Complex Regional Pain Syndrome (CRPS) / Justin Hata, MD Western Occupational Health Conference - Newport Beach, CA / September 30 - October 2, 2010 1 Complex Regional Pain Syndrome (CRPS) Justin Hata, MD UC Irvine Healthcare Assistant Clinical Professor Department of Anesthesiology & Perioperative Care Department of Physical Medicine & Rehabilitation Chief, Pain Medicine Division Director, UCI Center for Pain Management Co-Director, UCI Comprehensive Spine Program Disclosure Information Western Occupational Health Conference 2010 Justin Hata, MD Assistant Clinical Professor, UC Irvine Healthcare “I have nothing to disclose.” “I will not discuss off-label use and/or investigational use in my presentation.” Objectives 1. Define CRPS 2. Discuss work-up 3. Explore treatment options, including medications 4. Explore current concepts
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Complex Regional Pain Syndrome (CRPS)Complex Regional Pain Syndrome (CRPS) Justin Hata, MD UC Irvine Healthcare Assistant Clinical Professor Department of Anesthesiology & Perioperative
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Western Occupational Health Conference - Newport Beach, CA / September 30 - October 2, 2010 2
Definition
International Association for the Study ofPain (IASP): A variety of painful conditions following injury
which appears regionally having a distalpredominance of abnormal findings,exceeding in both magnitude and duration theexpected clinical course of the inciting eventand often resulting in significant impairment ofmotor function, and showing variableprogression over time.
History1600’s: Ambrose Paredescribed persistent pain& contractures afterbloodletting procedure forKing Charles IX1700’s: Percivall Pottreports burning pain andatrophy in injured limbs1800’s: Claude Bernardmentioned a syndrome ofpain associated with thesympathetic nervoussystem
Silas Weir-Mitchell1864: “Causalgia” in Civil Warsoldiers with limb injuries “…the most terrible of all tortures
which a nerve wound mayinflict…Its favorite site is the foot orhand. . . Its intensity varies fromthe most trivial burning to a state oftorture...The part itself is not alonesubject to an intense burningsensation, but becomes exquisitelyhyperanesthetic, so that a touch ortap of the finger increases thepain."
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SMP versus SIP
Pain relieved by blockade of the efferentsympathetic nervous system “RSD” previously used based on observation that
sympatholytic procedures relieved pain in manypatients
Not all patients with CRPS have SMP Not all SMP is CRPS
CRPS patient may have sympatheticallyindependent pain (SIP) introduced by Campbelland Meyer in 1992
Mechanism of SMP
Normal response to injury is activation ofsympathetic reflex arcSMP involves prolonged continuation ofthe sympathetic reflex arc Hyperdynamic state of vasoconstriction, tissue
ischemia, and pain Increased activity and _-adrenergic receptor
sensitivity of nociceptive neruons Nociceptors now activated by norepinephrine
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Autonomic Disturbances
Sympathetic deficit Warmth Loss of vasoconstrictor reflexes
Sympathetic over-activity Sweating Coldness
Cold pattern commonly in CRPS patientswith the longest duration of pain Warm, dry limb of CRPS can evolve into a cool
moist limb as the condition progresses
Motor Disorders (MDs)
Loss of voluntary controlBradykinesiaDystoniaMyoclonusTremorMay occur early in the disease coursePrevalence of MDs increases as thedisease duration lengthens
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Physical/Occupational Therapy
Both PT & OT have positive effectAcute Stage Immobilization Careful contralateral PT
Dystrophic Stage Passive PT with active isometric exercises Isotonic training Sensory desensitization program
2010 European EBM Guidelines forCRPS Type I
Multidisciplinary task forceLiterature review of treatment effects for CRPS IStudies published between 1980 – 2005Conclusions: For pain treatment: WHO analgesic ladder is advised For neuropathic pain: anticonvulsants and TCAs For inflammatory symptoms: free radical scavengers (DMSO or
N-acetylcysteine) To promote blood flow: vasadilatory medication and sympathetic
blockade show insufficient effect PT/OT advised to decrease functional limitations Vitamin C for primary prevention after wrist fx Further research needed!
Medications: 2010 European EBMGuidelines
No evidence or insufficient evidence forbeneficial effect Tylenol NSAIDs Opioids Local anesthetics Antidepressants Capsaicin Oral muscle relaxants Botulinum toxin Intrathecal baclofen administration
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InterventionsSympathetic blockade: Not useful for TxSympathectomy – Indications that may improvepain: surgical, chemical, or radiofrequencyIV Regional Block – No indication w/bretylium,guanethidine, local anesthetic, clonidine,ketoralac Possible improvement w/ketanserine or Infliximab*
Neuromodulation – Indication for painreduction and improved QOL: spinal cordstimulators (SCS)
Psychotherapy
Biofeedback
Stress Management
Relaxation Training
Family Therapy
Movement Disturbances Treatment
No RCT of PT, OT, or oral pharmacotherapy intreatment of MDs in CRPS.Splints or plaster casts are often ineffective May even worsen dystonic postures of CRPS
BZD and high doses of baclofen may bebeneficial in the treatment of dystonia andspasmsNo controlled studies for use of botulinum toxinin dystoniaIntrathecal baclofen: 1 study, small cohort,improved dystonia
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Sensory FactorsQuantify pain by visual analog scale (VAS), if practical.Document qualities of pain using the McGill short-form.Quantify temperature allodynia by a standard Peltier-type device.Quantify mechanical allodynia using von Frey testing.Measure deep mechanical sensitivity by algometer, overmuscle and joint.Functional imaging provides the best data: a fullyobjective correlate with evoked pain (and hyperalgesia)Quantitative Sensory Testing
Vasomotor FactorsLaser Doppler: direct, fully objectivemeasure of vasomotor toneLimb temperature: indirect, yet objectivemeasure of cutaneous and subcutaneousblood flowMethods in order of objectivity andquantification: Infrared telethermography, thermistors,
thermometers, and temperature tape“Space suits”: manipulate and measurevasomotor tone experimentally
Sudomotor/Edema Factors
Can be objectively measured Quantitative sudomotor axon response testing
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Motor FactorsSubjectively quantitate weakness by scoresFeatures of certain motor signs can be measured,such as bradykinesia and general activity (e.g.,accelerometer)Currently no reliable scores or metrics formyoclonus, athetosis, dystonia, or contractureSkin, nail, or hair trophic changes use subjectivemeasuresRange of motion: GoniometerBone density (Sudeck's atrophy) can be measuredSmall nerve density can be quantitated
Take Home Points
CRPS I (aka RSD) = NO nerve injuryCRPS II (aka causalgia) = nerve injuryNon-dermatomal pain out of proportion toinciting eventObjectification of autonomic, motor, trophic, orsensory changesSMP may or may not be presentMultidisciplinary treatment with medications, PT,interventions, psychotherapy
ReferencesProposed new diagnostic criteria for complex regional pain syndrome. Harden RN, Bruehl S,Stanton-Hicks M, Wilson PR. Pain Med. 2007 May-Jun;8(4):326-31.What does the mechanism of spinal cord stimulation tell us about complex regional painsyndrome? Prager JP. Pain Med. 2010 Aug;11(8):1278-83.Movement disorders in complex regional pain syndrome. van Hilten JJ. Pain Med. 2010Aug;11(8):1274-7.Vasomotor disturbances in complex regional pain syndrome--a review. Wasner G. Pain Med.2010 Aug;11(8):1267-73.Sensory disturbances in complex regional pain syndrome: clinical observations, autonomicinteractions, and possible mechanisms. Drummond PD. Pain Med. 2010 Aug;11(8):1257-66.Role of neuropeptide, cytokine, and growth factor signaling in complex regional pain syndrome.Kingery WS. Pain Med. 2010 Aug;11(8):1239-50.A hypothesis for the cause of complex regional pain syndrome-type I (reflex sympatheticdystrophy): pain due to deep-tissue microvascular pathology. Coderre TJ, Bennett GJ. Pain Med.2010 Aug;11(8):1224-38.Objectification of the diagnostic criteria for CRPS. Harden RN. Pain Med. 2010 Aug;11(8):1212-5.An update on the pathophysiology of complex regional pain syndrome. Bruehl S. Anesthesiology.2010 Sep;113(3):713-25.Evidence based guidelines for complex regional pain syndrome type 1. Perez RS, Zollinger PE,Dijkstra PU, Thomassen-Hilgersom IL, Zuurmond WW, Rosenbrand KC, Geertzen JH; CRPS Itask force. BMC Neurol. 2010 Mar 31;10:20.