Reflex sympathetic dystrophy following traumatic myelopathy

Two cases of reflex sympathetic dystrophy in the upper extremity of patients with traumatic cervical spinal cord injuries are reported. Both patients had very incomplete lesions with early neurological recovery, suggesting an underlying central cord syndrome. Although reflex sympathetic dystrophy is often seen following stroke, it has only rarely been documented in traumatic myelopathy, and it should be considered in the differential diagnosis of unexplained pain syndromes in the extremities of paraplegic or quadriplegic patients.     

Pain measurement in reflex sympathetic dystrophy syndrome

The reflex sympathetic dystrophy syndrome (RSDS) consists of a triad of pain, edema and sympathetic dysfunction of an extremity following trauma, peripheral nerve injury or central nervous system disorder. Reflex sympathetic dystrophy syndrome is a difficult and costly pain syndrome to treat. One of the difficulties in evaluating treatment efficacy is the objectification and quantification of patient findings. The purpose of this investigation was to develop a simple, reproducible and systematic evaluation of pain and neurologic impairment in RSDS. The protocol evaluation included the following measures of pain and impairment: (1) objectification of distal joint pain by palpation (0-4 scale); (2) volumetric measurement by water displacement of the distal limb; (3) skin temperature measurement; (4) active range of motion assessment of the affected limb (AROM); (5) McGill Pain Questionnaire (MPQ); and (6) visual analogue pain scale (VAS). Seventeen subjects with definite or probable RSDS were evaluated. The mean age of patients was 35.6 years +/- 8.0 years (+/- 2 S.E.M.), and the mean duration of symptoms was 11.8 +/- 4.8 months. There were an equal number of subjects with upper and lower extremity involvement. The VAS had significant correlations with limb volume, AROM-lower extremity and joint pain indices (P less than 0.0005). The MPQ subscales had robust correlation with the joint pain indices alone (P less than 0.0001). Skin temperature was not predictive of changes in joint pain score, AROM, limb volume or subjective pain measures. However, there was internal consistency between volumetric and AROM measures and joint pain indices. This protocol is recommended for use in therapeutic trials for the treatment of the RSDS.     

Treatment of reflex sympathetic dystrophy with topical capsaicin. Case report.

A 31-year-old woman with intractable reflex sympathetic dystrophy experienced nearly complete, though temporary, resolution of pain following 3 weeks of topical capsaicin. We propose that capsaicin may be a useful treatment for reflex sympathetic dystrophy, either by depleting substance P from primary afferent neurons that mediate allodynia, or by modulating sympathetic efferent activity.     

Ultrasound treatment of reflex sympathetic dystrophy

Three cases of lower extremity reflex sympathetic dystrophy (RSD) responded dramatically to a daily low dose ultrasound (0.5 watts/cm2 X 5 minutes) therapy to the tarsal tunnel and plantar nerve distribution, and the use of a shoe insert. Two of the three cases had been refractory to more standard therapy for RSD, including pharmacologic agents. All three patients preferred a conservative approach to surgical sympathectomy. No complications were observed, and all three cases are now symptom free. Daily ultrasound treatments are time-consuming and costly but are safe and may be useful for patients who refuse surgical sympathectomy. We hypothesize that ultrasound may have affected peripheral sympathetic nerve fibers. However, more indirect effects of ultrasound, such as increased blood flow to the limb, may be part of the action mechanism as well.     

A 2 1/2-year-old girl with reflex sympathetic dystrophy syndrome (CRPS type I): case report

An unusual case of a 2 1/2-year-old girl with reflex sympathetic dystrophy (RSD) of the left arm is described. She is the youngest RSD case ever presented in the literature. Upper extremity involvement is also rare in childhood RSD. She had both physical and psychological trauma in an earthquake preceding the disease. The association of RSD with a psychological disorder is stressed and awareness of the condition to the general paediatrician is recommended for early diagnosis and successful treatment.     

Norepinephrine in reflex sympathetic dystrophy: an hypothesis

Reflex sympathetic dystrophy (RSD) usually occurs in an individual who has been experiencing significant personal stress, a state associated with increased discharge of norepinephrine (NE) from perivascular postganglionic sympathetic neurons. RSD is often precipitated by this sequence: traumatic arterial spasm, regional ischemia, neurogenic inflammation, and ischemic/edematous damage to membranes of preterminal perivascular nociceptive neurons. In the natural repair of these membranes, it is suggested that adrenoceptors appear and are ordinarily transitory; but in RSD, they are retained by the increased adjacent NE. This process delays further healing, produces pain, and releases inflammatory substances, resulting in interacting pathophysiologic vicious cycles.     

Lumbosacral radiculopathy, reflex sympathetic dystrophy and tarsal tunnel syndrome: an unusual presentation

This case documents a patient with lumbosacral radiculopathy, reflex sympathetic dystrophy, and tarsal tunnel syndrome affecting one extremity. After lumbar laminectomy for L5-S1 radiculopathy, the patient developed foot pain diagnosed as secondary to reflex sympathetic dystrophy. Because of increasing foot pain despite long-term conservative therapy, the patient underwent further evaluation, including electrodiagnostic studies leading to the diagnosis of a superimposed tarsal tunnel syndrome. Following surgical decompression, pain decreased. Because of the unusual presentation, diagnosis and treatment of the tarsal tunnel syndrome was significantly delayed. To help understand the coexistence of these conditions, interrelating pathophysiologic mechanisms have been postulated, including the possibility that a "double-crush" phenomenon may have contributed to the development of tarsal tunnel syndrome. Earlier diagnosis and definitive treatment of the foot pain may have been possible had these mechanisms been better understood.     

Two unique shoulder disorders. Adhesive capsulitis and reflex sympathetic dystrophy syndrome

Adhesive capsulitis and reflex sympathetic dystrophy syndrome are unique, but not rare, shoulder disorders that occur most often in persons over 50 who have experienced recent trauma. Although the etiology and nature of the disorders are not fully understood, therapy is often effective when instituted early. Adhesive capsulitis is a self-limited disorder, and patients usually recover in time. Reflex sympathetic dystrophy syndrome, however, can cause serious impairment if not treated promptly. Early mobilization of persons at risk may help reduce the incidence of the disorders.     

Controversies surrounding reflex sympathetic dystrophy: A review article

The topic of reflex sympathetic dystrophy (RSD) has generated an increasingly significant volume of medical literature and controversy over the last decade. A search of PubMed, the online site of the National Library of Medicine, for papers on RSD reveals nearly 2200 articles on the topic (using algodystrophy as the search word, wherein RSD references are also included, and more older and European articles are also listed). From 1991 through 1998 inclusive there is an average of nearly 100 articles per year on the topic, which represents more than a third of all the articles referenced since 1965. In the decade of the 1980s, there is an average of 64 articles per year, 74 per year in the last half of the decade and 54 per year in the first half. Prior to the decade of the 1980s, one finds an average of 40 articles per year back to the mid-1960s. The controversy surrounding the disorder centers around the nature of the problem and whether it is a primary organic disorder or a primary psychogenic disorder associated with the accomplishment of some secondary gain. If it is the former, then clearly research should continue to determine the nature and etiology of the malfunctioning organ(s). If, on the other hand, RSD is a psychogenic disorder, then the medical community does well to focus mainly on the peripheral manifestations of the problem. In that instance, therapy should be primarily psychological and cognitive with regard to the secondary gain, and persistent organic treatments are unlikely to improve the condition in general and worsen individual cases.     

Reflex sympathetic dystrophy syndrome secondary to L5 radiculopathy

A 47-year-old woman developed radiating right lower extremity pain with weakness in the L5 myotomes. A CT scan, subsequent myelogram, and postmyelogram CT scan were reported as negative. Two months of bed rest diminished the radiating symptoms, but the weakness persisted. Three months post onset a severe burning dysesthesia developed in the right foot, and the patient became unable to bear weight on that extremity. Physical examination revealed 4-/5 weakness of the ankle dorsiflexors, foot evertors, toe extensors, and hip abductors. The entire right foot was swollen and had a red, mottled discoloration. An EMG was equivocal, and a three-phase bone scan was positive in the right foot in all three phases, which is characteristic of reflex sympathetic dystrophy. A repeat CT scan and review of the earlier scans revealed a high lateral disc fragment at the exit foramina of the L5 nerve root. Upon laminectomy, a free disc fragment at the exit foramina was removed, and the patient's symptoms resolved completely. Reflex sympathetic dystrophy syndrome is very rarely reported in association with lumbar radiculopathy. This case emphasizes the need to carefully evaluate the far lateral exit foramina on CT scan in patients with symptoms of radiculopathy. Myelogram is characteristically normal in these cases.     

Doppler sonographic assessment of posttraumatic reflex sympathetic dystrophy.

OBJECTIVE: To reveal the arterial Doppler sonographic findings in cases of posttraumatic reflex sympathetic dystrophy METHODS: Eleven patients had hand reflex sympathetic dystrophy, and 9 had foot reflex sympathetic dystrophy. The duration of symptoms ranged from 1 to 28 weeks, and the history of fracture ranged from 6 to 48 weeks. Bilateral brachial or popliteal arteries proximal to injuries were evaluated by Doppler sonography with a 7.5-MHz linear transducer. All patients also had triphasic bone scintigraphy and extremity thermography RESULTS: Two patients had monophasic waveforms and 4 had low-pulsatility triphasic waveforms on the affected limbs when compared with the asymptomatic limbs. All opposite asymptomatic limbs had normal triphasic waveforms in these 6 cases. Spectral analysis revealed a loss or decrease of a normal reversed flow component with a reduced pulsatility index on the affected limb. Fourteen other patients had symmetric triphasic waveforms. We observed that the patients who had stage 1 reflex sympathetic dystrophy and warm limbs with durations of symptoms of more than 2 weeks had positive Doppler sonographic findings, whereas all patients with stage 2 reflex sympathetic dystrophy and all with normal skin temperature, regardless of stage, had normal waveforms. CONCLUSIONS: Doppler sonography revealed loss of normal triphasic arterial waveforms in some of the cases of stage 1 disease, whereas many cases of stage 1 disease and all cases of stage 2 disease had normal findings. Therefore, we think that Doppler sonography cannot be used for the diagnosis of reflex sympathetic dystrophy but may help in assessing hemodynamic stages of the disease.