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.
Discussion
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.
Clinical Presentation
Patients may describe the pain as deep, burning, aching, tearing, crushing, or throbbing. Edema, vasomotor (skin temperature and color) and/or sudomotor (sweating) abnormalities are present in the affected region at some point in the history. Skin temperature changes and increased or decreased sweating may be seen. Symptoms often spread beyond their original location. In late stage CRPS, there are trophic changes including contractures, waxy skin changes, altered hair growth, brittle, ridged nails, and bony demineralization visible on radiography. It has been estimated that in 35% of cases there may be no identifiable precipitating event.² The diagnosis should be made only after excluding other conditions that could account for the symptomatology.
Physical examination typically reveals a nondermatomal or stocking and glove distribution of sensory deficits. Allodynia, hyperalgesia, and hyperpathia may be evoked. Allodynia is pain resulting from a stimulus that does not usually provoke pain, such as light touch. Criteria to be considered in assessing allodynia include failure for the stimulus to cause pain in other areas of the body, and a change in the quality of the sensation. Hyperalgesia is an increased response to a stimulus that is normally painful. Hyperpathia is an abnormally painful reaction to a stimulus that may be explosive in nature, may include the inability to identify or localize the stimulus, and may include a delayed radiating aftersensation. Anesthesia dolorosa, a complete absence of sensibility to touch in the area of severe pain, may also be present. The pain associated with CRPS is typically worse with movement. Motor dysfunction may include weakness, tremor, hyperreflexia, dystonia, and myoclonic jerks. The pain associated with RSD is typically reduced with elevation of the extremity and worsens with dependency. This has been referred to as the orthostatic component of RSD. The affected limb may also feel foreign in a phenomenon known as cognitive neglect.
The diagnosis of CRPS is primarily clinical. No diagnostic test proves conclusively that the patient has CRPS, as no test is sufficiently specific. Plain film radiographs may reveal mottled radiolucencies that look similar to those found in osteomyelitis. Other radiographic signs of CRPS include metaphyseal osteoporosis (Sudeck’s atrophy), tunneled cortices, and endosteal resorption. Findings on bone scintigraphy include a periarticular pattern of diffuse uptake, hypoactivity due to decreased vascular supply, and increased uptake secondary to vasomotor instability. Magnetic resonance imaging may show soft tissue swelling, skin thickening or thinning, tissue enhancement with contrast material, and muscle atrophy. A positive response to a regional sympathetic block is supportive of the diagnosis; however there is a substantial placebo effect. Needle electromyography (EMG) is not useful. Other, less common tests have also been proposed. Lowe et al. proposed that laboratory evaluation of autonomic indices improves the clinical evaluation.³ Vasomotor tone can be measured with laser Doppler flowmetry (DLF) and infrared thermometry. Vasomotor tone asymmetries were found in 80% of their cases, quantitative sudomotor axon reflex test asymmetries were seen in 75%, and resting sweat output asymmetries were seen in 67%. Bej and Schwartzman looked at cutaneous blood flow, finding that the rhythmic cycling of cutaneous blood flow that was present in a control group was absent in patients with CRPS.⁴
It is recommended that proper evaluation of CRPS requires examination on multiple occasions. To arrive at an early diagnosis after trauma, the symptoms should be typical and severe, even though patients do not always present with classic symptoms. One factor that complicates diagnosis is that patients usually investigate pain syndromes on their own and learn how to mimic the appropriate symptoms. The patient may present with pseudoparalysis, the inability to move the affected limb, although muscle contraction can be felt and needle EMG studies are normal. A study of abnormal movements in a cohort of CRPS patients enrolled in a study during the years 1989-1998 found that 100% of these patients exhibited non-organic signs, with malingering documented by surveillance in some cases.⁵ Interestingly, while it was the authors’ intention to enroll both RSD and causalgia patients, abnormal movements were found only in RSD patients but not in cases of causalgia (in which there is a specifically identifiable nerve lesion).
Epidemiology
Much research has been done on the epidemiology of RSD. Allen et al.⁶ performed a retrospective chart review on 134 patients with CRPS. The majority of the patients were female—by over a 2:1 ratio. The majority of patients (54%) had filed a workers’ compensation claim related to RSD. Seventeen percent were involved in a lawsuit. Bone scans were positive in 53% and negative in 47% of patients. Birklein et al.⁷ summarized findings in 145 CRPS patients, 122 of which had RSD. The gender ratio was also greater than 2:1 female over male. The average age of patients was 50 years old. The pain was described as hyperalgesic in 93%, allodynic in 26%, dysesthetic in 30%, tearing in 25%, stinging in 17%, burning in 16%, deep in 63%, superficial in 30%, lancinating in 27%, and constant in 59%. Examination showed edema in 78% of patients, sudomotor (sweating) abnormalities in 54%, trophic changes in 53%, motor weakness in 79%, tremor in 48%, altered reflexes in 47%, and dystonia or myoclonic jerking in 30%. A Turkish retrospective review of 168 patients found that the upper limb was affected 50% more commonly than the lower limb, fractures were the most common precipitating event, and 75% of cases were job-related.⁸ Sandorini et al.⁹ performed a retrospective population-based (cohort) study in Olmstead County, Minnesota for cases identified in 1989-1999. They calculated an incidence of 5.46 cases per 100,000 person years at risk and a prevalence of 20.57 per 100,000 persons. The female to male ratio was 4:1, with an average age of onset of 47 years old. The most common precipitating event was a fracture, occurring in 46% of patients. The vast majority of the cases involved the upper extremity. Patients gave subjective reports of swelling in 97% of cases, temperature change in 62%, weakness in 57%, allodynia in 54%, sweating changes in 28%, and color change in 77%. A Dutch cohort study¹⁰ of cases diagnosed during the period 1996-2005 provided an estimate of the incidence of 26.2 cases per 100,000 person years, which is close to that which was found in Minnesota. The female to male ratio was 3.4:1. Again, the precipitating event was most commonly a fracture, and the upper extremity was affected in the majority of cases. Another Dutch population-based study suggested that genetic factors are involved in the causation of CRPS.¹¹ Familial occurrence of CRPS was found in 31 families, 14 of which included three or more affected members. Further evidence of genetic factors was provided by findings of a twofold increase in HLA-A3, B7, and DR215 minor histocompatibility antigens in CRPS patients as compared to controls.¹² Geertzen et al.¹³ determined that psychological factors are risk factors for development of RSD. Stressful life events were reported nearly four times more commonly in RSD patients as compared to controls. Results on a psychological questionnaire showed that males with RSD were more anxious than healthy males. Females with RSD were more depressed than controls, had more feelings of inadequacy, and were emotionally less stable.
Pathophysiology
The pathophysiology of CRPS is not completely understood. Sympathetic nervous system, vascular, inflammatory, and central mechanisms have been proposed. Veldman et al.¹⁴ reported findings supportive of Sudeck’s theory of an exaggerated regional inflammatory response, in a study involving involving 829 patients. Sympathetically maintained pain may result when peripheral nerve injury results in a loss of inhibitory interneurons and a decrease in segmental inhibition at the spinal cord level. Blumberg et al.¹⁵ suggest that nociceptive afferent information decreases the threshold of spinal circuits, causes an abnormal discharge of efferent sympathetic neurons, and causes edema which increases tissue pressure. This, in turn, activates deep nociceptors ultimately affecting nonlesioned regions, and thus producing a vicious cycle. Neuropeptides may be involved in what has been considered a regional inflammatory process termed “neurogenic inflammation.” Neuropeptides can cause vasodilatation, increased vascular permeability, and excite surrounding sensory nerve fibers. Sensory nerve studies of A-delta fibers using the Neural Scan device were done of the upper extremities of a different patient who was diagnosed with RSD of the right elbow but was also subsequently found to be malingering (see Figure 1). The lack of abnormal results were consistent with a pseudo-RSD patient. Schinkel et al.¹⁶ found higher serum levels of the neuropeptide Substance P present in RSD patients, as compared to healthy subjects. Increased concentrations of pro-inflammatory cytokines IL-6 and tumor necrosis factor alpha have been found in skin fluid in the extremities of RSD patients.¹⁷ Significant increases in cerebrospinal fluid levels of pro-inflammatory cytokines IL-1 beta and IL-6 have been found in RSD patients as compared to controls.¹⁸ Central nervous system involvement has been suggested by several studies. Rommel et al.¹⁹ theorized that functional alterations in central processing of noxious incoming information was responsible for both motor and sensory abnormalities. Upon neurological examination of 24 RSD patients, they found that the sensory deficits frequently extend past the painful area of the affected limb, including affecting both of the limbs on the ipsilateral side in 33% of the cases. Baron et al.²⁰ suggested that cortical pathways are involved. They found that when RSD is treated with sympathetic blockade, myofascial trigger points disappear in the unaffected limb contralateral to the block, as well as in the affected limb. Malhofner et al.²¹ found—on magnetic source imaging—that CRPS patients show shrinkage in the cortical representation of an affected extremity in the primary somatosensory cortex, and also show cortical reorganization in other areas of the somatosensory cortex during recovery from CRPS. Hannington-Kiff²² suggested the involvement of natural opioid peptide modulation since the early features of RSD can resemble the effects of autonomic arousal seen in opioid withdrawal. A role for the failure of normally localized increase in opioid modulation in an affected limb may provide a pathophysiologic rationale for therapy. Oaklander et al.²³ hypothesized that RSD is associated specifically with posttraumatic focal distal degeneration of small-diameter nerve axons. They performed skin biopsies on eighteen RSD patients, and found that epidermal axonal densities were significantly decreased by an average of 29% at the affected site, as compared to an unaffected site on the patient’s contralateral limb. Symptom-matched controls with regional pain due to causes other than RSD did not show a decrease in axonal densities.
Impairment Determination in CRPS
Determination of impairment ratings for CRPS is fraught with difficulties. The AMA Guides to the Evaluation of Permanent Impairment (the Guides) has long been the most commonly used basis for determining impairment. It is used in state workers’ compensation systems, federal systems, and in automobile casualty and personal injury claims. It is widely used internationally, and is mandatory for adjudicating personal injury claims in New Zealand, as well as both workers compensation and personal injury claims in parts of Canada and Australia.²⁴ Use of the Guides is specifically required in 38 states. However, while they are used in most state workers’ compensation jurisdictions, physician examiners may be using different editions of the Guides in different states. State statutes may or may not specify which edition of the Guides to use. Connecticut specifically allows use of any of the Fourth, Fifth, or Sixth Editions. Currently only ten states require use of the most current edition, the Sixth Edition, which was released at the end of 2007. Those states are Alaska, Louisiana, Mississippi, Montana, New Mexico, Oklahoma, Pennsylvania, Rhode Island, Tennessee and Wyoming. Seventeen states (Arizona, California, Delaware, Georgia, Hawaii, Kentucky, New Hampshire, Idaho, Indiana, Iowa, Massachusetts, Nevada, North Dakota, Ohio, Utah, Vermont and Washington) require use of the Fifth Edition of the Guides. Nine states (Alabama, Arkansas, Connecticut, Kansas, Maine, Maryland, South Dakota, Texas, and West Virginia) still require that the Fourth Edition be used, and two states (Colorado and Oregon) still mandate that the Third Edition (Revised) be used. Six states (Florida, Illinois, Minnesota, New York, North Carolina, and Wisconsin) do not use the AMA Guides at all, instead requiring use of their own state specific guidelines. Six states (Michigan, Missouri, Nebraska, New Jersey, South Carolina, and Virginia) do not specify use of any specific guideline, presumably leaving it up to the individual examiner to choose whether to use the AMA Guides or some other set of guidelines. States may, or may not, specify how the Guides are to be utilized. Some states use their own guidelines for some specific problems while using the Guides for other problems. Some states generally use a statutory schedule but use the Guides for non-scheduled injuries, while others do not specify the use of any specific guidelines.
The methods used to assign impairment ratings for the diagnosis of RSD have undergone considerable evolution in the past fifteen years. In the Fourth Edition of the Guides published in 1993,²⁵ no distinction was made between RSD and causalgia. Major causalgia is described as “an extremely serious form of RSD...” There were no defined criteria by which a diagnosis of RSD is established. The Guides merely state that RSD and causalgia are described by pain which is constant, intense, and burning. According to the Fourth Edition, there are only four cardinal signs and symptoms of RSD: pain, swelling, stiffness, and discoloration. Remarkably, this edition of the Guides did not require that there be present any specific sign, symptom, test result, or combination thereof—beyond the general description of the pain given above—in order for the examiner to diagnose RSD and rate it accordingly. [Whereas, in fact, true stiffness (as opposed to voluntary guarding or decreased active range of motion) typically is only present in the latest stages of RSD.] The diagnosis may be supported by clinical studies such as a positive three-phase bone scan, or a response to sympathetic blockade followed by a recurrence of the pain after the block wears off. According to the Guides, the impairment rating is to be determined in a manner identical to that which is used for determining the impairment rating for peripheral nerve injuries. Separate ratings are made for the loss of motion of the involved joints, strength deficit, and sensory loss, or pain. Pain, with or without allodynia, which is forgotten during activity is determined to be a 1-25% sensory deficit; pain which interferes with activity is rated as a 26-60% sensory deficit; pain which prevents activities or requires major or minor changes is rated as a 60-80% deficit; severe pain with allodynia which prevents all activity is rated as an 81-100% sensory deficit. Although there is no definable nerve lesion in RSD, this rating protocol requires that the examiner impute a specific nerve to be responsible for the pain based upon the result of the sensory examination—interpreted using cutaneous innervation charts. The percentage sensory deficit is then multiplied by a maximum impairment corresponding to the specific affected nerve in order to yield the overall impairment of the extremity due to that nerve lesion.
The Fifth Edition of the Guides is ambiguous in its treatment of RSD and causalgia.²⁶ In section 13.8 (criteria for rating impairments related to chronic pain), it provides a more exhaustive list of symptoms, objective clinical signs, and objective clinical tests (three phase bone scan, laser Doppler flowmetry, and response to a sympathetic blockade), as compared to the Fourth Edition. However, as in the Fourth Edition, no minimum criteria for the diagnoses are specified. The impairment of the whole person (WPI) due to RSD or causalgia in an upper extremity is rated according to the degree of difficulty in using the extremity in self-care or daily activities, and whether the dominant or nondominant extremity is affected. Ratings vary from 1% to 4% WPI for a difficulty limited to the nondominant extremity, to a range of 40% to 60% for an inability to use the dominant extremity in self-care or daily activities. WPI of a lower extremity due to RSD or causalgia is rated according to the extent to which gait and station are affected. These ratings vary from a range of 1% to 9% WPI for difficulty limited to grades, stairs, standing from deep chairs, and long distances, to a range of 40% to 60% for inability to stand without help, mechanical support, or an assistive device.
On the other hand, the same Fifth Edition of the Guides, in chapter 16, section 16.5e (ratings for Complex Regional Pain Syndrome), is much more stringent in its requirements for a diagnosis of RSD or causalgia to be ratable. It also treats RSD (CRPS I) and causalgia (CRPS II) as distinctly different entities for the first time. It states that “the approach to the diagnosis of these syndromes should be conservative and based on objective findings.” Further discussion in this article will be limited to RSD, the diagnosis in the above clinical case presentation. Only objective signs and clinical test results are taken into account in establishing minimal criteria for the diagnosis. The symptoms are not included. At least eight of eleven objective findings (nine clinical signs and two radiographic findings) must be present in order to make the diagnosis and to determine a rating. The nine clinical signs are: changes in skin color; skin temperature changes; changes in skin texture; hair changes; nail changes; dry or overly moist skin; soft tissue atrophy; joint stiffness; and swelling. The two radiographic findings are osteopenia on plain x-rays and altered uptake on three-phase bone scan. If eight of these criteria are satisfied, then RSD is rated by combining the ratings for the impairments due to loss of motion, sensory deficits, and pain. The protocol given in the Fifth Edition of the Guides differs from that which was used in the Fourth Edition in that no impairments for any specific nerve structure are applied. Therefore, no multiplier is used in order to obtain the WPI. This Fifth Edition method may result in higher impairment ratings for the identical clinical situation as compared to ratings determined using the Fourth Edition.
A further ambiguity in the Fifth Edition is that chapter 13 states that a positive three-phase bone scan may be used as evidence supporting the diagnoses of RSD, but cautions that it cannot be used as a required diagnostic criterion because of the low sensitivity of 50% found by Werner et al.²⁷ However, as noted above, chapter 16 includes the three-phase bone scan as one of the eleven diagnostic criteria of which eight are required in order to make the diagnosis. Furthermore, whereas text in chapter 13 implies that a positive response to sympathetic blockade supports the diagnosis of RSD, chapter 16 states that “contrary to previous suggestions, regional sympathetic blockade has no role in the diagnosis of CRPS.” These inconsistencies reflect the general lack of consensus as to just what RSD is and how to diagnose it.
In addition to its more stringent diagnostic requirements for rating RSD as a chronic pain syndrome at all, the Fifth Edition is also more stringent in its rating of impairments due to sensory deficit according to severity. Some degree of allodynia is required for a deficit to be classified at greater than a 25% impairment whereas, in the Fourth Edition, allodynia is only required for deficits to be rated at greater than 80%. According to the Fifth Edition, for a 100% deficit the pain must be so severe that it prevents all activity. This degree of activity limitation is not required in the Fourth Edition.
Changes in the Sixth Edition continue the trend towards more stringent requirements for rating RSD.²⁸ This more conservative approach is advised because “scientific findings have actually indicated that whenever this diagnosis is made, it is probably incorrect.” RSD may be rated only if criteria put forth by a formal international consensus are met. These criteria are actually the “research criteria” proposed by Harden et al.²⁸ The Sixth Edition diagnostic criteria are:
continuing pain is disproportionate to the inciting event;
one symptom must be reported in three of the four categories of sensory, vasomotor, and motor/trophic changes;
one sign must be present simultaneously in two of the above four categories; and
there is no other diagnosis that better explains the aforementioned signs and symptoms.
The protocol for determining WPI in the Sixth Edition is also significantly more complex than that of the Fifth Edition. After the diagnosis is firmly established, the severity is classified according to scores obtained by using the objective diagnostic criteria given in chapter 16 of the Fifth Edition. One point is given for the presence of each of these criteria. In the Sixth Edition, RSD is ratable only if there are at least a total of four points (although the international consensus criteria permit that the diagnosis is made in situations where only two or three points can be given). If the score is four or five points, then the condition is assigned to severity class 1 (mild), corresponding to a rating in the range of 1% to 13% impairment of the extremity. If the score is six or seven points, then the condition is assigned to severity class 2 (moderate), corresponding to a rating in the range of 14% to 25% impairment of the extremity. A score greater than seven points can be assigned either to class 3 (severe) corresponding to a rating in the range of 26% to 49% impairment of the extremity, or to class 4 (very severe), corresponding to a rating in the range of 50% to 100%. The determination of class 3 versus class 4 status is based upon the (rounded) average of the Functional History, Physical Examination, and Clinical Studies adjustment factors. Note that if an impairment due to RSD was rated according to chapter 13 of the Fifth Edition of the Guides, it could be rated as high as 60% WPI, whereas the maximum rating of WPI using the Sixth Edition would be only 15% (after conversion from the degree of impairment of an extremity to impairment of the whole person). The international consensus criteria allow that a diagnosis of RSD may be confirmed with only two or three objective criteria points. In these cases, the impairment can still be rated using the rating system of chapter 3, Pain Related Impairment (PRI), however the maximum obtainable WPI is limited to 3%. The PRI is classified according to the patient’s score on the Pain Disability Questionnaire.²⁹ Depending on the score, the patient’s degree of pain-related impairment is classified as none, mild, moderate, severe, or extreme. The corresponding percentages of whole person impairment for these categories are 0% for none or mild, 1% for moderate, 2% for severe, and 3% for extreme. If the patient’s score on the PDQ would assign him or her to the extreme category, then the examiner has the option to downgrade the percentage if he or she feels that the patient is not credible. If the patient would be classified into one of the lower categories, then the examiner has the option to increase the award up to the 3% cap if the examiner believes that the patient has understated his or her limitations.
The Florida impairment guidelines³⁰ suggest the following ratings for the upper and lower extremities. Mild CRPS (objective involvement with little impact on functional use) is rated at 5% impairment. Moderate CRPS (objective involvement which prevents some functional use) is rated at 15%. Severe CRPS (objective involvement which prevents most functional use) is rated at 25%.
Conclusion
It is very difficult to assess impairment due to RSD for a variety of reasons. The diagnosis may be unclear, but it may also be subject to malingering. The methods to be used to determine impairment resulting from RSD vary greatly depending upon the purpose of the evaluation and the area of jurisdiction. Experience and clinical judgment continue to play a large role.