Neuropathic Faecal Incontinence: Correlation Between Peripheral Axonal Counts and Cortical Activation


Introduction and Objectives: Faecal incontinence is a devastating social and physical handicap affecting 2% of the general population. It is 8 times more common in females than males, largely due to the adverse effects of childbirth on vulnerable pudendal nerves. Our laboratory created 2 rat models simulating faecal incontinence in which the inferior rectal nerve (a terminal branch of the pudendal nerve that supplies the external anal sphincter) is either crushed or compressed. We aimed to determine the effects of these injuries on inferior rectal-nerve axonal counts and cross-sectional areas in our rat models, and to correlate these findings with somatosensory evoked potentials (SSEPs) from the same animals.

Methods: Eighteen female virgin Wistar rats were assigned equally to 3 groups: control, nerve crush, and nerve-balloon compression, respectively. The creation of the rat models (Healy et al. Dis Colon Rectum, in press) involves either: a) focal crush, or b) compression by catheter balloon inflation of the inferior rectal nerve. Four weeks following injury, inferior rectal nerves were harvested, resin embedded, sectioned (1μm thickness), and analyzed using Scion Image software following SSEP recordings.

Results: The inferior rectal nerve was successfully harvested in 14 of the 18 rats (4 control, 5 nerve crush, and 5 balloon compression). There was no significant difference in median inferior rectal-nerve total axonal counts (P = 0.69, Kruskal-Wallis test). No significant difference was demonstrated in the frequency distribution of the axonal cross-sectional area: control versus nerve crush and control versus balloon compression (P = 0.92, P =0.17, respectively, Kolmogorov-Smirnov test). A significant difference in the median axonal cross-sectional area was found: control: 12.6 μm2, nerve crush: 13.3 μm2, and balloon compression: 17.6 μm2 (P < 0.0001, Kruskal-Wallis test). The nerve crush and balloon compression rats had significantly smaller SSEPs than control rats (P = 0.024, P = 0.03, respectively, Dunnett post-hoc test).

Conclusion: There is a significant reduction of evoked cortical potentials in both models despite the fact that an equal number of axons were stimulated compared to controls. This suggests that the altered cortical drive in these models is a result of modified central processing and not peripheral axonal loss.

KEYWORDS: Faecal incontinence, somatosensory evoked potential