Features Of Reflex Sympathetic Dystrophy Research Articles

Locking Compression Plate in Long Standing Clavicular Nonunions With Poor Bone Stock

Aim of our study was to evaluate the use of Locking Compression Plate (LCP) in patients with long standing nonunions of the clavicle with osteoporotic bones. There were a total of 11 patients. Surgery was performed for painful nonunion with shoulder dysfunction. Average time since injury was 6.9 months (3-39 months). Nonunions were stabilized by a 3.5-mm LCP, applied on the antero-inferior surface of the clavicular shaft. A six-hole LCP was used in eight cases. In three patients seven-hole LCP and in one patient eight-hole LCP was used. The fixation was supplemented by autogenous cancellous bone graft (except in hypertrophic nonunions). Patients were followed for a mean of 2.8 (1-3) years. The average time of radiologic union was 5.3 months (3-9 months). Union was achieved in all patients. Subjective clinical assessment was performed using the Disabilities of the Arm, Shoulder, and Hand functional score (DASH). The mean DASH score preoperatively was 42 (25-52) and postoperatively was 24 (11-34). Superficial infection and features of reflex sympathetic dystrophy were seen in one patient each. Long standing clavicular nonunion with osteopenic bone is a difficult problem to treat. Our study shows that LCPs can be an improved implant option with good fracture healing.

Neurology (59)

Reflex sympathetic dystrophy. (Mount Sinai School of Medicine, New York, NY) Int J Dermatol 2000;39:481–486.This review aimed to familiarize the dermatologist with the essential features of reflex sympathetic dystrophy. It highlights areas that are most likely to be of interest to the dermatologist. Information regarding diagnosis, pathogenesis theories, and treatment are included. Comment by Enrique Reig, MD.This paper analyses RSD from the point of view of a specialist in dermatology. It addresses in depth the definition of RSD (or the new name, CRPS type I), the symptoms required for adequate diagnosis, some theories to explain this syndrome, and some of the treatments available. It highlights the clinical pictures, which can cause RSD (trauma, ischemia, tumors, infection, neurological and iatrogenic causes), and particularly dermatological syndromes (minor surgery, postherpetic neuralgia, Dupuytren, vasculitis …).The treatment has a bipolar objective: to relieve pain in order to be able to apply appropriate physical therapy, which will allow recovery of the involved limb. There are more than 60 treatments reported in the literature, suggesting that there is no universal protocol. However, prevention of RSD, and particularly the early onset of treatment are essential for achieving functional and pain relief. To suppress sympathetic hyperactivity, nerve blocks (somatic and sympathetic), intravenous regional blockade with guanethidine or reserpine, alpha blockers (phentolamine), beta blockers (propranolol), and calcitonine can be used.No reference is made to anticonvulsants (gabapentine, topiramate), antidepressants (ie, amitriptyline), intravenous lidocaine, or spinal cord stimulation.

The natural history of post-traumatic reflex sympathetic dystrophy

The paper presents the results of a prospective trial to examine the natural history of early reflex sympathetic dystrophy (RSD). Thirty patients with post-traumatic RSD of the hand were observed without treatment. They were reassessed 1, 2 and 6 months after diagnosis with a final assessment at 10 to 18 months (average 13 months). Twenty-seven patients completed the study. Three were withdrawn during the study because of persistence of signs and symptoms of RSD and were given further treatment. Of the 27 patients who completed the study, only one showed sufficient features of the condition to warrant the diagnosis of mild RSD. In the remaining 26, most features of RSD had resolved spontaneously. Pain and swelling disappeared more quickly than other features of RSD. Although the signs and symptoms of RSD had largely gone at 13 months, the hands were still functionally impaired because of weaker grip strength.

REFLEX SYMPATHETIC DYSTROPHY OF THE UPPER EXTREMITY

The weight of available evidence suggests that reflex sympathetic dystrophy (RSD) is a complex clinical entity that (1) occurs predominantly in young adult women; (2) has five clinical types but presents most frequently as minor traumatic dystrophy; (3) has primary signs and symptoms (e.g., pain, edema, stiffness, and discoloration) that are expressed highly in each clinical type, whereas secondary signs and symptoms are variable; (4) responds well to treatment, regardless of its clinical type; and (5) is managed best when treatment is started early. It can be concluded that RSD is a multifaceted disease that responds well when managed with a multimodal treatment program aimed at the various interacting components of the disorder. The recognition and documentation of the variation of the clinical features of RSD may allow for its earlier diagnosis and treatment and thus significantly improve the chances for a successful outcome.

Reflex sympathetic dystrophy in a patient with peripheral sympathetic denervation

Reflex sympathetic dystrophy (RSD) includes persistent pain in an extremity, associated with features of vasomotor dysfunction and, later, dystrophic changes. Many theories have been proposed to explain these clinical features and include sympathetic dysfunction. We report a unique case of RSD following an upper limb fracture in a patient with established severe peripheral sympathetic denervation as part of idiopathic chronic autonomic failure. This case provides evidence that the clinical features of RSD were not mediated via increased sympathetic nerve activity in the affected limb. Locally released neuropeptides or autocoids therefore may be involved in the pathogenesis of RSD. The term sympathetic in RSD may be inappropriate and require revision.

Innervation of hyperalgesic skin in patients with complex regional pain syndrome.

To look for anatomical and histochemical signs of interaction between sensory and sympathetic nerves in the hyperalgesic skin of patients with complex regional pain syndrome. Skin samples were obtained from eight patients whose condition developed after a suspected or confirmed peripheral nerve injury, and from nine patients with features of reflex sympathetic dystrophy (RSD) following a soft-tissue injury. A skin sample was also obtained from 18 control subjects of similar age and sex distribution to patients. In patients, skin samples were taken from an area of static mechanical hyperalgesia and from an equivalent site in the contralateral limb. In controls, skin samples were obtained from the dorsum of one hand or foot. HISTOCHEMICAL MARKERS: We used neuron-specific enolase for all classes of nerve fiber; tyrosine hydroxylase for noradrenergic fibers; vasoactive intestinal peptide for sympathetic sudomotor fibers; tyrosine hydroxylase co-existing with neuropeptide Y for sympathetic vasoconstrictor fibers; and calcitonin gene-related peptide with substance P or somatostatin for peptide-containing unmyelinated sensory fibers. In patients, the distribution of markers was similar in skin taken from an area of mechanical hyperalgesia and skin taken from an equivalent site contralaterally, and was unrelated to clinical features of RSD. The distribution of markers did not differ between patients and controls. Nerve tangles immunoreactive to neuron-specific enolase, but not to other markers, were detected in samples taken from four patients and two controls. The nerve tangles were present bilaterally in two patients, and only on the affected side in two other patients. The clinical condition was more fully developed in the four patients whose skin samples contained nerve tangles than in most other patients. A major difference in distribution or change in histochemical content of cutaneous autonomic or nociceptor fibers is unlikely to underly static mechanical hyperalgesia following a soft-tissue or peripheral nerve injury. The relevance of cutaneous nerve tangles for the pathophysiology of RSD is uncertain.

Complex regional pain syndrome

Reflex sympathetic dystrophy is a complex progressive and potentially devastating condition generally affecting the extremities. Because clinical presentation is variable, diagnosis can be difficult. Recently, the Special interest Group of Pain and the Sympathetic Nervous System of the International Association for the Study of Pain developed a new taxonomy to help acknowledge and differentiate the features of reflex sympathetic dystrophy and causalgia. These are categorized under the heading of complex regional pain syndrome. Sympathetically maintained pain is also recognized as a separate component to this group of conditions. The authors present this new taxonomy and present cases of each condition.

The sympathetic skin response in the shoulder-hand syndrome complicating tetraplegia.

To determine the utility of the sympathetic skin response (SSR) in studying sympathetic outflow in cervical spinal cord injury (CSCI) patients who develop features of reflex sympathetic dystrophy, we studied seven consecutive CSCI patients with the shoulder-hand syndrome (SHS), and seven patients with similar injuries but without the manifestations of the SHS. The mean SSR amplitude was more than three times greater in patients with the SHS, a statistically significant difference. We restudied six patients with a SHS after symptoms had improved following steroid treatment: the mean amplitude fell significantly, approaching the mean for the control group. When pain was asymmetric, the SSR amplitude was higher in the arm with greater pain. Four of the seven SHS patients demonstrated an unusual pattern of spontaneous cyclical electrical activity during a period of severe pain. We conclude that a SHS complicating CSCI is associated with increased amplitude of the SSR, supporting the theory that sympathetic hyperactivity is important in the pathophysiology of reflex sympathetic dystrophy in this setting.

Function Ten Years After Colles?? Fracture

There are no data in the literature concerning the outcome of Colles' fracture beyond six years. One hundred consecutive patients with displaced Colles' fractures were reviewed ten years after the injury. Function, radiographic anatomy, osteoarthrosis, and reflex sympathetic dystrophy (algodystrophy) were all objectively assessed. By the time of this review, 35 patients had died. Eighty-five percent of those surviving had a satisfactory outcome. Forty-two percent had improved functionally in ten years and 20% had deteriorated. Initial and ten-year radial shortening and early finger stiffness significantly correlated with final outcome. Dorsal angulation influenced early but not ten-year function. Sixty-two percent of those with an unsatisfactory result had objective features of reflex sympathetic dystrophy, compared with only 6% of those with a satisfactory result. Osteoarthrosis was found in 37%, but in only 4% was it associated with an unsatisfactory outcome.

Sympathetically mediated anterior knee pain

Nineteen patients with anterior knee pain without the classical features of reflex sympathetic dystrophy (RSD) were investigated by local anesthetic sympathetic blockade. Scintigraphy was performed before the sympathetic blockade in all the cases, and the scintigraphic appearances were correlated with the clinical response. Eleven patients responded to the blockade (9 good and 2 fair). Only 1 out of 10 patients with increased scintigraphic uptake failed to respond, whereas 7 out of 9 patients with normal uptake failed to respond. Our study suggests that a sympathetically mediated component may exist in patients with anterior knee pain without RSD, and that scintigraphy is useful in identifying those patients for whom sympathetic blockade may be helpful.

Does failed natural opioid modulation in regional sympathetic ganglia cause reflex sympathetic dystrophy?

Early features of reflex sympathetic dystrophy in a limb resemble the general effects of autonomic arousal associated with opioid withdrawal. It is suggested that natural opioid peptide modulation in regional sympathetic ganglia normally rises to prevent excessive autonomic activity in an injured limb. After an injury (especially a trivial one) to a susceptible subject, this localised increase in opioid modulation may fail or may rapidly wane so that autonomic features of opioid withdrawal appear in the affected limb. Florid dystrophic changes may then occur because of passive complications of disuse associated with pain, or as a result of more active processes. Preservation of an appropriate opioid bias in the regional sympathetic ganglia might be an important factor in the successful management and prevention of reflex sympathetic dystrophy.

REFLEX SYMPATHETIC DYSTROPHY: THE SIGNIFICANCE OF DIFFERING PLASMA CATECHOLAMINE CONCENTRATIONS IN AFFECTED AND UNAFFECTED LIMBS

In 26 patients with features of reflex sympathetic dystrophy, venous blood was collected from painful and unaffected limbs. Levels of plasma adrenaline, noradrenaline and its intracellular metabolite, 3,4-dihydroxyphenylethyleneglycol (DHPG), were measured by combined gas chromatography/mass spectrometry. Plasma DHPG was lower on the painful side. Concentration of plasma noradrenaline was also lower on the painful side in patients with widespread allodynia, and in those with hyperhidrosis in the affected hand or foot. These findings do not support the widely held view that autonomic disturbances in reflex sympathetic dystrophy are due to sympathetic overactivity. Rather, they suggest that sweating and changes in peripheral blood flow result from supersensitivity to sympathetic neurotransmitters. After injury, supersensitivity to noradrenaline may also contribute to spontaneous pain and allodynia by disrupting efferent sympathetic modulation of sensation. This would explain why pain and allodynia are relieved by sympathetic blockade, and why noradrenaline rekindles pain in sympathectomized skin.

Reflex Sympathetic Dystrophy in Children

Six patients with reflex sympathetic dystrophy were investigated during the period between 1973 and 1978. Children do not develop the severe, disabling pain nor the patchy osteoporosis (Sudeck's atrophy) which are considered essential features of reflex sympathetic dystrophy in adults. In contrast to the adult variety, reflex sympathetic dystrophy in children is a self-limiting condition which usually responds well to mild analgesics and physical therapy. Frequently it may be necessary to administer the physical therapy in an intensive, inpatient program, both to break the pain-disability cycle and to remove the patient from a stressful family environment that may have initiated or prolonged the syndrome. The use of steroids (dexamethasone) had no appreciable effect on the clinical course in these children.