Abstract

In the mid-1980s, a large number of children with myelomeningocele (MMC) were undergoing bladder augmentation for neurogenic bladder dysfunction leading to renal deterioration and incontinence. At that time, a small portion of the bladder was excised and submitted to pathology. We noted that pathology reports indicated “acute and chronic inflammation” but there was no mention of any other bladder wall abnormalities. This description did not explain the radiographic findings of trabeculation nor did it address the appearance of the bladder at cystoscopy or at the time of augmentation. On reviewing these bladders histologically, we noted that there was a significant increase in connective tissue and marked disruption of bladder muscle bundle formation by dense infiltrating collagen or extracellular matrix (ECM) protein.1 Some of the muscle cells appeared to be encased within collagen. These observations provided an explanation as to why these bladders develop significant problems with compliance and why they do not contract normally . We then embarked on investigations to determine when these bladder wall changes occurred since it was assumed at that time that the bladders were normal at birth and then deteriorated due to recurrent infection or hypercontractility and/or detrusor sphincter dyssynergia.

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