Neurogenic Bladder: As relevant to a Urogynecologist

The complicated function of the lower urinary tract (LUT) is regulated by the central and peripheral nervous system. Thus, any disturbance of the nervous system can affect the LUT function and cause neurogenic LUT dysfunction (N-LUTD). N-LUTD has replaced the term neurogenic bladder because not only the bladder but also the bladder outlet and the pelvic floor may be affected by the neurogenic deficit. The neurogenic insult may affect the storage phase or the emptying phase, or both phases of LUT function depending on the localization and severity of the neurogenic disease.

The neurogenic involvement may be anatomically classified into 3 groups (1) suprapontine, (2) infrapontine-suprasacral and (3) sacral-infrasacral lesions, which are in correlation with the functional classification of N-LUTD. For example, suprapontine lesions such as in Parkinson’s disease or cerebrovascular accidents (CVA) are associated with neurogenic detrusor overactivity (NDO) leading to urinary incontinence (UI) and synergic sphincters. In this group, patients may present with urgency UI and the upper urinary tract (UUT) deterioration is unlikely. Infrapontine-suprasacral lesions such as in spinal cord injury cause NDO UI with detrusor sphincter dyssynergia (DSD) meaning non-relaxation of the urethral sphincter(s). This type of N-LUTD leads to renal failure in almost all cases if left untreated. The sacral-infrasacral lesions are associated with peripheral neuropathy as seen in diabetes or after radical pelvic surgeries and cause neurogenic detrusor underactivity leading to high residual urine and overflow UI. The sphincters may be normo- or hypoactive. Still, UUT deterioration is possible in the long term.

Almost all known neurogenic diseases can lead to N-LUTD, which then necessitates a thorough clinical assessment with a focused neuro-urological physical examination, biochemical and radiological tests, and invasive urodynamic studies. The main goal of the management of N-LUTD is always to secure the upper UT (UUT) first and then to cure the lower urinary tract symptoms (LUTS) of the patient. The most significant complication of N-LUTD is the UUT damage. UUT damage is caused by the increased hydrostatic pressure within the urinary tract, basically due to NDO and DSD leading to vesicoureteral reflux, hydronephrosis, and chronic pyelonephritis that end up with end-stage renal disease. It is to note that LUTS and long-term complications do not correlate. It is, therefore, crucial to delineate patients with a high risk of subsequent complications during the initial assessment. The ICS standard urodynamic testing, including a filling cystometry and a pressure flow study, appears to be the most accurate tool for risk stratification.

The risk of developing upper UUT damage and renal failure is much higher in spinal cord injury or spina bifida patients compared with slowly progressive non-traumatic neurological disorders. Treatment and intensity of follow-up examinations should be planned depending on the type of neuro-urological disorder and the risk of UUT damage. The management depends on the type of N-LUTD and urodynamic finding. The gold standard treatment to empty a bladder with neurogenically impaired contractility is clean intermittent self-catheterization (CISC), which is also the most common treatment option to empty the bladder in the presence of DSD. A catheterizable stoma can be created on the anterior abdominal wall in patients with manual impairment or urethral problems that prevent CISC. The NDO may initially be managed with antimuscarinic medications. Intravesical botulinum neurotoxin injection is usually spared for refractory cases that do not respond to medical treatment. Several neuromodulation methods are being tested for the same indication but they are still considered as investigational. Bladder augmentation surgery or urinary diversion may be considered in severely non-compliant bladders.

The take-home message for the urogynecologist may be that neurogenic etiology is not always obvious and may be hidden at the time of the first presentation. For example, approximately 10% of patients with Multiple Sclerosis (MS) may primarily develop LUTS and may visit a urologist or urogynecologist before seeing a neurologist. Diabetic bladder, spinal cord tumors, or cranial pathologies may also manifest with LUTS before reaching a diagnosis of the underlying neurogenic disease. Thus, a high index of suspicion is needed for timely diagnosis and to prevent complications. N-LUTD should always be considered in the differential diagnosis and ruled out by necessary means in women who present with UI or other LUTS.

Case 1:

A 46-year-old female patient represented with the complaint of mixed urinary incontinence (UI) who was referred to undergo a mid-urethral sling surgery. She was on oral diabetics for her type 2 diabetes and had 2 vaginal deliveries. On physical examination, she was found to have Grade I anterior + posterior vaginal wall prolapse, a mobile urethra, and a negative ICS cough stress test and also negative accessory stress tests. Her quality of life was significantly affected by her UI, but she couldn’t delineate any predominant type of UI. Her urine analysis and urinary ultrasound were normal, and she had no residual urine after voiding.

With these findings, she underwent a standard ICS urodynamic testing, including a filling cystometry and a pressure flow study.

Her cystometry revealed a normosensitive, normocompliant bladder with a normal capacity

But with terminal detrusor overactivity, urinary incontinence. Her cough tests throughout the study again were negative. A standard pressure flow study could not be performed because she started to leak urine before the permission to void. But still, one could tell that her bladder outflow was not obstructed. The patient was started antimuscarinic treatment, thereafter her urgency component was completely resolved. She is happy now and occasionally experiencing stress urinary incontinence, only with very strong coughs and only when the bladder is full which does not affect her Q/L.

The management of mixed UI is challenging, and the predominant type is not always easy to understand. These cases need an invasive urodynamic study to objectively assess lower urinary tract dysfunction, besides a thorough clinical evaluation before irreversible therapies are applied.

Case 2: A 50-year-old lady presented with persistent stress incontinence with cough and exercise despite TO-MUS surgery 1 year ago.

She had 5 vaginal deliveries, no co-morbidity. On physical examination, she was found to have a urethra with limited mobility (Qtip tests <300) and a positive ICS cough stress test, no prolapse, and no mesh erosion. Her tape was palpated suburethrally in the correct localization without any other abnormality. She had normal uroflowmetry with no residual urine. Her biochemical and ultrasound assessment was unrevealing.

Her cystometry revealed normal bladder capacity and sensation, normal compliance, no detrusor overactivity but urodynamic stress UI with low ALPP (<60 cmH2O) which was manifest with every cough test after 300 ml of bladder volume. Her pressure flow study was normal.

Considering her limited urethral mobility and low ALPP she was offered to undergo autologous fascia pubovaginal sling surgery with vaginal partial mesh excision. Edward McGuire introduced intrinsic sphincter deficiency (ISD) as a distinct etiology of female SUI in the 1970s, which still includes many unanswered questions. ISD is the main reason for surgical failures. The classical triad of management options for ISD includes autologous fascia pubovaginal slings, artificial urinary sphincter implantation, and periurethral injection of bulking agents. Urodynamic parameters such as low urethral closure pressures, low abdominal leak point pressures, or both may define ISD, but the methodology is imprecise and variable. Still, the present case is a good example of ISD, as revealed by invasive urodynamic studies.