EXTERNAL ANAL-SPHINCTER HYPERREFLEXIA FOLLOWING SPINAL TRANSECTION INTHE RAT

Citation
Gm. Holmes et al., EXTERNAL ANAL-SPHINCTER HYPERREFLEXIA FOLLOWING SPINAL TRANSECTION INTHE RAT, Journal of neurotrauma, 15(6), 1998, pp. 451-457
Citations number
28
Categorie Soggetti
Neurosciences,"Clinical Neurology","Emergency Medicine & Critical Care
Journal title
ISSN journal
08977151
Volume
15
Issue
6
Year of publication
1998
Pages
451 - 457
Database
ISI
SICI code
0897-7151(1998)15:6<451:EAHFST>2.0.ZU;2-R
Abstract
In the present study, long-term and short-term rat preparations were u sed to develop a model for investigating external anal sphincter (EAS) reflexes in intact and spinal cord-injured (SCI) rats, In this model, EAS distension with an external probe elicits reflex contractions of the EAS in intact, unanesthetized animals, At 2 h after spinal cord tr ansection, none of the lesioned animals displayed EAS EMG activity, In fact, once distended, the EAS was incapable of maintaining closure of the anal orifice, Over a period of 4 days, spinalized animals develop ed a hyperreflexia of the EAS response, By 48 h, the rectified, integr ated EAS EMG was significantly elevated in comparison with nonlesioned controls (EAS hyperreflexia), In addition, the duration of the EAS EM G bursts in response to sphincter distension had significantly increas ed, At 6 weeks after injury, the EAS was significantly hyperreflexic a s measured by EMG burst duration and burst area, As with intact animal s, posttransection EAS reflexes were highly anesthesia sensitive, Thes e studies indicate that (1) brief distension of the anal orifice is su fficient to evoke a physiologically relevant reflexive activation of t he EAS in the rat, (2) the 2- to 24-h postinjury areflexia observed in these experiments may be a suitable model for the study of spinal sho ck, and (3) the observed EAS hyperreflexia after chronic SCI may repre sent the permanent effects of removing descending inhibitory circuits and segmental plasticity, making this reflex an appropriate measure of defecatory dysfunction after spinal cord injury.