What are the mechanisms by which spinal cord stimulation exerts its effect

The mechanism of spinal cord stimulation is conceptualized based on the gate control theory of pain. In simplistic terms, this theory states that peripheral nerve fibers carrying pain to the spinal cord may have their input modified at the spinal cord level prior to transmission to the brain. The synapses in the dorsal horns act as gates that can either close to keep impulses from reaching the brain or open to allow impulses to pass. Small-diameter nerve fibers (C-fibers and lightly myelinated A-delta fibers) transmit pain impulses. Excess small fiber activity at the dorsal horn of the spinal cord opens the gate and permits impulse transmission, leading to pain perception. Large nerve fibers (A-beta fibers) carry nonpainful impulses, such as touch and vibratory sensation, and have the capacity to close the gate and inhibit pain transmission. Spinal cord stimulation is thought to preferentially stimulate large nerve fibers because these fibers are myelinated and have a lower depolarization threshold than small-diameter nerve fibers.

Experimental evidence suggests a mechanism of action for spinal cord stimulation by increasing levels of gamma aminobutyric acid (GABA) within the dorsal horn of the spinal cord. GABA is an inhibitor of neural transmission in the spinal cord and suppresses hyperexcitability of wide dynamic range interneurons in the dorsal horn. Spinal cord stimulation may also exert a direct effect on brain activity, but this mechanism is not well understood at present.

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