Urinary incontinence and overactive bladder symptoms are more common in patients with myasthenia gravis (MG) than in the general population, with the late-onset subtype (LOMG) experiencing the earliest onset and fastest progression, according to a recent study published in Neurological Sciences.
The prevalence of urinary dysfunction in patients with MG has been underexplored despite its potential impact on quality of life. The authors aimed to explore the prevalence, severity and potential predictors of urinary incontinence and overactive bladder symptoms in MG patients, with a particular focus on the impact of MG severity and subtype on urinary dysfunction.
In this study, around 90 patients with MG and 90 matched controls were evaluated for urinary incontinence and overactive bladder symptoms using validated questionnaires. MG severity was assessed using the Myasthenia Gravis Activities of Daily Living (MG-ADL) scale, and patients were categorized into early-onset MG (EOMG), LOMG and very late-onset MG (VLOMG) subgroups.
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Results showed that nearly 52% of patients with MG had significant urinary incontinence symptoms compared to 12% of controls, with LOMG patients having the highest prevalence and the fastest progression.
The MG-ADL score was found to be an independent predictor of urinary incontinence. Higher MG-ADL scores — meaning greater disease severity — meant an increased risk of urinary incontinence.
About one in three patients with MG had severe incontinence, compared to only 2% of controls, and stress incontinence symptoms were higher in patients with MG than in the control group.
“This finding aligns with previously proposed theory that MG-related muscle weakness and fatigue may extend to the pelvic floor muscles, specifically the [external urethral sphincter], thereby impairing their ability to support normal bladder function, eventually leading to stress [urinary incontinence],” noted the study’s authors.
While the study found strong associations between MG and urinary dysfunction, the absence of urodynamic testing and detailed pyridostigmine usage data limits the understanding of the exact mechanisms at play. Future studies should incorporate these elements to draw more precise conclusions.
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