Progress in Chronic Pain Management Chronic Pain Syndromes

Module 2 Progress in Chronic Pain Management Chronic Pain Syndromes: Cancer Chronic Low Back Pain Osteoarthritis Fibromyalgia A National Pain Education Council Program Cancer Pain Epidemiology • Cancer pain is highly prevalent – 30%-50% of those in active therapy – 75%-90% of those with advanced disease – approximately 25% of those in nursing homes (Bernebei et al, 1998; Caraceni et al,1999; Cleeland et al, 1994; Heim et al, 1993; Portenoy, 1994; Portenoy et al, 1992; Serlin et al, 1995) Cancer Pain Inferred Pathophysiology • Nociceptive: deemed consistent with apparent degree of tissue injury – Somatic: related to ongoing activation of somatic primary afferents – Visceral: related to activation of primary afferent neurons that innervate viscera • Neuropathic: sustained by aberrant somatosensory processing in the peripheral nervous system or CNS (Portenoy, 2000) Cancer Pain Diagnosis: Clinical Considerations • Acute or chronic – tumor-related (e.g., metastatic bone disease, nerve compression or infiltration) – treatment-related (chemotherapy, radiation or surgery) – unrelated to cancer or treatment • Nociceptive, neuropathic or mixed pain (Portenoy , 2000; Portenoy et al, 1996) Cancer Pain Principles of Assessment • Pain History – – – – – chronicity intensity and severity pathophysiology and mechanism tumor type and stage of disease pattern of pain and syndrome • Physical and Neurologic Examination • Radiographic Findings (Cleeland CS et al, 1992; Jacox et al, 1994; Portenoy et al, 199; Turk et al, 1994; Wall et al, 1994) Cancer Pain Treatment Considerations • Identify the cause of the pain • Primary treatment if indicated • WHO ladder combined with etiology-specific therapies for syndromes – pharmacologic and nonpharmacologic interventions – long-acting + short-acting opoids – adjuvant medications for neuropathic pain – NSAIDs and steroids can be helpful when there is an inflammatory component to pain (Jacox et al, 1994) WHO Guidelines for Cancer Pain GOAL: Freedom From Pain STEP 3 Pain Persists • Step 3: Opioids for moderate-to-severe pain +/non-opioid +/-adjuvant therapy • Step 2: Opioids for mild- tomoderate pain +/- nonopioid +/- adjuvant therapy • Step 1: Non-opioid +/adjuvant therapy STEP 2 Pain Persists STEP 1 (Adapted from Portenoy et al, 1997) Chronic Low Back Pain Epidemiology • 60%–85% lifetime prevalence • Second most common complaint to prompt medical evaluation • Leading cause of long-term work disability • Most common reason for early Social Security disability in US • U.S. indirect costs: $33 billion annually • Disability and costs related to pain, not to the disease (Loesser et al, 2001; Wall et al, 1994) process Chronic Low Back Pain Pathophysiology • Activation and sensitization of the nerve root nervi nervorum from root compression/traction • Sensitization of the nociceptors of the annulus fibrosus, periosteal spinal structures, and ligaments, due to acute inflammation, e.g., status post-trauma • Hyperalgesia (deep spinal and dermatomal) due to central sensitization (Loesser et al, 2001) Chronic Low Back Pain Clinical Characteristics • • • • • Preoccupation with pain Consistently disabled from pain Depression and anxiety are common High incidence of psychiatric diagnoses Drug misuse is common, but addiction relatively rare (Wall et al, 1994) Chronic Low Back Pain Diagnosis • History – medical, psychosocial – pain: location, duration, severity, alleviating/ aggravating influences • Physical Examination – posture and range-of-motion evaluation – routine neurologic and vascular exams • Imaging Studies – X-rays with flexion/extension – MRI – CT in some (Wall et al, 1994) Chronic Low Back Pain Treatment Considerations • Analgesic Medications • Adjuvant Analgesics • Physical Therapy Approaches • Neural Stimulation • Psychologic Management • Multidisciplinary Pain Centers (Portenoy et al, 1994) Osteoarthritis (Degenerative Joint Disease) Epidemology • Most common form of arthritis worldwide • Occurs most in women and in adults over age 45 • Occurs in 80% of people over 55 years of age • Affects >40 million people in US (1 in 6) • 23% experience limitation of activities • Cost in medical care and lost wages ~$95 billion (Elders, 2000; Loeser et al, 2001; Merskey et al, 1994) Osteoarthritis Pathophysiology • Progressive loss of articular cartilage • Chondrocytes produce metalloproteinases that degrade cartilage and cause fissuring, pitting, erosion, and denuded areas • Subchondral bone thickens and osteophytes, or bone spurs, form • Synovium thickened (contains moderate amount of lymphocytes, plasma cells) • Joint capsule and ligaments hypertrophied (Loesser et al, 2001; Wall et al, 1994) Osteoarthritis Clinical Characteristics • Deep aching pain, poorly localized • May occur in one or two joints or be generalized • Pain occurs in involved joint and is relieved by rest • Joint stiffness in morning and after periods of inactivity • Aching “night pain” is common • If pain is severe on activity and asymptomatic at rest, evaluate for neurogenic claudication (Loesser et al, 2001) Osteoarthritis Diagnosis • History: age, functionality, degree of pain, stiffness, time of occurrence (e.g., morning, at rest, during activity) • Physical examination: range of motion, tenderness, bony enlargement of joint • Laboratory findings: radiograph, CBC, synovial fluid analysis (Loesser et al, 2001; Manek et al, 2000) Osteoarthritis Treatment Considerations: First, perform a comprehensive assessment of pain and function Mild-to-moderate pain Moderate-to-severe pain Severe arthritis pain: COX-2 drugs and non-specific NSAIDs do not provide substantial relief Drug therapy ineffective and function severely impaired (ACR, 2000; APS, 2002; Manek et al, 2000) Acetaminophen COX-2 NSAIDS Opioids Surgical Treatment Fibromyalgia Syndrome Epidemiology • 4–7 times more common in adult women than in men; highest prevalence in women 50–60 yrs • Approximately 2% of general population in U.S. and Canada have symptoms that could meet ACR criteria • Long-term follow-up studies suggest that fibromyalgia is not a syndrome representing a transition from one disorder to another (Loesser et al, 2001; Portenoy et al, 1996; Wall et al, 1994) Fibromyalgia Syndrome Pathophysiology Etiology is unknown: 3 views of pathophysiology have emerged: • Central Nervous System (neurogenic) – generalized pain – increase in CSF substance P – decrease in serum and CSF serotonin • Muscle Pathology – decreased oxygen tension and blood flow – abnormal muscle biopsies – weakness • Psychopathology – anxiety, depression (Loeser et al, 2001; Portenoy et al, 1996; Wall et al, 1994) Fibromyalgia Syndrome Clinical Characteristics • • • • • • • Pain (musculoskeletal tenderness) Lightheadedness, dizziness, syncope Fatigue Chronic insomnia; sleep disturbance Cognitive deficits/short-term memory loss Depression/anxiety Numbness, dysesthesia in hands and feet (Loeser et al, 2001) Fibromyalgia Syndrome Diagnosis Based on the 1990 ACR classification guidelines: • 1 historical feature + 1 physical finding • Historical feature = widespread (axial) pain of 3 months or more • Physical finding = pain in at least 3 of the 4 body segments + a finding of at least 11 tender points on digital palpation of 18 designated tender points (Merskey et al, 1994; Portenoy et al, 1996; Wall et al, 1994; Wolk M, 2002) Fibromyalgia Syndrome Treatment: A Multidisciplinary Approach • Patient Education – reading materials, videos, support groups • Physical Exercise – low-grade (muscle stretches, aerobic conditioning) • Pharmacologic Therapies – tricyclic antidepressants, NSAIDS, topical capsaicin, opioids* *Drug therapies have been used with varying degrees of success in treating fibromyalgia. (Portenoy et al, 1996; Wall et al, 1994) Pathophysiology of Pain • Inferred from characteristics, etiology or pathophysiology • Types – nociceptive – neuropathic – idiopathic • Therapeutic implications (Portenoy et al, 1996) Pathophysiology of Chronic Pain • In chronic pain, the nervous system remodels continuously in response to repeated pain signals – nerves become hypersensitive to pain – nerves become resistant to antinociceptive system • If untreated, pain signals will continue even after injury resolves • Chronic pain signals become embedded in the central nervous system (Marcus, 2000) Peripheral and Central Pathways for Pain Ascending Tracts Cortex Descending Tracts Thalamus Midbrain Pons Medulla Spinal Cord (Brookoff, 2000) Pain-Sensing System in the Malfunction in Chronic Pain Pain Sensing In chronic pain, pain signals are generated without physiologic significance Acute pain: Pain-sensing signals are initiated in response to a stimulus • They elicit a painrelieving response Chronic pain: Pain signals are generated for no reason and may be intensified • Pain-relieving mechanisms may be defective or deactivated (Illustration: Seward Hung, 2000) Nociceptive Pain Presumably results from ongoing activation of primary afferent neurons responding to noxious stimuli • Pain consistent with degree of tissue injury • Described as aching, squeezing, stabbing, throbbing • Subtypes: – Somatic: related to activation of somatic afferent neurons – Visceral: related to activation of visceral afferent neurons (Loeser et al, 2001; Portenoy et al, 1996) Neuropathic Pain • Initiated by a primary lesion in the nervous system; believed to be sustained by aberrant somatosensory processing in the peripheral or central nervous system • Independent of obvious ongoing nociceptive activation • Burning, shooting, electrical quality; may be aching, throbbing, sharp • Subtypes: – Presumed “central generator”  deafferentation pain (central pain, phantom pain)  Sympathetically-maintained pain – Presumed “peripheral generator”  Polyneuropathies and mononeuropathies (Portenoy et al, 1996) Idiopathic and Psychogenic Pain Idiopathic Pain • Usually exists in the absence of an identifiable physical or psychologic pathology that could account for pain • Uncommon in patients with progressive illness Psychogenic Pain • Presents positive evidence of a predominant psychologic contribution and may be labeled with a specific psychiatric diagnosis (Loeser et al, 2001; Merskey et al, 1994; Portenoy et al, 1996)