BACKGROUND AND OBJECTIVES: Glucose is a common component of anesthetic solutions used for spinal anesthesia. However, its possible contribution to recent injuries occurring with spinal anesthesia has not been adequately addressed. Accordingly, the present studies compare the functional and morphologic effects of intrathecally administered glucose with those of lidocaine. METHODS: Twenty rats, implanted with intrathecal catheters, were divided into three groups to receive a 1-hour infusion of 5% lidocaine (n = 6), 10% glucose (n = 7), or normal saline (n = 7). Four days after infusion, animals were evaluated for persistent sensory impairment using the tail-flick test. Three days later, the animals were sacrificed, and the spinal cord and nerve roots were examined by a neuropathologist blinded to the solution received and the results of sensory testing. RESULTS: Lidocaine-treated animals exhibited persistent sensory impairment, whereas glucose- and saline-treated animals did not. Neuropathologic evaluation revealed moderate to severe nerve root injury in lidocaine-treated animals. Histologic changes in glucose- and saline-treated animals were minimal, similar, and restricted to the area adjacent to the catheter. Morphologic damage associated with lidocaine preferentially affected the nerve roots, with relative sparing of the spinal cord and dorsal root ganglia. CONCLUSIONS: These results suggest that, at clinically relevant concentrations, glucose does not induce neurologic injury, providing indirect evidence that recent clinical injuries occurring after spinal anesthesia resulted from a neurotoxic effect of the local anesthetic. Additionally, the present studies suggest that deficits resulting from neurotoxicity of intrathecally administered anesthetic result from injury to the axon.
BACKGROUND AND OBJECTIVES:Glucose is a common component of anesthetic solutions used for spinal anesthesia. However, its possible contribution to recent injuries occurring with spinal anesthesia has not been adequately addressed. Accordingly, the present studies compare the functional and morphologic effects of intrathecally administered glucose with those of lidocaine. METHODS: Twenty rats, implanted with intrathecal catheters, were divided into three groups to receive a 1-hour infusion of 5% lidocaine (n = 6), 10% glucose (n = 7), or normal saline (n = 7). Four days after infusion, animals were evaluated for persistent sensory impairment using the tail-flick test. Three days later, the animals were sacrificed, and the spinal cord and nerve roots were examined by a neuropathologist blinded to the solution received and the results of sensory testing. RESULTS:Lidocaine-treated animals exhibited persistent sensory impairment, whereas glucose- and saline-treated animals did not. Neuropathologic evaluation revealed moderate to severe nerve root injury in lidocaine-treated animals. Histologic changes in glucose- and saline-treated animals were minimal, similar, and restricted to the area adjacent to the catheter. Morphologic damage associated with lidocaine preferentially affected the nerve roots, with relative sparing of the spinal cord and dorsal root ganglia. CONCLUSIONS: These results suggest that, at clinically relevant concentrations, glucose does not induce neurologic injury, providing indirect evidence that recent clinical injuries occurring after spinal anesthesia resulted from a neurotoxic effect of the local anesthetic. Additionally, the present studies suggest that deficits resulting from neurotoxicity of intrathecally administered anesthetic result from injury to the axon.