This document discusses the management of chronic pain. It begins with definitions and classifications of different types of pain. It then discusses the epidemiology, anatomy, pathophysiology, diagnosis, and common causes of chronic pain such as low back pain, peripheral neuropathies, postherpetic neuralgia, migraines, and fibromyalgia. The document also covers pharmacological treatments including analgesics like NSAIDs and opioids as well as psychological treatments.

1. Management Of Chronic Pain
MODERATOR– Dr SatyaKrishnaKumar
AssistantProfessor
PRESENTER– Dr MeghaKharyal
Post graduaTE

2.  DEFINITION AND COMPARATIVE NOSOLOGY
 EPIDEMIOLOGY
 ANATOMY ANDPATHOPHYSIOLOGY
 DIAGNOSIS AND CLINICAL FEATURES
 Pathology and Imaging Studies
 COMMON CHRONIC PAIN CONDITIONS
 PHARMACOLOGICAL TREATMENTS
 PsychologicalTreatments

3. DEFINITION AND COMPARATIVE NOSOLOGY
 Pain is a complex experience that involves cognitive, behavioral, and emotional
factors.
 The International Association for the Study of Pain defines pain as an
unpleasant sensory and emotional experience associated with actual or
potential tissue damage.
 Pain is subjective, and the patient's report of pain should be considered valid
unless there is evidence suggesting otherwise.

4.  Allodynia: A painful response to a normally non-noxious stimulus
 Deafferentation Pain: Pain resulting from loss of sensory input into the central
nervous system
 Dysesthesia: An abnormal pain that can be spontaneous or evoked
 Hyperalgesia: An exaggerated painful response to a normally noxious stimulus
 Hyperesthesia: Increased sensitivity to stimulation that excludes the special
senses
 Hyperpathia: An exaggerated painful response evoked by a noxious or non-
noxious stimulus
 Hypoesthesia: Diminished sensitivity to stimulation that excludes the special
Types of painful experience

7. Neuropathic Peripheral Central
Peripheral neuropathy Spinal cord injury Parkinson's disease
Postherpetic neuralgia Central poststroke pain Multiple sclerosis
Trigeminal neuralgia Seizure disorder
Chronic postsurgical pain
Phantom limb pain
Complex regional pain
syndrome
Radiculopathy
Nerve entrapment

8. Nociceptive Somatic Visceral
Arthritis Myofascial pain Irritable bowel syndrome
Fibromyalgia Endometriosis
Connective tissue disorders Interstitial cystitis
Surgical/trauma related pain Ulcers
Burn pain Appendicitis
Cholecystitis
Neuropathic and Nociceptive Pain Conditions

9. EPIDEMIOLOGY
 Pain is a major reason for medical visits and has a significant societal impact.
 Chronic back pain, severe headaches, arthralgias, and neck pain are common
conditions.
 Patients with chronic pain use more healthcare resources.
 Moderate to severe pain leads to work absenteeism.
 Women tend to experience more severe and frequent pain than men.
 Lower socioeconomic status is linked to higher prevalence of chronic pain.
 History of previous pain and greater acute pain intensity increase the risk of
chronic pain.

10. TRANSDUCTIO
N Conversion
of a noxious
stimuli
(chemical,
mechanical, or
thermal) into
electrical
energy.
TRANSMISSIO
N Electrical
stimulus is
sent to the
dorsal horn of
the spinal
cord and
synapse at the
2nd order
neuron.
ANATOMY OF PATHWAY

11. MODULATION
Inhibition vs
amplification of
signal
(facilitated by
EAA).
PERCEPTIO
N
Conscious
awareness
of pain as a
culmination
of previous
processes
in the
context of
the
individuals
experiences
.

12. PATHOPHYSIOLOGY

13.  Pain is an important defense mechanism that warns the
body of potential or actual injuries or diseases.
 Noxious signals send impulses to the spinal cord, which
relays the information to the brain.
 The brain interprets the information as pain, localizes it,
and sends back instructions for the body to react.
 Pain sensation is mediated by pain receptors or
nociceptors, which are present in the skin, superficial
tissues, and most organs except for the brain.
 First-order neurons, the nerve endings in the pain pathway,
transmit signals from the nociceptors. These neurons can
be myelinated (A fibers) or unmyelinated (C fibers).
 Myelinated A fibers conduct at fast speeds and are
responsible for initial sharp pain, while unmyelinated C
fibers conduct at slower speeds and cause longer-lasting,
dull, diffusing pain.
 First-order neurons travel via spinal nerves to the spinal
cord, where they synapse with second-order neurons in the
dorsal horn.

14. Second-order neurons cross over to the opposite
side of the cord before ascending to the brain,
allowing information of pain on one side of the
body to be transmitted to the opposite side of the
brain.
Two major pathways carry pain signals from the
spinal cord to the brain: the spinothalamic tract
and the Spinoreticular tract.
The spinothalamic tract is involved in the
localization of pain and carries signals from the
spinal cord to the thalamus, where they synapse
with third-order neurons that project to the
somatosensory cortex.
The Spinoreticular tract carries signals to the
reticular formation of the brainstem before
ascending to the thalamus, hypothalamus, and
cortex. This tract is responsible for the emotional
aspect of pain.
Pain signals from the face follow a different route
to the thalamus via the trigeminal nerve.

15. DIAGNOSIS AND CLINICAL FEATURES

16.  Pain is subjective and should be taken seriously.
 There are no diagnostic tests to confirm or measure the severity of pain.
 Evaluation of pain begins with a thorough history and physical examination.
 Chronic pain can have significant psychological effects compared to acute pain.
 Pain severity can be assessed using verbal, numerical, or visual analog scales
(VAS).
 Psychological factors and functional capacity should be evaluated alongside pain
severity.
 Distinguishing between neuropathic and nociceptive pain is important for
treatment approaches.
 Comorbid psychopathology, like depression and anxiety, is common in chronic
pain patients and should be treated concurrently.
 Physical examination, focusing on neurologic and musculoskeletal aspects, helps
identify underlying causes.
 The assessment of pain is individualized and encompasses a comprehensive
history, pain severity measurement, evaluation of psychological factors, and a

17. Pathology and Imaging Studies
 Imaging techniques have limitations in identifying the cause of chronic pain.
 MRI findings often have a poor correlation with pain severity.
 CT scans are better for detecting bone disease and bleeding, while ultrasound
is inexpensive and radiation-free.
 Electromyography and nerve conduction studies detect lesions in large nerves
but have limitations.
 Skin biopsies can help diagnose peripheral neuropathies.
 Brain imaging shows morphologic alterations in areas involved in pain
perception in chronic pain patients.
 Successful treatment can reverse these brain changes.

18. COMMON CHRONIC PAINS

19. Low BackPain
 Low back pain (LBP) is common,Psychological factors predict the transition to
chronic LBP.
 Poor functional status after treatment predicts chronic LBP.
 Economic and social rewards are associated with higher disability and
depression in chronic LBP.
 Depressive disorder increases the risk of chronic LBP and musculoskeletal pain.
 Chronic LBP can lead to significant psychopathology.
 Treatments for chronic LBP reduce symptoms, but effectiveness in improving
function and work outcomes varies.
 Thorough evaluation and individualized treatment plans are essential for LBP
patients.

20. Peripheral Neuropathic PAIN
 Peripheral neuropathy is caused by nerve damage, leading to pain,
numbness, and weakness.
 Common causes include diabetes and excessive alcohol consumption.
 Painful diabetic neuropathy affects about 25% of diabetic patients.
 The pain is often described as burning and lancinating, and can be constant
or episodic.
 It is caused by nerve degeneration and abnormal impulse generation.
 Voltage-dependent sodium channels and central sensitization contribute to
pain amplification.
 Treatment focuses on managing symptoms, as complete reversal of the
damage is rare.

21. PostherpeticNeuralgia
 Postherpetic neuralgia (PHN) causes persistent or recurrent pain at the site of
shingles.
 It occurs in about 10% of patients with acute herpes zoster.
 Risk factors include advanced age, cancer, diabetes, immunosuppression, and
greater pain severity.
 Over 50% of patients over the age of 65 develop PHN.
 PHN generally improves over time, but 25% of patients experience pain for over a
year.
 Acute herpes zoster damages motor and sensory fibers in the dorsal root
ganglion.
 Postherpetic neuralgia (PHN) involves additional neurologic damage and
inflammation.
 Early treatment of herpes zoster and vaccination can help prevent or reduce the
development of PHN.

22. Migraine and Chronic Daily Headache
 Migraine affects 18% of women and 6% of men.
 Typical onset is between the third to sixth decades of life.
 Migraine presents as unilateral, pulsatile pain with accompanying symptoms like
nausea, vomiting, photophobia, and phonophobia.
 Complicated migraine includes focal neurologic symptoms, and its exact cause is
unknown.
 Management involves identifying and controlling comorbidities and risk factors.
 Prophylactic agents and cognitive-behavioral therapy (CBT) are used for
prevention.
 Nonsteroidal anti-inflammatory medications and triptans are effective for acute
attacks.

23. Central Poststroke
 Central pain occurs due to CNS lesions (e.g., stroke, SCI) and is poorly
localized and fluctuating.
 Symptoms include allodynia, hyperalgesia, muscle and visceral pain, and
lancinating pain.
 It may emerge after a month or longer following the initial injury.
 Excitatory amino acids play a role in central sensitization and pain generation.
 Treatment options include analgesics, adjuvant medications, and electrical
stimulation.

24. Fibromyalgia
 Fibromyalgia is characterized by musculoskeletal pain, tenderness, and
stiffness.
 It involves central sensitization, leading to symptoms like fatigue, poor sleep,
cognitive difficulties, and depression.
 Treatment options for fibromyalgia pain include muscle relaxants, membrane
stabilizers, selective serotonin/norepinephrine reuptake inhibitors, and
tramadol.
 These medications have shown effectiveness in reducing fibromyalgia pain.

25. Complex Regional Pain Syndrome
• CRPS is a painful condition triggered by trauma or immobilization.
• It causes persistent pain, allodynia, and hyperalgesia.
• Around 3-5% of distal radial fracture patients develop CRPS.
• It involves sensory, motor, and sudomotor changes.
• Treatments include medications, physical therapy, and psychological
support.
• Rehabilitation promoting limb use and movement improves prognosis.

26. PhantomLimb pain
 Phantom limb pain is neuropathic pain occurring in the territory of an
amputated limb.
 It affects 50 to 80 percent of amputees and is described as stabbing,
throbbing, aching, burning, or cramping.
 Medications like morphine, calcitonin, and mexiletine show some reduction in
pain.
 Psychological interventions, such as cognitive-behavioral therapy (CBT) and
biofeedback, have varying effectiveness.

27. Orofacial Pain Trigeminal neuralgia,or tic douloureux
 Trigeminal neuralgia: Chronic facial pain, usually unilateral, with triggers or
spontaneous episodes. Treatments include carbamazepine and other options.
 Temporomandibular disorder (TMD): Jaw joint and muscle pain. Conservative
therapies recommended, surgery for refractory cases.
 Burning mouth syndrome: Oral and pharyngeal pain with dryness and taste
alterations. Common psychiatric comorbidities.
 Identifying causes and providing symptomatic treatments are important.
 Less common orofacial pain conditions include cluster headache, SUNCT, Tolosa-
Hunt syndrome, and atypical facial pain.

28. PARKINSON DISEASE
 The majority of patients with Parkinson disease have pain. The pain can be
musculoskeletal, neuropathic, or dystonic and is typically described as
cramping and aching in the low back and extremities.
 It is more common in women. The pain is often reduced when the patient is
treated with levodopa. This suggests a central origin that may be produced by
the lack of dopaminergic input.
 In addition to levodopa, analgesics and adjuvant medications can significantly
reduce the pain associated with Parkinson disease.
 Deep brain stimulation is also an option when symptoms are refractory to
other treatments.

29. COURSE AND PROGNOSIS
 In chronic pain, the course and prognosis varies widely and is difficult to
predict.
 Certainly, psychiatric comorbidities and their treatments influence the course
and prognosis greatly.

30. Somatic Symptom Disorder
 Pain in SSD is influenced by psychological factors, but it is not psychogenic pain.
 Neuroimaging studies show decreased gray matter in pain perception areas.
 Somatization disorders have multiple unexplained painful symptoms.
 Patients may believe their pain is imaginary, leading to excessive testing and
inappropriate treatments.
 It affects a larger portion of the population and overlaps with affective disorders.
 It causes functional disability and role impairment.

31. Substance Use Disorder
 Severe substance use disorder: 7-20% prevalence in chronic pain patients.
 Aberrant medication-taking behaviors ≠ abuse or addiction.
 Chronic pain can increase reliance on opioid analgesics.
 Pseudoaddiction: pain undertreatment mimics addiction.
 Substance abuse history or psychiatric comorbidity increases risk.
 Prescribed medications often involved in new substance use disorder cases.
 Risk prediction tools have limitations.
 Regular follow-up and monitoring needed for opioid prescriptions.
 Integrating pain care with substance abuse treatment improves outcomes.

32. Depressionand AffectiveIllness
 Pain and depression are closely interconnected.
 The rate of depression is more than three times higher in patients with chronic
low back pain.
 Depression is associated with more severe and persistent pain, increased
interference from pain, and observable pain behaviors.
 Patients with pain and depression are more likely to use medication on a daily
basis.
 Comorbid pain and depression increase the risk of suicidal thoughts and actions.
 Treating depression alongside pain is essential for improved outcomes, including
reduced pain, better functioning, and enhanced quality of life.
 The shared neurobiology between pain and depression contributes to these
outcomes.

33. AnxietyDisorders
 Anxiety symptoms are present in about half of chronic pain patients, with up
to 30% meeting criteria for anxiety disorders.
 PTSD is a common comorbid condition in chronic pain patients, associated
with increased pain, distress, and disability.
 Cognitive distortions like catastrophizing and fear-avoidance beliefs predict
poor coping and adjustment to chronic pain.
 Catastrophizing is also a predictor of suicidality, independent of pain
severity and depression.

34. PHARMACOLOGICAL TREATMENT

35. ANTIPYRETIC ANALGESICS
 Aspirin, acetaminophen, and NSAIDs are commonly used for acute pain.
 Aspirin inhibits prostaglandin production and is widely used as an analgesic.
 Acetaminophen acts primarily in the central nervous system and is weaker than
NSAIDs.
 NSAIDs work centrally and peripherally, effective for various types of pain.
 NSAIDs are more effective for nociceptive pain than neuropathic pain.
 Opioids may be needed for severe pain, as NSAIDs have a ceiling effect.
 NSAIDs have side effects including gastrointestinal issues, renal toxicity, and
cardiovascular risks.
 Selective inhibitors and acid-reducing agents may help reduce gastrointestinal
complications.
 Prescribing NSAIDs at the lowest effective dose for the shortest duration is
recommended.
 Topical NSAIDs can be used for regional pain and have similar efficacy.

36. Opioid Analgesics
 Opioids reduce pain through receptor interaction.
 Controversial long-term use for chronic pain.
 Side effects include sedation, nausea, constipation, and respiratory depression.
 Thorough evaluation and monitoring are necessary for opioid management.
 Tolerance, dependence, and addiction can develop with long-term use.
 Common opioids: morphine, oxycodone, hydrocodone, fentanyl.
 Methadone and newer analgesics have unique considerations and risks.

37. Pure agonists
Morphine 30 mg 3-6 hours
Oxycodone 20 mg 3-6 hours
Hydrocodone 30-60 mg 3-6 hours
Hydromorphone 3-6 mg 3-6 hours
Oxymorphone 10 mg 3-6 hours
Fentanyl 12.5 mcg/h (TD) 72 hours (TD)
800-1,000 mcg (TM) 1.5-3 hours (TM)
Codeine 200 mg 3-6 hours
Methadone 2-20 mg 6-12 hours for pain
Clinically Available Opioids Used in Chronic Pain Conditions

38. Agonist/Antagonists
Buprenorphine 0.3 mg (SL) 6-8 hours (SL)
5-70 mcg/h (TD) 7 days (TD)
Butorphanol 1 mg (IN) 3-4 hours
Weak, Dual-Action
Agonists
Tramadol 150-300 mg 4-6 hours
Tapentadol 75-110 mg 4-6 hours

39. Antidepressants
 Antidepressants have analgesic effects separate from their antidepressant
properties.
 These effects are mediated by inhibiting serotonin and norepinephrine
reuptake.
 Enhanced activation of inhibitory neurons in the spinal cord contributes to the
analgesic effects.
 Antidepressants modulate monoamines and interact with opioid systems, ion
channels, and various receptors.
 The potential analgesic properties of antidepressants are often
underestimated in chronic pain treatment.

40. Tricyclic Antidepressants
 Tricyclic antidepressants (TCAs) are highly effective for neuropathic pain,
headache syndromes, central pain syndromes, postherpetic neuralgia (PHN),
and painful neuropathies.
 Nortriptyline, a secondary amine TCA, is better tolerated than amitriptyline, a
tertiary amine TCA.
 Lower doses of TCAs can provide analgesia, independent of their
antidepressant effects.
 They are cost-effective and can be monitored through serum levels to ensure
proper dosage and avoid toxicity.
 They may not be effective for conditions like spinal cord injury pain,
phantom limb pain, or painful HIV neuropathy.

41. Serotonin-Norepinephrine
 SNRIs (duloxetine, venlafaxine, desvenlafaxine, milnacipran) inhibit serotonin and
norepinephrine reuptake.
 SNRIs have fewer side effects than TCAs, faster titration, and no serum monitoring.
 Duloxetine is potent in blocking serotonin and norepinephrine, while venlafaxine
is beneficial for neuropathic pain and migraines.
 Milnacipran is effective in reducing hyperalgesia in fibromyalgia.
 SSRIs have inconsistent efficacy in chronic pain conditions, but potential benefits
in migraines, fibromyalgia, irritable bowel syndrome, and painful diabetic
neuropathy.
 SSRIs are alternatives to TCAs or SNRIs when other medications are ineffective or
poorly tolerated.

42. Novel Antidepressants
 There is little evidence supporting the use of novel antidepressants such as
mirtazapine, bupropion, trazodone, vortioxetine, and vilazodone for the
treatment of pain.
 Mirtazapine has shown effectiveness in reducing chronic tension type
headaches, while bupropion has been effective in treating neuropathic pain.
 Trazodone has been suggested as a treatment for chronic pain, but its side
effects can limit dose titration. The efficacy of vortioxetine and vilazodone in
pain treatment is yet to be established.

43. Anticonvulsants

44. Calciumchannel blockers
 Calcium channel blockers, such as verapamil, are used to treat chronic pain
syndromes like migraine and cluster headaches.
 Ziconotide, derived from cone snail toxin, is a neuron-specific calcium
channel blocker used intrathecally for refractory cancer or AIDS pain.
 Caution is advised when prescribing benzodiazepines to chronic pain
patients due to side effects and potential negative outcomes, especially
when combined with opioids, which can increase mortality risk.

45. Psychological Treatments

46. Cognitive- Behavioral Models.
 Psychological treatments like CBT are important for managing chronic pain.
 CBT helps replace maladaptive behaviors with healthy ones, addresses beliefs
and attitudes about pain, and teaches coping strategies.
 Third-wave therapies focus on acceptance, changing the relationship with
pain, and enhancing overall quality of life.
BELIEF
 Beliefs impact chronic pain management and psychosocial functioning.
 Patient beliefs about pain, emotions, and activity affect well-being. Cognitive
factors (self-efficacy, expectations, locus of control) impact coping and pain
outcomes.
 Perceived control and acceptance predict positive treatment effects. Higher
self-efficacy and internal locus of control relate to lower pain and better
coping.
 Acceptance of pain yields positive outcomes, regardless of catastrophizing or
coping skills.

47. COPING
 Effective coping strategies are crucial for managing chronic pain.
 Active and adaptive coping strategies are beneficial, while passive or maladaptive
strategies lead to higher disability and poorer outcomes.
 Developing and implementing effective coping skills can decrease pain and
disability.
Placebo
 Placebo effects are complex and measurable, similar to active treatments.
 Differentiating treatment and placebo responses is clinically challenging.
 Controversy surrounds placebo use and evidence of significant effects.
 Using placebos to question the reality of pain is dishonest and counterproductive.
It erodes trust and diminishes future treatment effectiveness.

48. Multidisciplinary Rehabilitation
 Chronic pain affects well-being and quality of life.
 Multidisciplinary rehabilitation aims to improve functioning and reduce suffering.
Early treatment failures have long-term consequences.
 Comprehensive programs show pain reduction and functional improvements.
Interdisciplinary pain rehabilitation programs (IPRPs) aid return to work and
reduce economic burden.
 Evidence-based guidelines emphasize integrated treatment and patient
selection.

49. Invasive Treatments Nerve Blocks
 Injections are used for diagnosing and treating chronic pain.
 Local anesthetic injections improve blood flow, release entrapped nerves,
and interrupt central sensitization.
 Corticosteroids added to injections block inflammation and provide
additional pain relief.
 Nerve blocks offer temporary pain relief and assist in rehabilitation.
 Examples include trigger point, intra-articular, and direct nerve blocks.
 Spinal injections like epidural and facet injections target specific pain
sources.
 Neuro-ablative procedures using alcohol or glycerol can provide temporary
relief but should be avoided in nonmalignant pain conditions due to severe
rebound pain.

50. Electrical Stimulation
 Spinal cord stimulation (SCS) uses low-voltage electrical pulses for chronic
pain management.
 The procedure involves implanting a pulse generator, extension cable, and
leads near the pain-associated nerve root. Electrical stimulation induces
paresthesia to mask the pain.
Surgery Surgical interventions
 SCS is recommended for chronic pain patients unresponsive to conservative
treatments.
 Determining the cause of pain can be challenging before considering surgery.
 Removing a painful body part rarely provides long-term pain relief and can
sometimes worsen pain.
 Careful patient selection is crucial for determining suitability for surgery in
chronic pain management.

51. summary
 The International Association for the Study of Pain defines pain as an unpleasant
sensory and emotional experience associated with actual or potential tissue damage.
 Pain can be either acute or chronic
 They can be Nociceptive or Neuropathic
 Nociceptive pain –Caused by normal neural activity in response to tissue damage
stimuli
 Neuropathic pain – caused by lesion or disease affecting the nervous system
 Chronic pain serves as a defense mechanism, warning the body of potential injuries or
diseases.
 Pain is mediated by pain receptors or nociceptors present in various tissues and
organs.
 The pain pathway involves first-order neurons transmitting signals to the spinal cord,
where they synapse with second-order neurons in the dorsal horn.
 Two major pathways, the spinothalamic tract and the spinoreticular tract, carry pain
signals to the brain.
 The spinothalamic tract is involved in pain localization, while the spinoreticular tract
contributes to the emotional aspect of pain.

52. Different types of pain, such as somatic and visceral pain, have distinct
characteristics and pathways.
Treatment options for chronic pain include opioids, antidepressants, calcium
channel blockers, and injections.
Opioids interact with opioid receptors and carry risks of tolerance, dependence,
and addiction.
Antidepressants have analgesic effects independent of their antidepressant
properties, with tricyclic antidepressants being effective for neuropathic pain.
Calcium channel blockers, like verapamil, are used for migraine and cluster
headaches.
Injections, such as local anesthetic and corticosteroid injections, improve blood
flow, block inflammation, and provide pain relief.
Nerve blocks and spinal injections target specific pain sources and offer temporary

53. Managing chronic pain patients on opioids requires thorough evaluation,
documentation, treatment planning, patient education, consent, and close
monitoring.
Integration of chronic pain care with substance abuse treatment models can
improve outcomes.
Factors like pain condition, response, and potential for aberrant behaviors
should be considered before initiating opioid therapy.
Psychological treatment is an essential component of managing chronic
pain.
Cognitive-behavioral therapy (CBT) is a commonly used approach that helps
individuals identify and change negative thought patterns and behaviors
related to pain.
A multidisciplinary approach is essential in the management of chronic pain

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