学術データベース

Hypersensitivity caused by suppression of descending inhibitory pathways following lumbar intrathecal injection of lidocaine in rats.

著者名

田渕　正樹 (Tabuchi Masaki)

共著者名

Fuyuta M, Takasugi Y, Higashino H, Koga Y.

出版社／掲載誌名

Acta. Med. Kinki Univ.

巻号

33(1/2)

頁

47-54

出版日

2008/12

概要

Although the etiology of neural blockrelated transient neurological sequelae following spinal anesthesia, such as transient neurological symptoms (TNS) and less serious sensory disturbances, is still unclear, previous reports have described the facilitation of ascending nociceptive pathways as the source of complications resulting from local anesthetic toxicity, needle trauma, and patient positioning. We hypothesized that, in addition to the facilitation of ascending nociceptive pathways, the intrathecal injection of local anesthetics might interrupt descending inhibitory pathways, leading to hypersensitivity. To test this hypothesis, changes in tail flick (TF) latency were evaluated under lidocaine blockade of descending inhibitory pathways at the thoracic spinal cord level and under lumbar intrathecal lidocaine injection in rats. Furthermore, the effects of lumbar intrathecal lidocaine injection on cerebrospinal fluid (CSF) concentrations of neurotransmitters related to nociceptive transmission were investigated. The results revealed that thoracic intrathecal lidocaine shortened TF latency immediately after injection, while lumbar intrathecal lidocaine injection initially prolonged TF latency to the cut-off point and subsequently reduced TF latency compared to the baseline. Lumbar intrathecal lidocaine caused a significant reduction in norepinephrine concentrations in the CSF. These results indicate that the reduction of TF latency following lumbar intrathecal lidocaine injection was caused by the suppression of nor adrenergic descending inhibitory pathways. We concluded that the enhanced activity of dorsal horn neurons due to the suppression of descending inhibitory pathways by intrathecal lidocaine injection is one of the possible mechanisms of transient neurological sequelae.