How pain occurs is detailed in the publication - Pain .
And neuropathologists explain the pathogenesis of causalgia by the participation in its occurrence of fibers of the sympathetic nervous system innervating the affected area, which play an important role in the blood supply to the skin and the perception of pain. For more information, see - Neuropathic Pain .
But why does not all people with similar severity develop CRPS II, that is, causalgia? The multifactorial mechanism for the development of this condition has not yet been fully disclosed.
It is assumed that the causalgic syndrome is associated with an increased response to pain signals - an individual hypersensitivity of nerve fibers, which may be caused by an abnormality of the sensory axons of peripheral nerves, for example, in violation of their myelination (the formation of an insulating myelin sheath). 
There is a hypothesis for the development of an excessive inflammatory response to trauma, especially during the acute stage of CRPS II, with the release of proinflammatory cytokines by cells of damaged tissues, and the peripheral nerves release the corresponding neuropeptides (bradykinin, glutamate, substance P), which activate peripheral and secondary central nociceptive (transmitting pain impulses) neurons.
And the progression of this pain syndrome to a chronic state is seen in a decrease in the level of catecholamine neurotransmitters in the blood (in particular, norepinephrine) and subsequent compensatory activation of peripheral alpha-adrenergic receptors.