Michelangelo Buonocore1, Laura Demartini2. 1. Unit of Clinical Neurophysiology & Neurodiagnostic Skin Biopsy, Fondazione Salvatore Maugeri, Pavia, Italy. 2. Unit of Pain Medicine, Fondazione Salvatore Maugeri, Pavia, Italy.
Abstract
BACKGROUND: Although the number of patients with chronic neuropathic pain treated by spinal cord stimulation (SCS) is continuously increasing, its analgesic mechanism remains to be elucidated. Previous studies have demonstrated that classical SCS (low stimulation frequency evoking paresthesia) inhibits the somatosensory evoked potentials (SEPs). CASE PRESENTATION: We describe here the results of a series of SEPs recordings performed in a female patient with chronic pain, using four different types of SCS: the classical SCS (60 Hz, 250 μsec) and three paresthesia free SCS modalities: high frequency (10 kHz, 20 μsec) and two types of high-density SCS (500 Hz, 500 μsec and 200 Hz, 1000 μsec). All the tested SCS modalities completely inhibited the SEPs cortical responses, with an immediate recovery of the inhibition after turning the stimulator off. CONCLUSIONS: All the tested SCS modalities are able to inhibit SEPs and thus the lemniscal system. In particular, both paresthesia and paresthesia free SCS affect SEPs in the same manner. The presence of this inhibitory effect during paresthesia free modalities suggests that it is independent from the generation of action potentials, with a probable mechanism acting at the stimulation site. Further studies investigating the relationship between the inhibition of the lemniscal system and the analgesic effect of the SCS are, therefore, warranted.
BACKGROUND: Although the number of patients with chronic neuropathic pain treated by spinal cord stimulation (SCS) is continuously increasing, its analgesic mechanism remains to be elucidated. Previous studies have demonstrated that classical SCS (low stimulation frequency evoking paresthesia) inhibits the somatosensory evoked potentials (SEPs). CASE PRESENTATION: We describe here the results of a series of SEPs recordings performed in a female patient with chronic pain, using four different types of SCS: the classical SCS (60 Hz, 250 μsec) and three paresthesia free SCS modalities: high frequency (10 kHz, 20 μsec) and two types of high-density SCS (500 Hz, 500 μsec and 200 Hz, 1000 μsec). All the tested SCS modalities completely inhibited the SEPs cortical responses, with an immediate recovery of the inhibition after turning the stimulator off. CONCLUSIONS: All the tested SCS modalities are able to inhibit SEPs and thus the lemniscal system. In particular, both paresthesia and paresthesia free SCS affect SEPs in the same manner. The presence of this inhibitory effect during paresthesia free modalities suggests that it is independent from the generation of action potentials, with a probable mechanism acting at the stimulation site. Further studies investigating the relationship between the inhibition of the lemniscal system and the analgesic effect of the SCS are, therefore, warranted.