Urinary incontinence, diminished bladder capacity and abnormal bladder sensation are common hallmarks of neurogenic bladder due to central neuropathies, such as spinal cord injury, multiple sclerosis, stroke and Parkinson's disease. We have previously demonstrated that a novel neuromodulation technique (transcutaneous spinal cord neuromodulation) can acutely alter the function of the lower urinary tract in patients with spinal cord injury [1]. In that study, subjects exhibited increased bladder capacity and improved bladder sensation while stimulation was being delivered. However, these effects did not persist in the absence of stimulation. Therefore the aims of this study were: 1) to determine if a course of multiple stimulation sessions can lead to long term plasticity in lower urinary tract function and 2) to assess whether the effects of transcutaneous spinal cord neuromodulation that were observed in subjects with spinal cord injury would be translated in subjects with stroke.

Five patients (four males and one female) with stable spinal cord injury at T8 or above who used clean intermittent catheterization (CIC) and five patients with stable cortical stroke. Each subject had stable disease for at least one year. All subjects underwent a detailed history and physical examination, completed the neurogenic bladder symptom score, and were evaluated with a clinical urodynamic study performed according to ICS guidelines. 
Following the baseline evaluation, the patients were invited to return for an 8-week long course of stimulation. Stimulation was delivered using adhesive electrodes over the interspinous ligaments of T11 and L1 as cathode and two adhesive electrodes over the iliac crest serving as anode. The stimulation waveform consisted of two alternating pulses of opposite polarities separated by a 1 mS delay to form a delayed biphasic waveform. The pulses consisted of a high frequency biphasic carrier pulse (10 KHz) combined with a low frequency (30 Hz) burst pulse each with a pulse width of 1 ms. Subjects received stimulation for 90 minutes. Each subject completed three stimulation sessions a week. Within 1 week of the last stimulation session, all subjects completed a urodynamic study, a 4-day voiding diary and the neurogenic bladder symptom score.

Urodynamics in spinal cord injury subjects demonstrated a mean bladder capacity of 125  ml and voiding efficiency of 24%. Urodynamics after completion of the study revealed a mean bladder capacity of 253 ml (p < 0.05) and voiding efficiency of 32% (p < 0.05). Among stroke subjects, mean bladder capacity was 72 ml on initial urodynamics and 273 ml after completing the study (p < 0.05). 
Mean initial Neurogenic Bladder Symptom Score was 35 in spinal cord injury subjects and decreased to 28 after study completion (p < 0.05). Stroke subjects also demonstrated a decrease in the Neurogenic Bladder Symptom Score from 30 to 17 (p < 0.05). 
Subjects with SCI experienced an average of 2.2 leaks per day before and 1.35 leaks at study completion (p > 0.05). Stroke subjects also showed a nonsignificant decrease in the number of daily incontinence episodes (1 to 0.3 per day, p > 0.05). Mean number of nocturnal voids decreased from 1.7 to 0.65 in the spinal cord injury subjects (p < 0.05) and from 2.5 to 1.8 in the stroke subjects (p < 0.05).

Our findings indicate that transcutaneous neuromodulation of the spinal cord can modulate the activity of the lower urinary tract in subjects suffering from neurogenic bladder due to central neuropathies (i.e. spinal cord injury and stroke). A series of stimulation sessions resulted in increased bladder capacity on urodynamic assessment. Furthermore, subjects with stroke and spinal cord injury both reported significant and clinically meaningful decreases in the Neurogenic Bladder Symptom Score, and number of nocturia episodes.  The number of daily incontinence episodes also decreased, although that difference did not reach statistical significance. These findings suggest that the effects of transcutaneous neuromodulation of the spinal cord on the lower urinary tract can persist even in the absence of ongoing stimulation and that it may be of benefit to patients with neurogenic bladder due to pathologies other than spinal cord injury.

Transcutaneous spinal cord neuromodulation was initially developed to facilitate motor functional recovery after spinal cord injury. Our findings indicate that this modality also improves lower urinary tract parameters in patients with neurogenic bladder. We hypothesize that transcutaneous spinal cord neuromodulation may facilitate lower urinary tract recovery by modulating dysfunctional neural signaling that occurs due to loss of higher neural input in both spinal cord injury and stroke. Future studies will focus on replicating these results in a sham-controlled environment and evaluating transcutaneous spinal cord neuromodulation in other pathologies resulting in neurogenic bladder.

Gad PN, Kreydin E, Zhong H, Latack K, Edgerton VR. Non-invasive Neuromodulation of Spinal Cord Restores Lower Urinary Tract Function After Paralysis. Front Neurosci. 2018;12:432. Published 2018 Jun 29. doi:10.3389/fnins.2018.00432