Neurogenic bladder in lower motor neuron lesion: Long‐term assessment

We have comprehensively investigated 10 patients with lower motor neuron (LMN) lesions (mean duration of lesions: 14 years) who were managed with intermittent catheterization. All patients (9 males and 1 female) underwent complete neurologic examination and, if necessary, extensive electromyographic studies to define the level and completeness of the lesion. The causes of the LMN lesions were traumatic injury (5), congenital (2), inflammation (1), and surgery (2). Patients were arranged into 2 groups. Five patients had complete lesions (no sensory or motor function at sacral level) and 5 had incomplete lesions (some remaining function). All patients were continent between catheterizations. A detailed urodynamic investigation, including cystometrogram (CMG), urethral pressure profile (UPP), voiding cystourethrogram (VCUG), phentolamine (5 mg i.v.), and bethanechol (5 mg s.c.), Tests, was performed in all patients. Detrusor compliance (DC) at 100 ml was statistically the same in both groups (21.9 ml/cm H₂O in complete lesions and 37.2 ml/cm H₂O in incomplete lesions) and did not change at all after phentolamine in incomplete lesions (37.2 ml/cm H₂O) but was somewhat increased in complete ones (27.5 ml/cm H₂O). Bethanechol decreased DC in patients with complete and incomplete lesions (2.9 and 7.1 ml/cm H₂O, respectively). Maximal urethral pressure was the same in both groups before and after pharmacological tests. The bladder neck was completely closed (VCUG) in all 5 patients with incomplete lesions in comparison to only 1 from the other group. Phentolamine had only a slight effect on bladder neck in both groups. Bladder compliance is normal in patients with LMN lesions treated with intermittent catheterization and the bladder neck is opened only in complete lesions. This may also account for the absence of incontinence in these patients.