A 39-year-old woman comes to the office due to worsening urinary symptoms for the past several weeks. The patient has increasingly had sudden, intermittent urges to urinate followed by small-volume urine. On several occasions, she has had difficulty reaching the bathroom in time and has involuntarily leaked a small amount of urine. The patient reports no fever, dysuria, hematuria, abdominal pain, or abnormal vaginal discharge. She was diagnosed with multiple sclerosis 3 years ago after an episode of gait unsteadiness. Since then, she has had several acute exacerbations, most recently 2 months ago, which were treated with glucocorticoids. Her other medical conditions include hypertension and glucocorticoid-induced hyperglycemia. She does not use tobacco, alcohol, or illicit drugs. Vital signs are normal. Physical examination shows hyperreflexia of the lower extremities and mild intention tremor. The remainder of the examination shows no abnormalities. Urine dipstick is negative for leukocyte esterase and nitrite but positive for glucose. Postvoid bladder scan reveals a contracted, small bladder. Which of the following is the most likely cause of this patient's urinary symptoms?
Show Explanatory Sources
This patient with multiple sclerosis (MS) has developed urgency incontinence (also known as overactive bladder), which is the sudden-onset urge to void followed by an involuntary leakage of urine.
Sclerotic plaques of MS in the cerebral cortex can impair the upper motor neurons that exert inhibitory control of spinal neurons (eg, descending corticospinal tracts). This results in lower motor neuron overactivity, leading to spasticity, which can manifest as gait disturbances and hyperreflexia, as seen in this patient. Similarly, cerebral cortex MS plaques can impair upper motor neurons that inhibit the micturition reflex. This can lead to increased involuntary (ie, spastic) contractions and overactivity of the detrusor muscle, resulting in a small, contracted bladder (as seen in this patient's bladder scan). These bladder spasms do not allow adequate time between the sensation to void and the loss of urine, which can be worsened in patients with gait abnormalities that limit their ability to quickly reach a bathroom.
Treatment options of urgency incontinence include antimuscarinics (eg, oxybutynin) and β-3 receptor agonists (eg, mirabegron).
(Choices A and C) Demyelination of the sacral spinal cord (ie, cauda equina) can lead to impairment of the lower motor neuron input to the bladder, resulting in detrusor underactivity. Either detrusor underactivity or obstruction of the bladder outlet can lead to urinary retention and overflow incontinence. However, these patients would have a distended bladder and a large (>150 mL) postvoid residual urine volume.
(Choice B) Hyperglycemia can lead to polyuria due to glucosuria-induced osmotic diuresis, which can cause overflow incontinence. However, in contrast to this patient, patients with overflow incontinence typically have a constant dribbling of urine and a distended bladder with large postvoid residuals.
(Choice E) Weakness of pelvic floor muscles can lead to urethral hypermobility, which causes stress urinary incontinence, characterized by urine leakage with increased intraabdominal pressure (eg, Valsalva, cough, sneeze). This patient's sudden urge to urinate and inability to reach the bathroom are more consistent with urge incontinence.
Educational objective:
Patients with multiple sclerosis can develop urgency incontinence due to loss of cortical (ie, upper motor neuron) inhibition of detrusor contraction.