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Detrusor Areflexia

Detrusor areflexia is observed most commonly in cauda equina lesions where the sacral reflex is disrupted. However, people with cauda equina lesions may also present atypically with autonomic detrusor contraction which causes a continuous increase of intravesical pressure during urination (Shin et al. 2002). Detrusor areflexia can also occur below the S2 spinal cord level and involve the conus medularis or peripheral nerves. Clinically, this means that the bladder cannot 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, and upper urinary tract damage), 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 males 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 two other studies described in the sections pertaining to DESD therapy there were mixed samples with a few subjects with detrusor areflexia. 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., Table 20 for Other Miscellaneous Treatments).

Table 21 Destrusor Areflexia

Author Year

Country

Research Design

PEDro Score

Total Sample Size

MethodsOutcome
Shin et al. 2002

Korea
Observational

N=50

Population: Individuals with traumatic cauda equina injury:

Normal compliance group (n=36):

Mean age: 32.9 yr; Gender: males (n=20), females (n=16); Mean time from injury: 4.9 mo; Mean time interval between injury and rehabilitation: 3.4 mo; Voiding method: clean intermittent catheterization (n=20), reflex voiding (n=11), foley catheterization (n=3), normal voiding (n=2).

Low compliance group (n=14):

Mean age: 26.2 yr; Gender: males (n=6), females (n=8); Mean time from injury: 7.8 mo; Mean time interval between injury and rehabilitation: 5.9 months; Voiding method: clean intermittent catheterization (n=2), reflex voiding (n=7), foley catheterization (n=5), normal voiding (n=0).

Intervention: Urodynamic evaluation; normalization of compliance in individuals in the low compliance group via Oxybutynin and propiverine.

Outcome Measures: Presence of autonomous detrusor contraction (ADC), time since injury, voiding method prior to admission, maximal bladder capacity, maximal detrusor pressure, compliance,

1.     No significant difference between the normal compliance and low compliance for age and sex.

2.     There was a significantly longer time interval between rehabilitation and time from injury in the low compliance group (p<0.05).

3.     In the normal compliance group, clean intermittent catheterizations were used significantly more compared to the low compliance group (p<0.05).

4.     The low compliance group had significantly lower mean compliance and mean maximal bladder capacity than the normal compliance group (p<0.01).

5.     Mean maximal detrusor pressure was significantly higher in the low compliance group (p<0.01).

6.     ADC observed in 6/14 individuals in the low compliance group, these individuals had significantly lower mean compliance, maximal bladder capacity and higher maximal detrusor pressure (p<0.05).

7.     Normalization of low compliance group led to significantly higher compliances and maximal bladder pressures (p<0.05), as well as significantly lower maximal detrusor pressures (p<0.05).

8.     Follow-up of normalization showed ADC to disappear and compliance and maximal bladder capacity to return to normal in 4/6 ADC individuals.