Reduced somatosensory cortical activation in experimental models of neuropathic fecal incontinence.

Abstract

Alteration in cortical awareness may be the underlying abnormality in patients with neuropathic fecal incontinence. The cortical effects of inferior rectal nerve injury were determined using somatosensory evoked cortical potential recordings in an experimental model of neuropathic fecal incontinence. Eighteen female virgin Wistar rats were assigned equally to one of three groups: an unoperated control group, a nerve crush group (positive control), and a nerve balloon compression group. Four weeks following the injury, all animals underwent somatosensory evoked cortical potential recordings. Following this, the inferior rectal nerve was harvested, resin-embedded, sectioned (1 microm thickness), and axonal counts and axonal cross-sectional areas were analyzed using Scion Image software. Somatosensory evoked cortical potentials were reduced in the nerve crush and balloon compression groups compared with controls (P = 0.024, P = 0.03, respectively). The inferior rectal nerve was harvested in 14 of the 18 animals (4 control, 5 nerve crush, 5 balloon compression). There were no differences in median inferior rectal nerve total axonal counts (P = 0.69) or in the frequency distribution of axonal cross-sectional area between groups (control vs. nerve crush and control vs. balloon compression: P = 0.92, P = 0.17, respectively). Somatosensory evoked cortical potential amplitude is reduced following crush or compression injury to the inferior rectal nerve. In neuropathic fecal incontinence, alteration in cortical awareness may be the result of processing modification at a central and not peripheral level.