Urodynamic patterns after traumatic spinal cord injury

In the current issue of the Journal, the correlation between somatic neurologic findings, spinal imaging studies, and urodynamic findings in patients with spinal cord injury is reported ‘as not exact’.1 Unpredicted neurourologic findings are defined with careful urodynamic studies (UDS); therefore, bladder management should not completely rely only on clinical bladder evaluation or neurological examination alone, but should always include UDS. The aim of classifying neurogenic bladder is to help appreciate pathophysiology based on the clinical findings to guide the appropriate management. There is a fair correlation between the site of lesion and subsequent neurologic dysfunction. Lesions above pontine micturition center (MC) are associated with detrusor hyperreflexia and lesions below MC are almost always associated with detrusor sphincter dyssenergia (DSD) and autonomic dysreflexia (AD). Monitoring of blood pressure during cystomanometry can help presence of AD in such patients.2 In the study reported in this journal, there were some patients (9.25%) who did not show dyssenergia. It is possible that the neurologic lesion was incomplete. Previously reported studies show some dyssenergic response even in incomplete lesions. Ischemic spinal cord lesions will lead to an infarct which could result in lower motor neuron lesion and areflexia even in supraconal lesions as has also been reported in the current publication. Supraconal lesions in the spinal cord result in upper motor neuron lesions with hyperreflexia and spasticity. Infraconal lesions are associated with lower motor neuron involvement with areflexia and lack of muscle tonus. Cauda equina and conus lesions need careful neurologic and urodynamic evaluation for the proper diagnosis and management. In majority of such patients use of alpha blockers may be what is needed for bladder evacuation assisted with minimum attempted Valsalva maneuver. In such patients with enlarged prostate, urodynamic evaluation is further helpful to monitor voiding pressures, before and after a minimal procedure ‘transurethral incision of the prostate’ with enlarged prostate, rather than a ‘transurethral resection of the prostate’ which could result in incontinence. In females careful evaluation with urodynamics can be helpful for the bladder management to prevent incontinence with and without a small dose of anticholinergics. Studies have also shown that bladder neck in females has sparse alpha adrenergic activity. DSD may also be absent in some upper motor neuron lesions particularly in multipara with a damaged sphincter. As reported in the current journal from Jaipur, India,1 several factors merit consideration to this ‘inexact’ correlation between anatomic lesion and neurourologic clinical findings. First, arterial ischemia can initially lead to degeneration of the spinal cord. Any subsequent reorganization of crucial neural pathways distal to the lesion with or without neural sprouting at the level of injury may affect the neurologic and urodynamic findings. Second, spinal cord injury may be incomplete, thereby partially allowing the integration and modulation of complex micturition signals at multiple levels of the nervous system. Multiple injuries coexisting at different levels can result in unpredictable mixed voiding patterns. In fact, the multiplicity of levels of injury is occasionally unrecognized when based solely on urologic history and clinical evaluation in patients with new spinal cord injury. UDS seems essential for the precise neurourologic assessment to appropriately manage bladder dysfunctions in such patients.