Adult urologyCan neurologic examination predict type of detrusor sphincter-dyssynergia in patients with spinal cord injury?
Section snippets
Material and methods
A total of 105 patients with a spinal cord lesion, who were admitted for rehabilitation to our institution, were studied. All patients were assessed neurologically on the day of admission according to the American Spinal Cord Injury Association protocol.4 Only patients with American Spinal Cord Injury Association impairment grade A to D were included. Accordingly, the spinal cord lesion was classified as complete or incomplete. Incomplete was defined as the presence of any sensory or motor
Results
A total of 105 male patients could be analyzed. All but 10 had a traumatic spinal cord lesion. All 10 patients with a nontraumatic spinal cord lesion presented with a spinal injury as a consequence of vascular damage. The mean age at injury was 39.2 years (range 15 to 76 years). Of the 105 patients, 41 had tetraplegia (19 complete and 22 incomplete) and 64 had paraplegia (16 complete and 48 incomplete); 81 were in the early (less than 12 months) and 24 in the chronic (more than 1 year)
Comment
Previous data reported by Blaivas et al.,2 Yalla et al.,3 and Tanagho8 have demonstrated that micturition is normally preceded by relaxation of the external urethral sphincter followed within 1 to 15 seconds by a detrusor contraction. This sequence remains intact in patients with cranial neurologic lesions above the level of the pontine mesencephalic micturition center. However, in patients with a neurologic lesion of suprasacral cord, this orderly sequence is usually lost and bladder-external
Conclusions
Neurologic status and DSD type after SCI show statistically significant correlations and, therefore, neurologic examination and determination of DSD type may be helpful to complete neurourologic diagnosis and to assist in confirming completeness of the lesion after acute injury. Because DSD seems to become worse with time, regular urodynamic follow-up examinations are mandatory in patients with DSD to adjust treatment, if necessary.
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Cited by (41)
Detrusor Sphincter Dyssynergia
2024, Urologic Clinics of North AmericaDysfunction of lower urinary tract in patients with spinal cord injury
2015, Handbook of Clinical NeurologyCitation Excerpt :Weld and Dmochowski (2000a) found that, in a population of 243 patients with SCI, suprasacral lesions were associated with detrusor hyperreflexia and/or DSD in 94.9%, and sacral lesions with detrusor areflexia in 85.7% of cases. These results have been replicated by other authors (Schurch et al., 2004; Agrawal and Joshi, 2013). Even if this roughly corresponds to the classic differentiation in upper and lower motor neuron bladder, it should be kept in mind that the completeness or incompleteness of the lesion and the possible association of multiple injury levels can complicate the picture, so much so that a urodynamic evaluation is mandatory in order to correctly assess and classify LUTD in SCI patients (Stöhrer et al., 2009).
The effects of fetal allogeneic umbilical cord tissue transplant following experimental spinal cord injury on urinary bladder morphology
2013, Neurologia i Neurochirurgia PolskaCitation Excerpt :Primary afferent and efferent components of storage and micturition reflexes are distributed bilaterally in spinal cord and overlap extensively. Similarly, both the sensory ascending tract and motor descending tract are important for synergic voiding [20,21]. Incomplete SCI result in an initial loss and later partial recovery of lower urinary tract function.
Cortical substrate of bladder control in SCI and the effect of peripheral pudendal stimulation
2010, NeuroImageCitation Excerpt :Eventually, this leads to involuntary micturitions, incomplete bladder emptying, increased risk for bladder infections and high urine pressures damaging the upper urinary tracts. It is hypothesized that detrusor-sphincter dyssynergia in SCI is caused by injured ponto-spinal, as well as from emerging pathological peripheral reflexes (see e.g. Tai et al., 2006; Schurch et al., 2005). It is not clear whether suprapontine neural changes also contribute to, or at least follow, the pathological LUT function in SCI patients.