Reflex Sympathetic Dystrophy A Clinical, Histological, Histochemical and Experimental Study

Folkerts, J.F.; Wiertz-Hoessels, E. L. M. J.; Krediet, P; Sneep, A.J.

doi:10.1159/000103475

Cited by 7 publications

(1 citation statement)

References 2 publications

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“…The latter additionally demonstrated reduced cholineesterase reactions, pathologic changes of motor endplates and reduced adrenergic innervation. 34 Histologic examination of bone revealed signs of active remodelling of both the cancellous bone and the cortex. 35 Vascular Medicine 1998; 3: 207-214…”

Section: Diagnosismentioning

confidence: 99%

Reflex sympathetic dystrophy: facts and hypotheses

Kurvers

1998

Vasc Med

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Reflex sympathetic dystrophy (RSD) syndrome has been recognized clinically for many years. It is most often initiated by trauma to a nerve, neural plexus, or soft tissue. Diagnostic criteria are the presence of regional pain and other sensory changes following a noxious event. The pain is associated with changes in skin colour, skin temperature, abnormal sweating, oedema, and sometimes motor abnormalities. The clinical course is commonly divided into three stages: first (acute or hyperaemic), second (dystrophic or ischaemic), and third (atrophic) stage. The diagnosis is primarily clinical, but roentgenography, scintigraphy, thermography, electromyography and assessment of nerve conduction velocity can help to confirm the diagnosis. Although a wide variety of treatments have been recommended, the only therapies found to be effective in large studies aim at interfering with the activity of the sympathetic nervous system. To this end, efferent sympathetic nerve activity can be interrupted surgically or chemically. Alternatively, adrenoceptor blockers may be used to relieve pain. Numerous theories have been proposed to explain the pathophysiology. Sympathetic dysfunction, which often has been purported to play a pivotal role in RSD, has been suggested to consist of an increased rate of efferent sympathetic nerve impulses towards the involved extremity induced by increased afferent activity. However, the results of several experimental studies suggest that sympathetic dysfunction consists of supersensitivity to catecholamines induced by (partial) autonomic denervation. Besides, it has been suggested that excitation of sensory nerve fibres at axonal level causes release of neuropeptides at the peripheral endings of these fibres. These neuropeptides may induce vasodilation, increase vascular permeability, and excite surrounding sensory nerve fibres -- a phenomenon referred to as neurogenic inflammation. At the level of the central nervous system, it has been suggested that the increased input from peripheral nociceptors alters the central processing mechanisms.

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Section: Diagnosismentioning

confidence: 99%

Reflex sympathetic dystrophy: facts and hypotheses

Kurvers

1998

Vasc Med

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Zur Entstehung und Therapie des Schmerzsyndroms bei der sympathischen Reflexdystrophie

Blumberg

1988

Schmerz

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Reflex sympathetic dystrophy (RSD) is a disease of the extremities that can be elicited by different factors, occurring at different sites (e.g., trauma, herpes zoster, myocardial infarction). Independently of its etiology, however, the clinical symptoms of RSD are found most often in distal parts of the extremities affected (hand or foot). In a generalized distribution pattern, the following signs, representing a triad of autonomic, motoric and sensory disturbances, are commonly observed in these regions: 1. dysregulation of blood flow to the skin and of sweating, together with diffuse swelling, 2. impairment of movement and muscular strength; 3. diffuse sensory skin disturbances and spontaneous pain of ariable character (e.g., burning, throbbing, aching, shooting). Pain sensation is generally diffuse; in most cases it is deep and less often, superficial (probably representing bone or skin pain, respectively). This triad occurs at the very onset of RSD. If the distribution pattern is generalized, it can be used as a diagnostic criterion for RSD. Our experimental results support the idea of disturbances of skin blood flow related to abnormal vasoconstrictor outflow. This assumption is primarily based on two observations: 1. 73% of 97 RSD patients (upper extremity affected) showed systematic side differences in fingertip temperatures at room temperature. All points measured on the affected side had higher (n=51) or lower (n= 20) temperature values than corresponding sites on the healthy extremity. Such systematic side differences were found only in 16% out of 79 healthy subjects (p

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Neue Gesichtspunkte zur Klinik, Diagnostik und Pathophysiologie der sympathischen Reflexdystrophie (Morbus Sudeck)

1990

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Reflex sympathetic dystrophy can be elicited by various factors (e. g. trauma, herpes zoster, myocardial infarction). Independent of kind and site of a lesion, symptoms occur most often in the whole distal part of the affected extremity. There in most cases, a triad of autonomic, motor and sensory disturbances can be found clinically. For early diagnosis--beside clinical investigation--a comparative measurement of skin temperatures on both sides of finger or toe tips, respectively, is recommended. Hereby the clinical finding of a warmer or colder extremity can be proved, which supplies evidence of a disturbed skin blood flow. In case, the above mentioned triad and a disturbance of skin circulation is found, diagnosis of sympathetic reflex dystrophy can be made with great certainty. With regard to the underlying pathophysiology, symptoms can be explained at this time satisfactory only by the assumption of a vicious circle. Starting from a painful event (e.g. trauma, mark in a plaster cast, nerve lesion or myocardial infarction) a functional disturbance of the sympathetic nervous system is initiated. This results in a disturbance of the circulation in all of the affected tissues (skin, muscle, bone and joint), which finally gives rise to an abnormal excitation of afferent receptors, particularly of nociceptors. This excitation maintains the disturbance of the sympathetic nervous system at central nervous level (vicious circle). The most relevant pathomechanism in this process seems to be the occurrence of an imbalance between the activity of sympathetic vasoconstrictor neurons supplying arteries and those, supplying veins. A sympatholytic therapy, if applied in time, is able to cut off the vicious circle, which may lead to a restitutio ad integrum. Further investigations will show to what extent psychological factors are involved in developing the central nervous disturbance of the sympathetic nervous system and may also show if in addition the motor system is affected.

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Reflex Sympathetic Dystrophy A Clinical, Histological, Histochemical and Experimental Study

Cited by 7 publications

References 2 publications

Reflex sympathetic dystrophy: facts and hypotheses

Reflex sympathetic dystrophy: facts and hypotheses

Zur Entstehung und Therapie des Schmerzsyndroms bei der sympathischen Reflexdystrophie

Neue Gesichtspunkte zur Klinik, Diagnostik und Pathophysiologie der sympathischen Reflexdystrophie (Morbus Sudeck)

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