Gate control pain modulation theory explains transient improvements.
The dorsal horns are not merely passive transmission stations but sites at which dynamic activities (inhibition, excitation and modulation) occur. 
Via a series of filters and amplifiers, the nociceptive message is integrated and analysed in the cerebral cortex, with interconnections with various areas. 
The processing of pain takes place in an integrated matrix throughout the neuroaxis and occurs on at least three levels, at peripheral, spinal, and supraspinal sites. 
Knowledge of the modalities of pain control is essential to correctly adapt treatment strategies (drugs, neurostimulation, psycho-behavioural therapy, etc.).
Dysfunction of pain control systems causes neuropathic pain. 
Spinal Cord Stimulation modalities evolved from the gate-control theory postulating a spinal modulation of noxious inflow.             
It has been demonstrated in multiple studies that dorsal horn neuronal activity caused by peripheral noxious stimuli could be inhibited by concomitant stimulation of the dorsal columns. 
Pain relief was more prominent at pain ascending through C fibers than pain ascending through Adelta fibers 
Many theories on the mechanism of action of Spinal Cord Stimulation have been suggested, including activation of gate control mechanisms, conductance blockade of the spinothalamic tracts, activation of supraspinal mechanisms, blockade of supraspinal sympathetic mechanisms, and activation or release of putative neuromodulators. 
At present, Spinal Cord Stimulation is a well established form of treatment for failed back surgery syndrome, complex regional pain syndromes (CRPS), low back pain with radiculopathy and refractory pain due to ischemia.    
Stimulation produced analgesia can provide a level of analgesia and efficacy that is unattainable by other treatment modalities. 
Spinal Cord Stimulation for the treatment of chronic pain is cost- effective when used in the context of a pain treatment continuum. 
Precise subcutaneous field stimulation is targeted to specific areas of neuropathic pain. 
We aim at attenuation or blockade of pain through intervention at the periphery, by activation of inhibitory processes that gate pain at the spinal cord and brain. 
Segmental noxious stimulation produces a stronger analgesic effect than segmental innocuous stimulation. 
That is exactly what intradermal sterile water or subcutaneous saline injections do!
Chloride, used in subcutaneous "sham" injections, independently regulates the pain pathway. 
Intraspinal steroids should no longer be used since we can obtain better results using sterile water intradermal injections, especially for back pain.
Furthermore, intradermal injections are minimally invasive and absolutely NOT neurotoxic.
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