Chronic Pain

1. PAIN DISORDERS
By Dr Wasim
Under guidance of
Dr sanjay jain
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2. Pain
 “An unpleasant sensory and emotional experience
associated with actual or potential tissue damage or
described in terms of such damage”.
(International Association for the Study of Pain) (Merskey
et al, 1986)
 “The awareness of discomfort resulting from injury, disease
or emotional distress and evidence by biological and
behavioral changes”.
(U.S. Congress of Technology Assessment) (Webster,
1986)
 “A response to maladaptive, repressed, or unresolved
negative emotions”. (Sarno, 1991)
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3. Pain
 Pain is a product of:
 Nociception,
 Perception,
 Suffering,
 Pain behavior.
 Types:
 Somatic (skin, joints, muscles)
 Visceral
 Neuropathic pain (injury to nerves, spinal cord pathways, or
thalamus)
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4. CHRONIC PAIN
• Patients feel chronic pain in one or more areas of the body.
• This pain is caused by psychological stress and/or the over
exaggeration of an injury.
• Pain disorder is part of the category of somatoform disorders.
• Somatoform means that pain and symptoms are caused by
psychological factors.
• This pain can cause more problems such as distress and/or
impairment.
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5. 5
The problem is often difficult to diagnose, and pts may appear
emotionally distraught. Several factors can cause, perpetuate, or
exacerbate chronic pain:
(1) painful disease for which there is no cure (e.g., arthritis,
cancer, migraine headaches, diabetic neuropathy);
(2) neural factors initiated by a bodily disease that persist after the
disease has resolved (e.g., damaged sensory or sympathetic
nerves);
(3) psychological conditions. Pay special attention to the medical
history and to depression. Major depression is common,
treatable, and potentially fatal (suicide).

6. CAUSES
• Common places of pain is in the back, chest, abdomen, and
head.
• The causes of the pain changes according to the area of the
pain.
• There is no explanation for the duration and the severity of the
pain.
• The main cause is psychological stress.
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7. SYMPTOMS
 Negative or distorted cognition
 Disability, inactivity, and/or passivity
 Insomnia and fatigue.
 Disrupted social relationships with friends, family, and/or work.
 Depression and anxiety.
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8. DSM AND PAIN
• I (1952)
– Psychophysiological disorders“
– “Psychoneurotic Disorders”
• II (1968)
– Hysterical neurosis
• III (1980)
– Psychogenic Pain
• “incompatible” or “INXS”
• Etiologically related
• III-R (1987)
– Somatoform pain
– Dropped etiology part
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9. • IV
– Pain Disorder
• Pain=predominant focus
• Substantial distress/impairment
• Psych factors “have role”
– Onset or expression
• Not malingering/factitious disorder
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10. DSM IV – TR
A. Pain in one or more anatomical sites is the predominant focus
of the clinical presentation and is of sufficient severity to
warrant clinical attention.
B. The pain causes clinically significant distress or impairment in
social, occupational, or other important areas of functioning.
C. Psychological factors are judged to have an important role in
the onset, severity, exacerbation, or maintenance of the pain.
D. The symptom or deficit is not intentionally produced or feigned
(as in Factitious Disorder or Malingering).
E. The pain is not better accounted for by a Mood, Anxiety, or
Psychotic Disorder and does not meet criteria for Dyspareunia.
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11. 11
Code as follows
307.80 Pain Disorder Associated With Psychological Factors:
Specify if:
Acute: duration of less than 6 months
Chronic: duration of 6 months or longer
307.89 Pain Disorder Associated With Both Psychological
Factors and a General Medical Condition:
Specify if:
Acute: duration of less than 6 months
Chronic: duration of 6 months or longer

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DSM 5
Somatic Symptom Disorder Diagnostic Criteria
300.82 (F45.1)
A. One or more somatic symptoms that are distressing or result in
significant disruption of daily life.
B. Excessive thoughts, feelings, or behaviors related to the
somatic symptoms or associated health concerns as
manifested by at least one of the following:
1. Disproportionate and persistent thoughts about the
seriousness of one’s symptoms.
2. Persistently high level of anxiety about health or symptoms.
3. Excessive time and energy devoted to these symptoms or
health concerns.
C. Although any one somatic symptom may not be continuously
present, the state of being symptomatic is persistent (typically
more than 6 months).

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Specify if:
With predominant pain (previously pain disorder): This specifier is
for individuals whose somatic symptoms predominantly involve
pain.
Specify if:
Persistent: A persistent course is characterized by severe
symptoms, marked impairment, and long duration (more than 6
months).
Specify current severity:
Mild: Only one of the symptoms specified in Criterion B is fulfilled.
Moderate: Two or more of the symptoms specified in Criterion B
are fulfilled. Severe: Two or more of the symptoms specified in
Criterion B are fulfilled, plus there are multiple somatic complaints
(or one very severe somatic symptom).

14. ICD 10 AND PAIN
• F45.4 Persistent somatoform pain disorder
 The predominant complaint is of persistent, severe, and
distressing pain, which cannot be explained fully by a
physiological process or a physical disorder. Pain occurs in
association with emotional conflict or psychosocial problems
that are sufficient to allow the conclusion that they are the main
causative influences. The result is usually a marked increase in
support and attention, either personal or medical.
 Pain presumed to be of psychogenic origin occurring during the
course of depressive disorder or schizophrenia should not be
included here. Pain due to known or inferred
psychophysiological mechanisms such as muscle tension pain
or migraine, but still believed to have a psychogenic cause,
should be coded by the use of F54 (psychological or
behavioural factors associated with disorders or diseases
classified elsewhere) plus an additional code from elsewhere in
ICD-10 (e.g. migraine, G43.-). 14

15. Includes:
• psychalgia
• psychogenic backache or headache
• somatoform pain disorder
Differential diagnosis. The commonest problem is to
differentiate this disorder from the histrionic elaboration of
organically caused pain. Patients with organic pain for whom a
definite physical diagnosis has not yet been reached may easily
become frightened or resentful, with resulting attention-seeking
behaviour. A variety of aches and pains are common in
somatization disorders but are not so persistent or so dominant
over the other complaints.
Excludes:
• backache NOS (M54.9)
• pain NOS (acute/chronic) (R52.-)
• tension-type headache (G44.2
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16. Chronic Pain
 Chronic Pain:
 Duration ≥ 6 months,
 Poorly localized,
 Resistant to treatment, often referred to a psychiatrist.
 Classification (International association for the study of
pain) -This system is primarily focused on the physical
dimension of pain. There is room in the system for
suggesting a psychological role in pain, specifically in the
second and fifth axes.
 AXIS I Anatomical Regions
 AXIS II Organ Systems
 AXIS III Temporal characteristics
 AXIS IV Intensity,time since onset
 AXIS V Etiology (Merskey & Bogduk, 1994) 16

17. PATHOPHSIOLOGY OF PAIN
• Many theories of the etiology and pathophysiology of pain
involving both biological and psychological factors
BIOLOGICAL THEORY-
• neuropathway descends from the cerebral cortex and medulla,
which inhibits the firing of pain transmission neurons when it is
activated (Cloninger, 1993). This system is apparently mediated
by the endogenous opiate-like compounds, endorphins, and by
serotonin. Indeed, metabolites of both of these
neurotransmitters may be reduced in the cerebrospinal fluid of
chronic pain patients (von Knorring & Attkisson, 1979).
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18. 18
NORMAL PAIN MECHANISM
Pain-producing (nociceptive) sensory stimuli in skin and viscera activate
peripheral nerve endings of primary afferent neurons, which synapse on
second-order neurons in spinal cord or medulla . These second order neurons
form crossed ascending pathways that reach the thalamus and are projected to
the somatosensory cortex.
Parallel ascending neurons connect with brainstem nuclei and ventrocaudal and
medial thalamic nuclei. These parallel pathways project to the limbic system
and underlie the emotional aspect of pain. Pain transmission is regulated at the
dorsal horn level by descending bulbospinal pathways that contain serotonin,
norepinephrine, and several neuropeptides.
Agents that modify pain perception may act by reducing tissue inflammation
(NSAIDs, prostaglandin synthesis inhibitors), interfering with pain transmission
(narcotics), or enhancing descending modulation (narcotics and
antidepressants). Anticonvulsants (gabapentin, carbamazepine) may be
effective for aberrant pain sensations arising from peripheral nerve injury.

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Pain transmission and modulatory pathways.
A. Transmission system for nociceptive
messages. Noxious stimuli activate the
sensitive peripheral ending of the primary
afferent nociceptor by the process of
transduction. The message is then
transmitted over the peripheral nerve to the
spinal cord, where it synapses with cells of
origin of the major ascending pain pathway,
the spinothalamic tract. The message is
relayed in the thalamus to the anterior
cingulate (C), frontal insular (F), and
somatosensory cortex (SS).
B. Pain-modulation network. Inputs from
frontal cortex and hypothalamus activate cells
in the midbrain that control spinal pain-
transmission cells via cells in the medulla.

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The gate control theory developed by Melzack and Wall (1983), as reviewed
by King (1994), links biological and psychological factors. It hypothesizes a
gate-like mechanism involving the dorsal horn of the spinal cord by which
large A-beta fibers as well as small A-delta and C fibers carry impulses from
the periphery to the substantia gelatinosa and T-cells in the spinal cord.
Activation of the large fibers inhibits whereas activation of the small fibers
facilitates transmission to the T-cells. In addition,impulses descending from
the brain,influenced by cognitive processes, may either inhibit or facilitate
transmission of pain impulses. Such a mechanism may explain how
psychological processes affect pain perception.

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PSYCHOLOGICAL THEORY
As reviewed by Cloninger (1993), psychological constructs involving learning
theories, both operant and classical conditioning, may apply. In operant
paradigms, pain-related complaints are reinforced by increased
attention,relief from obligations,monetary compensation,and the pleasurable
effects of analgesics. In classical conditioning, originally neutral settings such
as a workplace or bedroom where pain was experienced come to evoke pain-
related behavior. Social and cultural attitudes may also have effects. Patients
with unexplained pain are more likely than others to have close relatives with
chronic pain.
Learning Theory Model
‘Operant’ & ‘Non-operant’ pain.
Operant is modified by positive or negative reinforcement.
Applicable in assessment & treatment.
Inappropriate beliefs contribute to pain behaviors, cognitive approaches
should be integrated.
Acute pain management policies need change – early mobilization to prevent
chronic pain.
(Fordyce, 1985)

22. Epidemiology of Chronic Pain
 Prevalence in general population 10 % to 55%.
(Karlsten & Gordh, 1997; Nickel & Raspe, 2001)
 WHO review mean prevalence of chronic pain was 31% in men,
40% in women, 25% in children up to 18 years, & 50% in > 65
years. (Ospina & Harstall, 2002)
 In a 24 year longitudinal study of chest, abdomen and
musculoskeletal pain, symptoms increased with age; women
reported more persistent & severe pain.
(Brattberg et al, 1997)
 In ≥ 65 yr musculoskeletal pain- three times more difficulty
performing ≥3 physical activities.
(Scudds & Robertson, 1998) 22

23. Factors in Chronic Pain
CAUSE, PERPETUATE, OR EXACERBATE
 Disease that is characteristically painful for which no
presently cure - arthritis, cancer.
 Secondary perpetuating factors initiated by disease and
persist after the disease resolved- include
 Damaged sensory nerves,
 Sympathetic efferent activity, and
 Painful reflex muscle contraction.
 Various psychological conditions can exacerbate, maintain,
modulate or even cause pain.
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24. Contribution of Emotional Disturbances
CLUES
o Pain that occurs in multiple unrelated sites
o A pattern of recurrent, but separate, pain problems
beginning in childhood or adolescence
o Pain beginning at a time of emotional trauma – as the loss
of parent or spouse
o History of physical or sexual abuse
o Past or present substance abuse. 24

25. Uncertain origin disorders presenting primarily with
pain
Generalized
 Fibromyalgia
Relatively Localized
 Tension headache – acute/chronic
 Temporomandibular pain & dysfunction syndrome
 Atypical facial pain
 Atypical (non-cardiac) chest pain
 Abdominal pain of psychological origin
 Non-ulcer dyspepsia
 Irritable bowel syndrome
 Chronic pelvic pain
 Irritable bladder syndrome
 Proctalgia fugax
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26. Pain Symptoms in Psychiatric Disorders
 About 38 % of psychiatric inpatients complained of pain.
(Delaplaine et al, 1978)
 On interview, 87% of psychiatric inpatients reported having
pain, 58% with duration of pain ≥ 2 years.
(King et al, 1998)
 59% of patients referred to psychiatry complained pain on
evaluation, only 6% patients were referred for this.
(King &Timko, 1999)
 Patients experiences of suffering, language & behaviors,
neurobiological conception of nociception all support a
psychological component.
(Hunt & Mantyh, 2001; Price, 2000)
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27. Psychiatrist’s role in the assessment
• Looking for pain / comorbid psychiatric syndromes,
• Psychological factors- cause, maintain, modulate pain.
• Current and past pain medications /other treatments.
• Comprehensive formulation to assess that patient is:
 Demoralized by sequence of meaningful events,
 Frustrated by psychological trait vulnerabilities,
 Upset by problematic behaviors, or specific disease.
(Clark MR, 1996) 27

28. Guidelines for Psychiatric approach
 Focus on improving function rather than alleviating pain.
 Unless clear evidence of malingering, accept the reported
pain as real.
 Explain psychiatrist’s involvement is not to suggest that they
do not have “real” pain or the pain is “all in their head.”
 Attempt to discern the roles of psychological factors /
medical condition in the onset & maintenance of the pain.
 Even when the medical condition is playing a major role,
psychological therapies are often efficacious. 28

29.  Psychosocial factors determine the responses, psychiatric
consultation is helpful before planning the treatment.
 Pain may be a symptom of mental disorders, lead to them, or
coexist.
 Effective management depends on the willingness, ability of
patients, to learn, practice strategies, to cope with pain.
 Be supportive, Patients often feel angry and frustrated about
issues & interactions with the health/ legal systems.
 Avoid therapeutic modalities that may worsen the patient’s
problems.
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30. 30
TREATMENT
Pharmacotherapy
Psychotherapy
Therapy-behavioral, physical, hypnosis, and/or
occupational
 The treatment may change according to the
severity of the pain.
Acute pain- goal is to relieve pain with medicine
Chronic pain-combination of medicine and therapy
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31. Pharmacological Treatment
 Ideally, pharmacotherapy - selected on the basis of:
 Etiology (ischemic, neuropathic),
 Pathophysiology (demyelination, central pain),
 Anatomy (C fibers, sympathetic nerves).
(Woolf & Decosterd, 1999)
 Unfortunately, medications are often underutilized and
under dosed.
 Physicians still attempt
 To alleviate pain with simple analgesics,
 Fail to appreciate the subtleties of the “adjuvant” drugs, which
possess multiple pharmacological actions.
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32. W.H.O. three step analgesic ladder
Guidelines in the pharmacologic treatment of pain:-
 STEP-1: For Mild Pain. Nonopioid analgesics +/- adjuvants.
 STEP-2: For Moderate Pain. Orally administered opioids, in
addition to
nonopioid analgesics +/- adjuvants.
 STEP-3: For Severe Pain. Parenteral opioids, in addition to
oral opioids,
nonopioids analgesics +/- adjuvants.
 Each step encourages the use of adjuvant analgesic agents.
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33. Guidelines for use of opioid analgesics
 May be used as initial treatment for severe acute pain
conditions.
 Cancer or chronic non-cancer related pain, initiate
treatment- non opioid & other analgesics, if needed milder
opioids.
 Even if opioid required, other modalities should be
continued if providing analgesia.
 In acute pain, a stronger opioid may be initially required.
 Prescribe on a fixed schedule rather than “as needed” basis.
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34. Opioid analgesics
 Effectiveness of opioids by RCTs, in reducing pain, pain related disability, depression,
insomnia, & physical dysfunction.
(Roth et al, 2000; Sittl et al, 2003)
 Acute withdrawal is not dangerous except in pt risk from increased sympathetic tone
- increased intracranial tension /unstable angina.
 Intermittent discontinuation /tapering of opioids results in exacerbation (opioid
abstinence/ induced hyperalgesia)- spinal sensitization.
(Li & Clark, 2002; Li et al, 2001)
 Loss of preexisting analgesia: tolerance, disease progression, new injury, worsening
neurological damage, comorbid psychiatric disorders, or medication - toxicity,
withdrawal, or opioid-induced hyperalgesia.
(Liu & Anand, 2001)
 Tolerance develops: administration of other agents, opioid rotation to more potent, &
intermittent cessation of agents (opioids , sedatives).
(Bolan et al, 2002; Pasternak, 2001) 34

35. Antidepressants
 Analgesic effect: reuptake blockade of NE & 5-HT, increasing descending inhibition.
(King, 1981; Magni, 1987)
TCAs (Collins et al, 2000; Sindrup & Jensen, 1999 & 2000)
 Cheaper, RCTs- no differences efficacy between TCAs.
 Analgesia at lower dose, earlier onset vs. depression.
 NE activity better analgesic effects than 5-HT alone.
SSRIs (Sindrup et al,1992; Rani et al, 1996)
 Paroxetine, Citalopram & Fluoxetine effective.
Others
 Duloxetine US-FDA approved diabetic peripheral neuropathy pain.
 Bupropion, Venlafaxine, Trazodone, Nefazodone,MAO – inhibitors
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36. Anticonvulsants
 Better compliance than TCAs because of fewer side effects.
 Phenytoin 1st successful drug for trigeminal neuralgia.
(Bergouignan,1942)
 Carbamazepine most studied for neuropathic pain.
(Tanelian & Victory, 1995)
 Valporate effective - 66-75% migraine & cluster headache.
(Gallagher at al, 2002)
 Gabapentin & Lamotrigine- reduce neuropathic pain.
(Pandey et al. 2002; Jensen, 2002)
 Combinations with complementary mechanisms of action increase
effectiveness & decrease adverse effects.
 Newer anticonvulsants evolving as first line therapy:
 Topiramate,Tiagabine, Pregabalin, Vigabatrin,
 Retigabine,Levetiracetam, and Zonisamide. (Cutrer, 2001) 36

37. Other Medications
LOCAL ANESTHETICS
 Topical Lidocaine & Oral Mexiletine- effective for neuropathic pain.
CALCIUM CHANNEL BLOCKERS
 Verapamil effective in migraine and cluster headache treatment.
 Diltiazem & Neuron specific CCB ziconotide & conopeptide.
BENZODIAZEPINES
 Clonazepam effective in episodic lancinating phantom limb pain.
(Bartusch et al, 1996)
 Associated with exacerbation of pain,interference with opioid analgesia &
increase the rate of developing tolerance to opioids.
(Nemmani & Mogil, 2003; Sawynok, 1985)
NSAIDS
TRIPTANS
LITHIUM 37

38. Psychological Treatment
 Biopsychosocial model recognizes number of factors, interrelationship,
contribution to ongoing suffering and successful treatment.
 Oriented toward self-management, with less perceptions of disability,
negative emotional response to pain- most likely to improve.
(McCracken & Turk, 2002)
 Three patient groups - based on Multidimensional Pain Inventory:
 Dysfunctional group – score- higher on pain severity, life interference,
distress & lower on perception of control & performance of daily activity.
 Interpersonally Distressed group – perception of poor support.
 Adaptive Copers – lower rating of pain severity, pain interference, affective
distress, disability & perception of being out of control.
(Cook & Chastain 2001; Greco et al, 2003)
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39. Cognitive behavioral therapy
 Identifying and correcting distorted attitude, belief and expectations.
 Believe problems inevitable & uncontrollable, experience more -negative
affective responses, pain, impaired physical/ psychological functioning.
 The components of CBT:
• Relaxation,
• Cognitive restructuring, and
• Coping self-statement training,
 Interrupt cycle of disability & enhance operant behavioral treatment.
(Turner & Chapman, 1982)
 Outcome studies of CBT demonstrated significant improvement in
• Pain intensity, Pain behavior, Pain symptoms,
• affective distress, Depression, Coping,
• physical functioning, Socio-economic costs Return to work.
(Hiller et al, 2003; Keefe et al, 1990; McCracken & Turk, 2002)
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40. Operant conditioning behavioral model
 For treatment of chronic pain pioneered by Fordyce, 1973.
 Based on the understanding of pain in a social context.
 Behavior of the patient is not only reinforce the behavior of
others but also reinforced by others.
 Productive behaviors are targeted for reinforcement and pain
behaviors are targeted for extinction.
 Helpful for reducing medication & improving activity level.
 Remains unclear what type of patient benefit most from what
type of behavioral treatment.
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41. Mind-Body Medicine (MBM)
 “The separation of psychology from the premises of biology is purely
artificial, because the human psyche lives in indissoluble union with the
body”. (Carl Jung)
 Patients complain that the system is disempowering, is expensive, fails to
manage chronic disease satisfactorily and emphasizes cure over prevention.
 MBM techniques offer patients greater control in their treatment, cheaper
alternatives, effective options for managing chronic conditions, and the
methods for maintaining wellness.
 MBM techniques are most effective are common problems most often
handled by primary care providers (e.g. chronic pain, anxiety, insomnia).
 MBM therapies include:
 Meditation Hypnosis Guided imagery
 Biofeedback Relaxation therapies Spiritual healing
 Yoga Art therapy Light therapy & others.
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42. Mind-Body Medicine (MBM)
Relaxation Techniques-
• Various techniques for helping patients cope with stress.
Biofeedback-
• That gives the patient conscious control over a physiologic function, not
normally under conscious control.
• Some find difficult to employ when not using the instrumentation.
• May result in patient over focusing on physiological parameters.
Hypnosis-
• It involves relaxation, increased suggestibility and dissociation.
• May resist receiving therapy due to invalid fears of losing control.
Meditation-
• It is the self regulation of attention, Two general types:
• Concentration meditation-Transcendental M. & Relaxation Response
• Mindfulness Meditation- Mindfulness-based stress reduction (MBSR).
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43. THANK YOU
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