H. Benveniste et al., In vivo diffusion-weighted magnetic resonance microscopy of rat spinal cord: Effect of ischemia and intrathecal hyperbaric 5% lidocaine, REG ANES PA, 24(4), 1999, pp. 311-318
Background and Objectives. Pathophysiologic mechanisms underlying persisten
t neurologic deficits after continuous spinal anesthesia using hyperbaric 5
% lidocaine are still not well understood. It has been suggested that high-
dose intrathecal lidocaine induces irreversible conduction block and even i
schemia in while matter tracts by breakdown of the blood-nerve barrier. In
this study, we use diffusion-weighted magnetic resonance microscopy to char
acterize the effect of intrathecal hyperbaric 5% lidocaine in rat spinal co
rd. The parameter measured with DWM, is an "apparent diffusion coefficient,
" (ADC), which can be used to exclude the presence of ischemia. Methods. Fe
male Fischer CDP rats were used. Group 1 (n = 5) was exposed to ischemia, g
roup 2 (n = 7) was exposed to intrathecal 5% hyperbaric lidocaine, and grou
p 3 (n = 5) was exposed to intrathecal 7.5% glucose. Diffusion-weighted MR
images in group 1 were acquired before and after ischemia induced by cardia
c arrest and in groups 2 and 3 rats prior to and during perfusion of the sp
inal catheter with either 5% hyperbaric lidocaine or 7.5% glucose. Results.
Ischemia decreased the ADC by 40% in gray matter and by 30% in white matte
r of spinal cord. Continuous intrathecal anesthesia with hyperbaric 5% lido
caine did not affect the spinal cord ADC. Further, 7.5% intrathecal glucose
had no effect on ADCs in gray or while matter of spinal cord. Conclusions.
Ischemia reduced the ADC in both spinal cord white and gray matter. Hyperb
aric 5% lidocaine did not affect the spinal cord ADC during the first 1.5 h
ours. We suggest that 5% hyperbaric lidocaine does not induce irreversible
neurologic deficits by causing spinal cord ischemia.