Hi folks,
Found this interesting article :-
Reflex Sympathetic Dystrophy Syndrome: A Chiropractic Perspective

by Edgar Romero, DC, DACNB, FIAMA
Reflex sympathetic dystrophy (RSD) syndrome, or complex regional pain syndrome, as it is now called, is, as the latter name implies, a complex series of symptoms that plagues many a patient. It is most commonly associated with pain/sensory abnormalities, vasomotor dysfunction, edema/sudomotor dysfunction, and motor/trophic changes.1 Some or all of these signs may be present with a diagnosis of RSD.
Research has shown that the predisposing factor for the condition generally lies in a peripheral nerve injury or some other injury that activates nociception at a high level, and can increase sensitization in the central nervous system.2 The pain can be in one limb or can progress to encompass the entire body. There is no psychological component to RSD, but many patients are severely depressed because of the constant pain, lack of sleep, and total disruption of lifestyle that occurs with the condition.2 It has been determined through further studies into this devastating condition that the etiology is in fact central, subsequent to the peripheral lesions that initiate the syndrome.3
According to the current medical model, physical therapy is the cornerstone of first-line treatment, with moderate cases requiring adjunctive analgesics, such as anticonvulsants and/or antidepressants. Use of opiods is not uncommon for those in too much pain to participate in physical therapy. For severe cases, anesthetic blockade, sympathetic/somatic blockades, spinal cord stimulation and spinal analgesia are all part of the treatments provided.4
A possible etiology of this pathology from a neurological point of view will be explained in this paper, with the proper treatment, including chiropractic, based on signs and symptoms. As stated previously, RSD is in many cases precipitated by some trauma or peripheral nerve injury that progresses over time to the syndrome, with associated pain and dysfunction. It must be assumed that the increased frequency of firing of the pain pathways has the effect of starting the imbalance that leads to RSD.
Nociceptive pathways have collaterals into the intermediolateral cell column (IML) of the spinal cord, which also happens to be the primary neuron of the sympathetic system. As a vasomotor component is one of the chief diagnostic indicators of the condition, one must assume that this pain barrage may be part of the initial syndrome. If this were the only factor, however, anyone who had ever been injured and felt pain would have at least some diagnostic indicators of RSD.
Although we all do experience a localized inflammatory response secondary to central vasoconstriction and peripheral dilation associated with increased sympathetic response after an injury, it is of course not to a degree that RSD would develop. Nociception does not in fact end at the spinal cord, obviously. It has rostral synapses, some of which proceed through the thalamus to the parietal cortex and consciousness. The greater numbers by far, however (76 percent, by some estimates), have collaterals that synapse in the reticular formation of the mesencephalon and the pons. The mesencephalic (or rostral) reticular formation has an excitatory effect on the cortex to increase perception. Thus, not only will a patient have difficulty sleeping secondary to an increased firing cortex, but the very perception of pain itself will also seem greater to the patient, even in the absence of continued nociception.
More importantly, the rostral reticular formation has an inhibitory effect on the medullary, or caudal, reticular formation. The caudal reticular formation itself inhibits the IML, which, to reiterate, is the primary neuron of the sympathetic system. Inhibition of an inhibitory center allows excitation to occur. Thus, the IML would be at a greater central integrative state than would normally be expected in the individual. This now gives us a possible double firing into the IML; when activated, the IML will produce a central vasoconstriction so powerful that there is likely an anoxic condition of the affected tissue.
Anoxic conditions in any tissue produce lactic acid and other nociceptive chemicals, further driving the nociceptive system and increasing the likelihood of IML firing. It can quickly become a catch-22 scenario, whereby nociception produces vasoconstriction, and vasoconstriction produces nociception. As described earlier, peripheral nerve injuries have a great likelihood of leading to RSD. With any peripheral nerve injury, it is large-diameter .


This is one article that I think gives a good explanation of how our vasoconstrictive and trophic tissue changes can be explained to be a part of a neurological disorder.
Cheers all
Tayla