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Purpose: Bladder outflow obstruction (BOO) is common in the elderly and can result in bladder voiding dysfunction (BVD) due to severe bladder muscle damage. The goal of this research was to evaluate the use of adult stem cells for the treatment of BVD due to decreased muscle contractility in a rat model. Materials and methods: Adipose-derived stem cells (ADSCs) and muscle precursor cells (MPCs) were harvested from male Lewis rats and expanded in culture. BOO was induced by tying a suture around the urethra. Six weeks after obstruction, the development of BVD was confirmed by cystometric analysis in conscious rats, histology and molecular investigations. Injection of ADSCs or MPCs into the bladder wall and synchronous deligation was performed 6weeks after the obstruction. After stem-cell treatment, morphological and functional changes were assessed. Age-matched rats and animals without cellular therapy but deligation-only served as controls. Results: Voiding pressures decreased progressively 6weeks after obstruction with increased bladder capacities. Structural changes of the detrusor muscle occurred during the time of obstruction with an increased connective tissue-to-smooth muscle ratio and decreased SMA/smoothelin expression. After stem-cell injection, improved voiding pressures and voiding volumes were observed together with recovered tissue architecture. RT-PCR and Western blotting showed an up-regulation of important contractile proteins. Conclusions: We established a reliable model for BVD and demonstrated that ADSCs and MPCs can prevent pathophysiological remodelling and provide regenerated bladder tissue and function.

Since its first description in 1952 neither the pathogenesis nor the localization of congenital ocular motor apraxia (COMA) have been cleared. There are reports indicating that COMA is more variable in its clinical expression and neuroradiological findings than previously assumed. In eight children with COMA neurological examination, developmental testing and neuroradiological investigation by CT or MRI were carried out. Ataxia was found in five, developmental delay in six of the patients. CT or MRI were normal in four children, the others had variable malformations such as hypoplasia of the cerebellum or corpus callosum, heterotopias of gray matter and maturational delays in the basal ganglia. No correlations between the clinical symptoms and the neuroradiological findings were found. The authors suggest that COMA is not an entity but rather a symptom, variably associated with malformations and maturational disorders of the brain.