• B A Meyerson, P Herregodts, B Linderoth, and B Ren.
• Karolinska Institute Center for Pain Research, Department of Neurosurgery, Karolinska Hospital, Stockholm, Sweden.
• Stereotact Funct Neurosurg. 1994 Jan 1;62(1-4):256-62.

AbstractIn spite of the routine usage of spinal cord stimulation (SCS) as treatment of chronic pain, there is an insufficient understanding of the mechanisms underlying its effect. The method was originally developed as a spin-off from experiments demonstrating the inhibitory control of nociceptive signals by the activation of large afferent fibers, and on the basis of these findings the gate-control theory was advanced. Later experiments showed that stimulation of the dorsal columns can inhibit the relay of nociceptive impulses to second-order neurons in the dorsal horn. It should be emphasized that all these experiments were performed with acute noxious stimuli; it is now universally recognized that SCS in patients is preferentially, or exclusively, effective for chronic neuropathic types of pain. For these and other reasons the mode of action of SCS in clinical pain cannot be inferred from these early animal experiments. In ongoing studies we have used animal models of mononeuropathy (rat) in which we have applied SCS acutely or chronically with stimulation parameters similar to those used in patients. In these animals the first component of the flexor reflex appears with a lower stimulus threshold in the nerve lesioned than in the intact, sham-operated leg. SCS was applied at the approximate level of Th-XII during 10-20 min and produced a marked augmentation of the stimulus threshold. This abnormally high threshold was not normalized until 30-60 min after the end of SCS. In awake animals SCS was applied via an implanted spinal electrode and the effect on behavior changes associated with mononeuropathy was studied.(ABSTRACT TRUNCATED AT 250 WORDS)

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