Complex Regional Pain Syndrome

2. COMPLEX REGIONAL PAIN
SYNDROME/REFLEX SYMPATHATIC
DYSTROHY
By: SAMI HALIM
(Senior Physiotherapist)
AKUH

3. OBJECTIVES
• Definition & Taxonomy
• History
• Epidemiology
• Pathophysiology
• Sigh & Symptoms
• Diagnostic Tests
• Differential Diagnosis
• Management
• Prevention

4. WHAT IS CRPS:
CRPS is a chronic, predominantly neuropathic and partly
musculoskeletal pain disorder often associated with
autonomic disturbance.
It is divided into two types.
oTYPE I
oTYPE II

6. McGILL PAIN INDEX

7. • TYPE I: (Reflex Sympathatic Dystrophy) 90%
Not linked to nerve damage in affected area.
e.g(fracture , amputation, sprains)
• TYPE II: (Causalgia) 15%
Linked with nerve damage in affected area or injury to
major peripheral nerves.
e.g (Median, Sciatic)

8. HISTORY
• During the Civil War, Silas Weir Mitchell,MD observed a
chronic pain syndrome in soldiers who suffered traumatic
nerve injuries
• Their symptoms included constant burning pain and
significant trophic changes
• He described this syndrome using the term Causalgia
(from the Greek kausis – “burning” and algos – “pain”)
• In the 1950’s, John Bonica (founder of the IASP)
introduced the phrase Reflex sympathetic dystrophy
after noticing the efficacy of temporary blockade of the
sympathetic nervous system in these patients.

9. • There have since been many confusing terms used to describe
the condition:
• Acute atrophy of the bone
• Algodystrophy
• Algoneurodystrophy
• Postinfarctional sclerodactyly
• Post-traumatic algodystrophy
• Post-traumatic dystrophy
• Post-traumatic sympathetic dystrophy
• Pseudodystrophy
• Reflex neurovascular dystrophy
• Shoulder hand syndrome
• Sudeck’s dystrophy
• Sympathalgia etc.

10. • In 1993, the International Association for the study of
pain [IASP] introduced the term Complex regional pain
syndrome to describe all pain states that previously
would have been diagnosed as RSD or causalgia-like
syndromes.

11. EPIDEMIOLOGY
• CRPS I: 21 per 100,000
• CRPS II: 4 per 100,000
• Female-to-Male ratio: 3:1
• Any age, but middle age predominates
• Median 42 years
• Onset 9 – 85 years of age

12. PATHOPHYSIOLOGY
• NOT KNOWN!!!
HYPOTHESIS:
• Increased Neurogenic Inflammation
Tissue trauma triggers the release of pro-inflammatory cytokines and
chemokines. These substances increase vasodilation, producing the
characteristic features of acute CRPS.
• Altered sympathetic nervous system function
In the chronic (cold) phase the CRPS-affected limb is cyanosed and
clammy as a result of vasoconstriction and sweating. This suggests that
excessive sympathetic nervous system outflow is a driving factor in
progression of the condition and maintenance of the pain.

13. • Autoimmunity
The presence of immunoglobulin G (IgG) autoantibodies against surface
antigens on autonomic neurons in the serum of patients with CRPS
suggests that autoimmunity may play a role in the development of this
condition.
• Genetic factors
Siblings of CRPS patients under 50 years were at three times higher risk of
developing the condition. HLA-B62 and HLA-DQ8 alleles were found to
strongly correlate with the development of CRPS.
• Central and peripheral sensitization
Increase the activity of local peripheral and secondary central nociceptive
neurons resulting in increased pain from noxious stimuli (hyperalgesia)
and pain in response to non-noxious stimuli (allodynia)

14. • Brain Plasticity
Neuroimaging studies of patients with CRPS have demonstrated a
decrease in area representing the CRPS-affected limb in the
somatosensory cortex compared to the unaffected limb. The
extent of reorganisation bears significant correlation with the pain
intensity and degree of hyperalgesia experienced by the patient.

15. SIGN & SYMPTOMS
• Major S/S:
• Distal edema – 80%
• Allodynia.
• Hyperalgesia
• Skin temperature changes – 80%
• Skin color changes
• Initially red, becomes pale in chronic disease
• Increase sweating
• Decreased ROM
• Nail and hair changes
• Increased growth in early disease

18. STAGES OF CRPS
CRPS Stage 1 (Acute)
0-3 months
“DYSFUNCTION STAGE”
• SKIN: Red, warm, swollen, dry, inflamed. Later color may change
to mottled and colder with marked hyperhyidrosis.
• DISTRIBUTION: Pain is not compatible with a single peripheral
nerve, trunk, or root lesion.
• MOTOR: Decreased ROM, weakness, spasm.
• X-RAYS: Normal.

19. CRPS Stage 2
3 – 6 months
“DYSTROPHIC STAGE”
• SKIN: Cool, moist, tight/shiny, swelling, Brittle hair,
brittle nails, discolored, edema.
• MOTOR: Weakness, Decreased ROM
• BONE SCAN: little helpful shows osteopenia.

20. CRPS Stage 3
6 months or after 1 year
“ATROPHIC STAGE”
• Pain is somewhat decreased (but still debilitating)
• less at rest, worse with passive motion
• Changes are irreversible, poor outcomes,
permanent disability
• SKIN: Atrophy, “waxy”, very thin, ulcerations, brittle nails.
• MOTOR: Decreased ROM, weakness, muscle & tendon
atrophy, contractures, dystonia, tremor. Nonfunctional limb.
• X-RAYS: Diffuse patchy osteoporosis (Sudeck’s Atrophy)

21. STAGE 1
STAGE 2
STAGE 3

22. DIAGNOSIS & TESTS

23. • Thermography.
• X-Ray
• fMRI
• Bone Scan
• EMG/NCS

24. DIFFERENTIAL DIAGNOSIS
• Unrecognized local pathology (fracture, sprain)
• Traumatic vasospasm
• Cellulitis
• Lymphedema
• Raynaud’s disease
• Thromboangiitis obliterans
• Erythromelalgia
• DVT
• Also, nerve entrapment syndromes, occupational overuse
syndromes, and diabetic neuropathy

25. MANAGEMENT
• Medication
• Physiotherapy/Occupational therapy
• Psychotherapy
• Nerve Blocks
• Implants
• Neurostimulator
• HBOT(Hyperbaric Oxygen Therapy)
• Sympathectomy
• Diet
• Alternative Therapies

26. MEDICATION:
• Prednisone (oral): anti-inflammatory, neuronal membrane
stabilizer
• Vitamin C (oral): antioxidant
• Alendronate (IV): osteoclast inhibitor
• Bretylium (IV): Autonomic ganglia blocker
• Ketansarin (IV): serotonin and alpha receptor antagonist
• Phentolamine (IV): alpha-1 receptor antagonist
• Lidocaine (IV): sodium channel blocker
• DMSO (topical): free radical scavenger
• Calcitonin (intranasal): osteoclast inhibitor
• Clonidine (epidural): alpha-2 receptor agonist
• Baclofen (intrathecal): GABA-B receptor agonist

27. PHYSIOTHERAPY/OCCUPATIONAL THERAPY:
• Treatment objectives for CRPS are to:
• Minimize pain
• Minimize edema,
• Normalize sensation,
• Promote normal positioning,
• Decrease muscle guarding and
• Increase activities of daily living (ADL)
• Active weight bearing exercises are emphasized

28. • TRANSCUTANEOUS ELECTRICAL NERVE STIMULATOR (TENS)
• EDEMA REDUCTION THERAPY
• KINESIO TAPING
• DESENSITIAZATION TECHQNIUE
Using different textures e.g feather, Cotton,Rice etc
• POSTURAL TRAINING
• STRESS LOADING
A stress loading program promotes active movement and compression of the affected joints
for a minimum of 3-5 consecutive minutes, three or more times each day.
Though stress loading may initially produce an increase in pain or swelling of the extremity,
after several days a decrease in symptoms will begin to be evident. Use of the affected
extremity in daily tasks is encouraged throughout rehabilitation to inhibit muscle guarding
and disuse atrophy.
Stress Loading consists of two principles: Scrubbing and Carrying

29. • CONSTRAINT INDUCED THERAPY (Constrain Unaffected Limb)
• GRADED MOTOR IMAGERY
• MIRROR THERAPY
• RELAXATION TECHNIQUES
• EXERCISE PROGRAM
PROM
Isometric exercises
Flexibility/Stretching
Aerobics
• POOL EXERCISES
MIRROR THERAPY
CONSTRAINT
THERAPY

30. GRADED MOTOR IMAGERY

31. VIRUALREHABILITATION

32. PSYCHOTHERAPY:
• Pain coping skills
• Biofeedback
• Relaxation training
• Cognitive behavioral therapy

33. NERVE BLOCKERS:
• Sympathetic Ganglion Blockers
• Regional/Pheripheral Nerve Blockers
• BOTOX
• Epidural

34. IMPLANTS:
• Spinal Cord Stimulator
• Dorsal Root Ganglion Stimulator
• Intrathecal Drug Pump
• Pain Controlled Analgesia
Intrathecal Drug Pump Spinal Cord Stimulator
Pain Controlled Analgesia Dorsal Root Ganglion Stimulator

35. NEUROSTIMULATOR:
Transcranial Magnetic Stimulation (Deep Brain Stimulation)

36. SYMPATHECTOMY:
• A sympathectomy is an irreversible procedure during which at least
one sympathetic ganglion is removed.
• It has an extremely high rate of failure.

37. HYPERBARIC OXYGEN THERAPY:
• Hyperbaric oxygen therapy involves breathing pure oxygen in a pressurized
room or tube.
• This helps fight bacteria and stimulate the release of substances called
growth factors and stem cells, which promote healing.
• The evidence is insufficient to support claims that hyperbaric oxygen
therapy can effectively treat CRPS.

38. DIET:
• RECOMMENDED FOOD
 Fresh Fruits/Veg’s
 Fish
 Fowl
 Lean Meats
 Low Fat Dairy products
 Whole Grains
 Olive oil
 Nuts / raisins
 Cooking Method Should be: Roasted, Grilled,Baking or Boiling.
• NON RECOMMENDED FOOD
 Cookies, cakes, chocolates, candies and cocktails
 Alcohol, fizzy drinks, Coffee.

39. ALTERNATIVE THERAPIES:
• Accupuncture
• Massage therapy
• Meditation
• Yoga or Tai Chi
• Reiki
• Hypnosis
• Vitamin D etc

41. PREVENTION
• Oral Vitamin C 500mg/Day for 50 days from injury

42. CRPS AWARENESS COMMUNITIES
• http://www.burningnightscrps.org
• http://www.rsdhope.org/
• http://rsds.org/

43. REFERENCES
• http://www.rsdhope.org/how-is-crps-diagnosed.html
• http://www.medicinenet.com/reflex_sympathetic_dystrophy_syn
drome/page2.htm
• http://www.burningnightscrps.org/sufferers/crps-rsd-
treatments/#noninvasive
• http://www.mayoclinic.org/diseases-conditions/complex-
regional-pain-syndrome/basics/causes/con-20022844
• https://en.wikipedia.org/wiki/Complex_regional_pain_syndrome#
Cause

44. THANK YOU…………… ANY QUESTION ?