PURPOSE: We standardize procedures for ultrastructural study of detrusor smooth muscle and intrinsic nerves in neurogenic bladder dysfunction in the human, and present an overview of the findings. MATERIALS AND METHODS: The study included 18 female and 33 male patients 7 to 96 years old. They had neurogenic bladder dysfunction with hyperreflexia for less than 1 to 43 years, resulting from upper motoneuron lesions (spinal cord injury 25, brain disorder 17) or combined upper and lower motoneuron deficit (meningomyelocele 9). Endoscopic or open bladder biopsies were processed for ultrastructural study of detrusor smooth muscle and intrinsic neural elements. Qualitative morphologic criteria of muscle cell arrangement, degeneration and cell-cell contacts, as well as those of degeneration and regeneration of intrinsic neural elements are defined. RESULTS: Five biopsies from the brain disorder group had insufficient smooth muscle and were excluded from study. The remaining 46 biopsies were evaluated by electron microscopy, and all displayed the complete dysjunction pattern of detrusor overactivity. Most displayed degeneration and regeneration of intrinsic axons but disproportionately limited muscle cell degeneration, irrespective of detrusor contractility. The brain disorder group biopsies displayed many more ultrastructurally normal axons than the meningomyelocele and spinal cord injury group biopsies (median 33% versus 8% or less). CONCLUSIONS: Upper motoneuron neurogenic bladder dysfunction in humans is associated with intrinsic neuromuscular defects in the detrusor. Ultrastructural features of these defects suggest morphologic markers that not only may distinguish neuropathic from nonneuropathic bladder dysfunction, but also may point to the anatomical level of the neurogenic deficit.
PURPOSE: We standardize procedures for ultrastructural study of detrusor smooth muscle and intrinsic nerves in neurogenic bladder dysfunction in the human, and present an overview of the findings. MATERIALS AND METHODS: The study included 18 female and 33 male patients 7 to 96 years old. They had neurogenic bladder dysfunction with hyperreflexia for less than 1 to 43 years, resulting from upper motoneuron lesions (spinal cord injury 25, brain disorder 17) or combined upper and lower motoneuron deficit (meningomyelocele 9). Endoscopic or open bladder biopsies were processed for ultrastructural study of detrusor smooth muscle and intrinsic neural elements. Qualitative morphologic criteria of muscle cell arrangement, degeneration and cell-cell contacts, as well as those of degeneration and regeneration of intrinsic neural elements are defined. RESULTS: Five biopsies from the brain disorder group had insufficient smooth muscle and were excluded from study. The remaining 46 biopsies were evaluated by electron microscopy, and all displayed the complete dysjunction pattern of detrusor overactivity. Most displayed degeneration and regeneration of intrinsic axons but disproportionately limited muscle cell degeneration, irrespective of detrusor contractility. The brain disorder group biopsies displayed many more ultrastructurally normal axons than the meningomyelocele and spinal cord injury group biopsies (median 33% versus 8% or less). CONCLUSIONS: Upper motoneuron neurogenic bladder dysfunction in humans is associated with intrinsic neuromuscular defects in the detrusor. Ultrastructural features of these defects suggest morphologic markers that not only may distinguish neuropathic from nonneuropathic bladder dysfunction, but also may point to the anatomical level of the neurogenic deficit.
Authors: Diaa E E Rizk; Rengasamy K Padmanabhan; Saeed Tariq; Mohamed Shafiullah; Ijaz Ahmed Journal: Int Urogynecol J Pelvic Floor Dysfunct Date: 2005-07-14