It remains uncertain to what extent lower urinary tract (LUT) symptom (LUTS) is a comorbidity of myasthenia gravis (MG). We prospectively administered a LUTS questionnaire devised for detecting neurogenic pelvic organ dysfunction (not validated) in an MG group and healthy control group and compared the results.

The MG group comprised 21 patients: 15 women, 6 men, age range 22‒73 (mean 47) years, illness duration range 0.2‒8 (mean 3.5) years, median MGFA grade 2, all walking independently. Therapies included thymectomy in 17, predonisolone 5‒20 mg/day in 10, and pyridostigmine bromide 60‒180 mg/day in 9. The control group, who were undergoing an annual health survey, comprised 235 consecutive subjects: 120 women, 115 men, age range 30‒69 (mean 48) years. The questionnaire had 9 questions. Each question was scored from 0 (none) to 3 (severe) with an additional quality of life (QOL) index scored from 0 (satisfied) to 3 (extremely dissatisfied). Statistical analysis was made using Student’s t-test.

Compared with the control subjects, the frequency of LUTS in the MG patients was significantly higher for daytime frequency (43%; p<0.01), nocturia (24%; p<0.01) and urinary incontinence (43%; p<0.05). The LUTS-related QOL index for the MG patients was significantly higher for MG patients as a whole than for all control patients (29%) (p<0.05).

Since we did not perform urodynamics in any of our patients, we do not know the exact pathological mechanism explaining the above findings of the storage dysfunction. However, looking at the urodynamic reports in MG and neuro-urology reports, there might be a direct cause and/or a secondary or associated cause producing LUTS in MG. Detrusor overactivity (as seen in Table 1) is usually attributed to the brain/supra-sacral spinal cord lesions, but it might also originate from partial peripheral nerve lesion (by irritation and ephaptic transmission of the nerve fibers). Another possibility for detrusor overactivity is that pyridostigmine, commonly prescribed to ameliorate muscular weakness in MG, stimulates bladder smooth muscles enough to generate detrusor overactivity. In our previous study, a 42-year-old man with MG (MGFA2, under 120 mg/day pyridostigmine) showed detrusor overactivity and small bladder capacity (150 ml) on urodynamics. He had no brain/ spinal cord diseases. Since anticholinergics are contraindicated for MG, we started him on 100 mg/day milnaciplan, a selective serotonin-noradrenaline reuptake inhibitor (SNRI). This medication ameliorated his OAB successfully (bladder capacity increased to 198 ml) without worsening of MG. Daytime urinary frequency (p<0.05) and stress urinary incontinence in females, though not statistically significant in the present study, have been shown to be common in MG, presumably reflecting pelvic floor descent on straining/coughing by muscle weakness as reported in muscular dystrophy and possibly, weakness of the external urethral sphincter muscle that is innervated by both somatic and sympathetic nerves. Nocturia in our MG cases might derive from nocturnal polyuria, since many patients were taking oral predonisolone, and polyuria induced by cortisol has been described.

Our study results showed that MG patients had significantly more LUTS (overactive bladder) than healthy control subjects and had worse LUTS-related QOL; therefore amelioration of LUTS in MG is important.