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- R J Schwartzman.
- Department of Neurology, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania.
- Neurol Clin. 1992 Nov 1;10(4):953-73.
AbstractConverging lines of research suggest that RSD is a form of reflex neurogenic inflammation. Early the sympathetic nervous system appears to have an initiating and sustaining role. In later states of the illness, structural changes at the DH level seem to correlate with centralization of the process. Neuropeptides and EAAs released from thin or unmyelinated nociceptive afferents may produce both the inflammation and the suspected central sensitization of DH neurons seen in later stages of the disease. Effective treatment will follow a clearer understanding of the physiology of each stage of the disease.
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