The chronic pain syndrome pathophysiology is disturbance in the process of acute nociception. The processes of transduction, transmission, modulation and perception have somehow got disturbed.
The pain stimuli which were supposed to be sent forward before closing of gate, get more and more intensely forwarded rather than getting modulated.
In addition, due to sustained partial depolarization of dorsal root horn cells, large input by small unmyelinated fibres keeps on getting forwarded through “open” gate. A stage in chronic pain syndrome pathophysiology comes when spontaneity of discharge rate goes on increasing, known as “Central Sensitization”.
The neurotransmitters and other chemicals like excitatory amino acids, viz, glutamate and aspartate, acting at N-methyl D aspartate receptors (NMDA) on WDR (wide dynamic range) neurons in lamina V cause the repetitive firing and more and more release of these as well as substance P when considering chronic pain syndrome pathophysiology .
Some other intracellular chronic pain syndrome pathophysiology processes like increased intracellular calcium, production of nitric oxide, production of prostaglandins, cause ultimately neuronal damage and irreversible dysfunction leading to chronicity of pain.
In addition, this damage leads to demyelination of larger fibres while (fibres loose their Schwann cell sheath); this leads to inter-axonal spread of impulses which may ascend up or down at spinal level.
The non-nociceptive neurons like sympathetic and mechanoreceptors afferents also start behaving abnormally. This type of pain is called neuropathic pain.
Reflex sympathetic dystrophic (RSD) type of pain: Again as described in chronic pain syndrome pathophysiology , similar type of process involving sympathetic afferents comes into play lending to these phenomenon of reflex sympathetic dystrophy.