Detrusor areflexia is seen most commonly in cauda equina lesions where the sacral reflex is disrupted. It can occasionally occur at other levels of spinal lesions. The clinical manifestation of this results in an inability for the bladder to empty completely or at all, leading to overdistension and stasis. Additionally, there is frequently incontinence due to lack of external sphincter tone, most often due to increased abdominal pressure on the bladder (i.e. stress incontinence). This can be especially problematic in persons with paraplegia that may require high valsalva forces for activities such as transferring from wheelchairs.

Unfortunately, there is a great paucity of research examining the impact and treatment of detrusor areflexia. Although the goals remain the same as with overactive bladder in SCI, (i.e., avoiding incontinence, stasis, UTI’s, and upper urinary tract damage, etc.), these goals may be achieved differently. In general, the goal is either: 1) stopping leakage and improving storage with medications and intermittent catheterization, or 2) improving emptying, either voluntarily in the incomplete injury, and/or into condom drainage in the person with more severe neurogenic bladder impairments. However, further discussion on detrusor areflexia will not occur in this chapter given the extremely sparse evidence base. It should be noted that in some studies described in the sections pertaining to DESD therapy there may have been mixed samples in which a few subjects with detrusor areflexia might have participated in addition to those with detrusor overactivity. In one instance, subjects with detrusor areflexia comprised all study participants providing level 4 evidence from a single case series (n=10) for the surgical anastomosis of the T11 ventral nerve root to the S2-S3 ventral nerve roots in improving bladder function (e.g., Lin et al. 2008 in Table 13.16 for Other Miscellaneous Treatments).