Pain Syndromes (Week 4--Pham and Melega) Flashcards
Complex Regional Pain Syndrome (CRPS)
Type I (Reflex Sympathetic Dystrophy–RSD) and Type II (causalgia–nerve damage)
Pain is hallmark and is regional/disproportionate
Signs of vasomotor and motor dysfunction
Diagnosis of exclusion
Usually preceded by injury to single limb
Female > male (3:1)
RSD and Causalgia
What Complex Regional Pain Syndrome (CRPS) used to be called? Now the two types??
RSD (Reflex Sympathetic Dystrophy): disproportionate pain, autonomic dysfunction, sympathetically maintained pain
Causalgia: described in WWII, persistent burning pain following gun shot wound
Causes of CRPS
Sprain/strain
Post-surgical
Spontaneous
Fracture
Contusion/crush
Mechanism of RSD
Original injury initiates pain impulse carried by sensory nerves to CNS
Pain impulse triggers impulse in sympathetic nervous system which returns to site of injury
Sympathetic impulse triggers inflammatory response causing vessels to spasm leading to swelling and increased pain (get burning extremity pain, red mottling of skin)
Pain triggers another response, establishing a cycle of pain and swelling
What can acute trauma cause?
Release of “algesic soup” that can result in sensitization of primary afferent neurons and neurogenic inflammation:
Substance P can increase vascular permeability, induce release of cytokines, attract leukocytes to site of injury (SP also causes release of bradykinin)
Bradykinin can cause vasodilation, increase SP release, sensitize nociceptors
Prostaglandins contribute to nociceptive sensitization
NE activation of peripheral nociceptive terminals (NE to alpha 1 sends out collaterals to activate C fibers)
Ectopic production of receptors (also expression of receptors of phenotype not normally expressed on nociceptor (NE, NGF))
Sprouting of new collaterals on nociceptor
Drugs used for descending inhibition
These drugs mildly enhance NE and 5HT release from descending neurons to inhibit ascenting nociceptive information
TCAs
SSRIs
SNRIs
Opioids
Tramadol
Drugs used for peripheral sensitization
These drugs block the Na+ channel to decrease the hyperactivity that occurs when you have peripheral sensitization
Carbamazepine
Phenytoin
TCAs
Topiramate
Lamotrigine
Lidocaine
Drugs used for central sensitization
These drugs block the NMDA receptor in the spinal cord to block incoming nociceptive signals to secondary neurons that occur when you have central sensitization
Ketamine
Topiramate
Dextromethorphan
Methadone
Others (don’t block NMDA receptor): capsaicin, NSAIDs, COX2 inhibitors, lidoderm patch
Gabapentin blocks Ca2+ channel
Clinical findings of CRPS
Pain: hyperalgesia, allodynia
Autonomic: edema, color change, temperature, sweating
Motor: tremor, weakness, contracture
Trophic: change in hair, nails, skin
Acute phase of CRPS
Tender
Edematous limb
Warm
Erythema
Reduced function
Progression: (?) increasing edema, hyperhidrosis, decreased limb temperature, nail thickening, hair coarseness increases
Dystrophic phase of CRPS
Ischemic phase
Still painful
Extremely cooling
Pale
Sweaty
Brittle nails
Brawny edema
Atrophy starting
Radiographic changes
Atrophic phase of CRPS
Whole limb involvement
Pain variable
Skin smooth, shiny
Cool extremity
Hair loss
Tapered digits
Contractures
Atrophy
Osteoporosis
Radiographic changes of CRPS
Periarticular osteopenia
Preservation of joint space though!
Prior ortho pin?
S/P Colles’ fracture?
Psychological changes of CRPS
Depression
Anxiety
Fear
Anger
Failure to cope
Diagnostic tests for CRPS
Plain film: osteopenia
Three phase bone scan: blood pooling; more blood in painful area (but if do this too early or too late, could be normal)
Thermography: hot zones
Sympathetic blocks: pain resolution after injection (for diagnosis need to catch it early) (put lidocaine near symp chain)