Complex Regional Pain Syndrome; causes, symptoms and treatment




Reflex sympathetic dystrophy (RDS) and causalgia are former diagnoses that are now classified as complex regional pain syndromes I and II, respectively (CPRS type I and CPRS type II). This revised taxonomic system was developed by a consensus conference in 1993 to clarify confusion about the meaning and interpretation of the previous diagnoses. Basically, this is a grouping of complex painful disorders that develop as a consequence of trauma affecting the extremities with or without an obvious nerve lesion.

Complex Regional Pain

Classification and Clinical Features of Complex Regional Pain Syndromes

CRPS type I (reflex sympathetic dystrophy)

Develops after an initiating noxious event

Spontaneous pain or allodynia/hyperalgesia

Edema, vascular abnormalities

Abnormal sudomotor activity

Non-nerve origin

CRPS type II (causalgia)

Develops after nerve injury

Not limited to territory of injured nerve

Edema; skin blood flow abnormality

Abnormal sudomotor activity

Clinical Features of CRPS (in addition to the differences listed above)

Symptoms more marked distally in an extremity

Symptoms progress in intensity and spread proximally

Symptoms vary with time

Disproportion of symptoms in relation to the causing event

A specific diagnosis, such as diabetes or fibromyalgia,has been excluded

Etiology and Symptoms

The underlying mechanism that stimulates the onset of these syndromes is unclear.1 They usually develop in association with a persistent, painful lesion, such as a painful shoulder; after a cardiovascular accident or myocardial infarction; with cervical osteoarthritis; after trauma such as a fracture or sprain; with burns or immobilization; or after surgery or cardiac catheterization.1 There may or may not be an obvious nerve lesion.

Three Stages of CRPS Type I (RSD)

Stage I: acute/reversible stage. This stage of vasodilation lasts 3 weeks to 6 months. Pain, the predominant feature, is usually out of proportion to the severity of the injury. There is hyperhidrosis, warmth, erythema, rapid nail growth, and edema in the distal extremity

Stage II: dystrophic or vasoconstriction (ischemic) stage. This stage lasts 3 to 6 months. It is characterized by sympathetic hyperactivity, burning pain, and hyperesthesia exacerbated by cold weather. There is mottling and coldness, brittle nails, and osteoporosis.

Stage III: atrophic stage. This stage is characterized by pain either decreasing or becoming worse and

by severe osteoporosis. Muscle wasting and contractures may occur. The condition can last for months or years, but spontaneous recovery often occurs within 18 to 24 months.

Common Impairments

Pain or hyperesthesia at the shoulder, wrist, or hand out of proportion to the injury.

Limitation of motion develops. Typically, the shoulder develops limitation in a capsular pattern with most restriction in lateral rotation and abduction. In the wrist and hand, the most common restrictions are limited wrist extension and metacarpophalangeal and proximal interphalangeal flexion. Edema of the hand and wrist secondary to circulatory impairment of the venous and lymphatic systems, which in turn precipitates stiffness in the hand.

Vasomotor instability. Trophic changes in the skin. As the condition progresses, the pain subsides but limitation of motion persists. The skin becomes cyanotic and shiny, the intrinsic muscles of the hand atrophy, subcutaneous tissue in the fingers and palmar fascia thicken, nail changes occur, and osteoporosis develops.


Early Intervention

It is a progressive disorder unless vigorous intervention is used during the acute stage. The best intervention is prevention when it is recognized that development of CRPS type I (RSD) is a possibility, such as when there has been trauma to the extremity or when the extremity is immobilized. It requires that the therapist motivate the patient to move the entire extremity safely, minimize edema and vascular stasis with elevation and activity of the distal segments (squeeze and open hand with upper extremity lesions, or ankle pumping and toe curls with lower extremity lesions), and be alert to the development of adverse symptomatology.

Stage I (early intervention)

Relieve pain and control edema


Retrograde massage

Elevate, elastic compression

Increase mobility (specific to involved tissues)

Tendon gliding in the hand

Nerve mobilization

Improve muscle performance

Stress loading in quadruped position


Improve total body circulation

Low impact aerobic exercise

Desensitize the area

Desensitization techniques for brief periods 5_/day

Educate the patient

Teach interventions that deal with variable vasomotor responses; when to use heat, cold, gentle exercises

Intervention—Stages II and III

Pain management. Modalities are often used as palliative interventions prior to or in conjunction with exercise to minimize pain.

Desensitization. Progress the desensitization techniques to increase the patient’s tolerance to various


Mobility. Use joint mobilization, neuromobilization, and stretching techniques to address tissues limiting mobility. Because of the pain and significant limitations, little progress is sometimes seen with the stretching maneuvers, so surgical intervention may be required to gain motion.

Muscle performance. Develop an exercise program to improve strength, endurance, and overall functional performance that meets the specific needs of the patient.

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