Complex Regional Pain Syndrome

Chronic progressive condition characterized by severe pain, swelling, and skin changes.


  • Type 1 (AKA RSD) : not associated with nerve injury, but may be associated with other trauma —
  • Type 2 (AKA causalgia): associated with nerve injury

Both types:

  • spontaneous pain or allodynia not limited to single peripheral nerve distribution — disporportionate to inciting event.
  • history of edema, blood flow abnormality, abnormal sweating.
  • no better explanation exists.


  • upregulation of NMDA receptors
  • elevated glutamate levels
  • immunogenic
  • cytokine release
  • neurogenic inflammation
  • adrenoreceptor pathology
  • sympathetic afferent coupling
  • …etc.


  • 3:1 female predominance
  • most common in 4th decade, but wide variation in age range affected.
  • 2-5% of patients with a peripheral nerve injury


  • at site of a previous injury (of varying severity)
  • spread beyond site of original injury.
  • most commonly burning pain
  • also muscle spasms, local swelling, joint tenderness / stiffness, nail and skin changes.
  • allodynia / hyperalgesia
  • eventually disuse atrophy and stiffness.


  1. Type one is characterized by severe, burning pain at the site of the injury. Muscle spasm, joint stiffness, restricted mobility, rapid hair and nail growth, and vasospasm.
  2. Type two is characterized by more intense pain. Swelling spreads, hair growth diminishes, nails become cracked, brittle, grooved, and spotty, osteoporosis becomes severe and diffuse, joints thicken, and muscles atrophy.
  3. Type three is characterized by irreversible changes in the skin and bones, while the pain becomes constant and may involve the entire limb. There is marked muscle atrophy, severely limited mobility of the affected area, and flexor tendon contractions.

Diagnosis is primarily clinical, but adjuncts are:

  • thermography
  • sweat testing
  • radiography – patchy osteoporosis;  bone scan, bone densitometry
  • electromyopgraphy (for type II)
  • nerve blocks


  • PT/OT: desensitization, mobilization
  • Medication: GABA agonists, steroids, antidepressants, NSAIDs
  • nerve blocks
  • neurostimulation
  • sympathectomy
  • ketamine

Collagen tubes for digital nerve

Retro review
12 patients
9 have outcomes data. 12-22 months

2pt: good/excellent 8/9
SW: 5 full/ dim lt touch 2 / dim prot.sens 1 / loss prot. Sens 1

BG: collagen vs PGA tubes avail.
PGA tubes have head to head comparison with primary repair and grafting. – weber 2000 randomized trial

Mat. & Methods:
2 yr period
2pd, sw, qdash
Seg loss 1-2 cm
Ci’s : infx, contam, systemic instability, primary repair possible w/o tension

Blinded evaluation
8 men 4 women. Avg 33yo
Hand dominance 50/50
4 isolated nerve injury 8 multiple trauma
2 f/u < 1yr
1had subsequent amputation
Avg fu 15 mos for remaining 9

Technique: 20 mm tubes, saline, 8-0 or 9-0, epineural
Post-op: std sensory reeducation protocol
Tt80avg. Surg time 140 avg


Promising results
Sensory model only (no motor nerves)
? Similar to primary nerve repair and repair with autograft?

Small size, 3 Pts lost to fu
No comparison cohort: primary repair/ repair with graft

Discussed other studies

The bow of the radius

“it has a slight lateral convexity or bowing.”
“the body is concave anteriorly in its proximal three-fourths and flattened in its distal one-fourth.”

  • Clinically oriented Anatomy. 3ed  KL Moore p.555

Saturday run

june 14
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running log

univ bridge to idylwyld loop
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Parallel Blog.

I started posting notes on a parallel blog:

Principles of Tendon Transfer

  1. correction of contracture
  2. adequate strength
  3. adequate amplitude (3/5/7 rule at hand & wrist)
  4. straight line of pull — artificial pulleys always attenuate
  5. 1 tendon : 1 function  (exception is FDS insertion allows natural split to 2 insertions — but definitely a fiddle)
  6. synergism
  7. expendable donor
  8. tissue equilibrium
N.B. timing of transfers.
3 key questions:
  1. What function is missing?
  2. What can be sacrificed?
  3. What does the patient need?