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Results for “Reflex Sympathetic Dystrophy”

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PubMed1995

The reflex sympathetic dystrophy syndrome in patients who have had a spinal cord injury.

Patients suffering from a spinal cord injury often present with a pain syndrome. Although the reflex sympathetic syndrome is a common diagnosis in some forms of neurological disease such as patients with a stroke, it is less frequent in those with a spinal lesion. The authors report eight patients with reflex sympathetic dystrophy who had a spinal cord injury. The diagnosis and treatment are discussed along with a review of literature.

Adult↗
PubMed1993

Reflex sympathetic dystrophy treated by electroconvulsive therapy: intractable pain, depression, and bilateral electrode ECT.

An adult female patient without previous history of pain or psychiatric disorder developed reflex sympathetic dystrophy (RSD) in her left hand and arm after 2 separate injuries, and subsequent arthroscopy and arthroscopic surgery. Traditional management with systemic medications, nerve blocks, and behavioral pain management were unsuccessful. With subsequent development of depression and suicide attempt, electroconvulsive therapy (ECT) was administered using bilateral lead placement. Total resolution of her pain occurred for several hours after the first treatment. Over the course of the full ECT series the pain, vasculature changes of RSD, and depression resolved completely. Prominent psychiatric disturbances were complications arising after ECT and the resolution of the RSD, and during long-term follow-up. A review of the literature from the 1940s revealed numerous cases of chronic, intractable pain treated successfully by ECT, although none of the case series were controlled studies. More recent literature questions if 'modified' ECT, using unilateral lead placement, is less effective than bilateral lead placement, in treating pain syndromes. Resolution of the vascular changes of RSD after ECT raises questions of possible cerebral contributions to the pathophysiology of RSD.

Adult↗
PubMed1991

Treatment of posttraumatic reflex sympathetic dystrophy syndrome (RSDS) with intravenous blocks of a mixture of corticosteroid and lidocaine: a retrospective review of 17 consecutive cases.

Seventeen consecutive patients with posttraumatic reflex sympathetic dystrophy syndrome (RSDS) were treated with one or more regional i.v. blocks of methylprednisolone sodium succinate and lidocaine HCL after physical therapy and oral medications had failed to produce satisfactory relief of their symptoms. In 12 of these patients the upper extremity was affected, and in five, it was the lower extremity. A fracture of the distal radius was the most frequent predisposing event. The average delay between injury and the manifestation of RSDS was 2.5 months (range 2 days to almost 6 months). The index treatment in all cases started within 3 months of the onset of symptoms. The number of i.v. blocks given ranged from one to four (average 2.4). The side effects and complications were negligible. The treatment, which in most cases was given exclusively on an outpatient basis, was well tolerated by all patients except one. Assessment of 16 of them at 6 months showed that 11 had total or almost total relief of their symptoms. When 15 of the patients were reassessed at an average follow-up of 28 months (range 12-48 months), it was noted that none of the patients with an early satisfactory response experienced recurrence of their symptoms. The condition of the symptomatic patients in the interim had improved overall. Analysis of the cases with an unsatisfactory outcome suggested that the primary reason for failure was inadequate treatment rather than ineffectiveness of the treatment used. It was concluded that this method is simple, safe, and well tolerated and should be regarded as a first choice for posttraumatic RSDS.

Adult↗
PubMed1994

[Reflex sympathetic dystrophy of the upper limb secondary to barbiturate treatment. A report of 3 cases and a review of the literature].

The authors describe three cases of reflex sympathetic dystrophy of the upper extremity associated with barbiturate therapy and evidence their common clinical aspects and differences. The most recent knowledge and the most important literature relating to this subject are also reported. On the basis of these, personal observations are discussed and some pathogenetic hypotheses formulated.

Aged↗
PubMed2001

The sequelae of reflex sympathetic dystrophy.

This paper presents the results of a retrospective analysis of 94 patients who were assessed at a mean of 11 months after successful treatment of reflex sympathetic dystrophy (RSD) of the hand. Fifty-four percent still complained of pain related to the weather, and many complained of cold intolerance (44%), slight pain after use (34%), nail and hair growth changes (34%), sensory disturbances (34%) and stiffness of fingers in the morning (28%). There were also complaints of reduced finger extension, pain and loss of movement in the shoulder joint and hand swelling after use, and 78% of patients had significantly reduced grip strength. These results suggest that, in spite of resolution of the acute RSD problem, significant long term sequelae of RSD continue to impair function of the hand in a proportion of patients.

Adult↗
PubMed1987

Reflex sympathetic dystrophy in a patient with pre-existing torsade de pointes.

A case is presented of a patient with pre-existing torsade de pointes who developed reflex sympathetic dystrophy. A trial of stellate ganglion blocks with ECG monitoring was instituted and the patient obtained relief. The pathophysiology of torsade de pointes is discussed with emphasis on the role of the stellate ganglion. Recommendations for management of similar patients are made.

Autonomic Nerve Block↗
PubMed1983

[Bone and phosphoro-calcium metabolism in reflex sympathetic dystrophy].

A combined study organised by the French Society of Rheumatology was devoted to the investigation of bone and phosphoro-calcium metabolism in cases of reflex sympathetic dystrophy. The following observations were made: the usual phosphoro-calcium parameters are not altered, apart from a slight elevation of the urinary calcium in multifocal forms of the disease, during the 3rd and 4th months; the level of PTH, studied in 11 patients, was normal in each case; the examination of 8 bone biopsies, one performed in the 7th week and six others performed during the 3rd and 4th months of the disease, showed, initially, invasion of the spongy tissue by oedema, signs of marrow stress and bone stress, with a reduction in the number of osteoblasts, without any marked alteration of bone remodelling. At a later stage, the biopsy shows intense bone remodelling with hyperosteoclastosis and hyperosteoblastosis and the formation of irregular bone tissue which later becomes lamellar. Electron microscopic study of two biopsies revealed signs of acellular demineralisation with normal appearance of the osteoblasts and osteoclasts.

Bone and Bones↗
PubMed1992

Reflex sympathetic dystrophy in brain-injured patients.

One-hundred consecutive patients were prospectively evaluated on admission to our Brain Injury Unit for signs and symptoms of reflex sympathetic dystrophy (RSD) in the upper extremity. Patients averaged 4 months postinjury and had an average age of 29 years. Thirteen patients had clinical signs and symptoms of RSD and were then evaluated with standard radiographs and 3-phase radionuclide scintigraphy. Twelve of 13 patients had 3-phase bone scans (TPBS) consistent with RSD (12% overall incidence). RSD was present exclusively in the spastic upper extremity. There were 9 patients with hemiparesis and 3 with quadraparesis. There was a significantly higher (P < 0.01) incidence of associated upper extremity injury in the group with RSD (75%). All patients had a mean Rancho Cognitive Level of V and initial Glasgow Coma Scores less than 8. Patients who developed RSD had lower Glasgow Coma Scores than the non-RSD patients. Brain-injured patients often display agitation, hyperalgesia, disuse or neglect of the RSD-involved extremity. In addition, these patients are often cognitively unable to vocalize complaints of pain. Undiagnosed RSD in these patients can result in a significant delay in rehabilitation and possible loss of the use of an otherwise functional upper extremity.

Accidents, Traffic↗
PubMed1998

Neurogenic inflammation and reflex sympathetic dystrophy (in vivo and in vitro assessment in an experimental model).

In the chronic constriction injury (CCI) model, signs and symptoms similar to those observed in reflex sympathetic dystrophy (RSD) can be induced by loosely ligating a rat sciatic nerve. Skin microcirculatory (inflammation-like) disorders may result from release of vasoactive neuropeptides at peripheral endings of antidromically acting nociceptive nerve fibers. These antidromic mechanisms may account for vasodilation and polymorphonuclear leukocyte (PMN) accumulation in the ligated hindpaw. We assessed skin blood flow (SBF) on the ligated side, by means of laser Doppler flowmetry, before as well as at day 4 after ligation. Postligation SBF measurements were performed before and after selective (capsaicin) conduction blockade of the ligated sciatic nerve. The extent of PMN accumulation was determined by measuring myeloperoxidase (MPO) activity in muscle biopsies obtained from the ligated and contralateral nonligated side. As compared to preligation SBF values, we observed an increase at day 4. SBF returned to preligation values consequent to capsaicin application. MPO activity, when compared to the nonligated side, was higher in biopsies obtained from the ligated side. These findings indicate that in the CCI-model, antidromically acting C-nociceptor nerve fibres increase SBF at 4 days after ligation. In addition, these antidromic mechanisms may induce an inflammatory response in the ipsilateral hindpaw, mediated by release of neuropeptides from the peripheral endings of antidromically acting C-nociceptor nerve fibers. This inflammatory response may account for various signs and symptoms as observed in the CCI model and may mirror pathophysiological mechanisms of RSD.

Animals↗