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10 Articles in Volume 8, Issue #8
Botulinum Toxin Type-A in Pain Management
Chronic Migraine: An Interactive Case History
Consistent Documentation Drives Compliance
Muscle Physiology, Kinetics, Assessment, and Rehabilitation
Non-surgical Decompression Treatment for Carpal Tunnel Syndrome
The Pseudo-RSD Pain Patient
Therapeutic Laser Evolution: Part 1
TMJ Pain and Temporal Tendonitis with Autonomic Features
Topical Use of Morphine
Toward a Neuroethics of Pain Medicine

The Pseudo-RSD Pain Patient

A case report of a patient successfully mimicking the signs and symptoms of reflex sympathetic dystrophy (RSD) together with a review of what is currently known about RSD presentation, epidemiology, pathophysiology, and a discussion on impairment determination for RSD sufferers.
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Reflex Sympathetic Dystrophy (RSD) is a challenging and very costly condition. In this article, we discuss a female who was injured on the job, and successfully mimicked the signs and symptoms of RSD. Subsequently several physicians opined that she was totally disabled and gave her a very high impairment rating. Here we review the clinical presentation, diagnosis, epidemiology, pathophysiology, and the problem of impairment rating in RSD.

Case Presentation

A 45-year-old female injured her right shoulder. Her symptoms included severe pain, numbness in her right arm, and “a cold feeling.” She had no history of pre-existing shoulder pathology. She was seen in the emergency room, where plain radiographs were unremarkable, and was told that she had a right shoulder contusion. She did not return to work. Nonsteroidal anti-inflammatory and physical therapy prescribed by her family practitioner were not helpful. A chiropractor diagnosed cervical brachial syndrome. He told her that she had subluxations in the cervical and thoracic spines and that she would need prolonged chiropractic treatment. After three months of chiropractic treatment there was no improvement. She was then referred to an orthopedic surgeon. An MRI scan of the right shoulder revealed degenerative changes. The orthopedic surgeon diagnosed osteoarthritis, frozen shoulder, and chronic shoulder sprain. He further said that there was no surgical problem and prescribed Lorcet. Lorcet taken four times daily did not relieve her pain adequately. The insurance carrier sent her for an Independent Medical Examination (IME). The IME doctor referred her to a neurologist for evaluation of the numbness. After performing needle electromyographic testing (which was negative), the neurologist prescribed Neurontin. Her family doctor prescribed Cymbalta for complaints of anxiety and depression. Next, she went to see a second chiropractor who also told her that subluxations in her neck were her main problem. She continued to take the Lorcet, Cymbalta, Neurontin, Motrin, and also additional Percocet for flare-ups. Her family doctor next referred her to a pain management specialist. This physician told her that she had reflex sympathetic dystrophy (RSD) and needed injections. A three-phase bone scan was negative. Her pain did not respond to the series of neural blocks performed by the pain management physician, but continued to get worse. She wore a shoulder sling most of the time. She was prescribed a series of different opioids, eventually ending with fentanyl patch 75 mcg a day. After being off work for three years, she applied for Social Security disability benefits. She reported intractable pain and severe limitations in activities of daily living. Her application was approved after a hearing in front of an administrative law judge. A neurologist at a tertiary care medical center told her that she had “the worst case of RSD” he had ever seen. The insurance carrier wanted to settle her case. They sent her to another independent medical examiner doctor who had 20 years experience. He opined a 55% whole person impairment based on the fourth edition of the Guides to the Evaluation of Permanent Impairment published by the American Medical Association (AMA). He noted severely decreased range of motion in the neck, right shoulder, right elbow, and right wrist. There was “bluish discoloration” and swelling of the right arm, associated with a “75% sensory loss.” A second opinion was requested of a university-based board-certified occupational medicine physician. His physical examination findings were consistent with the previous examiner. He reported that she kept her arm held in abduction and that the range of motion in the involved limb was nonfunctional. He opined a 60% whole person impairment, and that she was permanently and totally disabled as a result of her occupational injury. Shortly thereafter, a surveillance tape demonstrated that she was able to move her right arm without any difficulty. No evidence of discoloration, swelling, or limitation in range of motion could be seen.

In summary, a 45-year-old female presented with numerous physical findings consistent with reflex sympathetic dystrophy (RSD). Several well-trained, experienced physicians in neurology, pain management, chiropractic, and occupational medicine examined her and concluded that her complaints were legitimate and that she was disabled. Except for positive findings on physical examination, objective medical testing was not remarkable. She was determined to have a 60% whole person impairment which was the approximate equivalent of a $500,000 award for her injury. However, under surveillance it was apparent that she did not have any physical problem at all. How could her right arm have become swollen and discolored when she came to see her doctors? We hypothesize that she may have simulated these physical findings by applying a tight rubber band just below the shoulder, in order to constrict circulation to her arm. This would cause both swelling and discoloration, the stigmata of RSD. Removing this rubber band just before walking in to see the doctor would still leave these “positive” physical examination findings.


Reflex Sympathetic Dystrophy (RSD) is also known as Chronic Regional Pain Syndrome (CRPS) Type I. CRPS is defined by persistent regional pain and sensory changes, usually following a noxious event, after which the pain is disproportional to the inciting event. In CRPS Type I, there is no definable nerve lesion whereas in the less common CRPS Type II, a definable nerve lesion is present. Otherwise, there is no distinction. CRPS is an important condition for the specialist in disability medicine, as a large majority of these patients have permanent disability. Preceding events include traumatic injury, surgery, cerebrovascular accident, and myocardial infarction. The most common precipitating event is soft tissue injury. The clinical syndrome of CRPS was first described in the 1860s by French neurologist Claude Bernard, who considered the possibility of an association between the sympathetic nervous system and certain types of pain.1 Mitchell, an American army surgeon and student of Bernard, observed the characteristic symptoms of CRPS in soldiers who sustained nerve injuries consequent to gunshot wounds during the Civil War. He termed the syndrome causalgia. Historically, CRPS has been known by many other names. These include Sudeck’s atrophy, algodystrophy, post-infarction sclerodactyly, peripheral trophoneurosis, cervical sympathetic dystrophy, sympathetic dystrophy syndrome, osteoporosis-posttraumatic, shoulder-hand syndrome, causalgia-dystonia syndrome, acute bone atrophy, major traumatic dystrophy, and minor traumatic dystrophy.

Last updated on: October 30, 2012