bubble_chart Overview

Damage to the central or peripheral nervous system that controls urination, leading to bladder and urethral dysfunction, is called neurogenic bladder. The resulting urinary complications are the main cause of death in these patients. In 1972, Donnelly followed up with 370 paraplegic patients injured during World War II and found that 90% had pyelonephritis. Among the deceased paraplegic casualties, 405 died from renal failure.

bubble_chart Etiology

1. Spinal or cranial brain injury.
2. Central nervous system surgery or extensive pelvic surgery: such as radical surgery for intestinal cancer, radical surgery for uterine cancer, pelvic lymph node dissection, etc.
3. Congenital diseases: such as spina bifida, spinal meningocele, sacral deformity, sacral dysplasia, etc.
4. Drug effects: Drugs that affect the function of the sympathetic and parasympathetic nerves, such as propantheline, atropine, alcohol, nicotine, as well as drugs used for lowering blood pressure, desensitization, antihistamines, etc., can all affect the micturition central nervous system.
5. Certain diseases: diabetes, syphilis, tremor paralysis, poliomyelitis, encephalitis, apoplexy, myelitis, etc.
6. Unknown causes.

There are many classification methods for neurogenic bladder. In the past, the commonly used classification method was the Bors classification, which divides it into the following 5 categories:

1. Upper motor neuron lesions: Lesions are above the spinal cord center (S₂～S₄), including sensory and motor branches.
2. Lower motor neuron lesions: Lesions are located at the spinal cord center (S₂～S₄) or the peripheral nerves below the center, including sensory and motor branches.
3. Primary motor neuron lesions: Lesions are limited to the motor branch, with no lesions in the sensory branch, such as poliomyelitis.
4. Primary sensory neuron lesions: Lesions are limited to the sensory branch. Motor neuron lesions, such as neurogenic bladder caused by diabetes and tabes dorsalis.
5. "Mixed" lesions: The autonomic neuron lesions (parasympathetic nerves) related to micturition and the somatic motor neuron lesions are not at the same level, with one being in the upper motor neuron and the other in the lower motor neuron, or one having lesions while the other does not.

Although this classification method is quite detailed, it is too complex and lacks guiding significance for treatment selection. In recent years, internationally, it has been divided into two categories based on whether the detrusor muscle has uninhibited contractions during bladder filling:

1. Detrusor hyperreflexia: The detrusor muscle exhibits hyperreflexia in response to stimulation, showing uninhibited contractions during bladder pressure measurement. It may or may not be accompanied by dysfunction of the urethral sphincter.
2. Detrusor areflexia: In this type of neurogenic bladder, the detrusor muscle shows no reflex or hyporeflexia to stimulation. No uninhibited contractions appear during bladder pressure measurement. It may or may not be accompanied by dysfunction of the urethral sphincter.

bubble_chart Clinical Manifestations

An analysis of 102 cases with urinary symptoms from Shanghai Huashan Hospital showed that the urinary symptoms of neurogenic bladder are similar to those of general urinary system diseases, with the more distinctive ones being loss of urinary sensation, accompanied by defecation dysfunction and reflex voiding. Except for reflex voiding (which belongs to the category of detrusor hyperreflexia), there is little correlation between urinary symptoms and the types of neurogenic bladder. Therefore, symptom analysis is of little significance in distinguishing between the two types of neurogenic bladder.

bubble_chart Diagnosis

The diagnosis of neurogenic bladder consists of two parts: first, determining whether the voiding dysfunction is caused by neurological lesions, and second, identifying the type of neurogenic bladder.

### I. Determining Whether Voiding Dysfunction Is Caused by Neurological Lesions

1. **Medical History** ① Voiding dysfunction accompanied by bowel dysfunction (e.g., constipation, fecal incontinence) suggests the possibility of a neurogenic bladder due to neurological lesions. ② Note any history of trauma, surgery, diabetes, poliomyelitis, or medication use. ③ Assess for diminished or lost sensations such as the urge to void or bladder fullness. If bladder sensation is significantly diminished or absent, a neurogenic bladder can be confirmed.

2. **Examination** ① Reduced perineal sensation or altered anal sphincter tone (either decreased or increased) confirms a neurogenic bladder, though the absence of these signs does not rule it out. ② Check for abnormalities such as spina bifida, meningocele, or sacral dysplasia. ③ Presence of residual urine without mechanical lower urinary tract obstruction. ④ Electrical stimulation of the spinal reflex test: This primarily evaluates the integrity of the spinal reflex arc of the bladder and urethra (i.e., whether there is a lower motor neuron lesion) and whether there is a lesion in the neurons from the cerebral cortex to the pudendal nucleus (spinal center) (i.e., upper motor neuron lesion). Thus, this test not only diagnoses a neurogenic bladder but also distinguishes between lower motor neuron lesions (detrusor areflexia) and upper motor neuron lesions (detrusor hyperreflexia).

### II. Methods to Differentiate Between Two Types of Neurogenic Bladder

1. **Observing Uninhibited Contractions During Bladder Pressure Measurement** - If necessary, use provocative methods such as standing pressure measurement, coughing, or catheter traction. - If uninhibited contractions occur, it indicates detrusor hyperreflexia; otherwise, it suggests detrusor areflexia.

- **Note:** ① Non-neurogenic bladder patients with conditions like inflammation, stones, tumors, or lower urinary tract obstruction (e.g., benign prostatic hyperplasia) may also exhibit uninhibited contractions. ② Some patients with detrusor hyperreflexia may require provocation to show uninhibited contractions during supine pressure measurement.

2. **Ice Water Test** - After emptying the bladder with an F₁₆ catheter, rapidly inject 60 mL of 14°C ice water. - In detrusor hyperreflexia, the ice water (along with the catheter) is expelled forcefully within seconds. - In detrusor areflexia, the ice water drains slowly from the catheter.

3. **Anal Sphincter Tone** - A relaxed anal sphincter indicates detrusor areflexia.

4. **Urethral Closure Pressure Profile** - Normal or elevated maximum urethral closure pressure suggests detrusor hyperreflexia. - Reduced maximum urethral closure pressure indicates detrusor areflexia.

5. **Urethral Resistance Measurement** - Normal urethral resistance is 10.6 kPa (80 mmHg). - In detrusor areflexia, urethral resistance is lower than normal.

Among these tests, observing uninhibited contractions is the most accurate. Other tests have a higher chance of errors, possibly due to "mixed" lesions (Bors classification) in neurogenic bladder, where the neurological lesions of the detrusor and external urethral sphincter are not at the same level.

bubble_chart Treatment Measures

The primary goal in treating neurogenic bladder is to protect renal function, preventing pyelonephritis and hydronephrosis from leading to chronic renal failure. The secondary goal is to improve urinary symptoms to alleviate the patient's daily discomfort. Specific treatment measures involve employing various non-surgical or surgical methods to reduce residual urine volume. Once residual urine is eliminated or reduced to a minimal amount (below 50ml), urinary tract complications can be minimized. However, it is important to note that a small number of patients may still develop complications such as hydronephrosis, pyelonephritis, or renal dysfunction, even with little to no residual urine. This occurs because these patients exhibit strong detrusor muscle contractions during urination, with bladder pressure potentially exceeding 19.72 kPa (200 cmH₂O) (normal levels should be below 6.9 kPa or 7 cmH₂O). Such patients require prompt treatment to relieve lower urinary tract obstruction.

Below are several commonly used treatment methods:

1. **Non-surgical therapy**

- **Intermittent catheterization or continuous drainage**: For patients in the spinal shock phase after spinal cord injury or those with significant residual urine or urinary retention, intermittent catheterization can be used if renal function is normal. Initially performed by medical staff, patients in good overall condition can be trained to perform self-catheterization. Intermittent catheterization is particularly suitable for women. If all surgical treatments prove ineffective, lifelong self-intermittent catheterization may be necessary. For patients in poor overall health or with impaired renal function, continuous drainage with an indwelling catheter is recommended.

- **Medication**: Patients with significant residual urine, regardless of symptoms like urinary frequency, urgency, or urge incontinence due to detrusor hyperreflexia, should first be treated with α-receptor blockers to reduce residual urine. If α-receptor blockers alone are ineffective, drugs like urecholine or neostigmine, which enhance bladder contractility, can be added. For patients with detrusor hyperreflexia symptoms (e.g., urinary frequency, urgency, enuresis) but little to no residual urine, medications that suppress bladder contractions, such as Ditropan, Isoptin, or Probanthine, may be used. For patients with grade I stress incontinence and no residual urine, drugs like ephedrine or propranolol, which promote bladder neck and posterior urethral contraction, can be administered. For patients with impaired renal function, the priority is ensuring unobstructed urine drainage rather than using medications to improve urinary symptoms.

- **Acupuncture and moxibustion therapy**: Acupuncture has shown good efficacy in treating diabetic sensory paralytic bladder, particularly in early-stage cases.

- **Block therapy**: Proposed by Bors, this method is suitable for upper motor neuron lesions (detrusor hyperreflexia) but less effective for lower motor neuron lesions (detrusor areflexia). Patients who respond well to block therapy show significant reduction in residual urine and marked improvement in urinary symptoms. A few patients may maintain the effects for several months to a year after a single block, requiring only periodic follow-up without surgery.

The block therapy is performed in the following order: ① Mucous membrane block: Empty the bladder with a catheter, inject 90 ml of 0.25% Pontocaine solution, and drain after 10–20 minutes. ② Bilateral pudendal nerve block. ③ Selective sacral nerve block: Block one pair of sacral nerves (S_2–4). If ineffective, combined blocks of S₂ and S₄ or S₄ may be performed.

- **Bladder training and dilation**: For patients with severe urinary frequency and urgency but little to no residual urine, this method can be used. Patients are instructed to drink 200 ml of water hourly during the day and gradually extend the intervals between urination to help the bladder expand progressively.

2. **Surgical treatment**

Surgical treatment is generally performed when non-surgical therapy is ineffective and after the neuropathy has stabilized. For those equipped with 4-channel or 6-channel urodynamic testing instruments, surgery is conducted to relieve the obstruction after the examination results clearly identify the location and nature of functional lower urinary tract obstruction.

1. Surgical Principles ① For patients with mechanical obstruction in the urinary tract (e.g., benign prostatic hyperplasia), the mechanical obstruction should be removed first. ② For patients with detrusor areflexia, transurethral bladder neck incision should be considered first. ③ For patients with detrusor hyperreflexia or detrusor-sphincter dyssynergia, if pudendal nerve block provides only temporary relief, transurethral external sphincterotomy or resection may be performed. ④ For patients with detrusor hyperreflexia, if selective sacral nerve block provides temporary relief, corresponding sacral nerve anhydrous alcohol injection or sacral rhizotomy may be performed. ⑤ For severe urinary frequency and urgency (urgency syndrome) with little or no residual urine, if drug therapy, block therapy, bladder training, and dilation are ineffective, bladder denervation or transurethral injection of anhydrous alcohol or 6% phenol into the pelvic nerves on both sides of the bladder base may be considered. ⑥ For patients with detrusor hyperreflexia, if all block therapies are ineffective, bladder neck incision may be performed. ⑦ Full-length posterior urethrotomy: This procedure is only applicable to males, rendering the patient’s internal urethral sphincter incapable of controlling urine outflow from the bladder, resulting in unobstructed urinary incontinence. The patient will need to use a condom catheter and urine collection bag for life. After this procedure, complications such as urinary tract infections are reduced to less than 1%. The drawback is that it may inconvenience the patient’s daily life.

2. Indications for Full-Length Posterior Urethrotomy and Urinary Diversion ① Progressive renal function decline, hydronephrosis, or uncontrolled pyelonephritis persists after non-surgical and surgical treatments. ② Severe urinary symptoms persist after non-surgical and surgical treatments. ③ Severe renal impairment or chronic renal failure is already present.

In the above cases, urethral preservation is a good management approach for women with sexually transmitted diseases.

3. Management of Unobstructed Urinary Incontinence (Severe Incontinence with No Residual Urine) Male patients may use a penile clamp or urine collection bag, while female patients may use a urethral clamp or undergo urinary diversion surgery. For eligible patients, an artificial urinary sphincter device may be considered.

Patients with neurogenic bladder who achieve satisfactory treatment outcomes still require long-term follow-up. Annual residual urine measurement, urine culture, renal function tests, and intravenous urography (1–2 times per year) should be performed to monitor for any decline in urinary function or urinary tract complications.