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Dr. Jyoti Patel
SYNONYMS
 ERYTHROMELAGIA
 CAUSALGIA
 SUDECK’S ATROPHY
 TRAUMATIC ANGIOSPASMS
 RSD
 SHOULDER‐HAND SYNDROME
 SYMPATHALGIA
 HYPERPATHIC PAN
 SMP (SYMPATHETIC MEDIATED PAIN)
HISTORY
RSD /CAUSALGIA/SHOULDER HAND SYNDROME/SUDECK’S ATROPHY ETC Silas Weir Mitchell
Drs . Moorehouse and Keen
1993 Name Changed ISAP CRPS DEFINED




CHRONIC
PROGRESSIVE
NERVE DISORDER
DYSFUNCTION IN THE CONTROL OF THE CENTRAL AND PERIPHERAL NERVOUS SYSTEM
 A COMPLEX BETWEEN SENSORY, MOTOR, ANS AND IMMUNE SYSTEM
 CHARACTERIZED BY PAIN, SWELLING, AND SKIN CHANGES.
 AFFECT ANY BODY PART
 An injury that does not follow the normal healing path
 It does not depend on the magnitude of the injury
 Sympathetic nervous system responds abnormally
 rule out other possibilities
 DVT
 CTSMI
 MI
 Tumor
 DDD
SYMPATHETIC
INCREASE TEMPERATURE
INCREASE BLOOD PRESSURE, STRENGTHENS THE PROTECTIVE FUNCTIONS
INCREASES MUSCLE METABOLISM
INCREASES BONE CIRCULATION
PARASYMPATHETIC
PAIN IN CRPS
 PAIN – constant, burning, stabbing (causalgia) relentless , allodynia, hyperpathic
 SPASMS‐ blood vessels, muscles dystopia , weakness
 INFLAMMATION‐ color changes , swelling , decrease mobility
 PSYCHOLOGICAL‐ insomnia, emotional, depression , irritability agitation
PAIN IN CRPS
 HYPERPATHIA

UNMYELINATED C‐THERMORECEPTORS
 ALLODYNIA

MYELINATED A‐BETA  BURNING PAIN

UNMYELINATED CHEMORECEPTORS
 CAUSALGIA


SHORT BETWEEN MYELINATED AND UNMYELINATED FIBERS
TYPE I
 RSD – SUDECK’S ATROPHY
ALGONURODYSTROPHY
NO NERVE DAMAGE
A TRIGGERED TISSUE INJURY
TYPE II
 CAUSALGIA
 OBVIOUS NERVE DAMAGE









TRAUMA
CEREBRAL LESIONS
CAD, MI
CVA, HEMIPLEGIA, PARALYSIS
RADIATION
REPEATIVE MOTION
SURGERY
IMMOBILIZATION
NO CAUSE
SYMPTOMS
 BURNING PAIN
SKIN SENSITIVITY
CHANGE IN SKIN TEMP
CHANGE IN SKIN COLOR
CHANGE IN TEXTURE
CHANGE IN HAIR AND NAIL GROWTH
CHANGE IN MOVEMENT
DEPRESSION
ANXIETY
PATHOPHYSIOLOGY
WIND‐UP
CNS SENSITIZATION
NMDA CYTOKINASE RELEASE
GLUTAMATE
NEUROGENIC SYMPATHETIC AFFERENT COUPLING
ADRENORECEPTOR GLIAL CELL PATHOPHYSIOLOGY
CORTICAL OXIDATIVE CHANGES
IMMUNE RESPONSE
INFLAMMATORY RESPONSE
CRPS ?
DISTRUBANCE OF THE ANS
NEUROPATHIC PAIN SYNDROME
 DIABETIC NEUROPATHY
 POSTHERPETIC NEURALGIA
 AIDS NEUROPATHY
 SHOULDER HAND SYNDROME
 MS

•SUSCEPTIBILITY
ANY AGE
3 TIMES GREATER IN FEMALES
YOUNG ADUTLTS
30% CIGARETTE SMOKERS
GENETIC
INCIDENCE
2‐5% PERIPHERAL NERVE INJURY
13‐70% HEMIPLEGIA
1‐2% BONE FX
SYMPTOMS
 BURNING
ELECTRICAL SENSATIONS
SHOOTIN PAIN
MUSCLE SPASMS
LOCAL SWELLING
HYDROSIS
TEMP CHANGES SYMPTOMS
LOCAL SWELLING
HYDROSIS
TEMP CHANGES JOINT TENDERNESS
BONE CHANGES
SOFTENING AND THINNING OF BONES
RESTRICTED MOVEMENT
STAGE I
 SEVERE BURNING PAIN
 MUSCLE SPASMS
 JOINT STIFFNESS
 RESTRICTED MOBILITY
 RAPID HAIR GROWTH
 VASOSPASMS
 TEMP AND COLOR CHANGES
STAGE II
DYSTROPIC SWELLING SPREADS
DECREASED HAIR GROWTH
NAILS CRACKED,BRITTLED, GROOVED,SPOTTY
OSTEOPORSIS
JOINTS THICKEN
MUSCLE ATROPHY
INFECTIONS
PAIN
STAGE III
 ATROPHIC STAGE
IRREVERSIBLE CHANGES
CONSTANT P[AIN
MARKED MUSCLE ATROPHY
SEVERE MOBILITY LOSS
CONTRACTURES
BONE SOFTENING /THINNING
STAGE IV
 IMMUNE SYSTEM FAILURE
DECREASED HELPER T‐CELLS
INCREASED KILLER T‐CELLS
RTHOSTATIC HYPOTENSION
INTRACTABLE EDEMA
ULCERATIVE SKIN LESIONS
MI/ STROKES
INCEASED CANCER AND SUICIDE
EXHUSTED SYMPATHETIC AND IMMUNE SYSTEM
DIAGNOSIS
 SPONTANEOUS PAIN
 80 % HAVE TEMP DIFFRENCES
 ALLODYNIA
 EDEMA
 DIAGNOSIS OF EXCLUSION
 TYPES DIFFER ONLY IN NATURE
IASP CRITERIA
 THE PRESENCE OF AN INITIATING NOXIOUS EVENT THE IMMIBILIZATION OF A LIMB
CONTINUATION OF PAIN, ALLODYNIA, HYPERALGESIA
EVIDENCE AT SOMETIME OF EDEMA, CHANGE IN BLOOD FLOWW, SUDOMOTOR CHANGES
DIAGNOSIS OF EXCLUSION
SENSITIVITY 98‐100%
SPECIFITY 35‐55%
TESTS
DIAGNOSIS OF EXCLUSION
DIAGNOSIS OF SYMPTOOMS
X‐RAY
THERMOGRAPHY
ELECTRODIAGNOSTICS
SYMPTHETIC BLOCKS
SWEAT TEST
SOME PTS IMPROVE WITHOUT TREATMENT
TESTS
 Triple Phase Bone scan
 Thermography
 Diagnostic Blocks
 Infrared Thermal Imaging
 QST‐quantitative thermal sensory evoked test
 Not valuable‐EMG/NCV, CT Scan, MRI
TREATMENTS
 NSAID OF LIMITED USE
 PHYSICAL THERAPY
 PSYCHOTHERAPY
 SYMPATHETIC BLOCKS
 MEDICATIONS
 SURGICAL  SCS
 INTRATHECAL PUMPS
 AVOID INACTIVITY
TREATMENTS
 MIRROR BOX TRERAPY
 AVOID ICE
 CONSERVATIVE USAGE OF NARCOTICS
BUPRE NORPHINE
 ANTIDEPRESSANTS
 ANTICONVULSANTS
 PHYSICAL TX
 PARFIN,HYDRO AND HYPEROSMOLAR TREATMENTS
TREATMENTS
 PROPRIOTHERAPY
 MUSCLE RELAXANTS
 MANNITOL
 CONSERVATIVE USE OF BENZODIAZEPINE

KLONIPIN
 ALPHA BLOCKERS 

PHENOXYBENZAMINE
CLONIDINE PATCH
TREATMENTS
 Rational polypharmacy
 Drugs will no completely prevent the need for abortive/rescue agents
 Mixed evidence that pts are unique
 Traditional agents
 Tramadol, mexiletine, methadone,  Psychological interventions‐relaxation training, biofeedback, cognitive changes
 Centrally mediated
TREATMENTS
 BOTULIUM TOXIN
 KETAMINE
NMDA BLOCKING
 INFUSION
 COMA

CONCLUSION
 CRPS: complex form of neuropathic pain associated with hyperpathia, neurovasuclar ,instability, neuro‐
inflammation and limbic system dysfunction triggered by stimulation of neurovascular thermorecepetors c‐fibers sensitized to norepiephine this afferent sensory impulse leads to CRPS
 Early stages of up regulation super sensitivity  Chronic stages shows dysfunctional of the system
CONCLUSION
 ACCURATE DIAGNOSIS
 EARLY TREATMENT
 PSYCHOLOGICAL SUPPORT
1
 Crps both sympathetically independent pain
 And sympathetically maintained pain
 RF controversial
 Ablative controversial
 Stepwise progression for treatments