THE ROLE OF IMMOBILIZATION IN CRPS

There is strong clinical research supporting the disuse model as a basis for most of the signs and symptoms of CRPS. Most people diagnosed with CRPS have experienced an inciting injury, such as a fracture or an identifiable soft tissue trauma with a period of immobilization or an invasive procedure requiring immobilization. The explanation that most of the signs and symptoms of CRPS may be due to immobilization has been mostly ignored.¹⁰⁷ The IASP diagnostic criteria itself requires the presence of an initiating noxious event, or a cause of immobilization for diagnosing CRPS. Bonica’s 1953 Staging of RSD describes limitation of movement and limitation of motion as indicators of RSD.¹⁰⁸ Immobilization leads to both motor and sensory changes that have been the hallmark of CRPS.¹⁰⁹ A typical history involving a twisting injury or fracture involves casting, with the added complaint of burning pain, several more casts or walking boots may be applied for months.¹¹⁰ Signs and symptoms associated with CRPS are much like those seen shortly after cast immobilization. Symptoms of prolonged casting include muscle atrophy, stiffness, skin discoloration, and often coarseness of the skin, hair, and nails.

The person with CRPS typically has intense burning pain. This pain is excruciating, whereby touching just a sheet of paper or a bed sheet to the affected limb can feel like fire. The person with CRPS learns to guard that extremity. Since movement increases the pain, those with CRPS stop moving and using their affected limbs in efforts to minimize their suffering. Many of the CRPS signs and symptoms can be produced with disuse alone, and longstanding pain from the disuse encourages further immobilization. Research has shown that this causes a sensitization of the central nervous system.^{111, 112} The pain and other symptoms continue even after the original injury is healed because of the tissue changes which occurred from prolonged disuse of the limb. Most CRPS patients have reduced range of motion, however at times, passive range of motion is possible even when active range of motion is not. If the reduced range of motion was a motor function alteration then both passive and active range of motion should be affected. These deficits are thought to be due to specific alterations of central regulation of the motor functions caused by the disease. A proposed mechanism for this dysfunction is a change in the central representation induced by increased nociceptive input and by decreased sensory cutaneous and proprioceptive input due to immobilization.¹¹³ In essence, the prolonged immobilization causes the person to be more sensitive to movement because of increased sensitivity of the small autonomic nerves.^{114, 115}

Clinicians at the University of Washington Pain Center conducted a prospective study in collaboration with colleagues from Uppsala University and the Academic Hospital at Uppsala.¹¹⁶ Twenty-three volunteers were casted in the non-dominant forearm for four weeks. No painful stimulus was added, since the purpose of the study was to look at immobility alone. All volunteers had temperature differences between the limbs after the casts were removed. PET (positron emission tomography) scanning showed that the immobility of the limb caused increased cerebral blood flow in areas associated with sensory processing, motor function, and emotions. Other changes caused by the immobility involved abnormal sweating, skin, hair or nail changes, hyperpathia and hypersensitivity. All of these signs and symptoms resolved following an active course of physical therapy. The researchers noted that in animal studies involving immobilization of the wrist and hind paw of rats, there was a clear demonstration of sensory changes from non-noxious to noxious findings such as thermal hyperalgesia to warmth, mechanical allodynia, and cold allodynia.^{117, 118} In one study, just seven days of hind paw immobilization produced several weeks of both tactile and thermal allodynia in rats.¹¹⁸  In conclusion they wrote, “It seems evident from the available data that many of the signs and symptoms of CRPS can be produced by immobilization alone…These data suggest we consider these signs and symptoms as the normal response to disuse.”¹¹⁹

If disuse is primarily responsible for the signs and symptoms of CRPS, then increasing sensory input through activity and other sensory stimulation should improve the situation or at least prevent further changes.^120-122 While range of motion and physiotherapy remains one of the top priorities to prevent CRPS and to curb its symptoms, what about the person who received all of these therapies but is left with significant disabilities and pain? The question remains, if immobility is largely responsible for the chronic symptoms of CRPS/RSD is there something else that can be done to resolve the condition, once it becomes established?