Voiding Dysfunction in Mice With Experimental Autoimmune Encephalomyelitis: A Multiple Sclerosis-Like Disease

Lucie Even, Ourdia Bouali, Mathieu Roumiguie, Olivier Cuvillier, Bernard Malavaud, Xavier Game

Abstract


Background: Multiple sclerosis (MS) is the most common disabling neurological disorder affecting young adults. Lower urinary tract dysfunction (LUTD) is common during the course of MS and is responsible for an organic impact on the upper urinary tract and for impaired quality of life. Experimental autoimmune encephalomyelitis (EAE), an animal model of MS, is characterized in mice by paralysis of the tail and hind limbs progressing to paraplegia, but urinary parameters and voiding behavior are not well understood. We aimed to study micturition behavior of both healthy and EAE mice to determine changes induced by EAE.

Methods: Bladder function study included micturition behavior and filling cystometry.

Results: EAE mice developed profound bladder dysfunction characterized by a decrease in urine volume per micturition (138.8 ± 20 vs. 213 ± 17.5 µL, P = 0.018), significantly more frequent postvoid residual urine (30% vs. 61%, P = 0.0496), and increased postvoid residual volume (260 ± 15 vs. 197.5 ± 12 µL, P = 0.045). Cystometric analysis showed significantly more frequent detrusor overactivity (69% vs. 1%, P < 0.0001).

Conclusions: Our study, characterizing bladder dysfunction in EAE mice by clinical and cystometric examination, showed that dysfunction was similar to neurological bladder disorders found in human multiple sclerosis and makes this model promising to assess new compounds.




World J Nephrol Urol. 2016;5(1):4-10
doi: http://dx.doi.org/10.14740/wjnu245w


Keywords


Multiple sclerosis; Experimental autoimmune encephalomyelitis; Lower urinary tract dysfunction; Neurogenic bladder; Overactive bladder

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