Diabetic Neuropathy appears to have Diabetes as its etiology (cause). RSD, by contrast, may have several different etiologies. It has been accepted as fact for sometime - that RSD is sympathetically-mediated. That is - caused by an aberrant behavior of the Sympathetic Nervous System. Recent studies conducted by L. van der Laan, have shown a lack of conclusive evidence to support this conjecture.
Of the several possible categories of etiologies for RSD, antibody-mediation, injury to one or more nerves, or a malfunction of the Cortex or any of the Autonomic Nervous System ganglia may be responsible. Thus, RSD(abm - antibody-mediated) may be due to viral or bacterial infection. RSD(inj - injury-mediated) occurs often after trauma or injury, often it is an inconsequential injury. There may be additional but as of yet, unidentified etiological classes, say RSD(cns - Central Nervous System-mediated).
There are several unanswered questions regarding the onset of RSD(inj). Namely, what event has occurred to the physiology, to enable the mechanism or precursor to RSD on the event of the next trauma that may occur? Most patients that have contracted RSD as the result of an injury, report that this was not the first occurrence of such trauma.
Both Diabetic Neuropathy and RSD have in common, the failure of the vascular system and in particular, the failure of the microvascular system (mvs). RSD in addition, manifests in what appears to be, an inflammation of the tissues in the affected region. RSD usually appears initially in a limb, and more rarely, on the torso or thoracic area.
Both Diabetic Neuropathy and RSD are very nearly identical in their presentation. And both appear to spread from region to region in a similar manner. The underlying problem for both of these Neuropathies is reduced or constricted blood flow or circulation. The tissues attached to the mvs, in the affected region - suffer hypoxia (oxygen starvation) and a reduction of nutrients. The tissues so affected are: bone cells, muscle cells, nerve cells, skin cells and the mvs itself (the capillaries). After some time, these tissues become stressed and eventually die (cell necrosis).
Because of the stressing of and the death of these tissues, the patient experiences a variety of different and extremely severe pains. Unless this physical condition is treated it not only persists, but slowly spreads to adjacent (proximal) areas and at times, to distal (disjoint) areas. The pain is usually treated apart from the underlying disease. This provides temporary relief, but is not sufficient to block the ever growing pain - in the face of continuing growth of the disease, which in turn produces yet more pain.
