Hi,
I wrote this (I'm sorry I got a bit text-booky) but it indicates some of the reasons for some of the signs & symptoms of CRPS.

Please make with it what you will and ignore the rest. I offer it as it goes in a very small part to explain some of the lesser but intensely important actions of a small and oft forgotten part of the nervous system.

Also, I think it goes some way to explaining the simple "fight or flight" descriptor & perhaps a step or two further. I have purposely kept it general as I am avoiding trying to promote myself as "expert" in CRPS except that I have the rotten syndrome and have thought about a lot. You can all put your signs & symptoms in the right places should they fit.

Higher Control Of Autonomic Functions
Important centre for the regulation of autonomic functions are found in the brain-stem and hypothalamus. The latter is frequently considered to be the major higher centre of the autonomic nervous system. The role of these and other areas of the neural axis in autonomic control can be investigated by stimulation or ablation experiments and such investigations have shown that the cerebral cortex is also involved in autonomic control.

One function of the autonomic system is that of maintaining the internal environment within closely defined limits. To achieve this aim of maintaining homeostasis, the nervous system frequently utilizes the principles of a negative feedback mechanism, in which any change in the controlled variable will result in an effect on it in the opposite direction – for instance, a rise in blood pressure will be opposed and the standard level maintained. Positive feedback mechanisms do occur – the generation of a nerve action potential being an example – but are not generally involved in homeostatic control.

The basic components of a negative feedback homeostatic mechanism are:
1 The controlled variable is the parameter which is kept at a standard level, eg; blood pressure or arterial pCO2 (carbon dioxide pressure);
2 There is a specialized sensor element which responds specifically to changes in the controlled variable – eg: baroreceptors which monitor changes in pressure or chemoreceptors which may be neurons in the central nervous system or peripheral elements and which are selectively sensitive to specific agents such as carbon dioxide;
3 The afferent pathway along which information from the sensors is transmitted to the co-ordinating centre;
4 A co-ordinating centre those for respiratory and cardiovascular functions are located in the brain stem;
5 An efferent pathway which for the respiratory and cardiovascular systems may involve both somatic and autonomic nervous pathways; and
6 An effector mechanism, which is frequently muscle.
The operation of a feedback circuit such as this can be exemplified by the brain-stem systems which control blood-pressure and the partial pressure of carbon dioxide in the blood.

Effects of Autonomic Stimuli
The effects of stimulation of the sympathetic and parasympathetic nervous systems especially when the two systems innervate the same organ or tissue, are often antagonistic. For instance, the parasympathetic system inhibits the heart; the sympathetic system excites it.

However, there is no general principle about which system inhibits and which stimulates. Both systems excite sphincter muscles, but one innervates the constrictor muscles (SNS) and the other excites the dilator muscles (PSNS). The sympatheic system prepares the body for muscular exercise and reactions in emergencies. It exerts an important control over the cardiovascular system, increasing the strength and frequency of cardiac contractions and regulating the diameter of arterioles (peripheral) resistance). Both effects are intimately involved in the regulation of arterial blood-pressure.

Sympathetic activity causes adrenaline to be released by the adrenal gland in situations of severe stress – “fright, flight, or fight” – and during fatigue, cold and shock. The circulation of this hormone mimics sympathetic activity, causing increased blood-pressure, dilation of bronchioles and pupils, release of red-blood cells into the circulation from the spleen, increase blood sugar levels and elevation of body temperature.

Neurotransmitters at Autonomic Synapses
Details of the synthesis and release of acetylcholine, noradrenaline and adrenaline are complex reactions about which we are concerned.

Supersensitivity due to Androgenic Denervation
The action of circulating noradrenaline is mainly terminated by andrenergic nerve terminals which accumulate noradrenaline by energy-dependent mechanisms. When andrenergic nerve terminals are destroyed by surgical, chemical or IMMUNOLOGICAL methods, the action of circulating noradrenaline is greater and prolonged in comparison to normal. This phenomenon is called “supersensitivity” and is mainly due to the absence of re-uptake mechanisms in the denervated area.
What if a myelinated neurone becomes de-myelinated through these or any other mechanism. This results in a clearly crossed and exaggerated impulse that will interact with the limbic, endocrine reproductive , metabolic and bioenergetic: any body system.

Regrettably, the oversimplification of such complex systems leads to a misunderstanding and expectation that they are somewhat like a spark getting to a plug in a motor. This simple system can present enough problems to the average person so a system as complex as the one touched upon above is clearly complex and controls the whole body maintaining the homeostatic state in the normal organism.

Best regards
Please ignore if you think it nonsense.
Auberon