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Facts and Hypotheses
1: Vasc Med Reflex sympathetic dystrophy: facts and hypotheses.
Kurvers HA
Department of Surgery of the University Hospital Maastricht,
Cardiovascular
Research Institute, The Netherlands.
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.
Publication Types:
Review
Review, tutorial
PMID: 9892513, UI: 99107531
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