusing of attention
focus attention, and that a squash ball moving on the neutral task.
around on white walls, or a prompt blinking The mantra is a traditional Eastern
on a computer game screen can, at least in mechanism. It is usually a sound that is
part, perform the role of the mantra, allowing repeated aloud or experienced silently. It
freedom from intrusive concerns. becomes the focus of attention. These devices
Before concluding that the patient can are used as an aid in many popular forms of
gain nothing from office-based relaxation meditation. Mantras share some of the
techniques, however, it is obligatory for the features of counting sheep when sleep is
therapist to offer more than a single method. evasive.
To this end, some alternatives are described Focusing attention on breathing is a
below. neutral task that is used in most if not all
forms of relaxation, hypnosis and meditation.
Most commonly the patient is asked to slow
Methods of focusing
the breathing and to breathe with the
attention diaphragm rather than the ribs. (In
Central to these techniques is the exclusion diaphragmatic breathing, as the diaphragm
from the mind of worry and distressing descends, and air enters the lungs, the anterior
thoughts. This may be achieved by occupying abdominal wall, rather than the chest wall,
the mind with a task. It is possible to displace moves outward.) The patient may also be
distressing thoughts with happy thoughts; but asked to focus on the flow and feel of the air
in the initiation stage of relaxation, hypnosis as it enters the nose, trachea and lungs. In
and meditation, it is better to use a neutral some relaxation and hypnosis techniques
task. By focusing attention (concentrating) on attention to breathing is alternated with
the neutral task, awareness not only of worries attention to muscle relaxation. In some
and distress, but of the environment in meditation techniques attention to breathing
general, is reduced, and the mind becomes less (the counting to 10 breaths and then starting
critical and more open to imagery, suggestion again) is the only task (Wilson, 1995).
and autosuggestion. When the mind wanders Focusing attention on the muscles is a
neutral task that was pioneered by Jacobson Another perceptual exercise that is mainly
(1938). Like focusing on breathing, focusing used to deepen relaxation is creating the
on muscle relaxation achieves two ends experience of going down steps. Once some
simultaneously: it achieves one of the degree of relaxation is achieved the patient can
components of relaxation (decreased muscle be asked to see three steps leading down from
tension) and it provides a focus for attention, their present position. The patient can be
thereby assisting the avoidance of worry and asked to indicate when this task has been
the thoughts of everyday living. achieved. Patients are then asked to ‘feel’
themselves move down from the top to the
second step. As this occurs the patients are
Special technical details
asked to feel themselves ‘go deeper into
‘Visualization’ here means the formation of a relaxation’. The patient may be asked to
mental image as though objects were being seen indicate when this task has been achieved, and
through the eyes. This process can be used then to take the next step and go even deeper
either to initiate or to deepen the relaxed state into the relaxed state. The number of steps
or for both. The patient is asked to ‘see’ an can be altered to suit the therapist and the
image, often a serene water view. The patient patient.
must strongly focus to perform this task. The Ego-strengthening exercises have been
task can be made more exacting by asking the described in the hypnosis literature. Once
patient to ‘see’ things in greater detail. The hypnosis is induced the hypnotherapist makes
therapist may ask: ‘Try to see some small stones encouraging statements to the effect that the
over to one side.’ As a means of encouraging patient will become more confident, capable
continued participation the therapist may ask and contented. It is unlikely that this
the patient to indicate by lifting an index finger procedure modifies the ego as originally
when some particular object can be ‘seen’ intended. However, having relaxed patients
(details given below). Other perceptual relive events in which they were appreciated
modalities can be included. The patient may be and achieved positive results can serve as a
asked to try to ‘hear’ waves or lapping water. task on which to focus, and simultaneously as
The patient may be asked to ‘smell’ flowers. A a means of providing comfort and support. It
particularly useful task is to ask the patient to is necessary to discover in preliminary
‘feel’ the warmth of the sun on the face. discussion whether such an event can be
Patients may also be asked to ‘see’ themselves in identified. It is unhelpful to place this task
and ‘feel’ the rocking of a rowing boat while before deeply relaxed patients if they are
visualizing a beach scene. unable to identify events about which they
have positive memories and feelings. The but also to experience the associated feelings
Stein (1963) clenched fist technique may be and emotions. For example, as mentioned
useful. Relaxed patients are asked to re- above, the patient who is asked to slow the
experience an event associated with positive rate of breathing may also be asked to note the
thoughts and feelings; they are then asked to feeling of air going through the respiratory
make a fist and ‘keep hold’ of those feelings. passages. A more complex task is for the
The hand is kept closed until after completion patient who is asked to assume a peaceful
of the relaxation or hypnosis session. With attitude not simply to think of the concept of
practice, it is claimed that closing the hand peace, but also to achieve the feeling or
outside relaxation sessions may trigger the emotion of peace. These are more difficult
desired experience. tasks that require a greater degree of
It is possible to communicate with deeply concentration and provide a deeper level of
relaxed patients by asking them to indicate relaxation.
answers by the voluntary raising of the index Semantic and mystical issues arise. There is
finger of one hand. This does not cause no emotion called ‘peace’. It is possible to feel
disturbance of the relaxed state. (Experts in peaceful; but patients may be asked to go
hypnosis have described using the raising of a beyond ‘peaceful’. They may be asked to
finger as a means of communicating with the ‘become’ peace (for example), to allow their
unconscious; but that is a different matter.) body and mind, identity or essence to be
Questions can be phrased such that they transformed into or blend with nature, God,
require yes or no answers, one hand answering, the cosmos, or a universal serenity. At a more
yes, and the other, no. This feature should not secular level, patients may usefully be asked to
be overused, as it can have some temporary acquire or ‘get’ the feeling of drifting. It is
effect on the depth of relaxation. It can be used better for therapists to remain on the secular
to good effect as a means of indicating when a side of the border with mysticism. From the
task has been achieved, as in ‘When you have medical perspective and in medical parlance
been able to experience the feeling of inner such tasks foster a dissociative state.
peace, lift your index finger of your right hand.’ Dissociation is poorly defined, but includes
Such phraseology increases the chance of the separation of ordinarily integrated
success when the therapist is confident and behaviour, thought, feeling and consciousness.
positive: it is not a question of whether, but Thus, in so far as relaxation aims at producing
when the task will be achieved. a state of profound physical inactivity,
A valuable tool is to ask patients not only avoidance of the present environment, and
to follow instructions on an intellectual level, uncritical thought processes, there are
similarities to a dissociative state. Relaxation established in this field. For example, the
of the type described here could be considered original progressive muscular relaxation
as controlled dissociation. technique (Jacobson, 1938) called for repeated
Complications of relaxation are very few. muscular contraction and relaxation of
There is some danger of uncontrolled individual muscles or muscle groups, with
dissociation following treatment sessions. whole sessions being spent on small
These are averted by discussion following anatomical areas and coverage of the whole
treatments. The therapist ensures that the body taking many weeks. Abbreviated versions
patient is orientated in time and place and were appropriated. More recent relaxation
restored to normal consciousness. Positive or techniques have dispensed with the forceful
negative experiences need to be reviewed, and contraction of muscles; instead, the attention
the patient should be able to respond to of patients is directed to individual muscle
potentially dangerous painful conditions in groups, with the instruction simply to relax
the appropriate manner. them during slow expiration. Different
Audiotapes may be made of relaxation authors have drawn attention to the
sessions for use by patients at other times. importance of relaxing different muscle
This gives the patients an accurate account of groups (face, neck, hands); this appears to be a
the session and the opportunity to practise the matter of personal preference.
tasks at their own pace. A potential Suggestion (defined for present purposes)
disadvantage is that patients may become is a primitive process by which ideas can be
dependent on the therapist rather than accepted into the mind without critical
developing their own initiative and self- evaluation. Autosuggestion occurs when the
administered relaxation sessions. Opinions subjects present ideas to themselves. These
differ from one therapist to another and one procedures were first described in hypnosis.
from one patient to another. However, as relaxation techniques also focus
attention and increase receptivity, self-
delivered ego-strengthening exercises, and
Developing a unique method
positive self-messages, which constitute
It is recommended that therapists should autosuggestion by other names, have been
borrow from different techniques and develop included in many relaxation protocols.
a unique relaxation method with which they The relaxation technique described by
are personally comfortable and that suits their Meares (1968) borrows from meditation
clinical circumstances. techniques. The patient repeats thoughts: ‘It is
Borrowing and modifying is well good to relax. Relaxing is natural. It is the
natural way to calm and ease.’ This is similar process (this would be called
reminiscent of the repetition of a mantra. autohypnosis, if the therapy were considered
There is a difference, however, as these to be hypnosis) for a total of not less than 20
thoughts contain messages describing the minutes per day. Patients are advised that
desired mental state, which is not the case there may be minor setbacks, but progress can
with most mantras. be anticipated. Patients are also advised of the
risk of loss of enthusiasm, particularly if
progress is slower than desired.
Relaxation treatment of
The following scripts are provided as a
anxiety guide to the types of relaxation sessions that
Anxiety is common in pain states, and anxiety can be developed. The therapist is encouraged
increases the suffering associated with pain. to explore and modify.
For these reasons it is appropriate to reduce
anxiety in pain states. Relaxation (Fisher and Script 1
Durham, 1999), hypnosis (Ashton et al, The following monologue gives an idea of a
1997) and meditation (Miller et al, 1995) relaxation session early in the
have all been shown to reduce anxiety. The treatment/education process. Some repetition
system described in this essay is a hybrid, is given here, but in reality in a session lasting
elements having been drawn from across this more than 10 minutes even more repetition
therapeutic spectrum. would occur. In the initial phase of this
Relaxation, hypnosis and meditation are session the focus is mainly on the
frequently practised by healthy individuals musculature. That is not mandatory. Then
whose motives are many, including pleasure, the imagery of going down steps is used to
self-development and self-awareness. No deepen the relaxation. The patient is asked to
specific anti-anxiety component needs to be communicate with the therapist using finger
added for these to be considered effective movements. Toward the end, encouraging
treatments of anxiety. Obviously, these statements are made and the patient is
techniques produce a physical and mental encouraged to remain in touch with positive
state that is the antithesis of anxiety, and this feelings on cessation of the session.
is presumably relevant to their therapeutic
action. Please close your eyes . . . and try to follow
Patients can be taught to relax using scripts my suggestions . . . I can tell you the things
similar to the one that follows. They are to aim for . . . but you are the one who has
encouraged to self-direct themselves through a to do the work . . . First try to
concentrate on slowing your breathing retain and explore this relaxed feeling for
down . . . Calm, slow breathing . . . Calm yourself.
and relaxed . . . That’s good . . . Now I OK, that’s fine . . . You have calmed
want you to think about the muscles of your breathing and relaxed . . . Well done
your forehead . . . Let the muscles of your . . . Now try to see three steps in front of
forehead relax . . . Calm, slow breathing you . . . Calm and relaxed . . . See yourself
. . . Calm and relaxed . . . As you breathe standing on the top step . . . with a path at
out say ‘Relax’, inside . . . Thinking of the the bottom . . . See the details of these
muscles of your forehead . . . as you three steps . . . Slow your breathing down
breathe out think, ‘Relax’ . . . Let the . . . Very slow now . . . When you can see
muscles of your forehead relax . . . Now three steps . . . slowly move the index
think of the muscles of your face . . . your finger of your right hand.
eyes . . . and your mouth . . . as you OK, that’s great . . . Now see if you can
breath out say, ‘Relax’ . . . and let the get the feeling of stepping down from the
muscles of your eyes . . . your face . . . and top step to the second step . . . Feeling
your mouth, relax . . . You are doing very good . . . Calm and relaxed . . . as you step
well . . . You have control of your down try to get the feeling of going deeper
breathing . . . Now think of the muscles of into relaxation . . . Try to get that feeling
your neck and shoulders . . . Relax your of stepping down . . . I will let you
neck and shoulders . . . feel them sag a concentrate on stepping down . . . Move
little . . . feel them sink . . . feel them heavy that finger when you have been able to get
and relaxed . . . Calm and relaxed . . . down.
Think of the muscles of your chest and Good . . . Now can you get down to
your abdomen . . . let them relax . . . the next step? . . . As you go down you
deeply relax . . . Now think of the muscles will become more relaxed . . . Calm and
of your legs . . . as you breathe out . . . let relaxed . . . You are doing very well . . .
your legs relax . . . Now think of your feet Move your index finger when you have
. . . Now think of your hands . . . as you stepped down.
breathe out . . . let your feet and hands That’s good . . . OK . . . Why don’t
relax . . . Calm and relaxed . . . Everything you try to step down on to the path? . . .
is heavy and relaxed . . . You are feeling You have done very well . . . We will only
good . . . You sink into the chair . . . You go as far at the path today . . . Try to step
have done very well . . . I am going to stop down on to the path . . . As you do . . . feel
talking for a minute . . . In the silence, yourself go even deeper into relaxation . . .
Heavy and sinking into the chair . . . Face of relaxation by focusing on breathing. In a
relaxed . . . Neck relaxed . . . Chest relaxed preliminary discussion it is necessary to
. . . Legs relaxed . . . See if you can step establish whether the patient is able to breathe
down on to the path . . . As you step down through the nose. If not, it is necessary to
you will get more relaxed than ever . . . modify the wording to detail breathing
Move that finger when you make it down through the mouth. In this discussion it will
to the path. also be necessary to determine whether the
Well done. You should feel very patient is capable of diaphragmatic breathing.
pleased with yourself . . . You have taken If not, a lesson will be necessary. Finally, it
control of your mind and your body . . . will be necessary to discover a happy event in
You are in control . . . Take a moment to the life of the patient. This is preferably an
explore the feeling of relaxation . . . take event in which the patient played an active
note that you have produced this state of part. The preferred event was marked by the
profound relaxation . . . Let me know patient’s feeling capable and appreciated. It is
when you have been able to get a good used as a visualization task and a means of
feeling about what you have achieved. making supportive statements.
OK, now we are going to start to come
back up . . . Slowly turn around . . . See the Please close your eyes and focus on your
steps in front of you . . . Keep hold of that breathing . . . breathe in through your nose
good feeling about yourself . . . First, step . . . Feel the air going into your nostrils . . .
back up one step . . . Feeling good . . . Calm Slow the flow down . . . Concentrate only
and relaxed . . . Now back to the next step on your breathing . . . Concentrate on your
. . . Holding on to that good feeling . . . nostrils . . . Feel the air cool and flowing
Now finally up to the top step . . . You have freely . . . Now let yourself relax . . . Think
done very well . . . You have taken control of the air going down your neck . . .
of your mind and body . . . Gradually let Flowing freely . . . Slow your breathing . . .
your eyes open . . . Hold on to that good Feel the air go into your chest . . . You can
feeling . . . Don’t move too fast . . . You relax . . . Feel your body heavy and relaxed
have been deeply relaxed . . . You have in the chair . . . As the air enters your body
been in control . . . You have done well. . . . Feel your tummy rise . . . Relax your
OK. How do you feel? chest . . . Let your chest be heavy . . .
When the air comes into your body . . . let
Script 2 your tummy rise . . . Your breathing is
This monologue demonstrates the initiation much slower now . . . Your tummy rises
very slowly . . . You can hardly feel it rise treatment of anxiety. Hypnosis is used in
. . . Relaxed all over . . . I will stop talking acute dentistry, burns and surgery. The term
for a minute and let you concentrate on hypnoanalgesia is mainly restricted to the pain
your slow relaxed breathing. insensitivity induced in such acute settings.
Great, you’re doing fine . . . You are in While the mainstay of chronic pain treatment
control . . . Check your body . . . If you is the same set of techniques that are used in
have tension anywhere . . . Let go . . . See if the treatment of anxiety, the specific
you can get the feeling of drifting . . . As if hypnoanalgesic techniques may be co-opted
you are floating . . . Drifting . . . Let go and from acute care. These specific techniques
drift. may provide some relief in problematic cases
Now get in touch with that time we and provide some refreshing variation in
were talking about . . . See yourself in that clinical practice.
situation . . . See the details . . . Let yourself The term hypnoanalgesia will be avoided
drift . . . Now get in touch with that here, as similar effects can be obtained in
feeling of success . . . Get that feeling of relaxed states other than hypnosis. An early
being pleased . . . Get that feeling of specific relaxation/hypnosis pain reduction
confidence . . . Things went well . . . Hold method commences with the creation of local
on to that feeling of success . . . Let numbness/analgesia in the hand. The relaxed
yourself drift . . . I am going to be quiet patient is asked to create the experience of
now for a minute and let you get those having a hand in a bucket of ice water and to
feelings flowing over you. produce a feeling of coldness progressing to
Good. Now, hold on to that feeling as numbness or deadness. The hand may then be
you come back . . . Gradually coming up moved to a particular site, and the patient is
. . . hold on to that feeling . . . Feeling calm asked to experience the numbness of the hand
. . . Feeling Good. passing to the second site. This method is
How do you feel now? complicated, involving a number of steps, any
of which may be a source of difficulty, and is
not recommended. It was perhaps popular
Relaxation treatment of pain
because the passing of analgesia from one
Relaxation (NIH, 1996), hypnosis (Lang et al, region to another was spectacular and held
2000) and meditation (Kaplan et al, 1993) some entertainment value. It is included here
have been shown to reduce pain. Reduction in because it has historical value and gives us an
chronic pain (Lewis, 1992) may be achieved idea of the possibilities.
using exactly the same techniques used in the An alternative method is to ask the patient
to create the experience of numbness as it The lessons of Ainslie Meares (1968) are
occurs with the injection of local anaesthetic. most useful in helping people with pain. He
To assist in the creation of the effect the patient pointed out that pain is a warning sign that the
can be asked first to experience the prick of a body is being harmed, but it is when the patient
needle and then a sting as if a bolus had been becomes emotionally distressed that pain
injected, and finally a slowly spreading becomes aversive and excessive. ‘Unless we react
numbness. This numbness can be produced at to it there is little or no hurt in the painful
any site, and the technique can be used to stimulus.’ He makes the point that when a child
supplement the pain relief of general relaxation. falls and is distressed, mother’s kisses on the
Another technique that has been used in the cheek markedly reduce the crying. Her kisses (to
management of acute pain (burns dressing, the cheek, not the knee) ease the emotional
surgery, dental work) is ‘projection of the body distress, not the nociceptive focus. Thus Meares
image’ to a distant location. The patient is points to the need for the patient to understand
asked to create the experience of the body part the nature of pain and to be confident that
(or even the whole body) floating away to a when emotional distress can be controlled (by
distant place. In preparatory discussion, the relaxation) there is no need to be, or possibility
therapist and patient agree that if a particular of being overwhelmed, by pain.
piece of anatomy is at a distant location, it Meares (1968) described a range of
cannot be ‘here’ and thus cannot be painful. reactions to pain, including depression and
Whether this mechanistic explanation is hostility. In keeping with his insight that the
necessary is doubtful; as has been mentioned, amount of hurt associated with pain is
any task that requires focused attention has the proportional to the associated emotional
ability to reduce the experience of pain. distress, he recommends that patients are
Visualizing a scene has been described helped to a philosophical response. ‘It can’t be
above as a means of inducing relaxation. It is helped, but I will get over it.’ Relaxation
also reported to be useful in acute pain exercises can assist in shaping this response.
situations, under the designation, ‘reduction Finally, Meares (1968) acknowledges the
of awareness by distraction’. We are not possibility of pain relief by the above-
usually aware of the touch of our clothes; mentioned methods, but favours the ‘feeling
thus, if we are distracted, we may not be fully of pain in its pure form’. He supplies us with
aware of nociceptive stimuli. The more able the knowledge that pain is a signal; and, in a
the patient is to focus and the greater detail state of relaxation, the patient is able to
that can be experienced, the better will be the experience pain as information rather than as
analgesic effect. an unbearable sensation.
Script 3 . . . Calm and heavy . . . Now feel that

This monologue demonstrates a means of area going numb . . . Feel numbness
rapidly achieving relaxation. It is appropriate spreading out . . . dulling your pain . . .
for the patient who has had some earlier Let your pain become dull . . . Make your
lessons. It includes instructions on creating pain dull . . . Make that area numb and
local analgesia. your pain dull . . . I will let you focus on
making that area numb and your pain
Please close your eyes and follow my dull.
suggestions to the best of your ability . . . OK. Time to start coming back . . .
Let your legs relax . . . Let your back relax You are relaxed and feeling good . . . You
. . . Let your face relax . . . Let your whole have lessened your pain . . . You have been
body become pleasantly heavy and relaxed able to take charge . . . Try to keep your
. . . Let your shoulders and arms relax . . . pain area numb . . . Getting lighter . . . Still
Let your neck relax . . . Now you are in charge . . . Getting lighter . . . OK . . .
almost completely relaxed . . . Now you You can open your eyes whenever you
can slow your breathing . . . Let your feet want . . . You are still in control.
relax . . . Let your hands relax . . . I am
going to stop talking for a minute . . . Script 4
Think about every part of your body in This monologue demonstrates a very quick
turn . . . you are a detective . . . check every method of inducing deep relaxation. This is
part . . . make sure it is relaxed . . . If you only appropriate for patients who have learned
find a part that is still tense . . . relax it as the basic skill of relaxation. The monologue
you breathe out . . . Move your index also guides visualization of a beach scene and
finger when you are fully relaxed. ends with the patient’s accepting the pain as a
Great . . . You are relaxed and calm . . . nuisance, but something that can be tolerated.
Feel calm . . . Feel calm all over . . . Let the
feeling of calm float around you and Please close your eyes and relax . . . I am
through you . . . I will stop talking and let going to count to five . . . I want you to
you focus on being calm . . . deeply relaxed relax as I count . . . Five is very deeply
and calm. relaxed . . . One is where you are now . . .
Now think of where your pain is . . . just sitting quietly with your eyes closed
Try to imagine a local injection where . . . OK, getting ready . . . Starting at one,
your pain is . . . Feel a prick and a sting as now relax down to two . . . Feeling relaxed
the injection goes in . . . Calm and heavy . . . Going down now to three . . . Now
you are moderately relaxed . . . Heavy in in control . . . You are calm and feeling
your chair . . . Slow your breathing . . . Get good . . . You are feeling fine . . . in spite of
ready and now down to four . . . Now you your pain . . . Calm and peaceful . . . You
are deeply relaxed . . . Calm and relaxed can accept your pain . . . You are doing
. . . Heavy and relaxed . . . Get ready and well . . . Stay feeling calm . . . Now
now come down to five . . . very deeply gradually come back up . . . and open your
relaxed . . . I will give you a minute to eyes.
make the last step down.
That’s good . . . You are able to control
The problem of non-
your mind and body . . . Now try to
imagine sitting or lying at the beach . . .
compliance
Calm and relaxed . . . take your time and Most patients are able to obtain some relief
see the blue of the water and the sky . . . from anxiety and chronic pain through
Calm and relaxed . . . waiting to be able to relaxation, hypnosis or meditation. However,
see the water and the sky . . . Are there any many do not persist with these techniques.
clouds in the sky? . . . If there are some This is surprising, given that the pain is ever
clouds . . . move the index finger of your present and other treatment options are
left hand . . . If there are no clouds, move problematic and offer little relief. While these
the index finger of your right hand. techniques may have a modest temporary
OK, there are some clouds . . . Now effect, they are endlessly repeatable.
see the sand . . . focus on the sand . . . Try The reasons why they are abandoned, why
to see some seaweed on the sand . . . You patients cease claiming these analgesic
are doing well . . . Deeply relaxed . . . Now benefits, include the facts that the techniques
try to feel the sun on your face . . . try to are time-consuming, require effort and
feel the warmth on your face . . . provide only partial relief. Further, chronic
concentrate on the feeling of the sun on pain is distressing and exhausting, making
your face. effort more difficult. Finally, these techniques
Now, think about your pain . . . Stay can be boring.
calm and relaxed . . . Your pain is a There is little awareness that patients with
message . . . Your pain is a message you chronic pain often discontinue these
don’t need . . . Stay calm and relaxed . . . techniques. Patients often do not offer this
Accept your pain as a nuisance . . . information because they have been ‘sold’ the
Something you don’t need . . . But techniques as solutions to the pain, and they
something you can live with . . . You are therefore feel ungrateful and embarrassed
about their discontinuation. Therapists often 5. Create interpersonal relationships such

do not ask too closely, as they do not want to that patients will speak openly about the
know that the techniques have been difficulties they are having finding time
abandoned, because they have little else to and energy to continue.
offer. 6. Detect when the techniques have been
Why are these techniques presented as discontinued. Be accepting, but
being highly effective when clinically, more encourage re-commencement.
accurately, they are moderately effective? Part 7. Combat boredom by finding techniques
of the answer may be that they are purveyed that suit the patient, and provide a range
by therapists who are strongly biased in this of techniques.
direction. Another part may be that if these 8. Closely monitor progress and try to find
techniques are presented/accepted as being solutions to obstructions.
highly effective, then continuing pain means 9. Remember, nothing works for everyone,
failure of the patient to make use of the and these techniques are not a panacea.
prescribed treatment. The problem (pain) This does not mean that either the
then becomes the sole responsibility of the patient or the therapist has failed.
patient, and the therapist becomes an 10. If patients have become non-compliant
unappreciated healer. and return for treatment, it is not
As chronic pain is an area of limited enough simply to encourage them to
treatment options, and relaxation, hypnosis recommence their technique. It is usually
and meditation techniques can provide necessary to teach the technique again.
moderate relief, it is important to ensure full This may seem odd, but, as with the
utilization. The following may encourage behavioural treatment of agoraphobia
long-term compliance: and other phobias, relapsed patients need
re-education in something they have
1. Give realistic expectations. already been taught.
2. Emphasize that every option must be
fully utilized.
3. Emphasize the need for regular, References
indefinite practice. Ashton C, Whitworth G, Seldomridge J, Shapiro P,
4. Tell the patient that minimal benefits Weinberg A, Michler R, Smith C, Rose E,
Fisher S, Oz M. Self-hypnosis reduces anxiety
will be available initially, but that
following coronary artery bypass surgery. A
worthwhile benefits will be available after prospective trial. Journal of Cardiovascular
a few weeks of regular practice. Surgery 1997; 38: 69–75.
Fisher P, Durham R. Recovery rates in generalized Miller J, Fletcher K, Kabat-Zinn J. Three-year

anxiety disorder following psychological follow-up and clinical implications of a
therapy: an analysis of clinically significant mindfulness meditation-based stress reduction
change in the STSI-T across outcome studies intervention in the treatment of anxiety
since 1990. Psychological Medicine 1999; 29: disorders. General Hospital Psychiatry 1995; 17:
1425–34. 192–200.
Jacobson E. Progressive Relaxation. University of NIH Technology Assessment Panel on Integration
Chicago Press, Chicago, 1938. of Behavioral and Relaxation Approaches into
the Treatment of Chronic Pain and Insomnia.
Kaplan K, Goldenberg D, Galvin-Nadeau M. The
Integration of behavioral and relaxation
impact of a meditation-based stress reduction
approaches into the treatment of chronic pain
program on fibromyalgia. General Hospital
and insomnia. Journal of the American Medical
Psychiatry 1993; 15: 284–9.
Association 1996; 276: 313–18.
Lang E, Benotsch E, Fick L, Lutgendorf S,
Scott D. Modern Medical Hypnosis. Lloyd-Luke Ltd,
Berbaum M, Berbaum K, Logan H, Spiegel D.
London, 1974.
Adjunctive non-pharmacological analgesia for
invasive medical procedures: a randomised trial. Stein C. The clenched fist technique as a hypnotic
Lancet 2000; 355: 1486–90. procedure in clinical psychotherapy. American
Journal of Clinical Hypnosis 1963; 3: 113.
Lewis D. Hypnoanalgesia for chronic pain: the
response to multiple inductions at one session Wentworth-Rohr I. Symptom reduction through
and to separate single inductions. Journal of the clinical biofeedback. Human Sciences Press Inc,
Royal Society of Medicine 1992; 85: 620–4. New York, 1988.
Meares A. Relief without Drugs. Souvenir Press, Wilson P. The Calm Technique. Penguin Books,
London, 1968. Ringwood, Australia, 1995.
Psychotherapy in chronic pain
11 ‘. . . it has been consistently demonstrated by research that an

alliance built on trust and, above all, a warm, non-
judgmental and empathetic attitude in the therapist, lies at
the heart of good therapy.’
Bloch and Singh, 1997
Reasonable proficiency in relaxation techniques can be

developed through reading, attending short courses and
regular use of techniques in clinical practice. Proficiency in
psychotherapy, by contrast, requires extensive training and
supervision. A chapter such as this can provide only
preliminary information. Nevertheless, some useful principles
are introduced.
Psychotherapy is defined (Sullivan, 1954) as primarily a
verbal interchange between two individuals in which one of
these is designated an expert and the other a help-seeker (for
present purposes, a patient). They work together according to
an established theory of personality, psychopathology and
psychotherapy. They work together to identify the patient’s
characteristic problems in living, with the intention of achieving
behavioural change. The potential behavioural change depends
on the nature of the patient’s symptoms, and the type and goals
of psychotherapy, and may include shifts in An array of psychotherapies extends from

understanding and attitude about the self and deep lengthy psychoanalysis through to here-
the world, symptom reduction, and in the now and-now brief therapy, and from client-
less common, most intense form, fundamental centred therapy, in which nurturing empathy
changes in personality. is a principal feature to cognitive therapy,
While there are differences between which has thinking as the primary focus.
various forms of psychotherapy, universal Complete coverage is impossible; instead,
features have been identified (Frank, 1961), some points that have relevance to the chronic
and include (1) a confiding relationship in pain patient will be mentioned.
which the therapist remains dependable, The appropriate psychotherapy or
trustworthy and empathetic; (2) a rationale or psychotherapeutic elements in a given case
agreed approach to therapy; (3) the provision depend on the nature of the pain and its
of new information; (4) the gaining of hope origin, the premorbid personality and
by the patient; and (5) the experience of adjustment, the clinician’s training and the
success and mastery. Psychotherapy may also overall management plan.
be associated with arousal and expression of
emotion. Finally, the therapist is a model
Psychoanalysis
from which the patient learns attitudes and
behaviours. Such ‘socially determined Psychoanalysis is conducted in one-hour
learning’ (Bandura, 1977) is a feature of most sessions, four or five times a week, usually for
human relationships. about five years. It is held that subjective
The effectiveness of psychotherapy has experiences of childhood give rise to conflicts.
been established (Shapiro and Shapiro, 1982). These are usually conceptualized as involving
However, as with any other potent therapy, sexual or aggressive wishes. They are
the patient’s condition can also be made frequently unconscious, and it is the work of
worse. Strupp et al (1978) found that 3–6% psychoanalysis to bring them into awareness.
of patients are made worse. This outcome is Conflicts lead to anxiety, depression, somatic
possible only when patients are poorly selected symptoms, social and sexual inhibitions, and
and inadequately trained clinicians attempt difficulties in interpersonal relationships.
ambitious therapy. Such therapy is clumsily Understanding them enables the patient to
and rigidly applied. However, no harm, only change maladaptive patterns of behaviour.
good can come from building an alliance with A central tool is the interpretation of
a trusted and empathetic therapist (Bloch and transference. Transference involves the
Singh, 1997). bringing to new relationships of unconscious
Psychotherapy in chronic pain 83
attitudes, expectations and means of relating Where pain is due to psychological factors,
that were learnt in earlier relationships, it can be conceptualized as arising from
particularly those of the first few years of life. unconscious conflicts. For example, pain may
During the process of psychoanalysis the be a means of keeping a conflict from the
patient attributes to the analyst the conscious mind, or a manner of dealing with
characteristics of one or more important the guilt attached to a particular conflict. In
persons from the past, and eventually begins such circumstances, treatment using
to respond to him or her using unconscious psychoanalytic techniques could be applied.
attitudes and expectations from the past. Where pain has some physical basis but
Whenever evidence of transference emerges psychological difficulties are hampering
the analyst interprets or points out the recovery, psychoanalysis may be employed to
presumed origin of this material. There are reduce anxiety or depression and to improve
usually unconscious mechanisms within the interpersonal functioning. In such cases
patient that function to keep such conflicts improvement in pain and adjustment to
and attitudes from consciousness. These serve residual pain are features of a general
a defensive, homeostatic role. Commonly the improvement in self-understanding, the sense
interpretation is rejected; in psychoanalytic of self-worth and coping skills.
terminology, the interpretation is met with Psychoanalytic theory may be useful in
resistance. The resistance may then be understanding patients in a range of
interpreted, or exposed, by the analyst. When circumstances. For example, we may be able
the patient is able to accept an interpretation to detect the conflict underlying pain of
he or she is said to gain insight. Through psychological origin, or to recognize
serial insights the patient gains deep self- transference issues, when a patient responds to
understanding and is able to develop new helpful clinicians in an inappropriately
attitudes, expectations and means of relating. aggressive manner, which appears to have
origins in early life. Such understanding does
not lead automatically to psychoanalytic
Psychoanalysis in chronic pain
treatment, owing to practical issues such as
For a range of reasons, including the length cost or the unsuitability of many patients (for
and expense of training in psychoanalysis and example, patients need to have at least some
the length and expense of this treatment for ability to sustain effort and relationships).
individual patients, this form of treatment is Nevertheless, such understanding better
generally less available now than it was in the equips us to help such patients using
early to middle twentieth century. alternative methods.
Psychoanalysis has provided a basis for a supportive psychotherapy is the individual

range of less time-consuming and less who normally functions well in home, work
expensive forms of treatment. These are and social settings, but has experienced
known by various names including extraordinary life events that have caused
psychoanalytic psychotherapy, ‘dynamic emotional distress and overwhelmed the
psychotherapy’ and ‘brief ’ or ‘focal ability to function independently. Here the
psychotherapy’. Sessions may occur once or focus is on regaining the former high level of
twice per week and, from the outset, be functioning. Depending on the system of
limited to less than twenty. In these, classification, instead of supportive
transference phenomena are neither psychotherapy, some would call this ‘crisis
encouraged nor extensively interpreted. The intervention’ therapy. With such individuals,
therapist is more active, and seeks to clarify change-orientated therapy is usually not
and extend the patient’s understanding in an indicated, and supportive psychotherapy is a
empathetic setting. short-term treatment.
The methods used include helping the
individuals to understand their predicament,
Supportive psychotherapy
break complex tasks into manageable pieces,
Two quite different categories of patient explore a range of solutions, and decide on a
benefit from supportive psychotherapy. One is particular solution. Reassurance and
the patient who has a long history of coping encouragement are given as tasks are
poorly with the tasks of independent living. attempted. Patients are given information and
Such a person may find difficulty in reaching advised toward realistic expectations. Empathy
decisions, suffer feelings of low self-esteem, and even sympathy are important. There is a
worry excessively about the opinions of others place for catharsis, which is the relatively
and claim inability to sustain effort. These unbridled expression of anxiety, depression,
patients may be unsuitable for change- guilt, anger and the other distressing emotions
orientated therapy such as psychoanalysis. The that are stored up during a difficult life.
aim of supportive psychotherapy with such The risk in supportive psychotherapy is
patients is to help them regain and maintain that the patient may become increasingly
their best possible level of functioning, given dependent on the therapist. This issue must
their personality limitations and life be openly discussed; the patient should
circumstances. This is a form of long-term continue to use other supports and the
therapy. therapist should ensure that the patient
The other type of patient who receives continues to take some decisions and actions
as an independent individual. This issue is individuals lack the necessary psychological

discussed in the early stages, and it is wise to skills and personality strengths to engage in
place a time-limit on therapy. This may be a change-orientated psychotherapy. With
relatively long time, such as six months or one respect to chronic pain patients, two special
year. Then there should be a break in cases deserve mention. Alexithymia, which
supportive psychotherapy, or at least a change means being ‘without words to describe
of therapist; but a return is possible for a emotions’ (Sifneos, 1996) is a personality
further series of sessions in the future. feature that is reported to be an important
Supportive psychotherapy is sometimes factor in some cases of chronic pain. It is
criticized because the aim is not progressive proposed that, in the absence of the ability to
improvement in function. However, describe emotions, individuals respond to life
providing a ‘holding environment’, listening situations in maladaptive ways, including the
empathically and being a safe and reliable development of pain for which insufficient
support may, in fact, lead to strengthening of organic basis can be discovered. This inability
the personality (Ornstein, 1986). Change also to describe emotions and associated features
occurs through social learning (Bandura, such as a limited fantasy life make alexithymic
1977). individuals unsuitable for psychoanalytic-type
therapy.
Contrary to the expectations of some, the
Supportive psychotherapy in chronic
presence of ‘secondary gain’ from a condition
pain
(including chronic pain) generally means the
Those people who have healthy personalities patient is unsuitable for change-orientated
and have functioned well prior to an accident therapy. Where there are gains such as
or injury that has resulted in chronic pain may financial and emotional support, motivation
benefit from supportive psychotherapy. Of for psychological change is limited. Change-
course, chronic pain can mobilize previously orientated therapy calls for high levels of
contained conflicts, in such a way that motivation. Thus chronic pain patients who
dynamic psychotherapy may become are obtaining significant ‘secondary gains’ are
appropriate. usually better managed using supportive
For those patients who have pain of psychotherapy.
psychological origin or difficulty adjusting to
chronic pain, but are unsuitable for dynamic
psychotherapy, supportive psychotherapy may
have a place. As was mentioned above, some
Cognitive therapy (CT) and than the other way around (which may also be
cognitive behaviour therapy the case in certain circumstances). CT aims to
(CBT) correct errors in information processing as a
means of relieving emotional distress.
CT is usually a short-term treatment of 10 to Therapists explore the thinking style and
20 sessions, which are conducted once or, at habits of patients and offer and encourage the
most, twice per week. It is a system of use of logical perspectives and more adaptive
psychotherapy that aims at symptom removal responses. Where social withdrawal and other
rather than resolution of underlying conflicts, self-defeating behaviours have developed,
as in psychoanalysis and the related behavioural modification is also encouraged:
psychotherapies. CT is based on the theory examples include relaxation exercises and
that characteristic ‘errors in information assertiveness training.
processing’ occur in depression, anxiety, CT does not claim that errors of
personality disorder and other states of information processing are the sole or even the
emotional distress (Wright and Beck, 1996). initial causative feature of the syndromes of
These errors in information processing interest. The authors acknowledge the
have also been called ‘pathological importance of genetics, early life experiences,
information processing’, ‘cognitive distortions’ interpersonal conflict and other factors known
and ‘crooked thinking’ (Ellis, 1962). They do to have aetiological importance in mental
not arise from organic pathology, as do the disorders. Instead, CT is construed as a means
information processing or cognitive difficulties of treatment of certain symptoms, and as a
of dementia. Instead, these errors of helpful technique that can be used in
information processing relevant to CT are combination with medication (Simons et al,
more a matter of thinking style or habit. They 1984).
occur in response to environmental stimuli. CT is an expanding catalogue of
For example, if a person prone to depression techniques. Albert Ellis (1962), a pioneer in
makes a mistake at work, he or she might the field who coined the term ‘rational
think, ‘That just proves how dumb I am.’ The emotive therapy’ (RET), restricted his
person prone to anxiety, however, may avoid activities to disclosing ‘crooked thinking’ and
taking action, thinking, ‘If I make a mistake teaching logical thinking. Later workers added
they’ll think I’m absolutely stupid.’ behavioural techniques. Specific CT
Central to CT theory is that errors in approaches have been developed for the
information processing result in emotional treatment of depression (Beck et al, 1979),
distress and maladaptive behaviour, rather anxiety disorders (Beck et al, 1985),
personality disorders (Beck et al, 1990) and of how this may apply in chronic pain is taken
other conditions. from Turner and Romano (1990): a patient
Which particular techniques are included who thinks ‘I can’t take this any more’ is
under the CT umbrella is largely a matter of encouraged to more adaptive thinking, such as
personal opinion. With the addition of ‘Is it really true that I can’t deal with this? No.
behavioural components, some have used the It may be difficult, but I’ve done it before and
designation ‘cognitive behaviour therapy’ can again.’
(CBT) for this form of psychotherapy. There Coping skills is a range of techniques
is argument about the appropriateness of including relaxation, hypnosis and
subsuming age-old techniques such as meditation. ‘Coping self-statements’ may be
hypnosis and relaxation under the CT placed under the general heading of coping
heading, as this could be taken incorrectly to skills, or enjoy a separate heading. Examples
suggest that the clinician needs special CT from Turner and Romano (1990) include:
training to be qualified to deliver these ‘Relax’, ‘I can cope’ and ‘Focus on what you
services. have to do.’
CT has much to offer in the management
of the negative self-concepts and moods that
Cognitive therapy in chronic pain
may be associated with chronic pain and
All clinicians involved in the treatment of disability. CT and educational activities in
chronic pain provide accurate information to general help patients make the best possible
patients about the nature of chronic pain and adjustments to their situations.
encourage them to think logically and
constructively about their situation. A
Summary
particular example occurs when managing a
person with pain-related fear who is inactive Psychotherapy is a vast theoretical and service
and becoming disabled because of the landscape. Three points that represent
erroneous belief that pain indicates further different approaches have been described. All
structural damage. Appropriate interventions aim to reduce emotional distress.
are consistent with the CT approach. Psychoanalysis is a lengthy process that works
Current CT activities can be grouped to develop insight and resolution of
under two main headings: cognitive unconscious conflicts, thereby reducing
restructuring and coping skills. symptoms and encouraging growth of the
Cognitive restructuring is the correcting of personality. Supportive psychotherapy
errors in information processing. An example predominantly supports and encourages and
thereby maintains the best possible References

functioning of severely impaired individuals.
Bandura A. Social Learning Theory. Prentice-Hall,
Cognitive therapy is a short-term Englewood Cliffs, NJ, 1977.
psychotherapy that corrects errors in thinking
Beck A, Rush A, Shaw B, et al. Cognitive Therapy of
style, thereby easing secondary emotional Depression. Guilford, New York, 1979.
distress. It may also involve reversing Beck A, Emery G, Greenberg R. Anxiety Disorders
maladaptive behaviour. and Phobias: A Cognitive Perspective. Basic
No psychotherapy has been expressly Books, New York, 1985.
designed for application in chronic pain. Beck A, Freeman A, et al. Cognitive Therapy of
However, they can all contribute to the Personality Disorder. Guilford, New York, 1990.
general emotional well-being of chronic pain Bloch S, Singh B. Understanding Troubled Minds.
Melbourne University Press, Melbourne, 1997;
patients and favourably influence the
296.
experience of pain to some extent, depending
Ellis A. Reason and Emotion in Psychotherapy. Lyle
on the personality and life circumstances of
Stuart, New York, 1962.
the individual and the nature of the pain.
Frank J. Persuasion and Healing. Williams and
Psychotherapy alone is rarely a satisfactory Wilkins, Baltimore, MD, 1961.
treatment of chronic pain (Pilowsky and
Ornstein A. Supportive psychotherapy: a
Barrow, 1990), and this chapter does not contemporary view. Clinical Social Work Journal
pretend to teach psychotherapy. However, 1986; 14: 14–30.
psychotherapy provides useful advice about Pilowsky I, Barrow C. A controlled study of
the productive patient–clinician relationship psychotherapy and amitriptyline used
individually and in combination in the
and central elements of therapy. The
treatment of chronic intractable, ‘psychogenic’
psychotherapeutic relationship is confiding pain. Pain 1990; 40: 3–19.
and empathetic. The patient and clinician
Shapiro D, Shapiro D. Meta-analysis of
agree on the therapeutic approach, exchange comparative therapy outcome studies: a
information and ensure that each understands replication and refinement. Psychological Bulletin
1982; 92: 581–604.
the other. Hope and the trial of new or
regained skills are encouraged, attempts are Sifneos P. Alexithymia: past and present. American
Journal of Psychiatry 1996; 153 (7 Suppl):
acknowledged. The therapist is a model and
137–42.
the therapist’s attitudes, beliefs and behaviour
Simons A, Garfield S, Murphy G. The process of
are learned by the patient. change in cognitive therapy and
psychopharmacology for depression: sustained
improvement over one year. Archives of General
Psychiatry 1984; 41: 45–51.
Strupp H, Hadley S, Gomes-Schwartz B. Wright J, Beck A. Cognitive Therapy. In: Hales R,

Psychotherapy for Better or for Worse: The Yudofsky S (eds) The American Psychiatric Press
Problem of Negative Effects. J Aronson, New Synopsis of Psychiatry. American Psychiatric
York, 1978. Press, Washington, DC, 1996; 991–1010.
Sullivan H. The Psychiatric Interview. In: Perry H,
Gawel M (eds) WW Norton, New York, 1954.
Turner J, Romano J. Cognitive-Behavioral Therapy.
In: Bonica J (ed) The Management of Pain Lea
and Febiger, Philadelphia, 1990.
Fibromyalgia
12 ‘Merely corroborative detail, intended to give artistic

verisimilitude to an otherwise bald and unconvincing
narrative.’
WS Gilbert (The Mikado)
Introduction
Fibromyalgia (FM) is at the severe end of the spectrum of
widespread pain. With broad diagnostic criteria, widespread
pain was observed in 11.2% of a section of the British
population (Croft et al, 1993). Fibromyalgia has been
observed in 2% of a section of the North American
population (Wolfe et al, 1995; Lawrence et al, 1998).
FM (and its forerunner, fibrositis) has been a contentious
condition. Some authorities view the condition as a variant of
anxiety, and point out that panic disorder was, for many
decades, considered to be a heart condition (Skerritt, 1983).
However, The American College of Rheumatology adopted
diagnostic criteria in 1990 (Wolfe et al, 1990). These include
widespread pain (defined as pain in the left and right sides of
the body as well as above and below the waist), for at least 3
months. Axial pain (defined as pain in the cervical spine,
anterior chest, thoracic spine or low back) early life and in the previous year (Anderberg
must be present. In addition, the patient must et al, 2000a); this does not, however, resolve
report pain in at least 11 of 18 designated sites questions of cause and effect.
on digital palpation. While there may be The prognosis is poor. At 3-year follow-
problems with these criteria in so far as they up, only 3% of patients were found to be free
are restrictive, they have allowed of all pain (Felson and Goldenberg, 1986).
standardization of research. Current treatment is far from satisfactory.
Additional, commonly occurring FM is commonly associated with
symptoms/conditions, which are however not psychiatric disorders. Macfarlane et al (1999)
diagnostic criteria, include fatigue and non- found that over 25% of those with generalized
restorative sleep, irritable bowel syndrome pain (not precisely FM) had some
(IBS), Raynaud’s syndrome-like symptoms, concomitant mental disorder, most commonly
headache, subjective swelling, paraesthesia, depression. Anderberg et al (1999) found
palpitations, significant functional disability, higher figures for FM: 37% suffering
psychological distress (including depression or depression and 16% suffering anxiety.
anxiety) and cognitive complaints (particularly Depression in FM is independent of the
memory problems and inability to cardinal features of pain severity and
concentrate). hypersensitivity to pressure pain (Okifuji et al,
The aetiology of FM is unknown. Several 2000); however, it may contribute to the
mechanisms may be involved. A high inability fully to perform the activities of daily
prevalence in the female relatives of FM life.
patients suggests a genetic vulnerability FM patients tend to feature high levels of
(Buskila & Neumann, 1997). In the related harm avoidance (Anderberg et al, 1999) and a
condition of somatization, genetic factors strong tendency to catastrophizing (Hassett et
accounted for 25–50% of the total variance in al, 2000). There is evidence that unexplained
reports of symptoms, whereas familial and physical symptoms (which include FM) are
environmental effects accounted for virtually associated with abnormal attachment style
no variance (Kendler et al, 1995). Onset often (Taylor et al, 2000). This suggests that
appears to follow physical or psychological patients with poorer relationships will have
stress. The majority (70%) of patients identify poorer social and emotional supports and are
both physical and psychosocial factors more likely to present with such symptoms to
(Neerinckx et al, 2000). Compared to healthy the doctor.
individuals, there is evidence that those with
FM have suffered more stressful events in
Fibromyalgia 93
Overlap Pathophysiology
There is discussion about symptom overlap While the aetiology of FM remains uncertain,
between FM and chronic fatigue syndrome a range of pathophysiological phenomena
(CFS), temporo-mandibular joint disorder have been reported. Which (if any) are
(TMD), somatoform disorder and other primary and which are epiphenomena remains
medically unexplained syndromes. to be determined.
Some special interest groups want CFS to Naturally, the early studies focused on the
be accepted as separate condition. The structure of muscle. Fibres were sometimes
evidence to decide this point is still being described as ‘moth-eaten’ or in similar terms.
accumulated. However, such changes have not been
Clauw and Chrousos (1997) point out observed in controlled studies, and FM is no
that CFS has severe chronic fatigue as a longer considered to be a muscular disorder
necessary diagnostic feature, which must occur (Sims, 1998).
in the presence of four of eight symptoms The pain threshold of peripheral structures
(myalgia, arthralgia, sore throat, tender nodes, and viscera is globally diminished. Parallel
cognitive difficulty, headache, post-exertional phenomena have been demonstrated for
malaise, sleep disturbance), and that five of pressure, heat, cold and electrical stimulation
these are pain-based. FM, however, has pain (Dessein et al, 2000). These observations, in
as the single necessary and sufficient feature the absence of detectable peripheral
(albeit with particular conditions), and is pathology, have moved attention to the
frequently accompanied by fatigue, sleep central nervous system.
disorder, cognitive difficulties, headache, post- Somatosensory-induced
exertional malaise and sleep disturbance. electroencephalographic potentials in FM are
In a recent study 58% of females and 80% significantly different from those of normal
of males with fibromyalgia met the full criteria individuals, and objectify the subjective
for CFS (White et al, 2000). Thus significant reports of patients, indicating a lower pain
overlap between FM and CFS would seem to threshold. There is a significant amplitude
be beyond question. enhancement of cerebral potentials in
Also, FM and CFS have similar comorbid response to painful CO2-laser stimulation
illnesses/conditions, including IBS, interstitial (Gibson et al, 1994; Lorenz et al, 1996).
cystitis and generalized pain sensitivity. The Transcranial magnetic stimulation (TMS)
lifetime rates of IBS are 77% in FM and 92% was applied to the motor cortex of FM
in CFS (Aaron et al, 2000). patients in various conditions (e.g. single
pulse, paired pulse, relaxed and contracted in blunted secretion of thyrotropin and
muscles) (Salerno et al, 2000). Responses were thyroid hormone release in response to
captured from different sites and a range of thyroid-releasing hormone (TRH) (Clauw
calculations were performed. Motor cortical and Chrousos, 1997).
dysfunction was demonstrated in both On examining the HPA axis, the 24-hour
excitatory and inhibitory mechanisms. levels of free cortisol in urine are low and
However, similar findings were obtained from there is a blunted cortisol response to
rheumatoid arthritis patients, and they may be exogenous CRH (Crofford et al, 1994). It
a universal feature of chronic pain disorders. may be relevant that 24-hour levels of free
The autonomic system is impaired. The cortisol in urine are also significantly lower in
sympathetic system may manifest diminished CFS than in normal controls (Cleare et al,
baseline tone, lability and a reduced 2001). Returning to fibromyalgia, insulin-
responsiveness to stressors. Raj et al (2000) induced hypoglycaemia has been reported to
studied the heart rate over 24-hour periods both increase (Griep et al, 1993) and decrease
and during tilt-table experiments. Qiao et al (Alder et al, 1999) adrenocorticotropic
(1991) studied the conductance and blood hormone (ACTH) release. Very low levels of
flow of palmar skin during acoustic IGF-1 occur in one-third of FM patients, and
stimulation and cold pressor tests. The results may be specific to FM (Bennett et al, 1992).
of these studies suggest increased activity of The immune responses are frequently
cholinergic and decreased activity of abnormal. Low natural killer cell numbers and
adrenergic components of the peripheral function have been reported (Caro et al,
sympathetic nervous system. 1993). However, the enhanced humoral
Non-restorative sleep is reported by 75% immune responses that have been
of FM patients (Wolfe, 1989). There is a well- demonstrated in CFS do not appear to be a
established alpha wave intrusion during the feature of FM.
non-REM sleep stages 3 and 4 (Moldofsky et Alterations in neurotransmitters and
al, 1975). receptors are reported. The cerebrospinal fluid
Endocrine abnormalities have been (CSF) has a threefold increase in substance P
detected in hypothalamic–pituitary–adrenal (SP: Vaeroy et al, 1988) and decrease in
axis (HPA) function, in low levels of growth norepinephrine (NE: Russell et al, 1992a).
hormone (GH) and insulin-like growth Serum serotonin and tryptophan are decreased
factor-1 (IGF-1 which is produced in response and the density of serotonin receptors on
to GH and has many biological activities), in circulating platelets is increased (Russell et al,
varying degrees of gonadal hypofunction, and 1992b).
Fibromyalgia 95
There is evidence of decreased regional have been found to improve the sleep disorder
cerebral blood flow in women with without concomitant improvement in pain or
fibromyalgia. Comparing FM with healthy fatigue.
women, Montz et al (1995) found that those Sleep has not been extensively studied in
with FM demonstrated significantly lower FM, and it remains unclear whether sleep
regional cerebral blood flow (rCBF) of the disorder is a cause or consequence of the
cortex and thalamic and caudate nuclei. While condition. However, important pieces of the
this was a small study and replication is puzzle include the facts that (1) low ILGF-1
awaited, it points toward central changes in levels may be related to sleep pathology, as
FM. GH secretion occurs during stage 4 sleep
(Clauw and Chrousos, 1997), and (2)
serotonin modulates stage 4 sleep (Moldofsky,
Speculation
1982).
As has been mentioned, which (if any) of the
pathophysiological findings listed above are
primary and which are epiphenomena remains
FM as a consequence of CNS
sensitization
to be determined. Nor is it always clear in
which direction the biological events are The pain threshold of a range of modalities is
occurring. Nevertheless, attempts have been lower in FM than in normal controls. This
made to organize the existing information. has been objectified using evoked potentials.
This leads, as no abnormality with muscle has
been detected, to speculation regarding altered
FM as a sleep disorder
CNS sensory information processing. The
The hypothesis that FM is the result of sleep term ‘sensitization’ is used in such
disorder is suggested by the frequent clinical circumstances, and is defined as an increased
finding of disturbed and non-restorative sleep, excitability of spinal and supraspinal neural
and fatigue. It is supported by the findings of circuits.
alpha wave intrusion during the non-REM Sensitization develops consequent to
sleep stages 3 and 4 (Moldofsky et al, 1975) ongoing nociceptive input. Various forms
and the observation that disrupting the non- have been identified. One involves wide
REM sleep of normal subjects leads to dynamic range (WDR) neurones; these are
muscular aching and generalized tender points second-order dorsal horn neurones that
(Moldofsky and Scarisbrick, 1976). However, respond to either non-nociceptive or
temazepam, melatonin and other hypnotics nociceptive input. When WDR neurones
become sensitized, consequent upon ongoing systems in FM. A large number of reviews
nociceptive input, they respond to all input, support the stress response dysregulation
including non-nociceptive, as though it is hypothesis (Clauw and Chrousos, 1997;
nociceptive. Thus light touch or movement Dessein et al, 2000; Heim et al, 2000; Neek,
may cause pain (Gracely et al, 1992). 2000; Neek and Croford, 2000; Torpy et al,
Once central sensitization has occurred, 2000).
this mechanism could sustain painful muscles. Corticotropin-releasing hormone (CRH) is
It is possible that associated painful organ- a principal modulator in the stress response.
specific syndromes such as IBS have a similar The CRH neurones, which are mainly localized
basis. As to the initiating event, FM is often in the paraventricular nucleus of the
consequent upon insults such as rheumatoid hypothalamus, are widely distributed
arthritis and osteoarthritis and physical throughout the CNS. CRH has a profound
trauma (it may also have roots in effect on the function of the endocrine system.
psychological trauma). It also mediates arousal and stress-induced
As has already been noted, in FM, the CSF analgesia via beta-endorphin and excitatory
SP may be three times the normal. This is amino acid-secreting neurones that project
important, as SP is believed to be a major from the hypothalamus to the brain stem and
factor in the process of central sensitization spinal cord. It has input to the sympathetic
(Watkins et al, 1994). system, which exerts antinociception via the
spinal descending inhibitory pathways with the
release of noradrenaline, serotonin and
FM as dysregulation of the stress
neuropeptide Y at the dorsal horn.
response
Thus the biological consequences of low
This model posits that FM is a consequence of CRH state are the opposite of that seen in
dysregulation of the human stress response, acute stress and are similar to those noted in
which is mediated predominantly by the fibromyalgia and fatigue states: hypoarousal or
endocrine and sympathetic systems. It has fatigue and diffusely increased peripheral and
been argued that while the stress response was visceral nociception (generalized pain). Also,
adaptive during human evolution, it is along with the dysregulation of the autonomic
generally maladaptive for man in modern system may come dysregulation of smooth
society, who rarely faces threats to survival muscle and cardiovascular function, which
(Meaney et al, 1993). underpin at least some of the organ-specific
Mention has been made of reported syndromes (IBS, palpitations, Raynaud) that
impairments of the autonomic and endocrine occur in this spectrum of disorders.
Fibromyalgia 97
Various stressors can initiate the stress Speculation – summary

response. It is purported that continuous
FM may prove to be a range of disorders with
stress can cause the hypofunction and
separate pathophysiologies. All of the above
blunting of this response. The pain of FM is a
speculations have at least some underpinning
stressor, and may become involved in a
that has been replicated. How to integrate this
pathological self-sustaining cycle. It is
material is currently uncertain, but the final
proposed that CRH hyperactivity leads,
answer needs to address the following:
eventually, to alteration of the set points of
The evidence supporting FM as a primary
the various hormonal axes. Thus the observed
sleep disorder is not strong, but symptomatic
hormonal deviations in FM may represent a
fatigue and sleep problems and the non-REM
CNS adjustment to chronic pain and stress.
sleep abnormalities require explanation. The
Much attention in FM research has
observed low ILGF-1 levels may be related to
focused on the effect of CRH on the HPA
sleep pathology, as GH secretion occurs
axis. However, CRH also stimulates
during non-REM sleep.
somatostatin secretion at the hypothalamic
The evidence supporting a reduced pain
level, which in turn modulates GH secretion.
threshold and a CNS sensitization is strong.
(GH and IGF-1 levels have been reported as
This may be the result of various stressors. SP
low in FM.) Daily GH injections given to a
is elevated in CSF, and this may play a role in
subgroup of FM patients with low serum
the sensitization process.
IGF-1 levels produced a good response in
The evidence supporting dysregulation of
68% of subjects (Bennett et al, 1992). Thus
the stress response system is moderately
dysregulation of the stress response may also
strong. There is evidence for some changes in
influence GH levels.
endocrine and sympathetic systems function,
As has been mentioned, serum serotonin
but there is little to indicate whether this is
has been reported as low. Serotonin can
cause or consequence. Dysregulation could
stimulate HPA axis activity. It is therefore
logically follow sustained stress and could
possible that FM reflects a disorder of
explain the generalized pain, the reduced
serotonin concentration or function.
arousal and some organ-specific syndromes.
Alternatively, SP, which has been found
The dysregulation of the stress response
elevated in CSF in FM, may have a role in
mechanisms is compatible with sensitization
inhibiting CRH secretion.
of the nervous system, and these two may be
different faces of the same process. Abnormal
GH level is a component of both the stress
response dysregulation and the sleep restructuring, aerobic exercise and stretching,
disturbance, and may serve to integrate these activity pacing and patient and family
hypotheses. education. It is difficult for the clinician to
Serotonin in serum and SP in CSF may determine which of these elements is or are
both be abnormal in FM. Both of these agents responsible for any improvement.
can influence the endocrine system function Exercise programmes have produced
and play a role in CNS sensitization. Thus a significant reductions in pain and tender point
neurotransmitter hypothesis may warrant count (Martin et al, 1996). Sleep and level of
consideration in the future. fatigue are unaffected. Long-term benefits,
however, have not been demonstrated. In
spite of the initial improvement, patients have
Treatment
ceased to exercise (Wigers et al, 1996).
The response to treatment is poor. Most Courses of cognitive behaviour therapy
patients have used over-the-counter analgesics that aim to reduce the use of unhelpful
and a range of alternative treatments, such as behaviours such as excessive rest and over-
vitamins and prayer. Many have also used monitoring of bodily symptoms and
acupuncture (which is now being unhelpful attributions, and to increase
incorporated into mainstream medicine) with confidence in the ability to manage
some benefit (Berman et al, 1999). symptoms, and that teach relaxation
In this setting of relative therapeutic techniques, have produced promising results
impotence, it is especially important to attend (Goldenberg et al, 1992). Unfortunately,
to any concomitant psychiatric disorders. These long-term benefits have not been proved
can be anticipated in at least one-quarter of FM (Richards and Cleare, 2000).
patients, and respond to standard treatments. Goossens et al (1996) compared the
outcome of three treatment streams: (1)
educational; (2) education plus cognitive
Exercise, education and CBT
therapy; and (3) the waiting list. Both
Exercise, education and CBT have the treatment groups provided benefits. However,
advantage of being relatively free of side- there was no significant difference in
effects and involving the patients in the outcomes between the treatment groups. The
treatment process. There is some evidence of addition of a cognitive component to the
efficacy, but less of prolonged benefit. Many educational intervention led to significantly
treatment programmes include combinations higher health-care costs, but no additional
of relaxation, meditation, cognitive clinical benefit.
Fibromyalgia 99
Antidepressants they may be of value in the treatment of

concurrent depression (Anderberg et al, 2000b).
In a relatively bare armoury, the tricyclic
antidepressants, while only partially effective,
are widely used. Arnold et al (2000) Analgesics
performed a meta-analysis of nine randomized
Non-steroidal anti-inflammatory drugs
controlled trials and found significant clinical
(NSAIDs) have been disappointing. Ibuprofen
response in 25–37% of patients. The largest
was found to be no better, and naproxen only
improvements were in sleep quality, with
marginally better, than placebo (Richards and
other improvements in pain, stiffness, Cleare, 2000).
tenderness and fatigue. None of the studies Bennett (1999) makes the statement:
that were examined used the dose ranges that ‘Currently opiates are the most effective
are used in the treatment of depression; rather, medications for managing most chronic pain
the range was from 25 mg of amitriptyline to states.’ However, opioids have not been
75 mg of chlomipramine per day. extensively evaluated in fibromyalgia and
O’Malley et al (1999) conducted a meta- receive little support in reviews (Millea and
analysis of 94 placebo-controlled studies of Holloway, 2000).
antidepressants for unexplained symptoms Tramadol is an analgesic with weak opioid
and syndromes, 50 of which dealt with and monaminergic actions. It has minimal
fibromyalgia. A majority (69%) demonstrated respiratory depression, dependence and
benefit for at least one outcome measure, and tolerance, and is more appropriate for long-term
there was substantial benefit from medication. regular treatment than other forms of analgesia
The absolute percentage difference in (Richards and Cleare, 2000). Leventhal (1999)
improvement between the antidepressant and suggested ‘that tramadol may be useful for
placebo arms was 32%, yielding the treatment of fibromyalgia pain’. This was
conclusion that there would be a need to treat followed by a group of letters that cautioned
three persons for every person whose that this statement was premature and that side-
symptoms might be relieved. effects limited usefulness. Biasi et al (1998)
While the tricyclic antidepressants are conducted a double-blind placebo-controlled
useful, the selective serotonin reuptake trial using injectable preparations and found
inhibitors (SSRIs) have been disappointing in greater pain relief, but without reduction in the
treating the broad range of symptoms of number of tender points. Further studies are
fibromyalgia (O’Malley et al, 1999; Arnold et needed, but a clinical trial of the oral form of
al, 2000). However, there is some evidence that this drug in difficult cases can be justified.
Local anaesthetic injection and dry Ketamine, an N-methyl-D-aspartate

needling (NMDA) receptor antagonist anaesthetic,
given intravenously in sub-anaesthetic doses,
Injection of tender points with local
has attenuated pain, increased pain threshold
anaesthetic is used in the effort to provide
and improved muscle endurance in controlled
pain relief. Lignocaine has also been combined
trials (Sorensen et al, 1997). This agent has
with triamcinolone. Piercing a tender point
been associated with hallucinations, and
with a needle but injecting nothing (dry
further work is required.
needling) may also be of benefit, suggesting
There are many other drugs that have been
that the release of met-enkephalin may be an
found to have benefits in small studies that are
important factor (Figuerola et al, 1998).
awaiting replication.
These procedures require further examination,
but are unlikely to cause damage.
References
Aaron L, Burke M, Buchwald D. Overlapping
Hormones conditions among patients with chronic fatigue
syndrome, fibromyalgia and
Oral corticosteroids have not been useful. termporomandibular disorder. Archives of
Bennett et al (1992) found that in the Internal Medicine 2000; 164: 221–7.
subgroup of patients with low IGF-1, daily Alder G, Kinsley B, Hurwitz S, Mossey C,
injections of GH produced a good global Goldenberg D. Reduced hypothalamic–
response in 68% of patients. This was not pituitary and sympathoadrenal responses to
hyperglycemia in women with fibromyalgia
without side-effects: one-third of patients syndrome. American Journal of Medicine 1999;
developed carpal tunnel syndrome. This is an 106: 534–43.
expensive compound, and more work needs to Anderberg U, Forsgren T, Ekselius L,
be done before regular use could be Marteinsdottir I, Hallman J. Personality traits
considered. on the basis of the Temperament and Character
Inventory in female fibromyalgia syndrome
patients. Nordic Journal of Psychiatry 1999; 53:
353–9.
Other treatments
Anderberg U, Mareinsdottir I, Theorell T, von
Ondansetron, a selective 5HT3 receptor Knorring L. The impact of life events in female
patients with fibromyalgia and in female healthy
antagonist, has shown promise in a double- controls. European Psychiatry 2000a; 15;
blind cross-over trial (Hrycaj et al, 1996). This 295–301.
is another expensive compound that may find Anderberg U, Marteinsdottir I, von Knorring L.
a place in the treatment of FM in the future. Citalopram in patients with fibromyalgia – a
Fibromyalgia 101
randomised, double-blind, placebo-controlled Crofford L, Pillemer S, Kalogeras K, Cash J,

study. European Journal of Pain 2000b; 15: Michelson D, Kling M et al. Hypothalamic–
295–301. pituitary–adrenal axis perturbations in patients
with fibromyalgia. Arthritis and Rheumatism
Arnold L, Keck P, Welge J. Antidepressant
1994; 37: 1583–92.
treatment of fibromyalgia. A meta-analysis and
review. Psychosomatics 2000; 41: 104–13. Croft P, Rigby A, Boswell R, Schollum J, Silman A.
The prevalence of chronic widespread pain in
Bennett R. Emerging concepts in the neurobiology
the general population. Journal of Rheumatology
of chronic pain: evidence of abnormal sensory
1993; 20: 710–13.
processing in fibromyalgia. Mayo Clinic
Proceedings 1999; 74: 385–98. Dessein P, Shipton E, Stanwix A, Joffe B.
Bennett R, Clark S, Campbell S, Burckhardt C. Neuroendocrine deficiency-mediated development
Low levels of somatomedin C in patients with and persistence of pain in fibromyalgia: a
fibromyalgia syndrome. Arthritis and promising paradigm? Pain 2000; 86: 213–15.
Rheumatism 1992; 35: 1113–16. Felson D, Goldenberg D. The natural history of
Berman B, Ezzo J, Hadhazy V, Swyers J. Is fibromyalgia. Arthritis and Rheumatism 1986;
acupuncture effective in the treatment of 29: 1522–6.
fibromyalgia? Journal of Family Practice 1999; Figuerola M, Loe W, Sormani M, Barontini M.
48: 213–18. Met-enkephalin increase in patients with
Biasi G, Manca S, Manganelli S, Marccolongo R. fibromyalgia under local treatment. Functional
Tramadol in the fibromyalgia syndrome: a Neurology 1998; 13: 291–5.
controlled clinical trial versus placebo. Gibson S, Littlejohn G, Gorman M, Heime R,
International Journal of Pharmacological Research Granges G. Altered heat and pain thresholds
1998; 18: 13–19. and cerebral event-related potentials following
Buskila D, Neumann L. Fibromyalgia syndrome painful CO2 laser stimulation in subjects with
(FM) and nonarticular tenderness in relatives of fibromyalgia syndrome. Pain 1994; 58: 185–93.
patients with FM. Journal of Rheumatology Goldenberg D, Kaplan K, Nadeau M. A prospective
1997; 24: 941–4. study of stress reduction, relaxation response
Caro X, Ojo-Amaize E. Agopian M, Peter J. therapy in fibromyalgia. Scandinavian Journal of
Natural killer cell function in primary fibrositis Rheumatology 1992; S94: 47.
(fibromyalgia) syndrome. Arthritis and Goossens M, Rutten-van Molken M, Leidl R, Bos
Rheumatism 1993; 36(9S): D114. S, Vlaeyen J, Teeken-Gruben N. Cognitive-
Clauw D, Chrousos G. Chronic pain and fatigue educational treatment of fibromyalgia: a
syndromes: overlapping clinical and randomised clinical trial. II. Economic
neuroendocrine features and potential evaluation. Journal of Rheumatology 1996; 23:
pathogenic mechanisms. 1246–54.
Neuroimmunomodulation 1997; 4: 134–53. Gracely R, Lynch S, Bennett G. Painful
Cleare A, Blair D, Chambers S, Wessely S. Urinary neuropathy: altered central processing
free cortisol in chronic fatigue syndrome. maintained dynamically by peripheral input
American Journal of Psychiatry 2001; 158: (published erratum appears in Pain 1993; 52:
641–3. 251–3). Pain 1992; 51: 175–94.
Griep E, Boersma J, de Kloet E. Altered reactivity of Martin L, Nutting A, Macintosh B, et al. An exercise
the hypothalamic–pituitary–adrenal axis in the program in the treatment of fibromyalgia. Journal
primary fibromyalgia syndrome. Journal of of Rheumatology 1996; 23: 1050–3.
Meaney M, Bhatnagar S, Larocque S, McCormick
Hassett A, Cone J, Patella S, Sigal L. The role of C, et al. Individual differences in the
catastrophizing in the pain and depression of hypothalamic–pituitary–adrenal stress response
women with fibromyalgia syndrome. Arthritis and the hypothalamic CRH system. Annals of
and Rheumatism 2000; 43: 2493–500. the New York Academy of Sciences 1993; 697:
70–85.
Heim C, Ehlert U, Hellhammer D. The potential
role of hypocortisolism in the pathophysiology Millea P, Holloway R. Treating fibromyalgia.
of stress related bodily disorders. American Family Physician 2000; 62: 1575–82,
Psychoneuroendrocrinology 2000; 25: 1–35. 1587.
Hrycaj P, Stratz T, Mennet P, Muller W. Moldofsky H. Rheumatic pain modulation
Pathogenic aspects of responsiveness to syndrome: the interrelationships between sleep,
ondansetron (5HT type 3 receptor antagonist) central nervous system serotonin, and pain.
in patients with primary fibromyalgia syndrome Advances in Neurology 1982; 33: 51–7.
– a preliminary study. Journal of Rheumatology
Moldofsky H, Scarisbrick P. Induction of
1996; 23: 1418–23.
neurasthenic musculoskeletal pain syndrome by
Kendler K, Walters E, Truett K, Heath A, Neale M, selective sleep stage deprivation. Psychosomatic
Martin N. A twin-family study of self-report Medicine 1976; 38: 35–44.
symptoms of panic-phobia and somatization.
Moldofsky H, Scarisbrick P, England R, Smythe H.
Behavior and Genetics 1995; 25: 499–515.
Musculoskeletal symptoms and non-REM sleep
Lawrence R, Helmick C, Arnett F, et al. Estimated disturbance in patients with ‘fibrositis
prevalence of arthritis and selected syndrome’ and healthy subjects. Psychosomatic
musculoskeletal disorders in the United States. Medicine 1975; 37: 341–51.
Arthritis and Rheumatism 1998; 41: 778–99.
Montz J, Bradley L, Modell J, Alexander R, Trian-
Leventhal L. Management of fibromyalgia. Annals of Alexander M, Aaron L, et al. Fibromyalgia in
Internal Medicine 1999; 131: 850–8. women. Abnormalities of regional cerebral
blood flow in the caudate nucleus are associated
Lorenz J, Grasedyck K, Bromm B. Middle and long
with low pain threshold levels. Arthritis and
latent somatosensory evoked potentials after
Rheumatism 1995; 38: 926–38.
painful laser stimulation in patients with
fibromyalgia syndrome. Electroencephalography Neek G. Neuroendocrine and hormonal
and Clinical Neurophysiology 1996; 1000: perturbations and relations to the serotonergic
165–8. system in fibromyalgia patients. Scandinavian
Journal of Rheumatology 2000; 29 (Suppl 113):
Macfarlane G, Morris S, Hunt I, Benjamin S et al.
8–12.
Chronic widespread pain in the community: the
influence of psychological symptoms and Neek G, Crofford L. Neuroendocrine perturbations
mental disorders on healthcare seeking in fibromyalgia and chronic fatigue syndrome.
behaviour. Journal of Rheumatology 1999; 26: Rheumatic Diseases Clinics of North America
413–19. 2000; 26: 989–1002.
Fibromyalgia 103
Neerinckx E, Van Houdenhove B, Lysens R, stimulation in patients with fibromyalgia.

Vertommen H, Onghena P. Attributions in Clinical Neurophysiology 2000; 111: 994–1001.
chronic fatigue syndrome and fibromyalgia
Sims R. Fibromyalgia is not a muscular disorder.
syndrome in tertiary care. Journal of
American Journal of Medical Science 1998; 315:
346–50.
Okifuji A, Turk D, Sherman J. Evaluation of the
Skerritt P. Anxiety and the heart – a historical
relationship between depression and
review. Psychological Medicine 1983; 12: 17–25.
fibromyalgia syndrome: why aren’t they all
depressed? Journal of Rheumatology 2000; 27: Sorensen J, Bengtsson A, Backman E, Henriksson
212–19. K, Eksellus L, Bengtsson M. Fibromyalgia – are
there different mechanisms in the processing of
O’Malley P, Jackson J, Santoro J, Tomkins G,
pain? A double blind crossover comparison of
Balden E, Krownke K. Antidepressant therapy
analgesic drugs. Journal of Rheumatology 1997;
for unexplained symptoms and symptom
24: 1615–21.
syndromes. Journal of Family Practice 1999; 48:
980–90. Taylor R, Mann A, White N, Goldberg D.
Attachment style in patients with unexplained
Qiao Z, Vaeroy H, Morkrid L. Electrodermal and physical symptoms. Psychological Medicine 2000;
microcirculatory activity in patients with 30: 931–41.
fibromyalgia during baseline, acoustic
stimulation and cold pressor tests. Journal of Torpy D, Papanicolaou D, Lotsikas A, Wilder R,
Rheumatology 1991; 18: 1383–9. Chrousos G, Pillemer S. Responses of the
sympathetic nervous system and the
Raj S, Broullard D, Simpson C, Hopman W, hypothalamic–pituitary–adrenal axis to
Abdollah H. Dysautonomia among patients interleukin-6: a pilot study in fibromyalgia.
with fibromyalgia: a non invasive assessment. Arthritis and Rheumatism 2000; 43: 872–80.
Journal of Rheumatology 2000; 27: 2660–5.
Vaeroy H, Helle R, Forre O, Kass E, Terenius L.
Richards S, Cleare A. Treating fibromyalgia. Elevated CSF levels of substance P and high
Rheumatology 2000; 39: 343–6. incidence of Raynaud phenomenon in patients
with fibromyalgia: new features of the diagnosis.
Russell I, Vaeroy H, Javors M, Nyberg F.
Pain 1988; 32: 21–6.
Cerebrospinal fluid biogenic amine metabolites
in fibromyalgia/fibrositis syndrome and Watkins L, Wlertelak E, Furness L, Maler S. Illness-
rheumatoid arthritis. Arthritis and Rheumatism induced hyperalgesia is mediated by spinal
1992a; 35: 550–6. neuropeptides and excitatory amino acids. Brain
Research 1994; 664: 17–24.
Russell I, Mickalek J, Vipraio G, Fletcher E, Javors
M, Bowden C. Platelet 3H-imipramine uptake White K, Speechley M, Harth M, Ostbye T. Co-
receptor density and serum serotonin levels in existence of chronic fatigue syndrome with
patients with fibromyalgia/fibrositis syndrome. fibromyalgia syndrome in the general
Journal of Rheumatology 1992b; 19: 104–19. population. A controlled study. Scandinavian
Journal of Rheumatology 2000; 29: 44–51.
Salerno A, Thomas E, Olive P, Boltman F, Picot M,
Georgesco M. Motor cortical dysfunction Wigers S, Stiles T, Vogel P. Effects of aerobic
disclosed by single and double magnetic exercise versus stress management treatment in
fibromyalgia. A 4.5 year prospective study. The American College of Rheumatology 1990
Scandinavian Journal of Rheumatology 1996; 25: criteria for the classification of fibromyalgia.
77–86. Arthritis and Rheumatism 1990; 33: 160–72.
Wolfe F. Fibromyalgia: the clinical syndrome. Wolfe F, Ross K, Anderson J, Russell I, Hebert L.
Rheumatic Diseases Clinics of North America The prevalence and characteristics of
1989; 15: 1–18. fibromyalgia in the general population. Arthritis
and Rheumatism 1995; 38: 19–28.
Wolfe F, Smythe H, Yunus M, Bennett R, et al.
Headache
13 ‘The greater the ignorance the greater the dogmatism.’

Sir William Osler 1902
Headache is the most common pain disorder. In the USA the

prevalence was 78% among adult women and 68% among
adult males (Taylor 1985). In large community surveys,
headache had occurred in the last 14 days in 19% (Rasmussen
et al, 1991) and 21% (Wadsworth et al, 1971) of participants.
Headache is more common in women than men (partly
because of the higher prevalence in females of migraine and
tension-type headache). This may be due to female hormones
(Rasmussen, 1993). The prevalence decreases after middle
age, and many subjects become symptom-free.
The impact on the individual varies from minimal, in the
case of the individual with a mild occasional headache,
through to profound in the case of severe, frequent migraine.
Headache may cause considerable direct medical costs and
incapacitate people during their most productive years.
Headache research and therapy is a sophisticated field of
medicine. Comprehensive accounts are available (Olesen et al,
2000). This chapter only offers clinical suggestions for some
major, recurrent categories of headache.
The Headache Classification Committee Diagnostic criteria for migraine

of the International Headache Society (IHS, without aura (IHS, 1988)
1988) produced a comprehensive classification
1. Attacks last 4–72 hours
of headache disorders, cranial neuralgias, and
2. At least two of:
facial pain. Groups 1 to 4 are the primary
• unilateral
headaches, which include migraine, tension-
• pulsating
type headache and cluster headache, all of
• moderate to severe
which receive attention in this chapter.
• aggravated by movement.
Groups 5 to 11 are the secondary headaches.
3. At least one of:
This grouping includes headache associated
• nausea
with disorders of the neck, which also receives
• photophobia
mention later. Group 12 covers the cranial
• phonophobia.
neurologias and facial pain, and Group 13 is
concerned with ‘headache not classifiable’;
neither group receives further mention.
Diagnostic criteria for migraine with
aura (HIS, 1988)
Migraine 1. At least three of:
Migraine is a familial disorder characterized • one or more fully reversible aura
by periodic, commonly unilateral, pulsatile symptoms occur, indicating brain
headaches that begin in childhood, dysfunction
adolescence, or early adult life and recur with • at least one aura symptom develops
diminishing frequency during advancing years gradually over more than 4 minutes, or
(Adams et al, 1997). It is common, occurring two or more symptoms occur in
in 4–6% of men and 14–17% of women. The succession
diagnosis depends on the history and the • no single aura symptom lasts more
exclusion of other conditions. than 60 minutes
Two forms are described (migraine • headache follows aura with a free
without aura and migraine with aura). The interval of less than 60 minutes (it may
advantage of this distinction is unclear, as the also begin before or simultaneously
treatment is the same. with the aura).
2. History, physical examination, and where
appropriate, diagnostic tests exclude a
secondary cause.
Headache 107
Aura Headache diary

A subjective experience associated with A headache dairy is a means of keeping the
(usually proceeding) the headache. Visual patient involved in management and
auras are by far the most common. These may obtaining valuable information. It will
occur in one or both eyes. The patient cannot establish a baseline and chart response to
see clearly to one side of the fixation point. therapy. Details of dates (which give the
This area of defective vision may be foggy or frequency), severity, duration, auras,
shimmering; zigzag lines suggesting the top of associated symptoms and suspected triggers
a castle (fortification or teichopsia) are (e.g. stress, menstruation, foods, caffeine
common; coloured outlines and scotoma may withdrawal) should be recorded.
occur.
Less common auras include paraesthesia,
Non-drug therapy
motor weakness and aphasias.
Auras may occur in combination. A wide range of non-drug treatments, from
relaxation exercises, psychotherapy and
biofeedback to massage, chiropractic and
Pathophysiology
homeopathy, have enthusiastic exponents.
The definitive pathophysiological explanation Some may have value by reducing ‘stress’. Few
has not yet been achieved. Emotional stress have been examined in double-blind placebo-
and genetic factors may be important. controlled trials. Medical practitioners should
Vascular factors have been emphasized. not obstruct the pursuit of non-drug therapy
Distension and excessive pulsation of branches solutions; but where benefit is not obtained,
of the external carotid artery has been they should discourage exploitation.
speculated, and is supported by the
observation that the throbbing quality of the
Opioids
headache may be relieved by compression of
the parent artery (Iversen et al, 1990). Authoritative opinion is that opioids have
Reduction of regional cerebral blood flow has little place in the treatment of migraine. They
been demonstrated during attacks (Leao, compound the delayed gastric emptying that
1944). is a feature of the disorder. Codeine and
A neural hypothesis suggests an pethidine are short-acting, and recurrent
abnormality in the trigeminal nerve and headache (reappearance of a headache that
perhaps the hypothalamus (Lance, 1993). had been significantly relieved) may occur.
Also there is the danger of drug dependence, the migraine is of mild or moderate severity.
particularly where control is difficult. Finally, Like all migraine regimens, it is most effective
there is evidence that these drugs, taken over when commenced early.
time, may actually cause headache.
Pethidine, which is frequently sought and Aspirin (900 mg) or paracetamol
provided, has the additional disadvantage of (1000 mg) plus
having a metabolite (norpethidine) that is metoclopramide (10 mg) or
neurotoxic and a strong convulsant (Hassan et prochlorperazine (5 mg).
al, 2000).
The analgesic can be repeated every 4 hours.
Medication Points to remember:

a. Aspirin is contraindicated where there are
Abortive (treatment of acute episodes) and
enteric ulcers or bleeding disorders.
prophylactic medication is available. Many
b. In pregnancy, prochlorperazine to be used
medications are highly effective; the choice at
up to 32 weeks, metoclopramide to be
any point depends on confounding medical
used after 32 weeks.
conditions, past response, side-effects and
c. Give both the analgesic and the
cost. The aim in the following protocols is to
antiemetic, even if there is no nausea.
provide safe, effective and, importantly,
Metoclopramide will speed gastric
straightforward guidelines. Alternative, equally
emptying.
good, choices are possible.
d. Prochlorperazine has a mild sedative effect,
which is often an advantage.
e. If vomiting is a concern, consider
Medical treatment of the acute prochlorperazine 5 mg suppositories.
episode
f. Prochlorperazine has been associated with
Commence treatment at the first sign. acute dystonic reaction.
Withdraw to a quiet room with soft light and g. Both prochlorperazine and
relax; if possible, sleep. metoclopramide have been associated with
akathisia – a distressing emotional and
1. Regimen One: Simple analgesic plus anti- physical restlessness.
emetic h. Treat acute dystonia and akathisia with an
This regimen is suitable as the initial anticholinergic (e.g. benztropine 2 mg,
treatment for new patients, particularly when orally or imi), followed after one hour, if
Headache 109
there is insufficient response, by diazepam repeated only once, after one hour, if there
5 mg by mouth. has been no improvement.
e. Naproxen (500 mg) is available as a
2. Regimen Two: NSAID or 5-HT1D agonist suppository.
plus antiemetic
This regimen is appropriate as the routine 3. Regimen Three: Antiemetic plus dopamine
treatment where the patient has, in the past, blockade
failed to achieve satisfactory results with This is appropriate treatment where Regimen
Regimen One. It can also be implemented as a One has failed and the doctor is able to
second-wave treatment if there is no sign of provide a home visit.
improvement with the application of Regimen
One. Metoclopramide 10 mg imi plus
chlorpromazine 50 mg orally or imi.
Naproxen (1000 mg, oral) or sumatriptan
(50–100 mg, oral) plus an antiemetic, as Points to remember:
above. a. In pregnancy, metoclopramide may be
used only in the last trimester.
Naproxen can be repeated once, after 4 hours. b. Chlorpromazine can be used throughout
Sumatriptan (50 mg) can be repeated after pregnancy and can be used alone in the
one hour; administration above 100 mg offers first two trimesters. There is little point
no additional benefit. substituting prochlorperazine for
metoclopramide in the first two trimesters,
Points to remember: as prochlorperazine and chlorpromazine
a. Sumatriptan is contraindicated in are from the same drug family
pregnancy and where there are risk factors (phenothiazines).
for cardiovascular or cerebrovascular c. Metoclopramide is given by imi at this
accident. stage of the episode irrespective of
b. Naproxen is contraindicated where there vomiting. It reverses gastroparesis and
are enteric ulcers or bleeding disorders. reduces nausea.
c. Sumatriptan is commenced with the onset d. Chlorpromazine given by imi is
of pain, not during the aura. uncomfortable and may (rarely) lead to a
d. Sumatriptan (6 mg) is also available as a sterile abscess. These are relatively low-
patient- or professional-administered priority issues at this stage of severe
subcutaneous injection. This can be migraine. If vomiting is not a major
problem and metoclopramide has been 60 minutes after commencement of

administered, oral chlorpromazine may be infusion. Pulse rate, blood pressure and
considered. further ECGs to be performed according
e. Chlorpromazine will cause sedation, which to local protocols.
will be an advantage.
f. Chlorpromazine may cause hypotension
Medical prophylaxis
via an alpha-blocking action. Dizziness
may be reported. This needs no specific A 50% reduction in headache frequency is a
therapy other than care with rising from realistic goal of medical prophylaxis; fewer than
sitting or lying and with walking. 10% of patients achieve headache-free status.
g. Chlorpromazine theoretically can lead to Avoidance of triggers is the best
acute dystonia and akathisia, but this is prophylactic. But often there are no clear
unlikely at this low dose. In such an event triggers, and in any case, avoidance may not
administer an anticholinergic and later, if give the desired degree of prophylaxis.
necessary, a benzodiazepine, as outlined in Most of the commonly used prophylactic
Regimen One. agents produce a satisfactory response in
h. Ergotamines should not be administered about 60% of patients, and there is little
within 24 hours of 5HT1D agonists. evidence that one is superior to the rest. (A
warning against undue confidence, however:
4. Regimen Four: Lignocaine/lidocaine infusion the placebo response for most medical
This is appropriate for status migranosus conditions is around 50%.) The choice of
(migraine lasting longer than three days), and agent therefore depends on pre-existing
hospital admission is indicated. medical conditions and adverse effects. With
continuous administration there is greater
Lignocaine 2 mg/min delivered by pump. probability of developing adverse effects. The
Duration not to exceed 14 days. adverse effects of each medication should be
discussed so that the patient can be fully
Points to remember: involved in selection.
a. Contraindications: significant cardiac
disease, epileptic seizures, severe degrees of 1. Beta-blocker
sinoatrial, atrioventricular or Propranolol 40 to 300 mg per day or
intraventricular heart block, or allergic metoprolol 50 to 200 mg per day.
reactions to lignocaine. Start at low doses and increase gradually at
b. An ECG should be performed before and two- to four-week intervals.
Headache 111
Points to remember: epilepsy. Beneficial effects may be achieved

a. Contraindications: congestive heart before reaching the anti-epileptic range.
failure, atrioventricular conduction
defects and peripheral vascular disease. Points to remember:
They must be used with caution in a. Contraindications: pregnancy, liver disease
diabetes, as they may mask some early and thrombocytopenia.
signs of hypoglycaemia. b. Fulminant hepatitis is a serious but rare
b. Propranolol is a non-selective beta-blocker, side-effect of these drugs, and is not
and is therefore contraindicated in patients consistently preceded by abnormal liver
with asthma. Metoprolol is a selective function tests.
beta-1-blocker, and can be used with c. Common adverse effects include nausea,
caution in patients with asthma. weight gain, tremor and hair loss.
c. Propranolol passes the blood–brain barrier, d. Baseline and regular full blood
and depression is an important side-effect. examination and liver function tests are
Metoprolol passes the blood–brain barrier recommended.
much less easily, and has not been e. Gradual dose increases will reduce the
associated with depression. likelihood of adverse effects.
d. Other beta-blocker side-effects include
fatigue, orthostatic hypotension, diarrhoea 3. Tricyclic antidepressant (TCA)
and insomnia. Amitriptyline 10 to 150 mg at night.
e. Failure to respond to one beta-blocker Commence at 10 mg at night and increase
does not predict failure to all; hence slowly. Some authorities limit the dose to
another selective drug with proven 150 mg, but higher doses can be used,
prophylactic efficacy, such as atenolol, depending on tolerance of adverse effects.
could also be trialled.
f. Beta-blockers will not prevent the aura, Points to remember:
but they can be used in migraine both a. Contraindications: pregnancy, narrow-
with and without aura. angle glaucoma and urinary retention.
b. Adverse effects: drowsiness, dry mouth,
2. Anticonvulsant weight gain, orthostatic hypotension,
Sodium valproate 800 to 2000 mg per day in constipation.
divided doses. c. Dangerous in overdose.
Start at low dose (400 mg) and slowly d. Amitriptyline is the only TCA with
titrate up to the plasma concentrations used in established efficacy in migraine
prophylaxis. Imipramine and and bring it to appointments. The doctor

clomipramine appear to be effective. should reassure, emphasize the importance of
e. The anti-migraine effect is unrelated to early treatment and give information. They
antidepressant effect. should work together in the assessment of
f. To date, the SSRIs have not been shown response to non-medical treatment and to
to be effective. acute and prophylactic medical treatment.
They should discuss the patient’s daily routine
4. NSAID with a view to establishing regular sleep, and
Naproxen 500 mg twice daily explore psychosocial factors.
Points to remember:
Tension-type headache
a. Contraindications: peptic ulceration, liver
or kidney disease and coagulation Tension headache is the most common form
disorder/treatment. of headache. It is more common in females,
b. Side-effects: erosive gastritis, diarrhoea, and onset may be in middle life. Chronic
fluid retention, haematological anxiety or depression is frequently present.
complications. Tension headache is usually bilateral, but
d. For migraine associated with may occur on one side. It does not always
menstruation: naproxen for one week occur in the same location. In order of
before through to one week after frequency it occurs in occipital, parietal,
menstruation. temporal and frontal regions. It is described as
e. Where erosive gastritis complicates dull, aching, full or tight; often as if the head
successful prophylaxis, consider combining were encircled by a tight band. There may be
naproxen with a proton pump inhibitor throbbing. Sleep is usually not disturbed, but
such as omeprazole 20 mg daily. the headache may be noticed soon after
waking. There may be grinding of the teeth
and tenderness around the head.
The patient and the doctor A thorough history and physical (including
In the management of migraine, the patient neurological) examination is mandatory. The
and the doctor must work as a team. There aim is not only to exclude other diagnoses, but
may also be other team players, including to confirm the diagnosis of tension-type
family members, a psychologist, employers headache. In the physical examination a
and doctors from various fields. manual examination of pericranial muscles
The patient should keep a headache diary may identify tender points (manual pressure
Headache 113
produces localized pain) and trigger points • mild to moderate severity

(sustained manual pressure resulting in pain • bilateral location
referred to another area). • no aggravation by walking stairs or
The aetiology of tension-type headache is similar routine physical activity.
likely to be multifactorial. There is a genetic D. Both of the following:
predisposition, but environmental factors are • No nausea or vomiting (anorexia may
also important. In addition to anxiety and occur)
depression, stressful life circumstances may • Photophobia and phonophobia are
play a part. The pathophysiology is unclear. absent (one but not the other may be
The theory of increased scalp muscle tension present).
has not been substantiated (Anderson and E. History, physical examination and special
Frank, 1981). investigations (as necessary) exclude other
Chronic tension-type headache usually diagnoses.
evolves from the episodic form. It is speculated
that prolonged painful input from the
Diagnostic criteria for chronic
periphery causes central sensitization. A self-
tension-type headache (IHS, 1988)
perpetuating disturbance is then established,
with all peripheral afferents, including normal As for episodic tension-type headache, except
proprioception, being capable of causing pain. that the headache occurs 15 days per
Chronic head pain may also attend month for 6 months.
excessive and prolonged analgesic use
(rebound headache). On cessation of such use,
Management
such patients may be completely headache-
free, or headache may return episodically. Overt depression and anxiety disorders must
be diagnosed and treated appropriately.
The condition may be explained to the
Diagnostic criteria for episodic
patient as a disturbance of the central pain-
tension-type headache (IHS, 1988)
modulating system, such that normally
A. At least ten previous headache episodes innocuous stimuli are perceived as painful,
fulfilling the following criteria: with the secondary development of muscle
B. Headache lasting 30 min to 7 days tension, anxiety and depression. Advise that
C. At least two of the following characteristics cure is rare but that control is usually attained.
• pressing/tightening (non-pulsating Eliminate aggravating factors, especially
quality) analgesic abuse. Female sex hormones,
particularly the combined pill, but also the Cluster headache

progesterone-only pill, have been implicated,
and discontinuation for a trial period of three Cluster headache is categorized by a constant
months may be helpful. While ‘stress’ may unilateral orbital localization, and
play an aetiological role, it is impossible to live predominantly occurs in young men. The
a totally stress-free life, and stress-reduction pain is felt deep in and around the eye. It is
strategies rarely provide a complete answer. It intense and not usually throbbing. There may
is best to recommend adequate sleep and be radiation to the cheek, ear or other parts of
exercise. the head.
Relaxation therapy, biofeedback and The headache tends to commence about
special exercise regimens have shown promise an hour after the onset of sleep. It usually
in some small trials. However, it is difficult to recurs nightly (often at exactly the same time)
recommend such treatments, particularly at for periods of six weeks or more. Periods of
public expense, without convincing double- freedom may be of months or years; however,
blind trials. Psychotherapy may help in the a small proportion may not remit.
resolution of distressing issues. The pain and associated features, which
Mertin (1993) provides an overview of the may include conjunctival injection,
psychophysiological distinctions between the lacrimation, blocked nostril and others listed
muscle tension and vascular headache and the as diagnostic criteria, last about 45 minutes.
treatment implications. Suggestions on The same-side temporal artery may become
psychological management are provided. prominent and tender during an attack. The
Mild analgesics (paracetamol skin of the face and scalp may also be
500–1000 mg) and NSAIDs (ibuprofen hyperalgesic.
400 mg) are recommended in acute episodic The presentation of cluster headache is
tension-type headache. Opioids are to be sufficiently typical that it permits a clinical
avoided. Anxiolytics are also better avoided, diagnosis without additional investigations.
unless there are clear indications of anxiety. Prodromal symptoms may be present.
Patients must be made aware of the possible They start minutes before the pain, and
consequences of chronic medication use. include sensations in the head and neck,
Tricyclics are the drug of choice in the alimentary symptoms and mood alterations.
prophylaxis. Amitriptyline 75 to 150 mg per Alcohol is known to precipitate attacks
day is recommended. The specific serotonin during active periods, but not during
reuptake inhibitors (SSRIs) have not been remissions.
shown to have the same effect. The cause and mechanism of cluster
Headache 115
headache are unknown (Adams et al, 1997). Management

Theories have included (1) paroxysmal
The patient should be advised that the
parasympathetic discharge mediated through
condition is not associated with structural
the greater superficial petrosal nerve and
disease, and reassured that treatment is
sphenopalatine ganglion; (2) swelling of the
available to abort and prevent attacks.
internal carotid artery in the canal through
Alcohol should be avoided during cluster
which it ascends in the petrous portion of the
periods. Afternoon naps should be avoided
temporal bone; (3) dysregulation of
because they precipitate attacks.
hypothalamic mechanisms governing
circadian rhythm; and (4) spontaneous release Acute treatment
of histamine. 1. Oxygen
Oxygen inhalation aborts acute attacks. 100%
Diagnostic criteria for cluster oxygen is administered at 7 L per minute.
headache (IHS, 1988) Over 90% of individuals are reported to have
relief in less than 10 minutes, and 100% have
A. At least five attacks satisfying the following relief within 15 minutes. There are no side-
criteria: effects, and oxygen is not contraindicated in
B. Severe unilateral orbital, supraorbital, or any condition (unlike ergotamine). Tanks and
temporal pain lasting 15 to 80 minutes regulators can be rented from suppliers.
without treatment.
C. Headache is associated with at least one of 2. Sumatriptan
the following signs, which have to be Sumatriptan 6 mg by subcutaneous injection
present on the pain side: has been found effective and free of serious
• Conjunctival injection side-effects. Generally, no more than two
• Lacrimation injections in 24 hours. Sumatriptan has been
• Nasal congestion found to be more convenient than oxygen by
• Rhinorrhoea some patients. Sumatriptan 100 mg orally
• Forehead and facial swelling may also be effective.
• Miosis
• Ptosis 3. Naproxen
• Eyelid oedema. Naproxen 500 mg may be useful as first aid in
D. Frequency of attacks: from one every acute attacks, before other arrangements are
other day to eight per day. made. Naproxen 500 mg twice daily may
E. Not due to another disorder. reduce attacks during the expected period.
Prophylaxis Headache from cervical

1. Lithium carbonate pathology
Lithium carbonate is recommended (Kudrow,
1980). The average dose is 1 g per day, which Headache from cervical pathology is rare.
can be given in a single dose at night. While being listed in newspaper
However, dosage is determined by serum level, advertisements posted by spinal manipulation
the range being 0.8–1.2 mM. Serum steady exponents, it receives little space in certain
state is not reached for 5 days, blood to be classic works on pain (Bonica, 1990) and
taken 12 hours after last ingestion. Baseline neurology (Adams et al, 1997).
thyroid function tests and urea and electrolyte Gobel and Edmeads (2000) list the
levels are necessary. When used with a diuretic cervical conditions that are accepted as the
there may be retention of lithium and cause of headache: developmental
depletion of sodium, necessitating the close abnormalities, tumours, Paget’s disease,
monitoring of electrolytes. Reversible rheumatoid arthritis and craniocervical
hypothyroidism may develop, and can be dystonia. These will be suggested by the
treated by withdrawal of lithium or addition of history and stigmata of the underlying
thyroid hormone. There may be polyuria and diseases. There is controversy as to whether
polydipsia. Lithium should be avoided during disc disease and spondylosis, or ‘whiplash’
the first trimester of pregnancy. While there injury, cause headache.
may be some annoying side-effects, lithium is
generally free of major adverse effects.
Diagnostic criteria for headache
associated with disorders of the
2. Verapamil
cervical spine (IHS, 1988)
Verapamil commenced at a low dose and
titrated to 320 mg per day in divided doses is A. Pain is localized to the neck and occipital
recommended. Although the physiological region. May project to forehead, orbital
effect is rapid, the maximal clinical effect may region, temples, vertex, or ears.
be delayed for some weeks. B. Pain is precipitated or aggravated by
special neck movements or sustained neck
3. Naproxen pressure.
Naproxen 500 mg twice daily may be C. At least one of the following occurs:
effective. It is relatively straightforward to use, • Resistance to or limitation of passive
but the evidence for efficacy in prophylaxis is neck movements
not well established. • Changes in neck muscle contour,
Headache 117
texture, tone, or response to active and with paracetamol, NSAIDs or tramadol (up to
passive stretching and contraction. 400 mg/day). Tramadol may cause
• Abnormal tenderness of neck muscles. gastrointestinal side-effects and sweating, and
D. Radiological examination reveals at least should be used with caution in combination
one of : with serotonin-enhancing antidepressants,
• Movement abnormalities in flexion and because of the potential for the serotonin
extension syndrome (characterized by restlessness,
• Abnormal posture myoclonus, diaphoresis, tremor and mental
• Fractures, congenital abnormalities, status changes, such as confusion).
tumours, RA, or other distinct Continuous use of analgesics should be
pathology (not spondylosis or avoided, owing to the danger of worsening the
osteochondrosis). headache. Opioid substances are best avoided.
A trial of TCAs (amitriptyline 25–50 mg/day)
is worthy of consideration (adverse effects are
Management
mentioned above).
Causes should be identified and treated.
Symptomatic pharmacological, surgical and
chiropractic treatments do not produce lasting References
relief. Physiotherapy, muscle relaxation and Adams R, Victor M, Ropper A. Principles of
psychotherapy may provide temporary relief. Neurology, 6th edn. McGraw-Hill, New York,
1997.
It has been claimed that ipsilateral
Anderson C, Frank R. Migraine and tension
blockades of the C2 root of the occipital nerve
headache: Is there a physiological difference?
may allow differentiation between headache Headache 1981; 21: 63–GGG.
due to irritation of the C2 nerve root and
Bonica J. The Management of Pain, 2nd edn. Lea &
primary headache, such as migraine and Febiger, Philadelphia, 1990.
tension-type headache. However, the effect is Gobel H, Edmeads J. Disorders of the skull and
short-lived and the differentiation can be cervical spine. In: Olesen J, Tfelt-Hansen P,
achieved on history (Gobel and Edmeads, Welch K (eds) The Headaches. Lippincott
Williams and Wilkins, Philadelphia, 2000;
2000).
891–8.
Craniocervical dystonia is a disorder that
Hassan H, Bastani B, Gellens M. Successful
calls for special skills and experience, treatment of normeperidine neurotoxicity by
including the use of intramuscular injection of hemodialysis. American Journal of Kidney Disease
botulinum, thalamotomy and nerve resection. 2000; 35: 146–9.
Symptomatic treatment may be achieved IHS (Headache Classification Committee of the
International Headache Society). Classification Olesen J, Tfelt-Hansen P, Welch K. The Headaches,

and diagnostic criteria for headache disorders, 2nd edn. Lippincott Williams and Wilkins,
cranial neuralgias and facial pain. Cephalgia Philadelphia, 2000.
1988; 8(Suppl 7): 1–96.
Rasmussen B. Migraine and tension-type headache
Iversen H, Nielsen T, Olesen J. Arterial responses in a general population: precipitating factors,
during migraine headache. Lancet 1990; 336: female hormones, sleep pattern and relation to
837–FFF lifestyle. Pain 1993; 53: 65–72.
Kudrow L. Cluster Headache: Mechanisms and Rasmussen B, Jensen R, Schroll M, Olsen J.
Management. Oxford University Press, Oxford, Epidemiology of headache in a general
1980. population – a prevalence study. Journal of
Epidemiology 1991; 44: 1147–57.
Lance J. The Mechanisms and Management of
Headache, 5th edn. Butterworth-Heinemann, Taylor H. The Nuprin Pain Report. Lewis Harris
Boston, 1993. and Associates, New York, 1985.
Leao A. Spreading depression of activity in cerebral Wadsworth M, Butterfield W, Blaney R. Health
cortex. Journal of Neurophysiology 1944; 7: and sickness. The choice of treatment. In
359–KKK Perception of Illness and Use of Services in an
Urban Community. Tavistock, London, 1971.
Mertin P. Psychological Management of Chronic
Headaches. Guilford, New York, 1993.
Low back pain and sciatica
14 ‘The trouble with being a hypochondriac these days is that

antibiotics have cured all the good diseases.’
Caskie Stinnett
This book deals predominantly with chronic pain. When

considering back pain, however, the acute condition is also
discussed, as optimal treatment in the early stages may help
prevent the chronic condition. ‘Acute’ is generally applied to a
duration of less than 4 weeks, ‘subacute’, to 4 to 12 weeks,
and ‘chronic’ is to durations of greater than 12 weeks.
‘Back pain’ refers to symptoms in the spinal and paraspinal
region. It has an annual prevalence of 15–20% and is the
second most common symptom leading to medical
consultation (respiratory symptoms occupying first place).
‘Sciatica’ is pain radiating down the posterior or lateral aspect
of the leg, often to the ankle or foot. It is usually due to nerve-
root involvement. One per cent of patients with acute back
pain have nerve-root symptoms. Back pain and sciatica are
expensive to the individual and the community, and are the
cause of great suffering and disability.
The important issues in back pain and sciatica include the
facts that (1) the vast majority of cases are the result of benign
non-specific mechanical problems; (2) acute The differential diagnosis

non-specific mechanical pain improves in one
month in 75–90% of cases, and sciatica The differential diagnosis of low back pain has
improves in six weeks in more than 50% of been divided into mechanical and non-
cases; (3) very rarely are these pains the result mechanical conditions (Deyo, 1986). The
of serious progressive disorders; (4) a short list mechanical conditions include muscle and
of symptoms is available, ‘red flags’, that warn ligament strains, degenerative disease of the
of serious progressive conditions; (5) a spine, facet joint disease, bulging and
comprehensive history and physical herniated disc, fracture, spondylolisthesis and
examination, with particular attention to ‘red spinal stenosis (narrowing of the spinal canal).
flags’, is the starting-point; (6) when there is It is difficult to distinguish between the
clear evidence of a serious, progressive mechanical problems by physical examination
disorder, immediate special investigation and and diagnostic testing. Imaging is frequently
referral are appropriate; (7) when there is unhelpful; when imaging reveals pathology, it
suspicion of a serious progressive condition, is often impossible to be certain that a
regular, close review by the primary care candidate finding is causing a particular pain
physician is appropriate and will clarify the (Jensen et al, 1994). For example, 60% of
situation; (8) the primary care physician is pain free imaged individuals over the age of
well placed to manage the majority of cases of 60 years demonstrate disc degeneration
back pain with and without sciatica; (9) the (Wiesel et al, 1984; Powell et al, 1986).
important features of acute management are As was mentioned in the earlier chapter on
rapid return to normal activities, education of Plasticity and neuropathic pain, nociceptive
the patient about the condition and mild input has been associated with plastic changes
analgesia as required; (10) special in the spinal cord and brain such that the
investigations should be used sparingly, and nervous system may become sensitized and
only when there is a clear indication; (11) respond to mild nociceptive and non-
chronic back pain has a poor prognosis and is nociceptive input as though it were strongly
often associated with psychosocial and nociceptive. Using magnetic resonance
compensation issues; and (12) rapid spectroscopy, Grachev et al (2000)
resumption of daily activities, the avoidance of demonstrated reductions in N-acetyl aspartate
powerful analgesics and modification of the and glucose in the dorsolateral prefrontal
workplace may help prevent the chronic cortex of patients with back pain. These
condition. changes in the brain chemistry substantiate
the view that back pain is associated with
Low back pain and sciatica 121
brain changes, and raise the possibility that pain still have symptoms at three months
sensitization may occur. (Frymoyer et al, 1983), at least 10% report
The presence or absence of neurological persistent symptoms at one year, and 25–50%
symptoms is a straightforward and useful report relapse within one year (Croft et al,
distinction. Sciatica may compound back pain 1998). This relatively small group of patients
and is usually associated with disc herniation, with chronic pain accounts for the greater part
but may also accompany other pathology, of disability, compensation and public costs in
including spinal stenosis and degenerative general.
bony conditions (Atlas and Deyo, 2001).
The non-mechanical conditions can be
The diagnostic process
divided into those that directly involve the
spine, such as neoplasia, infection and The assessment of back pain is daunting, as
inflammatory arthritis, and those that involve the differential diagnosis is extensive and
other systems, such as vascular disease and includes serious progressive conditions.
diseases of pelvic, renal and gastrointestinal Guidelines have been developed that protect
organs. These are all uncommon (Deyo et al, both the patient and the doctor (Bigos et al,
1992). 1994). The first task is to identify the serious
progressive conditions and investigate and
refer as appropriate. A thorough history and
Clinical course of benign back physical examination, taking account of a
pain and sciatica short list of symptoms, ‘red flags’, will achieve
The clinical course of the serious progressive this end with reasonable sensitivity and
conditions will depend on the nature of the certainty (Deyo et al, 1992).
specific condition. Mechanical problems are
by far the most common causes of back pain, Red flags
and the majority are non-specific and self- 1. Recent severe trauma
limiting (Atlas and Deyo, 2001). Seventy-five 2. Weight loss, night sweats, fever
to 90% of such cases improve in one month 3. Past history of carcinoma, steroids, IV
(Croft et al, 1998) and more than 50% of drug use
sciatica cases improve in six weeks (Andersson 4. Severe night pain
et al, 1983). 5. Structural deformity
The above figures are encouraging, and 6. Progressive neurological deficits
support the conservative approach. 7. Inflammatory character pain
Nevertheless, at least 5% of those with back 8. Features of cauda equina syndrome
(urinary retention, saddle anaesthesia, range of circumstances, but this can usually be
bilateral neurological symptoms and signs) discussed with, and performed on the way to,
the specialist. When a red flag condition is
Not considered a red flag, but worth suspected, it is reasonable to schedule further
remembering is the fact that complaints of visits and keep the case under close review
back pain in the presence of normal (Bogduk, 1999).
movements and the absence of tenderness
suggest a visceral or vascular source of pain. In
Special investigations
practice, most of the red flags noted by
clinicians prove to be false positives; but It is important to order special investigations
caution is recommended. only when the results will influence treatment.
The physical examination should Imaging studies may not be helpful, as
commence with the patient standing and findings are poorly associated with symptoms.
unclothed. The important features are The most common causes of nerve root
posture, flexibility and tenderness. Straight-leg irritation, herniated disc and spinal stenosis
raising in lying is a good screening test for cannot be demonstrated with plain
nerve-root complications. A history of sciatica radiographs.
or straight-leg raising limited by pain to less CT and MRI studies should be ordered
than 60 degrees calls for a more detailed when the history and examination strongly
neurological examination of the lower limb. suggest a serious progressive disorder such as
Full details are available in texts on physical cauda equina syndrome, infection or tumour.
examination and neurology. In 98% of cases, When sciatica is probably due to a herniated
disc herniation involves the L5 and S1 nerves disc or spinal stenosis, and neurological signs
(Spangfort, 1972). Screening for L5 pathology are slight, early imaging is unnecessary, as
includes extension of the great toe and patients can be expected to recover with
walking on the heels, and loss of sensation on conservative management (Atlas and Deyo,
the dorsum of the foot. Screening for S1 2001). If improvement is slow with
pathology includes walking on the toes, conservative treatment, imaging studies
decreased sensation on the lateral aspect of the should be conducted. However, in chronic
sole, and reduced ankle reflex. back pain, extensive evaluations usually show
When there is strong evidence of a serious no surgically correctable lesions (Frymoyer,
progressive condition, immediate referral to a 1988).
specialist is appropriate. Whether special The patient may have expectations that
investigations are conducted will depend on a imaging will be performed. When
appropriate, it will be possible to reassure the al, 1995) and sciatica (Vroomen et al, 1999),
patient, and not ordering special return to usual activities has produced better
investigations may reassure that this is a outcomes than formal bed rest. It is
benign condition, familiar to the doctor. recommended that bed rest should be
Alternatively, it may not be possible to retain available as necessary and that activities that
the confidence of the patient without promote pain should be avoided.
performing some screening tests. It is not In the acute situation, the patient is in
uncommon to encounter patents who have pain and movement makes it worse. This is a
had repeated imaging studies only months or most distressing situation. The patient fears
even weeks apart, sometimes ordered by the the pain and fears that it will not be relieved
same doctor. Unless there are excellent and may even get worse, and further, that an
indications that change has occurred, repeat inability to perform the usual duties will have
studies cannot be justified. dire financial and social consequences for the
Routine laboratory tests are not needed. individual and the family. Fear of pain and
When other than benign mechanical movement is a major cause of chronicity
conditions are considered, erythrocyte (Croft et al, 1995), and has been discussed at
sedimentation rate (ESR), full blood count length in an earlier chapter. Thus the
and urinalysis are useful and relatively importance of early reassurance, an
inexpensive screening tests. Testing for the explanation of the nature of the condition and
HLA-B27 antigen has been useful in an exposition of the rationale of treatment
suspected ankylosing spondylitis. cannot be overemphasized.
Nuclear medicine and clinical Psychosocial factors frequently play a role
neurophysiology studies are better conducted in the persistence of back pain and disability.
in collaboration with a specialist. Accordingly, experts recommend identifying,
early in the acute stage, those patients with
psychosocial risk factors, in the hope that
Management in the acute
appropriate management will prevent the
stage
chronic condition. While this approach makes
The conservative approach emphasizes the sense and guides modern management, the
need for reassurance, and education of the study has not yet been performed that
patient regarding the nature of the condition substantiates the approach. It is relevant,
and its probable prognosis, and the however, that studies of rapid return to usual
opportunity for recovery. Extended bed rest is activities have had favourable outcomes. This
unhelpful. In both back pain (Malmivaara et process protects income, status and self-
esteem. It also helps to avoid conflict between unacceptably slow and psychosocial factors
patient, employer and insurer, and can be excluded as influential factors. While
resentment, anger and protracted legal battles. going to surgery too soon should be avoided,
Further, early return to work is associated delaying herniated disc surgery beyond 12
with less use of problematic medication, and weeks has been found to compromise
consequently, less risk of drug-use outcome (Weber, 1978). However, no more
complications. than 5 to 10 per cent of patients with
Other risk factors for persistent symptoms unremitting sciatica require operation
include a history of painful disorders, (Frymoyer, 1988). One study found that
depression, personality disorder, substance surgical treatment of lumbar disc herniation
abuse and current litigation and dissatisfaction produced a better functional ability and fewer
with work (Andersson et al, 1983; Deyo and symptoms than non-surgical management at
Diehl, 1988). Psychiatric, social work and one and two years, but that this was no longer
occupational therapy assessments should be evident at four and ten years (Weber, 1978).
conducted as appropriate. Psychiatric Physical treatments such as spinal
disorder, such as depression, should be manipulation, facet joint injection, epidural
vigorously treated. For the patient who finds steroid injection and ligamentous injection
work unrewarding, it may be possible for the and acupuncture are said to be of value, but
employer to provide alternative, more others claim efficacy has yet to be proved
satisfying duties. The occupational therapist (Atlas and Deyo, 2001).
may choose to take part in such negotiations.
Medication in the acute stage should be
Management of the chronic
limited, whenever possible, to non-steroidal
stage
anti-inflammatory drugs (NSAIDs), mild
analgesics such as paracetamol, and tricyclic Typically, patients with chronic back pain
antidepressants. When stronger analgesics are have suffered a benign mechanical problem.
necessary, non-addictive tramadol may have a Some have received back surgery but have
place. Avoidance of potent opioids and continued to suffer pain and disability. It is
benzodiazepines, whenever possible, will help important to treat existing mechanical
to prevent addiction and iatrogenic problems, but it is unwise to pursue a physical
complications. lesion relentlessly.
Referral for specialist consultation is As emphasized above, it is important to try
appropriate when there is good evidence of to identify those cases at risk of developing
serious progressive disorder or recovery is chronic problems and to take preventive
action. This is the theoretical ideal, which can education in the short term, and may be
be difficult to achieve in practice. Psychiatric superior to acupuncture at one-year follow-up
consultation is indicated, and existing (Cherkin et al, 2001).
psychiatric disorders should be treated. Chronic pain may be helped by
In the chronic stage, efforts to reassure and medication. The patient needs to understand
educate the patient regarding the role of fear and accept that medication can usually
of pain and movement in perpetuating the provide moderate symptomatic relief, but that
condition should be redoubled. Patients often complete eradication of pain is unlikely. Side-
believe that pain is an indication that their effects frequently cause problems; some
body is undergoing further damage, and this information on reducing side-effects can be
discourages them from any activity. found in the final chapter on
Consequently, they lose muscle strength, joint Pharmacotherapy. It is better, when possible,
flexibility and aerobic fitness, which further to avoid opioid use because of the problems of
increases the likelihood of experiencing pain. tolerance and addiction.
Patients need to learn that while acute pain Symptoms accompanying chronic pain
indicates damage and serves to immobilize the include fear (anxiety), depression, insomnia
injured part, chronic pain does not indicate and irritability. It is often very difficult, in
new damage – it serves no useful purpose, and particular cases, to disentangle and make
is, in fact, maladaptive, as it discourages return definitive statements about these symptoms.
to normal function. Patients are encouraged The most parsimonious approach is to regard
gradually to increase their daily activity. them as components of a depressive
However, they are also taught to pace syndrome, such as major depressive disorder,
themselves, meaning that they are taught to which might be expected to develop secondary
avoid exerting themselves to the degree that to unrelenting pain. However, clinical
will cause a flare-up of symptoms. Thus, experience is that some of these symptoms can
‘pacing’ means dividing tasks into manageable present alone, or in combination, without
quantities that extend the patient, perhaps on being part of a depressive syndrome. This
subsequent days, without causing setbacks. issue has not been fully researched, but clearly,
Psychological techniques including relaxation insomnia and irritability may present alone or
and cognitive restructuring may have a place in combination, in the absence of a full
in reducing anxiety and chronic pain. depressive syndrome. Again, it is reasonable to
Multidisciplinary programmes offer expect these symptoms as a consequence of
advantages (Nicholas et al, 2000). Massage unrelenting pain. In practice, patients often
may be superior to acupuncture and self-care complain most about their irritability. This is
because of angry outbursts toward family (Fishbain, 2000). Thus, the TCAs may have
members, who have been loving and multiple benefits in the management of this
supportive, which leave the patient feeling condition.
regretful and self-critical. The anticonvulsants have traditionally
The above paragraph is, to some extent, an been recommended in the treatment of
academic exercise, as the antidepressants are neuropathic pain. However, in practice they
useful and recommended for the management are also used in the management of chronic
of anxiety, depression, insomnia and back pain, irrespective of the possibility of a
irritability, whether as separate symptoms or neuropathic contribution. In view of the wide
as part of a depressive syndrome. When the range of actions of these drugs, Caraceni et al
full depressive syndrome is present, the (2000) speculate that the anticonvulsants may
normal antidepressant dose is usually required. prove to have a wide range of applications in
However, symptomatic relief from anxiety, pain. In chronic back pain, as with the TCAs,
insomnia and irritability is usually achieved at the anticonvulsants have the advantage of
smaller doses. The choice of antidepressant is beneficial effects in anxiety and depression.
important. While the newer antidepressants, Carbamazepine and sodium valproate are well
venlafaxine and the selective serotonin established in the treatment of chronic pain;
reuptake inhibitors (SSRIs) such as fluoxetine, however, gabapentin is now being used, and
may be useful in full doses in the treatment of appears to be as effective, but with less
the depressive syndrome, they are less useful troublesome side-effects.
in the symptomatic treatment of anxiety, The NSAIDs have a place in chronic back
insomnia and irritability. In symptomatic pain, particularly where degenerative
treatment, the older, tricyclic antidepressants conditions contribute. They have troublesome
(TCAs), are more useful. The TCAs cause dry gastrointestinal effects, but the
mouth and other anticholinergic side-effects; cyclooxygenase-2 inhibitors, such as celecoxib,
but this may be minimized by using smaller have relatively fewer.
doses of the more tolerable agents, such as When opioids are being contemplated,
nortriptyline. Twenty-five or 50 mg of tramadol deserves consideration. It displays
amitriptyline or nortriptyline will greatly assist both weak opioid and monaminergic actions.
pain-related insomnia, and 10 or 25 mg once It is thought to be free of euphoria,
or twice per day will assist anxiety and withdrawal and addiction problems. There is
irritability. minimal respiratory depression, but nausea
The TCAs also have an important, first- and somnolence are common side-effects. In
line role in the analgesia of back pain at least one study benefit has been
demonstrated in chronic low back pain Atlas S, Deyo R. Evaluating and managing acute
(Schnitzer et al, 2000). low back pain in the primary care setting.
Journal of General Internal Medicine 2001; 16:
The use of opioids for non-cancer pain 120–31.
remains controversial, but there is good
Bigos S, Bowyer O, Braen G. Acute low back
evidence that they relieve chronic back pain problems in adults. Clinical Practice Guidelines
(Jamison et al, 1998). In comparisons of no. 14. Rockville, MD, Department of Health
populations who receive and do not receive and Human Services, 1994. (AHCPR
publication no. 95–0642.)
opioids, it emerges that the factor that
Bogduk N. Management of low back pain. In:
determines the decision to provide opioids is
Update in the Management of Musculoskeletal
not the quantity of pain suffered, but the Pain. Alpha Biomedical Communications,
amount of emotional distress experienced. It is Darlinghurst, 1999; 85–102.
important, therefore, specifically to assess the Caraceni, A, Cheville A, Portenoy R. Pain
mental state and reduce emotional distress management: pharmacological and
nonpharmacological treatments. In: Massie MJ
with antidepressants and psychological
(ed) Pain: What Psychiatrists Need to Know.
therapies before resorting to the opioids. Once (Review of Psychiatry Series, Vol. 19, No 2;
the decision is made, the choice of agent will Oldham J and Riba M, series eds). American
depend on experience and availability. An Psychiatric Press, Washington, DC, 2000;
23–88.
acceptable approach is the combination of a
Cherkin D, Eisenberg D, Sherman K, Barlow W,
long-acting medication taken regularly (daily
Kaptchuk T, Street J, Deyo R. Randomized trial
or twice daily) and a short-acting medication comparing traditional Chinese medical
taken as required, for breakthrough pain. See acupuncture, therapeutic massage, and self-care
the final chapter on pharmacotherapy for education for chronic low back pain. Archives of
Internal Medicine 2001; 161: 1081–8.
details.
Croft P, Papageorgiou A, Ferry S, Thomas E,
When oral opioids are deemed to have
Jayson M, Silman A. Psychological distress and
failed, in highly specialized centres devices low back pain: evidence from a prospective
such as morphine pumps and epidural study in the general population. Spine 1995; 20:
stimulators may be implanted. There are no 2731–7.
controlled trials that support the use of these Croft P, Macfarlane G, Papageorgiou A, Thomas E,
Silman A. Outcome of low back pain in general
devices.
practice: a prospective study. British Medical
Journal 1998; 316: 1356–9.
References Deyo R. Early diagnostic evaluation of low back
pain. Journal of General Internal Medicine 1986;
Andersson G, Svensson H-O, Oden A. The
1: 328–38.
intensity of work recovery in low back pain.
Spine 1983; 8: 880–4. Deyo R, Diehl A. Psychosocial predictors of
disability in patients with low back pain. Journal Nicholas M, Molloy A, Tonkin L, Beeston L.
of Rheumatology 1988; 15: 1557–64. Manage Your Pain: Practical and Positive Ways of
Adapting to Chronic Pain. Australian
Deyo R, Rainville J, Kent D. What can the history
Broadcasting Commission, Sydney, 2000.
and physical examination tell us about low back
pain? Journal of the American Medical Association Powell M, Wilson M, Szypryt P, Symonds E,
1992; 268: 760–4. Worthington B. Prevalence of lumbar disc
degeneration observed by magnetic resonance in
Fishbain D. Evidence-based data on pain relief with
symptomless women. Lancet 1986; 2: 1366–7.
antidepressants. Annals of Medicine 2000; 32:
305–16. Schnitzer T, Gray W, Paster R, Kamin M. Efficacy
of tramadol in treatment of chronic low back
Frymoyer J, Pope M, Clements J, Wilder D,
pain. Journal of Rheumatology 2000; 27: 772–8.
MacPherson B, Ashikaga T. Risk factors in low-
back pain: an epidemiological survey. Journal of Spangfort E. The lumbar disk herniation: a
Bone and Joint Surgery [Am] 1983; 64-A: computer-aided analysis of 2,504 operations.
213–18. Acta Orthopaedica Scandinavica [Suppl] 1972;
142: 1–95.
Frymoyer J. Back pain and sciatica. New England
Journal of Medicine 1988; 318: 291–300. Vroomen P, de Krom M, Wilmink J, Kester A,
Knottnerus J. Lack of effectiveness of bed rest
Grachev I, Fredrickson B, Apkarian A. Abnormal
for sciatica. New England Journal of Medicine
brain chemistry in chronic back pain: an in vivo
1999; 340: 418–23.
proton magnetic resonance spectroscopy study.
Pain 2000; 89: 7–18. Weber H. Lumbar disc herniation: a prospective
study of prognostic factors including a controlled
Jamison R, Raymond S, Slawsby E, Nedeljkovic S,
trial. Part I. Journal of Oslo City Hospital 1978;
Katz N. Opioid therapy for chronic noncancer
28: 33–61.
back pain. A randomized prospective study.
Spine 1998; 23: 2591–600. Wiesel S, Tsourmas N, Feffer H, Citrin C, Patronas
N. A study of computer-assisted topography. I.
Jensen M, Brant-Zawadzki M, Obuchowski N,
The incidence of positive CAT scans in an
Modic M, Malkasian D, Ross J. Magnetic
asymptomatic group of patients. Spine 1984; 9:
resonance imaging of the lumbar spine in
549–51.
people without back pain. New England Journal
of Medicine 1994; 331: 69–73.
Malmivaara A, Hakkinen U, Aro T. The treatment
of acute low back pain – bed rest, or ordinary
activity. New England Journal of Medicine 1995;
332: 351–5.
Pharmacotherapy
15 ‘The desire to take medicine is perhaps the greatest feature

which distinguishes man from the animals.’
Sir William Osler 1904
Pain relief may be sought from a range of non-pharmacological

procedures (relaxation therapy, hypnosis, CBT, acupuncture,
and invasive techniques), but pharmacotherapy remains the
most widely used and effective component, and is usually
indispensable to chronic pain management.
Patients may be reluctant to take medication. There are
pragmatic concerns regarding adverse effects and addiction
and cultural concerns. Many cultures view the origin of pain
in religious terms or maintain attitudes that idolize pain. They
equate the acceptance of pain with faith and the toleration of
pain with character strength. It is the task of the clinician to
help the patient avoid adverse effects, drug abuse and
unnecessary suffering.
Adverse effects in general

Adverse effects are frequent and may lead to non-compliance
and subsequent treatment failure. The clinician should be
aware of the potential adverse effects of each frequently with gradual introduction. For
medication and monitor patient progress. example, carbamazepine and lamotrigene are
One current view, supported by the patients’ much less likely to cause characteristic skin
rights movements and legal systems, is that reactions if they are introduced slowly.
the patient must be informed about every When a patient is troubled by a particular
known adverse effect of every medication. adverse effect, it may be possible to change to
Another view is that patients are ill prepared another medication in the same family that is
to weigh the risks and benefits of specific less troublesome. For example, when a first-
medications. Exhaustive information may generation tricyclic antidepressant (TCA; e.g.
increase patient apprehension and the rate of amitriptyline) produces an unacceptably dry
detection/reporting of adverse effects, for no mouth, a second-generation TCA (e.g.
clinical gain. Thus some recommend giving desipramine), which has less anticholinergic
only a brief account of possible adverse effects, action, may be an answer.
encouraging contact at the first sign of Adverse effects may also be diminished by
problems, and arranging a follow-up visit for altering the time of administration. When
the near future. At follow-up, the clinician possible, give the majority of the sedating
asks non-leading questions about the body drugs of the regimen at night. This depends
systems that may be affected. It is legally safer on the purpose and half-life of the
for the clinician to take the comprehensive medication. Amitriptyline (half life 21 hours)
warning approach, which is often less given for depression, can be given all at night,
beneficial for the patient. while codeine (half life 2.9 hours) given for
It is sometimes possible to reduce the pain, is better given throughout the day.
impact of adverse effects. Always use the Likewise, activating agents such as stimulants
minimal effective dose. Commencing at full should be given in the morning. Different
dose produces the strongest adverse effects. patients may report different sedating or
This frightens and discourages and carries the alerting effects from the same medication. A
strongest likelihood of rejection of both this careful history will reveal the problem and the
medication in particular and all other necessary accommodation can be made.
medications. As a general rule, start with low The use of multiple pharmacological
doses and gradually increase. This allows the agents for the same or concurrent illnesses
patients gradually to become aware of and increases the likelihood of adverse effects.
gradually to accept adverse effects, and for Clinicians need to be informed regarding
physiological adjustments that will minimize interactions that cause adverse effects or
them. Some adverse effects occur much less reduce the efficacy of specific agents. For
Pharmacotherapy 131
example, selective serotonin reuptake (metoclopramide and prochlorperazine) and

inhibitors (SSRIs) will raise the blood level of the antiserotonergics (ondansetron). The
concomitantly administered TCAs, and vestibular system is stimulated by movement;
carbamazepine will lower the blood level of a thus it is better to rest than move during these
range of drugs, including oral contraceptives. periods. The sensitivity of the vestibular
Pharmacological agents introduced to system can be reduced by anticholinergics
correct adverse effects initiated by therapeutic (scopolamine and benztropine) and
agents may introduce their own adverse antihistamines (diphenhydramine). The
effects. For example, choline esters introduced opioids decrease the activity of the
to correct the effects of anticholinergic drugs gastrointestinal tract, which produces
may themselves cause tremor, diarrhoea, abnormal feedback to the vomiting centre.
abdominal cramps, and excessive eye watering; Metoclopramide 10 mg (up to 3 times
misoprostol, a prostaglandin analogue used to daily, if necessary) is the treatment of choice,
prevent gastric ulceration by NSAIDs, may as it has a dopamine-blocking action and also
cause abdominal pain and diarrhoea. Inquiries increases gastrointestinal activity. Adverse
regarding the concomitant use of over-the- effects include dystonic reactions (which may
counter medications, herbal remedies, need treatment with an anticholinergic and/or
caffeine, nicotine, and alcohol are mandatory. benzodiazepine) and sedation.
In general, the elderly are at greater risk of Prochlorperazine 10 mg (up to 3 times
adverse effects, and for them smaller daily) is a strong alternative. This may also
medication doses are indicated. cause dystonia and sedation. Ondansetron is a
useful but expensive alternative that may cause
Common adverse effects headache and constipation. Diphenhydramine
25 mg (up to 4 times daily) is inexpensive, but
1. Nausea and vomiting will increase sedation.
Nausea and vomiting are common adverse Scopolamine patches have been
effects of the opioids and the antiarrhythmics recommended, but these are no longer available
(mexiletine). The vomiting centre, which is in some countries (including Australia).
situated in the brain stem, is stimulated by
input from the chemoreceptor trigger zone,
2. Constipation
the vestibular system and the gastrointestinal
tract. The chemoreceptor trigger zone is Constipation is a frequent consequence of
stimulated by the opioids. This stimulation is anticholinergic activity, and of stimulation of
blocked by the antidopaminergics mu and delta opioid receptors.
Helpful agents include the following: Bethanechol has been suggested for
anticholinergic constipation. This choline ester
Eat more fruit and drink larger amounts of has been associated with adverse effects of
water. asthma, hyperthyroidism, coronary insufficiency
Fibre supplements (ispaghula, Fybogel; and peptic ulcer. Regular use for drug-induced
methylcellulose, Cellulone) constipation is not recommended; it is not
Faecal softener by mouth (docusate, Coloxyl). particularly effective, and is therefore not worth
Faecal softeners stimulate intestinal secretions, the risk of further adverse effects.
which enter and soften the stool. Thus oral Use of laxatives may be necessary where
administration may not be effective for two or high-dose opioid use is unavoidable. In many
three days. cases it is possible to reduce or change the
Peristaltic stimulant (sennosides a and b, offending medication, and increased intake of
Senokot) fruit, water and some fibre supplement will be
Combinations of faecal softener and peristaltic sufficient.
stimulant are available.
Suppositories (glycerol; Glycerine
3. Pruritus
Suppositories; docusate, Coloxyl
Suppositories) Pruritus results from spinal cord mu receptors.
Enema (docusate; Coloxyl Enema) It is relieved by diphenhydramine 25 mg (up
to 4 times daily).
Laxatives should be used with caution.
They are contraindicated in suspected
obstruction and certain other medical
4. Orthostatic hypotension
conditions. They may increase the absorption Orthostatic hypotension may result from
and hepatic uptake of other drugs. blockade of alpha 1-adrenergic receptors.
Continuous high-dose use may lead to Affected patients should be advised to change
dependence and should be avoided. However, posture slowly and to sit down immediately
regular intake of fibre supplement with faecal upon experiencing dizziness. Supportive
softener as required should be safe in the stockings to prevent venous pooling are
otherwise healthy individual. recommended by some authors, but are rarely
Some tolerance develops to the effects of used in clinical practice. Other measures may
opioids on gastrointestinal motility; however, include adding salt to the diet, and the use of
patients who take opioids chronically remain fludrocortisone. This adverse effect usually
constipated. subsides over time.
Pharmacotherapy 133
Orthostatic hypotension may also result is the most widely used TCA in pain
from opioid use. There is peripheral arteriolar management, but is the most sedating.
and venous dilation, produced by several Nortriptyline is a metabolite of amitriptyline.
mechanisms, including provoked histamine It is less sedating but retains analgesic effects,
release. There is also blunting of reflex and can be used to replace the parent drug.
vasoconstriction in response to plasma CO2. Desipramine is a TCA that is stimulating in
There is no specific treatment; reduce the dose some individuals. It is not used extensively in
and consider an alternative analgesic agent. pain management, where a degree of sedation
is often valuable.
Where the antidepressant is being used
5. Sedation
exclusively in the treatment of depression, an
Sedation may result from stimulation of mu SSRI will provide a non-sedating alternative.
and kappa receptors by opioid drugs and
stimulation of histamine receptors by
6. Urinary retention
antidepressant drugs.
Sedation due to opioid drugs in the Urinary retention may result from the use of
terminally ill may be managed with a anticholinergic drugs. It is rare that active
stimulant such as methylphenidate 5 mg (up treatment is needed. Bethanechol has a good
to 3 times daily). For non-cancer chronic pain effect, and can be use in oral or in
patients, however, the currently available subcutaneous form in acute situations.
stimulants, which are addictive and have other Urinary retention may occur when
adverse effects, are not recommended. For stimulation of the mu and delta opioid
these patients, dose reduction or changing to receptors inhibits the voiding reflex.
another opioid may be beneficial. Catheterization may be necessary in acute
The tricyclic antidepressants (TCAs) are situations. Tolerance develops to the effect of
the most frequently used antidepressants for opioids on the bladder.
chronic pain patients, because they have an
analgesic effect. This has not been
7. Dry mouth
satisfactorily demonstrated in the selective
serotonin reuptake inhibitors (SSRIs). The Dry mouth may be caused by anticholinergic
SSRIs have insignificant sedative effects. If a drugs. Oral bethanechol has been suggested,
TCA is being used for analgesic effects, and but may cause other adverse effects. Some
sedation is a problem, replacement with an relief may be obtained from chewing sugarless
SSRI cannot be recommended. Amitriptyline gum or sweets. It is important to use sugarless
products, as a dry mouth makes teeth Sildenafil is effective in drug-induced

particularly prone to caries. The impotence and impaired ejaculation and has
cholinomimetic alkaloid pilocarpine used as a relatively trivial adverse effects (most
1% solution mouthwash used three times daily commonly, headache, flushing and dyspepsia).
has the advantage of being relatively effective; It may also have a place in the treatment of
and, as a topical preparation, the risk of further female sexual dysfunction. Bethanecol has
adverse effects carried is slight. This use of been use for impotence. Neostigmine by
pilocarpine is not listed in some authoritative mouth half an hour before sexual intercourse
pharmacological texts (Taylor, 1990). may help impaired ejaculation, but is no
longer available in some countries (including
Australia). Cyproheptadine as a regular
8. Blurred vision
morning dose, or one to two hours before
Blurred vision may be caused by anticipated sexual activity, may help inhibited
anticholinergic drugs. Pilocarpine 1% one orgasm (Grebb, 1995).
drop four times daily can be beneficial and is When sexual dysfunction is the adverse
free of adverse effects. The frequency of effect of an SSRI, the addition of a small dose
application depends on the individual. of bupropion usually produces good results
Miosis may result from stimulation of mu (Labbate and Pollack, 1994).
and kappa opioid receptors, but rarely impairs
vision.
10. Gastric irritation and ulcer
Gastrointestinal (GI) symptoms occur in 10%
9. Sexual dysfunction
of patients treated with traditional NSAIDs.
Sexual dysfunction (decreased libido, Ulcers occur in 2%. GI symptoms are poor
impotence, impaired ejaculation, inhibition of predictors, and haemorrhage and perforation
female orgasm) can be associated with a range of ulcers may occur without warning.
of drugs acting on the nervous system. The analgesic properties of the NSAIDs
Sexual dysfunction is an uncommon result from inhibition of the enzyme
complication of analgesic use. Opioids inhibit cyclooxygenase (COX), which is central to the
the release of gonadotropin-releasing hormone production of prostaglandins. COX exists in
(GnRH) and corticotropin-releasing factor at least two physiological forms (COX-1 and
(CRF) and increase the concentration of COX-2). COX-1 inhibition is associated with
prolactin (PRL): thus sexual dysfunction is GI (and renal) toxicity, while COX-2
possible. inhibition reduces inflammation and pain.
Pharmacotherapy 135
Most currently used NSAIDs are non- Among the antipsychotic drugs,
specific inhibitors of both isoforms of COX. olanzapine causes marked weight gain, while
When using these, when symptoms or risk quetiapine causes almost none. The
factors (past history, heavy alcohol use, older antihistamines are notorious for weight gain,
age) cause concern, gastroprotective therapy is and should be avoided as regular treatment
indicated. Misoprostol (800 micrograms in where overweight is a problem.
divided doses), a prostaglandin analogue, reduces Patients should attempt to restrict fats and
the incidence of ulcers. This treatment may lead carbohydrates. Where dry mouth is a
to abdominal pain and diarrhoea. A proton problem, pilocarpine mouthwash may be
pump inhibitor such as omeprazole (20 mg useful, but most important is to alert the
daily) or a histamine H2 receptor antagonist such patient to the calorie content of drinks and
as cimetidine (400 mg in divided doses) may encourage the drinking of plain water or other
also be effective. Both are associated with a range calorie-free beverages. The involvement of a
of generally mild adverse effects. dietician may be helpful. Exercise is
With regard to gastric irritation and ulcer, encouraged. When weight gain has been
the selective COX-2 inhibitors such as unavoidable, discussions may help the patient
celecoxib have advantages. Where they can be accept this altered condition.
afforded, such drugs are recommended.
Opioids (opioid receptor

11. Weight gain actors)
Weight gain is a common and troublesome The opioid drugs are the strongest analgesics
adverse effect of many drugs that act on the available. They are similar to the endogenous
CNS. Fluid retention, increased appetite and opioids, the endorphins. The human has at
caloric intake, dry mouth leading to frequent least five opiate receptors (mu, kappa, sigma,
drinks, sedation and decreased exercise, and delta, epsilon), which have different
altered metabolism may all play a part. constellations of actions. The mu, kappa and
The TCAs cause significant weight gain; delta receptors have analgesic effects. The mu
the SSRIs cause little. When a TCA is being receptor has euphoric and the kappa and
used for its analgesic effects, it cannot be sigma receptors have dysphoric effects. The
replaced by an SSRI. However, when a TCA mu, kappa and delta receptors cause
is being used exclusively as an antidepressant, respiratory depression, while the sigma
and weight gain is a problem, replacement receptor causes increased respiration.
with an SSRI is recommended. Brain opiate receptors are mainly located
in the periaqueductal grey matter. Stimulation Tolerance also develops to drugs other than
activates dorsal column noradrenaline and the opioids. For example, carbamazepine
serotonin-transmitting neurones that inhibit doses have to be increased subsequent to the
afferent input in the dorsal horns. Spinal induction of metabolizing enzymes.
opiate receptors are mainly located in the In humans tolerance to constipation does
dorsal horns. Their stimulation has a direct not develop. This means that the starting
inhibitory effect on afferent transmission. dose, or relatively small doses, continue to
cause this problem. Fortunately, tolerance to
respiratory depression and sedation develops
Tolerance, dependency and
over a few weeks, so that the starting dose, or
addiction
another particular dose, will cease to cause
These conditions are poorly understood, a these problems. However, at very high doses,
situation that creates difficulties for people tolerance finally ceases and the persistence of
with chronic pain and doctors alike. The adverse effects prevents further dose
principles are simple. They should be clearly escalation.
communicated and understood, and returned Tolerance to the euphoric effect develops
to, should clinical practice become in days to weeks. This is at the root of the
problematic. psychological dependency of addiction, which
will be discussed below. Where the euphoric
effect is a primary goal, or becomes an
Tolerance
important goal, tolerance will result in the
Tolerance is the condition that a certain dose seeking of higher doses.
of medication produces a decreased effect Tolerance also, unfortunately, develops to
following repeated administration. the analgesic effects. However, clinically, this
Consequently, a greater dose is thereafter is usually a gradual process, and it is common
required to achieve the desired effect. for patients to remain on a stable dose for
Tolerance is a normal, adaptive response to years (Brescia et al, 1992). There are a number
drugs, and is demonstrated in a wide range of of confounding factors. Rapid escalation of
animals. Various bodily changes may dose by the doctor encourages tolerance. On
contribute to tolerance, including the the other hand, requests from the patient for
induction of metabolizing enzymes, rapid escalation call for physical and mental
moderation via negative feedback of endocrine re-evaluation. However, there is no ceiling
gland activity, and the alteration of receptor effect, and as long as the adverse effects are
density in the ‘plastic’ nervous system. tolerable, increasing the dose will restore the
Pharmacotherapy 137
analgesic effect. When approaching very high physiology. This is clearly the case where
doses, the clinician should involve colleagues tolerance has developed. Opioids suppress the
in the decision to increase. production of endogenous endorphins, and
Tolerance is soon lost. This means that if on cessation of medication the body is left
opioids can be tapered and ceased for three or with less than normal levels of a physiological
four weeks, the analgesic effects of lower doses agent.
will be restored (at least for a time). Withdrawal effects, albeit less dramatic,
are associated with the withdrawal of the
antiepileptics, venlafaxine, clonidine and
Dependence
many others.
There are two types of dependence: physical Withdrawal effects can be avoided by
and psychological dependence. There is much tapering rather than suddenly ceasing
to recommend replacing physical dependence medication.
with the term ‘neuroadaptation’ (Edwards,
cited in Jaffe, 1990); but this has not
Addiction (psychological
happened. For discussions with patients it is
dependence)
better to refer to psychological dependence as
‘addiction’. This topic will be dealt with Addiction or psychological dependence refers to
separately. compulsive drug use, an overwhelming interest
Physical dependence develops with the in securing a supply and the return to drug use
opioids and various other drugs. Physical after detoxification despite advice to the
dependence has developed when, if contrary. The term ‘compulsive’ is used here as it
administration is suddenly ceased, the patient relates to ‘compelled’, which means to be forced
demonstrates an abstinence syndrome, or or driven. Such behaviour causes the individual
physical withdrawal. The common picture in physical, psychological, or social harm.
opioid withdrawal includes muscle spasms, Addiction is observed with drugs that have
diarrhoea, and autonomic effects including euphoric or other comforting psychological
tachycardia and piloerection (the source of the effects.
term, ‘cold turkey’). These events can be both Addiction is suggested by aberrant drug-
painful (not to mention the re-emergence of related behaviour, which includes increasing
the pain that was the focus of treatment) and the amount of drug taken without medical
frightening. direction, hoarding drugs ‘in case’ they are
Withdrawal effects are an expected needed, obtaining drugs from different
response when drug use has altered doctors and buying drugs illegally.
Many patients are reluctant to accept and their management has been detailed
opioids because they fear addiction. Iatrogenic above.
addiction can occur; however, the risk is low
in the majority of patients, especially if
Management principles
clinicians are cautious and watch for aberrant
drug-related behaviour. The risks are higher Opioids are not a panacea for chronic pain,
for those who are excessively impulsive or and they all carry significant risks. Use in non-
dependent. Where there is a history of drug cancer pain is controversial by some accounts
abuse, treatment should proceed according to (Ward et al, 1993). However, Bouckoms et al
clear guidelines, preferably in collaboration (1992) reported the long-term treatment of
with a clinician with special experience in large series of patients with non-cancer
addiction. chronic pain in which 2/3 achieved effective
Many pain centres provide written pain relief. One-third demonstrated tolerance,
information and require all patients to sign physical dependency or drug abuse over a
opioid treatment contracts (Bouckoms, 1996; three-year period. Bennett (1999) recently
Irving and Wallace, 1997). Information is stated that opiates are the most effective
provided regarding tolerance, dependence and currently available treatment for most chronic
addiction. Before receiving the patient must pain states.
agree to adhere to directions, not to consult Opioids are considered to be more
other doctors, hoard medication, or buy/sell effective in non-neuropathic pain (Dellemijn,
drugs illegally, and not to use illegal drugs. 1999). Nevertheless, beneficial effects are
Most contracts state that contravention of reported with neuropathic pain (Watson and
these conditions will result in discontinuation Babul, 1998).
of the prescription of opioids. Opioids should only be considered when
all other avenues for relief (non-opioid and
co-analgesics) have been exhausted.
Adverse effects
It is not possible to predict whether an
There is no organ toxicity, and thus no fatal opioid will be helpful in a particular case. This
adverse effects, when opioids are used can only be determined through a clinical trial
according to directions. Respiratory arrest may in which the dose is gradually escalated till
occur in overdose. pain relief occurs or intolerable adverse effects
Nausea and vomiting, constipation, are experienced. Opioids differ from each
sedation, pruritus, urinary retention, and other; so that if one fails to provide relief, it is
sexual dysfunction are possible adverse effects, worth trying others.
Pharmacotherapy 139
Brose and Spiegel (1992) caution against of long-acting drug taken twice daily (once
using inadequate doses. They advise that there daily if this provides sufficient relief), with a
is great individual variability, and that, for a limited supply of short-acting opioids to be
particular drug, one patient may need five or taken for breakthrough pain. This
six times the dose of another. However, arrangement provides a monitoring system. If
Caraceni et al (2000) caution that failure to the patient is needing an increased amount of
achieve at least partial analgesia with relatively short-acting opioid, and after consideration
low doses in the non-tolerant individual must there is no evidence of aberrant drug
raise doubts about the potential for opioid behaviour, it is time to increase the dose of the
treatment. load-bearing long-acting medication.
Long-acting opioids taken twice daily As was mentioned above, patients must be
(once daily if possible, depending on the case made aware of the potential risks and benefits.
and the available preparations) are a Many pain centres require the signature of an
fundamental of good opioid use in chronic opioid management contract.
pain. They allow the serum levels to be kept Improved physical and social functioning
relatively constant. Fluctuations in serum should be stressed. Pain relief should enable
levels lead to the frequent return of pain. The the patient to engage more actively with the
return of pain is frightening. Attempts to gain world. Such changes in behaviour bring
relief in these circumstances lead to excessive additional benefits.
opioid use. With short-acting opioids Only one practitioner should prescribe the
fluctuations in serum levels are unavoidable. opioid for a particular patient. However, other
Thus short-acting opioids should not be used clinicians should be involved in decisions to
as the basis of chronic pain management. use very high doses, and when the treatment
Further supporting this position is the fact of patients with a history of drug abuse is
that frequent ingestion of drugs followed by being considered.
immediate relief and then the return of At each appointment the doctor should
symptoms carries a greater risk of engendering enquire into and record the degree of
addiction. analgesia, adverse effects, physical and social
Even with stable serum opioid levels, activity and aberrant drug behaviour
patients may experience severe ‘breakthrough’ (preoccupation with drugs, hoarding, dose
pain, sometimes for explicable reasons, such as escalation, obtaining drugs from other
increased activity, but often for no apparent sources).
reason.
The recommended regimen is a fixed dose
Examples of opioids Available as 5, 10, 30, 60, 100, 200 mg tablets

Recommended starting dose: 30 mg twice
A large range of opioid products are available.
daily.
A selection is presented, using manufacturer
recommendations: for complete details a
Oxycodone hydrochloride in the controlled-
pharmacology text should be consulted.
release form, marketed as Oxycontin
Clinical practice may vary from these
Administered twice daily
guidelines.
Available as 10, 20, 40 and 80 mg tablets
Chronic pain is generally managed using
Recommended starting dose: 10 mg twice
oral medication. Unless otherwise mentioned,
daily
the following details refer to the oral forms.
Fentanyl as a transdermal system (patch),

marketed as Durogesic
Long-acting drugs
A patch lasts 3 days.
These preparations form the backbone of Available as 25, 50, 75 and 100 micrograms
opioid management of chronic pain. per hour
Recommended starting dose, for opioid-naïve
Morphine sulphate in sustained-release form, patients, 25 micrograms per hour. Peak
marketed as Kapanol concentrations of fentanyl occur between 24 to
Administered once, or at most twice, daily 72 hours after application. After the initial 72
Available as 10, 20, 50 and 100 mg capsules hours, subsequent patches maintain a steady
Recommended starting dose: 20 mg twice serum concentration. Conversion from other
daily, or 40 mg once daily opioids : the fentanyl dose is based on the
Conversion from other opioids depends on a average daily use of opioids expressed as oral
variety of factors, and must be performed with morphine equivalent, e.g. an equivalent of
caution. Oral morphine has a potency 135–224 mg of oral morphine per 24 hours is
equivalent to oral oxycodone. When replaced with fentanyl 50 micrograms per hour.
methadone is given regularly, it is 3–4 times Tables are provided by the manufacturer.
more potent than oral morphine. Injected Individual titration will be necessary.
morphine has 3 times the potency of oral Short-acting opioid may be added for
morphine. breakthrough pain and subsequently
Morphine sulphate in the sustained-release converted into this form of fentanyl.
form, marketed as MS Contin This is a new and expensive product, and
Administered twice daily experience is limited.
Pharmacotherapy 141
Medium-acting drugs increasing the availability in the CNS of the

neurotransmitters serotonin and
Methadone marketed as Physeptone
norepinephrine. There are no serious adverse
Administered 3 times daily
effects: nausea is the most common; others
Available as 5 and 10 mg tablets
include somnolence and dizziness. It has been
Recommended starting dose: 10 mg 3 times
found effective in the pain of diabetic
daily
neuropathy (Harati et al, 1998), pain and
Methadone has less euphoric effect than the
allodynia in polyneuropathy (Sindrup et al,
other opioids, and is less likely to be associated
1999) and chronic low back pain (Schnitzer et
with addiction. It has an extremely long half
al, 2000).
life, which makes it valuable in preventing
withdrawal in addicts, and can be given as a
once-a-day dose. The analgesic half life,
however, is much shorter; and for chronic Short-acting drugs
pain relief purposes it must be taken more
In chronic pain management, these
frequently. Inter-individual variability in the
preparations are best reserved for
analgesic half life is a disadvantage, and many
breakthrough pain:
clinicians favour alternative, sustained-release
products.
Morphine sulphate immediate-release
preparation, marketed as Anamorph (and
Tramadol marketed as Tramal others)
Administered three times daily Administered on an as-needed basis.
Available as 50 and 100 mg capsules Available as 30 mg tablets.
Recommended starting dose 50 mg three Onset is rapid, at 15–20 minutes. Duration of
times daily. Manufacturer recommended action is 3–4 hours.
maximum dose: 400 mg daily
This medication is difficult to classify. It has Codeine phosphate marketed as Codeine
two actions (an opioid and a non-opioid phosphate (and others)
action). It has a mu receptor affinity 6000 Administered on an as-needed basis.
times less than morphine. There is no Available as 30 mg tablet.
euphoria and there are no withdrawal or This is a weak opioid. It has a quicker onset
addiction problems. Thus some authorities list and a shorter duration than morphine. In
tramadol as a non-opioid drug. The primary some products it is in combination with
analgesic effect appears to be through paracetamol, aspirin or acetaminophen.
Oxycodone hydrochloride immediate-release histamine H2 receptor antagonist) should be

preparation, marketed as Endone considered. Selective COX-2 inhibiting
Administered on an as-needed basis. NSAIDs have a clear advantage.
Available as 5 mg tablet. Inhibition of platelet aggregation is a
serious concern, particularly for patients with
pre-existing bleeding problems, those
Non-steroidal anti-
receiving anticoagulant therapy and the
inflammatory drugs (NSAIDs) medically frail.
(cyclooxygenase inhibitors) Nephrotoxicity from NSAIDs is rare in
The NSAIDs are antipyretic, and their anti- the healthy patient. However, the risk is
inflammatory action provides useful analgesic increased in patients with renal disease,
effects. The prostaglandins induce volume depletion, congestive heart failure or
inflammation and sensitize primary afferent cirrhosis.
nerves. The NSAIDs inhibit the enzyme Exacerbation of bronchospasm can occur,
cyclooxygenase (COX), thereby reducing the and may cause coughing at night.
production of prostaglandins. The NSAIDs Hypersensitivity reactions are rare: they range
probably also have central analgesic effects. from mild cutaneous eruptions to life-
COX exists in at least two physiological threatening anaphylaxis.
forms (COX-1 and COX-2). Most currently An interaction with lithium has been
available NSAIDs are non-specific inhibitors claimed. However, to this point the author
of both isoforms. COX-1 inhibition is has been able to find only case reports
associated with GI (and renal) toxicity, while regarding piroxicam and dicolfenac raising the
COX-2 inhibition reduces inflammation and serum level of lithium. Sulindac may have a
pain. minimal effect.
Monitoring may include tests for occult
faecal blood, haemoglobin level and renal and
Adverse effects hepatic function. Endoscopy is indicated
Adverse effects are related to COX inhibition. when GI symptoms are experienced.
As was stated above, GI symptoms occur
in 10% of patients treated. Ulcers and
haemorrhage may occur without warning.
When there are previous symptoms or risk NSAIDs are used for mild to moderate pain,
factors, gastric protection (a prostaglandin especially pain secondary to an inflammatory
analogue, a proton pump inhibitor or a component. They have a ceiling effect. There
Pharmacotherapy 143
is individual variation between patients with Selective COX-2 inhibitor

respect to the optimal drug and dose. Serial Celecoxib
trials of different NSAIDs, working up to Administered once or twice daily
maximal doses, are justified. They are Available as 100 and 200 mg capsules
generally believed to be less effective in Recommended starting dose: 100 mg once
neuropathic pain, but they may offer some daily
relief in this situation. They enhance opioid Maximum dose: 200 mg twice daily
analgesia and reduce the opioid requirement.
Selective COX-2 inhibitors are becoming Non-selective COX inhibitors – arranged in
available (celecoxib, rofecoxib and nimesulide) order of increasing frequency of
and are recommended where they can be administration
afforded.
Treatment should commence at a low Ketoprofen marketed in slow release form as
dose, and can be increased at the end of one Orudis
week if analgesia is not achieved. The Administered once daily
following list is composed from Available as 100 and 200 mg capsules
manufacturers’ product information, Recommended starting dose: 100 mg daily
supplemented from papers and leading texts. Maximum dose 300 mg daily (Insel, 1990)
Some manufacturers do not state that their
medications should be taken with food. Piroxicam
Owing to the high prevalence of GI Administered once a day
symptoms, however, this would be sensible Available as 10 and 20 mg capsules
advice. Recommended starting dose: 10 mg once
daily
Maximum dose limit is not available.
Examples of NSAIDs
Good response has been obtained with 20 mg
A large range of NSAID products are daily.
available. A selection is presented, using
manufacturer recommendations: for complete Sulindac
details a pharmacology text should be Administered once (at night) or twice daily
consulted. Clinical practice may vary from with food or fluid
these guidelines. Available as 100 and 200 mg tablets
Recommended starting dose: 100 mg daily
Maximum dose: 400 mg daily
Diflunisal place in the management of chronic pain

Administered twice daily (McQuay and Moore, 1998). This analgesic
Available as 250 and 500 mg tablets effect is not due to antidepressant effects,
Recommended starting dose: 500 mg twice although relieving any existing depression
daily makes the patient more able to tolerate pain.
Maximum dose: 2000 mg daily A protective mechanism in the CNS works
to reduce pain experienced by the organism.
Naproxen Norepinephrine and serotonin pathways
Administered twice a day descend in the dorsal column to the dorsal
Available as 250 and 500 mg tablets horns, where they inhibit nociceptor input
Recommended starting dose: 250 mg twice into the second-order neurones. Certain
daily antidepressants significantly increase this
Maximum dose: 3200 mg daily (Insel, 1990) dorsal horn inhibition.
Other actions of the TCAs that potentially
Diclofenac contribute to the analgesic effects are the
Administered three or four times daily: usually undesired features of alpha-1 and
swallow with liquid NMDA blockade. The TCAs also have an
Available as 25 mg and 50 mg tablets antihistamine action that may play an
Recommended starting dose: 50 mg twice analgesic role. Bouckoms (1996) suggested
daily that their ability to upregulate mesolimbic
Maximum dose: 200 mg daily dopamine may be important.
Fishbain (2000) conducted an evidence-
Ibuprofen based review and concluded that
Administered three to six times daily with antidepressants have an analgesic effect, which
food or fluid was particularly evident in neuropathic pain.
Available as 400 mg tablet Sindrup and Jensen (2000), using different
Recommended starting dose: 1200–1600 mg statistical methodology, compared the drugs
daily used for pain in polyneuropathy and
Maximum dose: 2400 mg daily concluded that TCAs remain the drugs of first
choice. Kanazi et al (2000) found TCAs to be
as effective as the other existing treatments of
Antidepressants
postherpetic neuralgia. Fishbain (2000) found
The antidepressants, particularly the tricyclic TCAs were effective in some specific pain
antidepressants (TCAs), have an important syndromes, including chronic low back pain,
Pharmacotherapy 145
osteoarthritis, rheumatoid arthritis, dependent, and doses of 150 mg amitriptyline

fibromyalgia and ulcer healing. O’Malley et al (Max et al, 1987) and beyond have been used
(1999) and Arnold et al (2000) also found with good effect.
TCAs to be valuable in the treatment of As was mentioned above, the sedative
fibromyalgia. effect of tertiary amine TCAs (amitriptyline,
The drugs that increase both imipramine) may be beneficial when there are
norepinephrine and serotonin in the synaptic sleep problems. Where daytime sedation
cleft are effective in pain. The SSRIs have remains a problem, the secondary amines
much less analgesic effect (O’Malley et al, should be offered (nortriptyline, desipramine).
1999; Arnold et al, 2000; Fishbain, 2000). Very slow TCA metabolism leading to
Venlafaxine is a novel serotonin and excessive side-effects results from the absence
norepinephrine reuptake inhibitor that, while of certain liver enzymes in about 5% of
safer in overdose, is similar in action to the people.
TCAs at high dose. It has not yet been studied Plasma levels of TCAs may be determined.
as an analgesic, but it may have a place in This may be useful where non-compliance or
migraine and tension headache prophylaxis very rapid or slow metabolism are suspected.
(Adelman et al, 2000). Levels may also serve as legal protection if
The monoamine oxidase inhibitors high doses are employed.
(MAOIs) may have some analgesic effects, but
they have not been studied and are little used
Adverse effects
in the field. There is a potentially dangerous
interaction of MAOIs and pethidine. The The adverse effects of sedation, constipation,
reversible MAOI, moclobemide, was found to orthostatic hypotension, dry mouth, blurred
ease pain in fibromyalgia, but overall, it was vision, urinary retention and sexual
not helpful, as sleep was not improved dysfunction have been discussed above. The
(Hannonen et al, 1998). TCAs are relatively contraindicated for
The analgesic effects of the TCAs usually patients with significant cardiac arrhythmia,
commence at lower doses than are commonly prostatic hypertrophy or narrow angle
employed for the treatment of depression. glaucoma due to anticholinergic actions. They
These effects usually occur in less than a week, may cause fatal cardiac conduction problems
and where pain and depression coexist, the in overdose.
pain responds first. TCAs can be commenced
at low doses of 25 mg nocte and increased over
several weeks. Analgesic effects are dose-
Selection of antidepressants is the least sedating TCA, and in some

patients may even have a stimulating effect.
A large range of antidepressant products are
available. A selection is presented, using
* Manufacturer recommendations. In clinical
manufacturer recommendations: for complete
practice these doses have been exceeded using
details, a pharmacology text should be
serum concentration guidelines.
consulted. Clinical practice may vary from
these guidelines.
SSRIs
Fluoxetine
TCAs
Administered in the morning, increasing to
Amitriptyline twice daily if necessary
Administered as a single dose at night or Available as 20 mg capsules
divided doses through the day Recommended starting dose: 20 mg
Available as 10, 25 and 50 mg tablets Maximum dose: 80 mg daily
Recommended starting dose: 25 mg
Maximum dose: 300 mg daily Other SSRI preparations are commonly used
in the treatment of depression (fluvoxamine,
Nortriptyline sertraline, paroxetine, citalopram). Evidence
Administered as a single dose at night or suggests they are equally effective in
divided doses through the day depression, but are poor analgesics.
Available as 10 and 25 mg tablets
Recommended stating dose 25 mg
Maximum dose: 100 mg daily*
Anticonvulsants
Nortriptyline is a metabolite, and less sedating The anticonvulsants are a group of unrelated
than amitriptyline. drugs with generally similar, but different,
actions, adverse effects and clinical
Desipramine applications. Members have a role in the
Administered in divided doses through the management of neuropathic pain and
day headache prophylaxis (see the chapter on
Available as 25 mg tablets headache).
Recommended stating dose: 25 mg mane Neuropathic pain may have many
Maximum dose: 200 mg* pathophysiologic features. One may be
Desipramine is a metabolite of imipramine. It ectopic firing of damaged peripheral neurones
Pharmacotherapy 147
secondary to instability of sodium channels. Other reviews focusing on gabapentin

Another is purported to be central sensitivity to (Laird and Gidal, 2000; Ross, 2000;
nociception mediated by activation of Tremont-Lukats et al, 2000) have concluded
N-methyl-D-aspartate (NMDA) receptors. that this drug has an analgesic effect in
These receptors are activated by inflow of neuropathic pain, and is better tolerated than
calcium ions into the post-synaptic dorsal horn the older antidepressants. Laird and Gidal
cells. The usefulness of the anticonvulsants in (2000) and Termont-Lukats et al (2000)
neuropathic pain may arise from ability to found that gabapentin should be the drug of
influence these or other processes, including first choice in the treatment of neuropathic
modulation of gamma-aminobutyric acid pain. Laird and Gidal (2000) added that the
(GABA). expense of this drug was a disincentive to use.
Carbamazepine blocks both sodium and Caraceni et al (2000) point out that future
calcium channels. Valproate blocks sodium studies may show the anticonvulsants to be as
channels and increases GABA levels. Gabapentin non-specific as the TCAs. They point out that
blocks both sodium and calcium channels and patients may have markedly different
increases GABA levels. Our knowledge is responses to drugs, and hence sequential trials
preliminary, however, and these may not be the of the anticonvulsants are justified.
important pharmacological effects.
Carbamazepine (Blom, 1962) and
valproate (Raftery, 1979) have been used in
Adverse effects
the treatment of neuropathic pain for decades.
Gabapentin has been shown effective in As the anticonvulsants are chemically
postherpetic neuralgia (Rowbotham et al, unrelated they have different constellations of
1998) and painful diabetic neuropathy adverse effects. They all have effects on neural
(Backonja et al, 1998). tissue, and therefore can be expected to cause
A review (Wiffen et al, 2000) looking at lethargy, somnolence, dizziness, ataxia and
the efficacy and adverse effects of the tremor. This is less severe in gabapentin. They
anticonvulsants, however, concluded that, in can all cause nausea, vomiting and diarrhoea,
chronic pain syndromes other than trigeminal again, less severely with gabapentin.
neuralgia, the anticonvulsants should be Additional non-serious adverse effects
withheld until other interventions have been include fluid retention and rash/itch with
tried. The authors also found that the carbamazepine, weight gain and hair loss with
evidence suggested that gabapentin is not valproate and non-pitting oedema with
superior to carbamazepine. gabapentin. (The hair loss associated with
valproate is eminently treatable with zinc tropiramate, have yet to be evaluated as

supplementation.) analgesics. Clinical practice may vary from
Rare life-threatening idiosyncratic these guidelines.
reactions are similar for carbamazepine and
valproate, and include agranulocytosis, Carbamazepine
Stevens–Johnson syndrome, aplastic anaemia, Administered 3 to 4 times daily for
thrombocytopenia, hepatic failure, dermatitis, conventional tablets and liquid; twice daily for
serum sickness and pancreatitis. Gabapentin the controlled-release tablets; swallow during
does not have severe adverse effects. or after meals with fluid.
Available as 100 and 200 mg conventional
tablets; liquid 100 mg/5 ml; 200 and 400 mg
controlled-release tablets
Drugs should be started at low levels and Starting dose (trigeminal neuralgia):
gradually increased to reduce the occurrence 200–400 mg daily
of adverse effects. The serum levels used in Maximal dose: 1200 mg daily
epilepsy do not apply in pain management
(Irving and Wallace, 1997) and the dose is Valproate
determined by balancing therapeutic response Administered twice daily
and adverse effects. Serum levels may provide Available as 100, 200, 500 mg tablets and
legal protection for the clinician when high syrup and sugar-free liquid 200 mg/5 ml
doses are used. Starting dose: 600 mg daily
Liver function tests (LFTs) and full blood Maximum dose: 2500 mg daily
count (FBC) are taken at baseline. Except for
gabapentin (which is not metabolized in the Gabapentin
liver) these are repeated monthly for three Administered three times daily
months, and then three- to six-monthly. Available as 300 and 400 mg capsules
Starting dose 300 mg on day 1, 600 mg on
day 2, 900 mg on day 3. To minimize adverse
Examples of anticonvulsants effects, the day 1 dose should be given at
A large range of anticonvulsants is available. A bedtime.
selection is presented, using manufacturer Maximum dose: 2400 mg daily (reports in the
recommendations: for complete details, a literature to 3600 mg daily).
pharmacology text should be consulted. The
newer anticonvulsants, lamotrigine and
Pharmacotherapy 149
Local anaesthetic/ lignocaine. It is available as an oral

antiarrhythmic agents (sodium preparation and has been used in the
channel blockers) treatment of painful neuropathy. Reviews
found little support for mexiletine in the
These drugs have been classified both as local treatment of chronic pain (Kalso et al, 1998)
anaesthetics and as antiarrhythmic agents, these and painful diabetic neuropathy (Jarvis and
labels perhaps reflecting the backgrounds of Coukell, 1998), but concluded that the drug
different authors. While they have other may have a place when other treatments have
actions, the most important action appears to failed. More recently, no benefit was
be sodium channel blockade. This is an action determined in the treatment of HIV-related
they share with the anticonvulsants. painful peripheral neuropathy (Kemper et al,
These agents are applied systemically 1998) or neuropathic pain with prominent
(intravenously or orally). A sodium channel allodynia (Wallace et al, 2000). This evidence
blocker suppresses abnormal activity in indicates that mexiletine is, at best, a second-
damaged neurones, without blocking normal line drug in the treatment of neuropathic
nerve conduction. Thus they have been used pain.
in neuropathic pain. However, central effects
have also been postulated, and intravenous
lignocaine has been found useful for
intractable headache. Patients with significant heart disease should
Intravenous lignocaine has also been found not receive intravenous lignocaine. Those who
effective in various conditions in reviews of could be at risk should obtain a cardiology
the treatment of general neuropathic pain consultation.
(Mao and Chen, 2000; Kalso et al, 1998; A lignocaine infusion is 1–5 mg/kg
Kingery, 1997) and postherpetic neuralgia administered over 20–30 minutes
(Bonezzi and Demartini, 1999). A Japanese (Baranowski et al, 1999). As dose-dependent
report indicated a favourable response in the effects have been reported, treatment should
painful neuropathy of multiple sclerosis commence within the lower level of the range.
(Sakurai and Kanazawa, 1999). The effect of If the low-dose infusion is unsuccessful, a
an infusion may last many months. A trial of higher dose infusion should be considered.
intravenous lignocaine is appropriate for Constant ECG and blood pressure
patients with neuropathic pain who are monitoring is necessary, and resuscitative
otherwise healthy. equipment and drugs, including oxygen,
Mexiletine is structurally related to should be immediately available.
Similarly, mexiletine should be Selection of local

commenced when the risk of cardiac anaesthetic/antiarrhythmic agents
complications has been appropriately
The following is derived from manufacturer
considered. The starting dose should be low,
recommendations and leading research papers.
and increases should be gradual. The serum
For complete details a pharmacology text
levels used in cardiology are not relevant when
should be consulted. Clinical practice may
the drug is used for pain relief.
vary from these guidelines.
Adverse effects Lignocaine

Administered by elective intravenous infusion
The adverse effects of lignocaine and
Available as 10 mg/ml, in 10 ml ampoules,
mexiletine are similar, but the emphasis is
and 20 mg/ml, in 5 ml ampoules
different, reflecting the different modes of
Starting dose at the low level of the range
administration. They include lightheadedness,
1–5 mg/kg, over 20–30 minutes.
drowsiness, apprehension, euphoria, tinnitus,
Maximal dose: 5 mg/kg.
blurred vision, nystagmus, gastrointestinal
symptoms, vomiting, twitching tremors,
Mexiletine
disorientation, confusion, dyspnoea, slurred
Administered three times daily
speech, convulsions, unconsciousness,
Available as 50 and 200 mg capsules
respiratory arrest, hypotension, arrhythmia,
Starting dose: 50 mg three times daily,
heart block, bradycardia, cardiac arrest and
increasing by 50 mg daily
allergic skin reactions.
Maximum dose: 10 mg/kg daily, or 900 mg,
Mexiletine causes more gastric discomfort,
whichever is the lower.
vomiting, unpleasant taste and oesophageal
ulceration (if a capsule is lodged in the
oesophagus because inadequate liquid has
Alpha-1 antagonists and alpha-
been swallowed). Transient tachycardia and
2 agonists
palpitations but not serious cardiac
arrhythmias have been reported in pain Sympathetically maintained pain (SMP) is a
studies (Jarvis and Coukell, 1998; Kemper et purported form of neuropathic pain that is
al, 1998; Wallace et al, 2000). sustained by efferent activity in the
sympathetic nervous system. The most severe
type is complex regional pain syndrome
(CRPS), or causalgia. This provides a
Pharmacotherapy 151
theoretical basis for specific use of alpha-1 profiles, and, with their modest efficacy, they
antagonists and alpha-2 agonists. The picture are generally thought to be drugs of second
is not yet clear, however, and some (Caraceni choice.
et al, 2000) consider the alpha-2 agonists to Some evidence suggests clonidine may be
be non-specific analgesics. combined with opioids, when tolerance to
Peripheral nerve terminals support alpha-1 opioids has developed (Bouckoms, 1996).
receptors. Stimulation of these receptors on Clonidine has been used in combination with
damaged nerves by ephedrine from other analgesics administered by intraspinal
sympathetic nerve terminals may be a cause of injection.
pain. Preganglionic nerves have pre-synaptic Doctors with special experience use
alpha-2 receptors. Stimulation of these phentolamine, an alpha-1 and alpha-2
receptors reduces the release of ephedrine into blocker, to determine whether oral treatment
the ganglionic synapse and, thereby, activity is likely to provide relief. Phentolamine,
in the post-ganglionic cell and release of 0.5–1.0 mg/kg, is infused intravenously over
ephedrine on to the peripheral nerve terminal. 30 minutes. Pain relief with this procedure
Thus a chemical sympathectomy can be supports a trial of oral medication. This test is
achieved by alpha-2 agonistic activity on the not universally employed, however, and a trial
preganglionic cell and alpha-1 antagonism of of oral medication will reveal whether it offers
target receptors. benefits.
Both types of drugs have neurological
effects; thus any analgesic effect may be
Adverse effects
mediated partially or wholly by central
actions. The adverse effects of these drugs can be
While the theory is attractive, oral and minimized by starting with low doses and
transdermal alpha-1 antagonists and alpha-2 increasing gradually, and many subside over
agonists have not achieved clinical two to three weeks. Both types of drug may
prominence. The alpha-1 antagonist, cause hypotension, drowsiness, nausea and
phenoxybenzamine, has been used with some vomiting.
success in CRPS (Ghostine et al, 1984; Clonidine may cause sinus bradycardia
Muizelaar et al, 1997). The alpha-2 agonist, and atrioventricular block; phenoxybenzamine
clonidine, administered transdermally has may cause tachycardia.
been useful for a small proportion of patients These drugs are also associated with a wide
with postherpetic neuralgia (Byas-Smith et al, range of less common effects, including nasal
1995). They have significant adverse effects congestion, dry mouth, hair loss, blurred
vision, diarrhoea, constipation, depression, Alpha-2 agonist

psychotic symptoms, pruritus, rash, Clonidine
impotence, fever and diaphoresis (this is not Administered twice daily
an exhaustive list). Available as 100 and 150 microgram tablets
In two studies of phenoxybenzamine for Starting dose: 50 micrograms twice daily.
CRPS (Ghostine et al, 1984; Muizelaar et al, Increase by 50 micrograms, every other day
1997), with a total of 99 patients, the adverse Maximum dose: 600 micrograms
effects were considered to be minimal and
transient.
NMDA receptor antagonists
Recent advances in our knowledge of the
Examples of alpha-1 antagonists N-methyl-D-aspartate (NMDA) and related
and alpha-2 agonists
receptors appear to set the stage for important
A small range of oral alpha-1 antagonists is developments in the management of chronic
available; only one is presented. For complete pain. We await the ready availability of proven
details a pharmacology text should be non-toxic, potent NMDA receptor blockers.
consulted. Clinical practice may vary from Dorsal horn cells, which process nociceptive
these guidelines. input, display, along with a range of others, mu
opioid and NMDA receptors. Part of the basis
Alpha-1 antagonist of the centrally mediated hyperalgesia that
Phenoxybenzamine occurs in chronic pain states is the sensitization
Administered twice daily of NMDA receptors, as a consequence of
Available 10 mg capsules continuous input from the periphery. The mu
Starting dose: 10 mg twice daily. Increase by opioid and NMDA receptors share certain
10 mg every other day intracellular processes such that the NMDA
Maximum dose: 60 mg daily receptor may also become progressively
sensitized as a result of progressive opioid
Phentolamine administration. Theory suggests that NMDA
Administered as a test of responsiveness of receptor blockers will have analgesic properties,
pain to alpha antagonism that hyperalgesia and opioid tolerance will
Available 10 mg/1 ml. occur together, and that NMDA blockade will
prevent/reverse opioid tolerance. There are
consistent experimental findings (Mao et al,
1995; Price et al, 2000).
Pharmacotherapy 153
As was pointed out above, some of the group of drugs; therefore they have different
analgesic effects of the anticonvulsants may constellations of adverse effects. Mention has
derive from NMDA blockade. A collection of been made of the adverse effects of the
other blockers is being researched as analgesics anticonvulsants.
(ketamine, dextromethorphan, amantadine), Ketamine has a wide range of adverse
but none have become routine treatment. effects. Heart rate and blood pressure have
The effects of oral ketamine on chronic been both raised and lowered. Arrhythmia has
neuropathic pain were retrospectively occurred. Respiration is frequently stimulated;
examined in 21 patients (Enarson et al, 1999). however, respiratory depression, laryngospasm
Only three obtained substantial benefits. and obstruction may occur. Diplopia and
Better results may be possible using the nystagmus have been noted. Hallucinations
intravenous route (Galer et al, 1993). A review and delirium occur. (These have been thought
(Weinbroun et al, 2000) of the clinical to occur only at anaesthetic doses. However,
benefits of dextromethorphan in chronic pain Mercadante et al (2000) report them at sub-
found unsatisfactory pain relief. The authors anaesthetic doses.) Tonic and clonic
also examined the evidence for movements, anorexia, nausea, vomiting and
dextromethorphan in acute pain, and found morbiliform rash have been reported.
an attenuation of pain, with tolerable adverse
effects. Intravenous amantadine has been
Selection of NMDA blocking drugs
shown to be effective in surgical neuropathic
pain (Pud et al, 1998), but not in sciatica Ketamine is the only NMDA blocking drug
(Medrik-Goldberg et al, 1999). (apart from the anticonvulsants) that is
Exciting evidence suggests that ketamine commercially available in a form that might
(Mercadante et al, 2000) and dextromethorphan be useful in chronic pain management.
(Price et al, 2000) increase the analgesic effects of Dextromethorphan is available as an
morphine. These studies suggest a capacity to antitussive syrup and amantadine is available
reduce tolerance to morphine that is considered as a capsule (and is used as an antiviral and
probable. Such a capacity would have wide antiparkinsonian agent).
application within pain management and
potentially in addiction medicine. Ketamine
Available as ampoules and vials, 200 mg
(base)/2 ml
Adverse effects
Oral administration: Enarson et al (1999)
The NMDA receptor blockers are a disparate started at 100 mg daily in divided doses and
increased by 40 mg daily till relief or till Monoamine receptor blockers

symptoms became intolerable. The highest (antipsychotics)
dose they used was 500 mg daily.
Intravenous administration: Galer et al (1993) Blockers of combinations of dopamine and
provided 5 mg/kg/hour for 60 to 90 minutes. serotonin (along with other) receptors are
used in the management of psychosis. These
medications have a place when there is
GABA-potentiators comorbid psychosis or delirium.
(benzodiazepine receptor Prochlorperazine has a place in the treatment
agonists/anxiolytics) of nausea. There is little evidence to support
Gamma-amino-butyric acid (GABA) is an claims that these drugs have useful analgesic
abundant neurotransmitter. GABA A receptors effects (Patt et al, 1994).
are the gatekeepers of chloride channels.
Stimulation of the receptor opens the channel Histamine receptor blockers
and inhibits the neurone. There is a specific (antihistamines)
benzodiazepine receptor on the GABA A
receptor. When the benzodiazepine receptor is Histamine receptors are found throughout the
occupied, GABA has a greater effect, causing nervous system. The mechanism by which
wider opening of the chloride channel and analgesia may be achieved remains theoretical
greater neuronal inhibition than when the (Galeotti et al, 1999). There is some evidence
benzodiazepine receptor is unoccupied. that diphenhydramine, hydroxyzine,
Clonazepam may be grouped with the orphenadrine and pyrilamine have analgesic
anticonvulsants, as this is a clinical role, but its effects (Rumore and Schlichting, 1986). The
action is distinct and there is some evidence antihistamines have been used in
for use in neuropathic pain (Reddy and Patt, combination, in the hope of augmenting
1994; Bartusch et al, 1996). known analgesics.
Tolerance and withdrawal may develop Sedation is a complication of most of these
with the benzodiazepines, which can further drugs, and, as there is no strong evidence of
complicate the management of difficult cases. analgesic benefit, they are better considered a
These drugs have a place in the management last choice strategy.
of anxiety and, to some extent, muscle spasm.
With the possible exception of clonazepam in
neuropathic pain, these drugs do not have a
place as analgesics.
Pharmacotherapy 155
Sympathomimetic agents Baranowski A, De Courcey J, Bonello E. A trial of

intravenous lidocaine on the pain and allodynia
(stimulants) of postherpetic neuralgia. Journal of Pain and
Symptom Management 1999; 17: 429–33.
Dextroamphetamine, methylphenidate and
Bartusch S, Sanders B, D’Alessio J, Jernigan J.
caffeine, along with other actions, stimulate
Clonazepam for the treatment of lancinating
adrenoreceptors. There is some evidence that phantom limb pain. Clinical Journal of Pain
these agents possess intrinsic analgesic 1996; 12: 59–62.
properties; but this is minor and does not Bennett R. Emerging concepts in the neurobiology
justify use. There is also evidence that the of chronic pain: evidence of abnormal sensory
processing in fibromyalgia. Mayo Clinic
amphetamines can enhance opioids (Dalal Proceedings 1999; 74: 385–98.
and Melzack, 1998). Caffeine has been used
Blom S. Trigeminal neuralgia: its treatment with a
to potentiate the effects of ibuprofen in new anticonvulsant drug (G32883). Lancet
tension-type headache (Diamond et al, 2000). 1962; 1: 839–40.
The main place of the stimulants in pain Bonezzi C, Demartini L. Treatment options in
medicine is in the management of opioid- postherpetic neuralgia. Acta Neurologica
Scandinavica Suppl 1999; 173: 25–35.
induced fatigue and insomnia (Corey et al,
1999). This is an infrequent use in chronic Bouckoms A. Chronic pain:
neuropsychopharmacology and adjunctive
non-cancer pain. Owing to their adverse psychiatric treatment. In: Rundell J, Wise M
effects, addiction and psychosis, these drugs (eds) Textbook of Consultation-Liaison Psychiatry.
are best avoided whenever possible. American Psychiatric Press, Washington, DC,
1996; 1007–36.
Bouckoms A, Masand P, Murray G, et al. Non-
References malignant pain treated with long term oral
Adelman L, Adelman J, Von Seggern R, Mannix L. narcotics. Annals of Clinical Psychiatry 1992; 4:
Venlafaxine extended release (XR) for the 185–92.
prophylaxis of migraine and tension-type Brescia J, Portenoy R, Ryan M, et al. Pain, opioid
headache: A retrospective study in a clinical use and survival in hospitalized patients with
setting. Headache 2000; 40: 572–80. advanced cancer. Journal of Clinical Oncology
Arnold L, Keck P, Welge J. Antidepressant 1992; 10: 149–55.
treatment of fibromyalgia. A meta-analysis and Brose W, Spiegel D. Neuropsychiatric aspects of
review. Psychosomatics 2000; 41: 104–13. pain management. In: Yudofsky S and Hales R
(eds) The American Psychiatric Textbook of
Backonja M, Beydoun A, Edwards K, et al.
Neuropsychiatry, 2nd edn. American Psychiatric
Gabapentin for the symptomatic treatment of
Press, Washington, DC, 1992; 245–75.
painful neuropathy in patients with diabetes
mellitus: a randomized controlled trial. Journal Byas-Smith M, Max M, Muir H, Kingman A.
of the American Medical Association 1998; 280: Transdermal clonidine compared to placebo in
1831–6. painful diabetic neuropathy using a two-staged
‘enriched enrollment’ design. Pain 1995; 60: Grebb J. General principles of psychopharmacology.
67–74. In: Kaplan H, Sadock B (eds) Comprehensive
Textbook of Psychiatry, 6th edn. Williams &
Caraceni A, Cheville A, Portenoy R. Pain
Wilkins, Baltimore, MD, 1995; 1895–909.
management: pharmacological and
nonpharmacological treatments. In: Massie MJ Hannonen P, Milminiemi K, Yli-Kerttula U,
(ed) Pain: What Psychiatrists Need to Know Isomeri R, Roponen P. A randomized, double-
(Review of Psychiatry Series, Vol. 19, No 2; blind, placebo-controlled study of moclobemide
Oldham J and Riba M, series eds). American and amitriptyline in the treatment of
Psychiatric Press, Washington, DC, 2000; 23–88. fibromyalgia in females without psychiatric
disorder. British Journal of Rheumatology 1998;
Corey P, Heck A, Weathermon R. Amphetamine to
1279–86.
counteract opioid-induced sedation. Annals of
Pharmacotherapy 1999; 33: 1362–6. Harati Y, Gooch C, Swenson M, Edelman S,
Greene D, Raskin P, Donofrio P, Cornblath D,
Dalal S, Melzack R. Potentiation of opioid analgesia Sachdeo R, Siu C, Kamin M. Double-blind
by psychostimulant drugs: a review. Journal of randomized trial of tramadol for the treatment
Pain and Symptom Management 1998; 16: of the pain of diabetic neuropathy. Neurology
245–53. 1998; 50: 1842–6.
Dellemijn P. Are opioids effective in relieving Insel P. Analgesic-antipyretics and antiinflammatory
neuropathic pain? Pain 1999; 80: 453–62. agents; drugs employed in the treatment of
Diamond S, Balm T, Freitag F. Ibuprofen plus rheumatoid arthritis and gout. In: Gilman A,
caffeine in the treatment of tension-type Rall T, Nies A, Taylor P (eds) The
headache. Clinics in Pharmacological Therapy Pharmacological Basis of Therapeutics, 8th edn.
2000; 68: 312–19. Pergamon Press, New York, 1990; 638–81.
Enarson M, Hays H, Woodroffe M. Clinical Irving G, Wallace M. Pain Management for the
experience with oral ketamine. Journal of Pain Practicing Physician. Churchill Livingstone,
and Symptom Management 1999; 17: 384–6. Philadelphia, 1997.
Fishbain D. Evidence-based data on pain relief with Jaffe J. Drug addiction and drug abuse. In: Gilman
antidepressants. Annals of Medicine 2000; 32: A, Rall T, Nies A, Taylor P (eds) The
305–16. Pharmacological Basis of Therapeutics, 8th edn.
Pergamon Press, New York, 1990; 522–30.
Galer B, Miller K, Rowbotham M. Response to
intravenous lidocaine infusion differs based on Jarvis B, Coukell A. Mexiletine. A review of its
clinical diagnosis and site of nervous system therapeutic use in painful diabetic neuropathy.
injury. Neurology 1993; 43: 1233–5. Drugs 1998; 56: 691–707.
Kalso E, Tramer M, McQuay H, Moore R.
Galeotti N, Ghelardini C, Bartolini A. The role of
Systematic local-anaesthetic-type drugs in
potassium channels in antihistamine analgesia.
chronic pain: a systematic review. European
Neuropharmacology 1999; 38: 1893–901.
Journal of Pain 1998; 2: 3–14.
Ghostine S, Comair Y, Turner D, Kassell N, Azar
Kanazi G, Johnson R, Dworkin R. Treatment of
C. Phenoxybenzamine in the treatment of
postherpetic neuralgia. Drugs 2000; 59: 1113–26.
causalgia. Report of 40 cases. Journal of
Neurosurgery 1984; 60: 1263–8. Kemper C, Kent G, Burton S, Deresinski S.
Pharmacotherapy 157
Mexiletine for HIV-infected patients with randomized, controlled, double-blind,

painful peripheral neuropathy: a double-blind, crossover, double-dose study. Journal of Pain
placebo-controlled, crossover treatment trial. and Symptom Management 2000; 20: 246–52.
Journal of Acquired Immune Deficiency Syndrome
Muizelaar J, Kleyer M, Hertogs I, DeLange D.
and Human Retrovirology 1998; 19: 367–72.
Complex regional pain syndrome (reflex
Kingery W. A critical review of controlled clinical sympathetic dystrophy and causalgia):
trials for peripheral neuropathic pain and management with the calcium channel blocker
complex regional pain syndrome. Pain 1997; nifedipine and/or the alpha-sympathetic blocker
73: 123–39. phenoxybenzamine in 59 patients. Clinical
Neurology and Neurosurgery 1997; 99: 26–30.
Labbate L, Pollack M. Treatment of fluoxetine-
induced sexual dysfunction with bupropion: a O’Malley P, Jackson J, Santoro J, Tomkins G,
case report. Annals of Clinical Psychiatry 1994; Balden E, Krownke K. Antidepressant therapy
6: 13–15. for unexplained symptoms and symptom
syndromes. Journal of Family Practice 1999; 48:
Laird M, Gidal B. Use of gabapentin in the
980–90.
treatment of neuropathic pain. Annals
Pharmacotherapy 2000; 34: 802–7. Patt R, Proper G, Reddy S. The neuroleptics as
adjuvant analgesics. Journal of Pain and
Mao J, Chen L. Systemic lidocaine for neuropathic
Symptom Management 1994; 9: 446–53.
pain relief. Pain 2000; 87: 7–17.
Pud D, Eisenberg E, Spitzer A, Adler R, Fried G,
Mao J, Price D, Mayer D. Mechanisms of
Yarnitsky D. The NMDA receptor antagonist
hyperalgesia and morphine tolerance: a current
reduces surgical neuropathic pain in cancer
view of their possible interactions. Pain 1995;
patients: a double blind, randomized, placebo
62: 259–74.
controlled trial. Pain 1998; 75: 349–54.
Max M, Culnane M, Schafer S, Gracely R, Walther
Price D, Mayer D, Mao J. NMDA-receptor and
D, Smoller B, Dubner R. Amitriptyline relieves
opioid receptor interactions as related to
diabetic neuropathy pain in patients with
analgesia and tolerance. Journal of Pain and
normal or depressed mood. Neurology 1987; 37:
Symptom Management 2000; 19: S7–11.
589–96.
Raftery H. The management of post herpetic pain
McQuay H, Moore A. An Evidence-Based Resource
using sodium valproate and amitriptyline. Irish
for Pain Relief. Oxford, Oxford University Press,
Medical Journal 1979; 72: 399–401.
1998.
Reddy S, Patt R. The benzodiazepines as adjuvant
Medrik-Goldberg T, Lifschitz D, Pud D, Adler R,
analgesics. Journal of Pain and Symptom
Eisenberg E. Intravenous lidocaine, amantadine,
Management 1994; 9: 510–14.
and placebo in the treatment of sciatica: a
double-blind, randomized, controlled study. Ross E. The evolving role of antiepileptic drugs
Regional Anesthesia and Pain Medicine 1999; 24: in treating neuropathic pain. Neurology 2000;
534–40. 55(5 Suppl 1): S41–6, discussion S54–8.
Mercadante S, Arcuri E, Tirelli W, Casuccio A. Rowbotham M, Harden N, Stacey B, Bernstein P,
Analgesic effects of intravenous ketamine in Magnus-Miller L. Gabapentin for the treatment
cancer patients or on morphine therapy. A of postherpetic neuralgia: a randomized
controlled trial. Journal of the American Medical Tremont-Lukats I, Megeff C, Backonja M.

Association 1998; 280: 1837–43. Anticonvulsants for neuropathic pain
syndromes: mechanisms of action and place in
Rumore M, Schlichting D. Clinical efficacy of
therapy. Drugs 2000; 60: 1029–52.
antihistaminics as analgesics. Pain 1986; 25:
7–22. Wallace M, Magnuson S, Ridgeway B. Efficacy of
oral mexiletine for neuropathic pain with
Sakurai M, Kanazawa I. Positive symptoms in
allodynia: a double-blind, placebo-controlled
multiple sclerosis: their treatment with sodium
crossover study. Regional Anesthesia and Pain
channel blockers, lidocaine and mexiletine.
Medicine 2000; 25: 459–67.
Journal of Neurological Sciences 1999; 162:
162–8. Ward S, Goldberg N, Miller-McCauley V. Pain-
related barriers to management of cancer pain.
Schnitzer T, Gray W, Paster R, Kamin M. Efficacy
Pain 1993; 52: 319–24.
of tramadol in treatment of chronic low back
pain. Journal of Rheumatology 2000; 27: 772–8. Watson C, Babul N. Efficiency of oxycodone in
neuropathic pain: a randomized trial in
Sindrup S, Jensen T. Pharmacologic treatment of
postherpetic neuralgia. Neurology 1998; 50:
pain in polyneuropathy. Neurology 2000; 55:
1833–41.
915–20.
Weinbroun A, Rudick V, Paret G, Ben-Abraham R.
Sindrup S, Andersen G, Madsen C, Smith T,
The role of dextromethorphan in pain control.
Brosen K, Jensen T. Tramadol relieves pain and
Canadian Journal of Anaesthesia 2000; 47:
allodynia in polyneuropathy: a randomised,
585–96.
double-blind, controlled trial. Pain 1999; 83:
85–90. Wiffen P, Collins S, McQuay H, Carroll D, Jadad
A, Moore A. Anticonvulsant drugs for acute and
Taylor P. Cholinergic agonists. In: Gilman A, Rall
chronic pain. Cochrane Database System Review
T, Nies A, Taylor P (eds) The Pharmacological
2000; 3: CD001133.
Basis of Therapeutics, 8th edn. Pergamon Press,
New York, 1990; 122–30.
670_Chronic Pain.index 19/02/2002 9 37 am Page 159
Index
A-beta fibres 10, 11 alpha 1-adrenergic receptor antagonists 132,

in neuropathic pain 20, 21 150–2
abnormal illness behaviour (AIB) 33, 52–3, alpha-2 agonists 150–2
55 alpha-adrenoceptors 21
activity amantadine 153
in back pain 123, 125 amitriptyline 146
graded 61, 125 adverse effects 130, 133
pacing 7, 125 in chronic back pain 126
pain related to 6–7 in fibromyalgia 99
promoting normal/near-normal 7, 23–4, in headache 111–12, 114, 117
56–7 amphetamines 155
acupuncture 98, 125 amputation 22
acute pain 1–2, 17, 18 analgesics
addiction 137–8 abuse/excessive use 113
A-delta fibres 10 in back pain 124
adrenaline 21 in fibromyalgia 99
adrenocorticotropic hormone (ACTH) 94 in headache 108–9, 114, 117
adverse drug effects 129–35 in somatization 56
akathisia 108–9, 110 see also non-steroidal anti-inflammatory
alcohol, cluster headache and 114, 115 drugs; opioids; pharmacotherapy;
alexithymia 32, 50, 85 specific drugs
allodynia 18–19, 21 Anamorph 141
160 Index
anatomy of pain 9–15 aura 106, 107

ankylosing spondylitis 123 autohypnosis see self-hypnosis
anterolateral funiculus 11 autonomic nervous system 30, 31
anthropology, medical 52, 55 in fibromyalgia 94, 96
antiarrhythmic agents 149–50 see also sympathetic nervous system
anticholinergic drugs autosuggestion 70
for adverse drug effects 108–9, 110, 131
adverse effects of 131–2, 133–4 back pain, low 119–27
anticonvulsants 146–8, 153 acute 119, 120
adverse effects 130, 147–8 management 123–4
in chronic back pain 126 chronic 119, 120
management principles 148 depression 44–5, 125–6
migraine prophylaxis 111 management 124–7, 144–5
in neuropathic pain 23 pathophysiology 22, 120–1
antidepressants 144–6 clinical course 121
adverse effects 133 diagnostic process 121–2
in chronic back pain 126 differential diagnosis 120–1
in fibromyalgia 99 ‘red flags’ 120, 121–2
see also selective serotonin reuptake special investigations 122–3
inhibitors; tricyclic antidepressants basal ganglia 22
antiemetics 108–10, 131 bed rest, in acute back pain 123
antihistamines 135, 154 behaviourism 7
antipsychotic drugs 154 benzodiazepine receptor agonists 154
anxiety 23, 44, 45 benzodiazepines 154
in chronic back pain 125, 126 benztropine 108–9
cognitive therapy 86–7 beta-blockers 110–11
fibromyalgia and 92 bethanechol 132, 133, 134
relaxation therapy 71–4 biofeedback 114
tension headache and 113 biomedical model 27–8
anxiolytics 114, 154 biopsychosocial model 3, 6, 27, 29–34
ascending sensory pathways 11–14 biological/medical component 29
Asians 33 diagnostic systems and 37–41
aspirin 108 psychological/psychiatric
attachment style, abnormal 92 component 29–33
attention, methods of focusing 67–8 social/environmental/cultural
attribution theory 52, 55 component 33–4
audiotapes, relaxation 70 somatization and 54
Index 161
bradykinin 10 headache 106

brain-stem pain 2, 17, 18
in neuropathic pain 22 Classification of Chronic Pain (IASP
relays 14 1994) 37–9
breakthrough pain 139 clenched fist technique, Stein 69
breathing, relaxed 73–4 clinical pain 17, 18
brief psychotherapy 84 clomipramine 99
bupropion 134 clonazepam 154
clonidine 151–2
caffeine 155 codeine 107, 130, 141
carbamazepine 23, 147, 148 cognition
adverse effects 130, 148 fear and 60–1
in chronic back pain 126 somatization and 50, 54–5
catastrophizing 92 cognitive behaviour therapy (CBT) 8,
catecholamines 10, 20–1 86–7
see also noradrenaline in fibromyalgia 98
catharsis 84 for pain-related fear 61
cauda equina syndrome 121–2 cognitive distortions 86
causalgia 150–1 cognitive restructuring 87
celecoxib 126, 135, 143 cognitive therapy (CT) 23, 86–7, 88
central (CNS) sensitization see sensitization, communication, patient 6, 69
central complex regional pain syndrome (CRPS) 22,
cerebral blood flow, regional 95, 107 150–1, 152
cerebral cortex 12, 14–15 compliance 77–8
cervical pathology, headache from 116–17 computed tomography (CT), in back
C fibres 10, 20, 21 pain 122
Chinese 33–4 constipation, drug-induced 131–2, 136
chlorpromazine 109–10 coping skills 87
cholecystokinin 22 corticosteroids, in fibromyalgia 100
chronic fatigue syndrome (CFS) 93, 94 corticotropin-releasing hormone (CRH) 96,
chronic pain 2 97
defined 2 cortisol 30, 94
predisposition to 19–20, 29 cranial neuralgias 106
reduction see management, chronic pain craniocervical dystonia 116, 117
types 17, 18 crisis intervention therapy 84
cimetidine 135 ‘crooked thinking’ 86
classification cultural factors 3, 33–4
162 Index
cyclooxygenase (COX) 134, 142 distraction 75

inhibitors see non-steroidal anti- distress, mental 31
inflammatory drugs disuse syndrome 60
cyclooxygenase (COX)-2 inhibitors 126, 135, dopamine blockade 109–10
142, 143 dorsal column 14, 15
cyproheptadine 134 stimulation 23
cytokines 30–1 dorsal horn
ascending pathways 11–14
delta opioid receptors 135 descending influences 12, 13, 15
delusions, pain 39 in neuropathic pain 21
dependence primary afferent terminals 10–11
physical 137 dorsal noradrenergic bundle (DNB) 30
psychological 137–8 dorsal root ganglion (DRG) neurones 20, 21
depression drug therapy see pharmacotherapy
in chronic back pain 44–5, 125–6 dry mouth 133–4
chronic pain as 32 dry needling 100
cognitive therapy 86–7 Durogesic 140
concurrent 20, 23, 44–5 dynamic psychotherapy 84
demanding, hypochondriacal 45 dynorphin 21
fibromyalgia and 9, 92 ‘dysfunctional’ pain 38
pain classification and 39 dystonia
tension headache and 113 acute 108–9, 110
descending pain pathways 15, 22 craniocervical 116, 117
desipramine 133, 146
dextroamphetamine 155 early life experiences, disturbing 19–20, 29
dextromethorphan 153 education, patient 61, 98
diabetic neuropathy, painful 147 ego-strengthening exercises 68–9, 70
Diagnostic and Statistical Manual, 4th edition elderly, adverse drug effects 131
(DSM-IV) 40–1 emotional experience 29–30
diagnostic systems, biopsychosocial pain endocrine abnormalities, in fibromyalgia 94,
and 37–41 96–7
diclofenac 142, 144 Endone 142
diflunisal 144 environmental factors 33–4
diphenhydramine 131, 132, 154 epidural analgesia, chronic 23, 127
disc herniation 121, 122, 124 ergotamines 110
disease 33, 52 ethnic differences 3, 33–4
dissociation 69–70 examination, physical 5, 122
Index 163
exercise 98, 114 genetic factors 92

see also activity group activities/therapy 34
expectations, realistic 6 growth hormone (GH)
levels, in fibromyalgia 94, 95, 97–8
facial pain 106 therapy, in fibromyalgia 100
family involvement 6, 57
fear 45, 59–62 hallucinations, pain 39, 40
avoidance 45, 59 harm avoidance 92
in back pain 125 headache 2, 105–17
clinical implications 61–2 cluster 106, 114–16
cognitive functions and 60–1 diagnostic criteria 115
cognitive therapy 87 management 115–16
of movement see movement, fear of diary 107
of pain 54–5, 59, 60, 123, 125 from cervical pathology 116–17
Fear Avoidance Beliefs Questionnaire migraine 105, 106–12
(FABQ) 61 rebound 113
fentanyl, transdermal 140 secondary 106
fibromyalgia (FM) 2, 91–100 tension 39, 45, 106, 112–14
diagnostic criteria 91–2 chronic 113
overlapping conditions 93 diagnostic criteria 113
pathophysiology 22, 92, 93–5 episodic 113
speculation 95–8 management 113–14
treatment 98–100, 145 health-care utilization 8
fibrositis 91 histamine 10
fight or flight reaction 31 histamine H2 receptor antagonist 135
fluctuations in pain 6–7 histamine receptor blockers
fluoxetine 146 (antihistamines) 135, 154
focal psychotherapy 84 histrionic elaboration 40
forearm pain 32 HIV-related painful peripheral
neuropathy 149
gabapentin 23, 126, 147, 148 5-HT see serotonin
gamma-aminobutyric acid (GABA) 22, 147, 5-HT1D agonists 109
154 hydroxyzine 154
potentiating drugs 154 hyperalgesia 9, 19
gastrointestinal (GI) side effects 134–5, 142 defined 18
gating mechanism 15 pathophysiology 10, 152
gender differences, headache 105 hypnoanalgesia 74
164 Index
hypnosis 15, 63–78 insomnia 23

for anxiety 71–4 in chronic back pain 125, 126
definition/overview 64 see also sleep
developing a unique method 70–1 insulin-induced hypoglycaemia 94
general techniques 65–7 insulin-like growth factor-1 (IGF-1) 94, 95, 97
methods of focusing attention 67–8 interleukin-1 30
non-compliance 77–8 International Association for the Study of
for pain 74–7 Pain (IASP) 29, 37–8
persistence of benefits 64–5 International Classification of Disease, 10th
special techniques 68–70 edition (ICD-10) 39–40
hypochondriasis 49, 51, 54 International Headache Society (IHS) 106
management 56 invasive treatments 3, 55
hypotension, orthostatic 132–3 investigations 5, 55
hypothalamic–pituitary–adrenal (HPA) in back pain 122–3
axis 94, 97 irritability, in back pain 125–6
hypothalamus irritable bowel syndrome (IBS) 92, 93, 96
function 30
pathways 12, 13, 14 Kapanol 140
hysteria 32, 39, 49, 51 kappa opioid receptors 135
conversion 38 ketamine 100, 153–4
see also somatization ketoprofen 143
ibuprofen 99, 114, 144 laminae, dorsal horn 10–11

illness 33, 52 lamotrigine 23, 130
illness behaviour 52 laxatives 132
abnormal (AIB) 33, 52–3, 55 learning
imaging, in back pain 120, 122–3 in pain disorder 51–2
immune system 30–1, 94 socially determined 82
inactivity 7, 60 theory 28
see also activity lignocaine (lidocaine)
inflammation 9–10, 17–18 adverse effects 150
information processing intravenous infusion 110, 149, 150
correcting errors 87 local injections 100
deficits 50, 54, 55, 86 limbic system
pathological 86 function 30
information provision 6, 55, 130, 138 pathways 12, 13, 14
insight 83 limits, setting 55–6
Index 165
lithium (carbonate) 116, 142 met-enkephalin 100

local anaesthetics methadone 141
adverse effects 150 methylphenidate 133, 155
injections/blocks 100, 117 metoclopramide 108, 109, 131
systemic administration 149–50 metoprolol 110–11
locus coeruleus 14, 30 mexiletine 149, 150
migraine 105, 106–12
magnetic resonance imaging (MRI), in back diagnostic criteria 106
pain 122 non-drug therapy 107
malingering 7 opioids 107–8
management, chronic pain pathophysiology 107
approach 5–8 prophylaxis 110–12
invasive techniques 3, 55 treatment of acute episode 108–10
non-invasive techniques 2–3, 5 miosis, opioid-induced 134
physical/medical methods 29 misoprostol 131, 135
relaxation methods 74–7 moclobemide 145
somatization aspects 55–7 monoamine oxidase inhibitors (MAOIs) 145
see also pharmacotherapy; psychotherapy monoamine receptor blockers 154
mantra 67, 71 morphine 127, 153
massage 125 immediate-release 141
mast cells 9–10 sustained-release 140
median forebrain bundle (MFB) 30 motor cortex dysfunction 22, 94
medical anthropology 52, 55 mouth, dry 133–4
medicalization 53–4 movement, fear of 54–5, 59, 60
medication see pharmacotherapy in back pain 123, 125
meditation 8, 63–78 MS Contin 140
for anxiety 71–4 multiple sclerosis, painful neuropathy of 149
developing a unique method 70–1 multisynaptic ascending system 14
general techniques 65–7 mu opioid receptors 135, 152
methods of focusing attention 67–8 muscle
in neuropathic pain 23 changes in fibromyalgia 93
non-compliance 77–8 relaxation 67–8
overview 63–4 tension 31, 113
for pain 74–7
persistence of benefits 64–5 naproxen 144
special techniques 68–70 in fibromyalgia 99
mental distress 31 in headache 109, 112, 115, 116
166 Index
nausea, drug-induced 131 NSAIDs see non-steroidal anti-inflammatory

needling, dry 100 drugs
neospinothalamic tract 11, 12, 14
neostigmine 134 occupational therapy, in back pain 124
neuroadaptation 137 olanzapine 135
neuropathic pain 2, 17–24 omeprazole 112, 135
defined 18 ondansetron 100, 131
mechanisms 19, 20–2, 146–7 operant pain model 7, 28–9, 34
symptoms 18–19 opiate receptors 135–6
treatment 23–4, 144, 149–50, 153 opioids 135–42
neuroplasticity 18, 20–2 addiction 137–8
neurotransmitters adverse effects 131–3, 134, 138
in fibromyalgia 94, 98 in chronic back pain 126–7
in neuropathic pain 20 clonidine with 151
N-methyl-D-aspartate (NMDA) receptor dependence 137
antagonists 100, 152–4 endogenous 21
adverse effects 153 in fibromyalgia 99
choice of agent 153–4 in headache 107–8, 114, 117
N-methyl-D-aspartate (NMDA) long-acting 140
receptors 147, 152 management principles 138–9
nociception 1–2 medium-acting 141
nociceptive pain 2 in neuropathic pain 23
nociceptors 1, 10 short-acting 141–2
sensitization 20 tolerance 136–7
non-compliance 77–8 withdrawal effects 137
non-steroidal anti-inflammatory drugs oral contraceptive pill 114
(NSAIDs) 142–4 orphenadrine 154
adverse effects 134–5, 142 orthostatic hypotension 132–3
in back pain 124, 126 Orudis 143
in fibromyalgia 99 over-the-counter medications 131
in headache 109, 112, 114, 117 oxycodone hydrochloride 140, 142
management principles 142–3 Oxycontin 140
in neuropathic pain 23 oxygen therapy, in cluster headache 115
noradrenaline (norepinephrine) 21, 23, 94,
144 pacing behaviour 7, 125
normal pain 17, 18 Paget’s disease 116
nortriptyline 126, 133, 146 pain
Index 167
classification 2, 17, 18 plasticity, neuropathic pain and 18, 20–2

defined 1, 29 postherpetic neuralgia 23, 144, 147, 149,
Pain Anxiety Symptoms Scale (PASS) 61 151
pain behaviour 7, 28–9, 34 predisposition to chronic pain 19–20, 29
pain disorder 51–2, 54 primary sensory neurones (afferents) 10
diagnostic criteria 40–1 terminals 10–11
management 56 prochlorperazine 108, 131, 154
pain experience 2 progressive muscular relaxation 70
Pain and Impairment Relationship Scale propranolol 110–11
(PAIRS) 61 prostaglandins 10, 134, 142
pain-prone disorder 32, 44 proton pump inhibitors 112, 135
pain-prone personality disorder 39 pruritus, opioid-induced 132
pain threshold, in fibromyalgia 93, 97 psychiatric disorders
palaeospinothalamic tract 11, 12, 14, 15 comorbid 43–6, 56
paracetamol 108, 114, 117 fibromyalgia and 92, 98
patient–therapist relationship 6, 88, 112 low back pain and 124
periaqueductal grey 12, 13, 14, 15 pain arising from 39–40
persistent somatoform pain disorder 39 see also anxiety; depression
personality disorder 44, 45–6 psychoanalysis 82–4, 87
cognitive therapy 87 psychoanalytic psychotherapy 84
pethidine 107–8 psychogenic pain 2, 32
pharmacotherapy 8, 129–55 psychological factors 29–33
adverse effects 129–35 aetiology 31–2
in back pain 125 in diagnostic systems 38, 40–1
for migraine 108–12 treatment 32–3
multiple agent 130–1 psychosocial factors, in back pain 123–4
in somatization 56 psychotherapy 8, 32–3, 81–8
see also specific drugs and classes of drugs in neuropathic pain 23
phenothiazines 109 in tension headache 114
phenoxybenzamine 151, 152 pyrilamine 154
phentolamine 151, 152
Physeptone 141 quetiapine 135
physical activity see activity
physiological pain 17, 18 railway spine 54
physiology of pain 9–15 rational emotive therapy (RET) 86
pilocarpine 134, 135 relaxation 8, 15, 63–78
piroxicam 142, 143 for anxiety 71–4
168 Index
relaxation continued in fibromyalgia 95–6, 97–8

complications 70 peripheral sensory terminals 20
definition/overview 63–4 sensory neurones
developing a unique method 70–1 cross-excitation 20
general techniques 65–7 primary 10–11
methods of focusing attention 67–8 spontaneous ectopic discharge 20
non-compliance 77–8 sympathetic coupling 20–1
for pain 74–7 sensory pathways, ascending 11–14
persistence of benefits 64–5 serotonin 10, 23, 144
special techniques 68–70 in fibromyalgia 94, 95, 97, 98
in tension headache 114 syndrome 117
repetitive strain syndrome 32 sex differences, headache 105
respiratory depression 136 sex hormones, female 113–14
reticular formation 13, 14, 15, 30 sexual dysfunction, drug-induced 134
rewards/reinforcers 7, 28, 34 sick 33
rheumatoid arthritis (RA) 22, 94, 96 role 33, 52–3
cervical pathology 116, 117 sigma opioid receptors 135
pharmacotherapy 145 sildenafil 134
sleep
schizophrenia 40 cluster headache and 114
sciatica 119–27 disorder, fibromyalgia as 94, 95, 97
see also back pain, low pain and 31
scopolamine 131 see also insomnia
secondary gains 51, 54, 85 social disadvantage 20
sedation, drug-induced 133, 136, 145 social factors 33–4
selective serotonin reuptake inhibitors social models, prior 51, 54
(SSRIs) 145, 146 social problems, medicalization 53
adverse effects 133, 134, 135 socioeconomic class 50
in chronic back pain 126 sodium channel blockers 149–50
in fibromyalgia 99 somatization 49–57, 92
in tension headache 114 conceptual underpinning 52–4
self-hypnosis 8, 70, 71 defined 49–50
see also hypnosis disorder 50–1, 56
self-messages, positive 70 management recommendations 55–7
sensitization overlapping conditions 49–52
central (CNS) 21–2 synthesis/summary 54–5
in back pain 120–1 somatoform disorder 54, 93
Index 169
somatoform pain disorder, persistent 39 substantia gelatinosa (lamina II) 10–11, 21

somatosensory cortex suggestion 70
primary (SI) 14 sulindac 143
secondary (SII) 15 sumatriptan 109, 115
spatial reorganization 22 supportive environments 7, 28–9, 32, 34
somatosensory-induced supportive psychotherapy 84–5, 87–8
electroencephalographic potentials 93 supraspinal influences 15, 22
somatostatin 97 surgery, in low back pain 124
spinal cord Survey of Pain Attitudes (SOPA) 61
ascending pathways 11–14 sympathetically maintained pain
decreased inhibition 22 (SMP) 150–1
increased excitability 21–2 sympathetic nervous system
opiate receptors 136 in fibromyalgia 94, 96
reorganization 21 sensory system coupling 20–1
terminals of primary afferents 10–11 see also autonomic nervous system
spinal stenosis 121, 122 sympathomimetic agents 155
spinocervical tract 14
spinomesencephalic tract 14 Tampa Scale for Kinesiophobia (TSK) 61
spinoreticular tract TCAs see tricyclic antidepressants
function 30 temporo-mandibular joint disorder (TMD) 93
pathways 11, 13, 14, 15 tender points
spinothalamic tract dry needling 100
function 30 local anaesthetic injection 100
pathways 11, 12, 14, 15 in tension headache 112–13
spontaneous pain 18, 19 thalamus 12, 13, 14
SSRIs see selective serotonin reuptake inhibitors in neuropathic pain 22
status migranosus 110 therapist–patient relationship 6, 88, 112
Stein clenched fist technique 69 thyroid hormones 94
stimulants 133, 155 tolerance, opioid 136–7
straight-leg raising 122 topiramate 23
stress tramadol 23–4, 141
fibromyalgia and 92 in chronic back pain 126–7
tension headache and 113, 114 in fibromyalgia 99
stress response dysregulation hypothesis, in headache 117
fibromyalgia 96–7 Tramal see tramadol
substance P (SP) 10, 20 transcranial magnetic stimulation (TMS) 22,
in fibromyalgia 94, 96, 97, 98 93–4
170 Index
transference 64, 82–3 migraine prophylaxis 111

trauma, local response 9–10, 17–18 venlafaxine 126, 145
triamcinolone 100 ventral noradrenergic bundle (VNB) 30
tricyclic antidepressants (TCAs) 144–6 verapamil 116
adverse effects 130, 133, 135, 145 vision
in chronic back pain 126, 144–5 blurred 134
in fibromyalgia 99, 145 in migraine aura 107
in headache 111–12, 114, 117 visualization 68, 75
mechanisms of action 19 vomiting
in neuropathic pain 23, 144 drug-induced 131
trigeminal neuralgia 23, 147, 148 in migraine 109–10
trigger points, in tension headache 113
tryptophan 94 weight gain, drug-induced 135
whiplash syndrome/disorder 54, 55, 116
unconscious mind 82–3 wide dynamic range (WDR) neurones 95–6
urinary retention 133 withdrawal effects 137
work-related problems 124
valproate, sodium 23, 147, 148 worry 31–2
in chronic back pain 126

Managing Chronic Pain Biopsychosocial

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Managing Chronic Pain Biopsychosocial

Uploaded by

Copyright:

Available Formats

670_Chronic Pain.

prelims 19/02/2002 9 27 am Page i

Managing Chronic Pain:

Managing Chronic Pain:

© 2002 by Taylor & Francis Group, LLC

No claim to original U.S. Government works

International Standard Book Number-13: 978-1-4822-0752-1 (eBook - PDF)

Visit the Taylor & Francis Web site at

and the CRC Press Web site at

Said a faith-healer from Brazil

1 ‘To help the patient to cope the psychiatrist must be a teacher,

Pain is a common human experience, but difficult to describe.

2 Managing Chronic Pain: A Biopsychosocial Approach

activity. Nociception, through identified hard- symptom (rheumatologists, oncologists)

2 ‘Doctors think a lot of patients are cured who have simply

Woven together, the following points form a useful approach

1. The fundamental Hippocratic principle of ‘first do no

6 Managing Chronic Pain: A Biopsychosocial Approach

3. The health professionals working in relative or friend. Such an individual can

A reasonable approach to chronic pain reduction 7

fluctuations and to continue (rather than pattern of behaviour. It is also an

8 Managing Chronic Pain: A Biopsychosocial Approach

Anatomy and physiology

3 ‘Symptoms, then, are in reality nothing but the cry from

The anatomic and physiologic basis of pain is a highly

Local response to trauma/inflammation

10 Managing Chronic Pain: A Biopsychosocial Approach

releasing histamine from preformed a range of stimuli. They transmit slowly

Anatomy and physiology 11

other laminae. They are important in the Ascending sensory pathways

12 Managing Chronic Pain: A Biopsychosocial Approach

to dorsal horn cells spinothalamic

Anatomy and physiology 13

to dorsal horn cells

14 Managing Chronic Pain: A Biopsychosocial Approach

Other ascending nociceptive pathways are Thalamus

Anatomy and physiology 15

The medial/intralaminar thalamic regulation mechanism that allows us to ignore

16 Managing Chronic Pain: A Biopsychosocial Approach

Treede R, Apkarian A, Bromm B. Cortical Woolf C, Mannion R. Neuropathic pain: aetiology,

Plasticity and neuropathic pain

4 ‘To every human problem there is a neat and easy solution –

Acute pain is a warning signal that serves a necessary survival

18 Managing Chronic Pain: A Biopsychosocial Approach

Nociceptive Neuropathic Psychogenic

Plasticity and neuropathic pain 19

20 Managing Chronic Pain: A Biopsychosocial Approach

predisposition to depression. Depression is directions, and such agents are released by

Plasticity and neuropathic pain 21

22 Managing Chronic Pain: A Biopsychosocial Approach

Plasticity and neuropathic pain 23

Treatment implications an established role in trigeminal neuralgia,

24 Managing Chronic Pain: A Biopsychosocial Approach

Plasticity and neuropathic pain 25

The biopsychosocial model in

5 ‘A biopsychosocial model . . . includes the patient as well as the

Before focusing on the biopsychosocial model, it is worth

28 Managing Chronic Pain: A Biopsychosocial Approach

The biopsychosocial model in chronic pain 29

30 Managing Chronic Pain: A Biopsychosocial Approach

The biopsychosocial model in chronic pain 31

32 Managing Chronic Pain: A Biopsychosocial Approach

The biopsychosocial model in chronic pain 33

34 Managing Chronic Pain: A Biopsychosocial Approach