PRESENTED BY: Dr CHITTRAMODERATED BY: Dr GIAN CHAUHAN

CHRONIC PAIN MANAGEMENT

IASP defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”

pain is always subjective and it is a sensation in part of the body, is unpleasant and also has an emotional component

If patients regard their experience as pain or if they report it in the same way as pain caused by tissue damage, it should be accepted as pain

ASA defines chronic pain as “pain of any etiology not directly related to neoplastic involvement, associated with chronic medical condition or extending in duration beyond the expected temporal boundary of tissue injury and normal healing, and adversely affecting the function or well-being of individual”

IASP defines it as “pain without apparent biological value that has persisted beyond the normal tissue healing time usually taken to be 3 months”

DEFINITION

PREVALENCE 20% to 60%higher prevalence in women and the elderly CLASSIFICATIONMalignant nonmalignant

inflammatory musculoskeletal neuropathic (arthritic) (low back pain) post herpetic phantom limb CRPS diabeticheadaches visceral

Chronic pain patients have in common complex influences of biologic, cognitive , emotional , and environmental factors

patients have limited mobility, lack of motivation, depression, anger, anxiety, and fear of reinjury, these hamper return to normal work or recreational activities

may become preoccupied with pain and somatic processes, which disrupt sleep ,cause irritability and social withdrawal

The interplay between these biologic, psychological, and social factors results in persistence of pain and illness behavior

Management of pain addresses physical, psychological, and social skills and underscores patients' active responsibility to regain control over life by improving function and well-being

BIOPHYSICAL CONCEPT

PATHWAY OF CHRONIC PAIN

› Repeated nociceptor stimulation sensitize both peripheral and central neurons (activity-dependent plasticity)

› progressive increase in output in response to persistent nociceptor excitation is known as“wind-up

› sustained by transcriptional changes in the expression of genes coding for various neuropeptides, transmitters, ion channels, receptors, and signaling molecules in both nociceptors and spinal neurons

› physical rearrangement of neuronal circuits by apoptosis, nerve growth, and sprouting occurs in the peripheral and central nervous systems

CHRONICITY

Mode of onsetsitechronicity and durationcharacter and severity(visc pain- dull aching,

neuralgic pain – stabbing, myofascial pain)investigations, operations, drugs,treatments doneassociated factors ( premonitory symptoms,ppt

factors,environmental factors, family history,pat medical and surgicl history, psychiatry history, medications drugs ,alcohol abuse, kinesiophobia

PATIENT EVALUATIONHISTORY

1. GPE (Skin lesions, jt deformities etc)2. PAIN RELATED BEHAVIOUR (facial

expression, emotional)3. SYSTEMIC EXAMINATION4. NEUROLOGICAL EXAMINATIONa) cranial nerve fxnb) msc strength gradingc) DTRd) Sensatione) musculoskeletal system

PHYSICAL EVALUATION

OLFACTORY:Familiar odors, individual naresOPTIC:Vision, fundus, fields of visionOCULOMOTOR,TROCHLEAR,ABDUCENSptosis, light response, nystagmus, fields of gaze,

asymmetric extraocular movementsTRIGEMINAL NERVEjaw msc strengthsuperficial pain and touch senation in each branch

CRANIAL NERVE EXAMINATION

The ophthalmic, maxillary, and mandibular nerves provide sensation to the eye and forehead, midface and upper jaw, and lower jaw, respectively

FACIAL › Corneal reflex, symmetryACOUSTIC› Sense of hearing, bone and air conductionGLOSSOPHARYNGEAL› Gag reflex, ability to swallowVAGUS› Palate and uvula inspection, nasal twangSPINAL ACCESSORY› Trapezius and SCM strengthHYPOGLOSSAL› Tongue inspection and strength

CLINICAL FINDING GRADENo contractility 0Slight flicker 1Full movement, gravity eliminated 2Full movement with gravity 3Full movement against gravity some resistance

4

Full movement against gravity full resistance

5

MOTOR SYSTEM

GRADE RESPONSE0 No response1+ Sluggish2+ Normal3+ Brisk4+ Exaggerated with clonus

DTR SCALE

› Pain,touch,temperature› vibration ,proprioception

SENSORY SYSTEM

1. Inspection2. Palpation3. Movement4. Range of motion

MUSCULOSKELETAL SYSTEM

› SLRT› Spinal flexibility› Tinel’s test› Phalen’s test› Adson’s test

SPECIFIC TESTS

› CATEGORY SCALE› RUPEE ANALOG SCALE› NUMERICAL RATING SCALE› VISUAL ANALOG SCALE› DESCRIPTOR DIFFERENTIAL SCALE

PAIN MEASUREMENT AND ASSESSMENT

› THE OUCHERS SCALE› HAPPY-SAD FACE SCALES› COLOR ANALOG SCALE› POKER CHIP TOOL› LADDER SCALE› LINEAR ANALOGUE SCALE

ASSESSING PAIN IN PRE-SCHOOLERS

OPERATING ROOM FLUOROSCOPY:› Anterior elements› Posterior elements› Space componentsProcedures performed:1. Caudal epidural steroids/catheter placement2. Celiac plexus block3. Hypogastric plexus block4. Sympathetic plexus block5. Trigeminal ganglion block6. Stellate ganglion block7. Transforaminal steroid injection

RADIOGRAPHY AND IMAGING

EPIDUROGRAPHY› Opacification of epidural space with aqueous

contrast mediumSPINAL ENDOSCOPY› Percutaneous minimally invasive endoscopic

investigation of epidural space to enable color visualisation anatomical structures inside the spinal canal

› Direct drug application› Direct lysis of scarring› Placement of catheter and electrode system

CT› Trauma› Abscess› Neoplasm› Metastasis› LAPSuperior bone detailMRI› More contrast resolution› Better soft tissue detail

BONE SCAN› Imaging of entire skeleton› Early detection of abnormal areas› Metastaic disease› CRPS› Joint diseases

MULTIMODAL MODALITYfacilities to evaluate and treat biomedical,

psychosocial, and occupational aspects Pain physician, psychologist, physical

therapist, and occupational therapistSINGLE MODALITY MANAGEMENTused as part of multimodal management

1) pharmacologic management2) ablative techniques3) acupuncture4) blocks (i.e., joint and nerve or nerve root)5) botulinum toxin injections6) electrical nerve stimulation7) epidural steroids with or without local anesthetics8) intrathecal drug therapies9) minimally invasive spinal procedures10) physical or restorative therapy11) psychologic treatment12) trigger point injections

TREATMENT OPTIONS

1) NSAIDs2) opioid therapy3) Serotonergic drugs4) anticonvulsants5) anti-depressants6) benzodiazepines7) NMDA receptor antagonists8) skeletal muscle relaxants9) topical agents

PHARMACOLOGIC MANAGEMENT

NSAIDs inhibit COXsCOX-1 and COX-2, are constitutively expressed in peripheral

tissues and in central nervous systemBy blocking one or both enzymes prostaglandin formation

diminishesLess severe pain states ( early arthritis, headache,backache) are

commonly treated with nonselective NSAIDs or antipyretic analgesics mostly used orally

↓Sensitization of sensory neurons,↑ Inhibition of spinal neuronsCOX-2 expression is constitutive in many tissues, gastrointestinal

epithelium, vascular endothelium, spinal cord and inhibition of COX-2 may exacerbate inflammation, impair ulcer healing

Selective COX-2 inhibitors confer an increased risk for thrombosis, myocardial infarction, renal impairment, hypertension, stroke, and liver toxicity

NSAIDS

ASA RECOMMENDS:controlled or extended release opioid therapy provides

effective pain relief for patients with low back pain or neuropathic pain for assessment periods ranging from 1 to 9 weeks, with nausea or vomiting and constipation as side effects

Tramadol provides effective pain relief for assessment periods ranging from 4 to 6 weeks

immediate release opioids, transdermal opioids, and sublingual opioids provide relief for back, neck, leg, and neuropathic pain for assessment periods ranging from 2 weeks to 3 months

Dizziness, somnolence, and pruritus are among reported side effects associated with opioid therapy

OPIOIDS

All three receptors (µ, δ, κ) mediate analgesia, but with differing side effects

Tolerance and physical dependence may occur with prolonged administration of pure agonists, and abrupt discontinuation or administration of an antagonist can result in withdrawal syndrome

Proposed mechanisms involved in pharmacodynamic tolerance include opioid receptor–G protein uncoupling, decreased receptor internalization/recycling, and increased sensitivity of the NMDA receptor

Increased nociceptive stimulation by tumor growth, inflammation, or neuroma formation are possible reasons for increased dose requirements

Opioids are effective in periphery ,at neuraxis and systemically

Systemically and spinally administered opioids can produce similar side effects, depending on the dosage and rostral/systemic redistribution

most effective drugs for severe acute and cancer-related chronic pain

prevalence of addiction is as high as 50% in patients treated with opioids for chronic nonmalignant pain

Thus, consistent with the multifactorial nature of chronic pain, it is highly questionable whether opioids alone can produce an analgesic response

Thus, the use of opioids as a sole treatment modality in chronic nonmalignant pain is not recommended

monoamine neurotransmitter found in sympathetic nervous system, gastrointestinal tract, and in platelets

Within the dorsal horn of the spinal cord, serotonergic neurons contribute to endogenous pain inhibition

5-HT1B/1D agonists are effective against neurovascular headachesTriptans inhibit neurogenic inflammation via 5-HT1D receptors on

trigeminal afferents, with additional sites of action on thalamic neurons and in the periaqueductal gray matter

Activation of vascular 5-HT1B receptors constricts meningeal and coronary vessels

Triptans can be applied orally, subcutaneously, or transnasally and have been used for the treatment of migraine

All triptans narrow coronary arteries via 5-HT1B receptors by up to 20% at clinical doses and should not be administered to patients with risk factors or coronary, cerebrovascular, or peripheral vascular disease

SEROTONERGIC DRUGS

used for treatment of neuropathic pain resulting from lesions to peripheral or central nervous system

cause may be ectopic activity in sensitized nociceptors from regenerating nerve sprouts, recruitment of previously “silent” nociceptors, or spontaneous neuronal activity

increased expression and trafficking of ion channels (e.g., Na+, Ca2+, TRP) and increased activity at glutamate receptor sites

stabilization of neuronal membrane by blockage of pathologically active voltage-sensitive Na+ channels (carbamazepine, phenytoin, lamotrigine, topiramate), blockage of voltage-dependent Ca2+ channels (gabapentin, pregabalin), inhibition of presynaptic release of excitatory neurotransmitters (gabapentin, lamotrigine), and enhancement of the activity of GABA receptors (topiramate)

Their most common adverse effects are impaired mental and motor function which limit their clinical use, particularly in elderly patients

Serious side effects have been reported, including hepatotoxicity, thrombocytopenia, and life-threatening dermatologic and hematologic reactions

ANTIEPILEPTIC DRUGS

Carbamazapine:first line treatment for trigeminal neuralgia used in acute onset PDN, post herpetic,central

pain, phantom limb, neural invasion by tumor,radiation fibrosis

monitor CBC, LFT, every 3 mnths100mg bd/day ↑by 100 mgbd-tds weekly to

600-800mg/dayOXCARBAZEPINE:300mg hs weekly ↑ 300mg/day max

1200mg/day

GABAPENTINFirst choice for neuropathic pain in eldrly,

PDN, post herpetic neuralgia and radiculopathy300mg hs-↑1st week to 300mg bd, ↑3rd week to

300mg tds- ↑ max of 1200-1600mg/deffect starts in 3 or 4 days and pain relief in 2

weeks dizziness, seadtion, nausea, rashesPREGABALIN

ASA recommends:delta calcium-channel antagonists provide

effective neuropathic pain relief for assessment periods ranging from 5 to 12 weeks

a meta-analysis found that sodium-channel antagonists provide effective pain relief for assessment periods ranging from 2 to 18 weeks

used for treatment of neuropathic pain – post herpetic, PDN- tension headache migraine,atypical facial pain- 1st line of treatment

nonselective norepinephrine/5-HT reuptake inhibitors (amitriptyline, imipramine, clomipramine, venlafaxine), preferential norepinephrine reuptake inhibitors (desipramine, nortriptyline), and selective 5-HT reuptake inhibitors (citalopram, paroxetine, fluoxetine)

The reuptake blockade leads to stimulation of endogenous monoaminergic pain inhibition in the spinal cord and brain

In addition, tricyclic antidepressants have NMDA receptor antagonist, endogenous opioid–enhancing, Na+ channel–blocking, and K+ channel–opening effects that can suppress peripheral and central sensitization

require monitoring of plasma drug concentrations to achieve optimal effect and avoid toxicity, unless sufficient pain relief is obtained with low doses

Patients with ischemic heart disease may have an increased risk for sudden arrhythmia, and patients with recent myocardial infarction, arrhythmia, or cardiac decompensation should not take tricyclic antidepressants at all

Adverse events include sedation, nausea, dry mouth, constipation, dizziness, sleep disturbance, and blurred vision

ANTIDEPRESSANTS

amitryptilline10mg/d hs-inc 25mg/d after 1 wk, 2-3 wks inc

50mg/d- max 75mg/dayASA recommends:tricyclic antidepressants provide effective pain

relief for variety of chronic pain etiologies for assessment periods ranging from 2 to 8 weeks, with dry mouth and somnolence or sedation as reported side effects

selective serotonin–norepinephrine reuptake inhibitors provide effective pain relief for variety of chronic pain etiologies for assessment periods ranging from 3 to 6 months

NMDA receptors involved in central sensitisation and wind up long term potentiation of pain

ASA RECOMMENDS:dextromethorphan and memantine are

equivocal regarding pain relief for patients with diabetic neuropathy, postherpetic neuralgia, or other neuropathic pain conditions (phantom limb pain, peripheral nerve injury, and CRPS)

provide pain relief for neuropathic pain for assessment periods ranging from 2 to 16 weeks

NMDA RECEPTOR ANTAGONISTS

many chronic pain syndromes depend to some degree on peripheral activation of primary afferent neurons

Localized administration can potentially optimize drug concentrations at site of pain generation while avoiding high plasma levels, systemic side effects, drug interactions, and need to titrate doses into therapeutic range

Topical NSAIDs are effective for a limited period (2 weeks) for chronic musculoskeletal pain

Local adverse effects included rash and pruritustopical tricyclic antidepressant (doxepin) has shown

efficacy in mixed group of patients with neuropathic pain and, as a mouthwash, in patients with chemotherapy-induced oral mucositis

TOPICAL AGENTS

Topically applied capsaicin interacts with nociceptive neurons via the vanilloid receptor (TRPV1)

after repeated application depletion of substance P in sensory neurons, direct neurotoxic effect that results in degeneration of small-diameter sensory nerve fibers

supplement for treatment of neuropathic pain in a small number of patients unresponsive to or intolerant of other therapeutic approaches

Topical formulations of local anesthetics block Na+ channels in primary afferent neurons,reduces impulse generation in both normal and damaged sensory neurons

Such neurons exhibit spontaneous and ectopic firing, which possibly contributes to certain conditions of chronic neuropathic pain

pain relief can be achieved with local anesthetic concentrations below those that totally block conduction of impulses

lidocaine patches and gels showed pain reduction in patients with postherpetic neuralgia and allodynia

patients with painful diabetic polyneuropathy, CRPS, postmastectomy syndrome, or post-thoracotomy syndrome can achieve relief of pain

Topically applied or locally injected opioids produce analgesia by activating opioid receptors on primary afferent neurons

upregulation and accelerated centrifugal transport of opioid receptors in sensory neurons and facilitation of access of opioid agonists to their receptors by disruption of the perineural barrier

Intra-articular morphine produces analgesia in chronic rheumatoid and osteoarthritis

Baclofen activates GABAB receptors presynaptically and postsynaptically, leads to decrease in excitatory and an increase in inhibitory neurotransmission

trigeminal neuralgia and central neuropathic pain side effects are drowsiness, dizziness, and

gastrointestinal distressBotulinum toxin is assumed to inhibit release of

acetylcholine at neuromuscular junction ,alleviate muscle spasticity

Side effects include pain and erythema at the injection site and unintended paralysis of adjacent muscles

OTHER ANALGESICS

THANKS