Neurogenic bladder

　　1. Causes of Disease

　　1. Brain Diseases

　　(1) Cerebrovascular Diseases: Commonly include hypertensive intracerebral hemorrhage, atherosclerotic cerebral infarction, cerebral embolism, intracranial arteritis, subarachnoid hemorrhage, cerebrovascular malformations, and rupture of basilar aneurysms, with intracerebral hemorrhage being the most common. Studies have shown that the neural pathways controlling the detrusor and external urinary sphincter are almost identical to those controlling somatosensory and motor functions, therefore, they are often damaged simultaneously. The brain has many nerve nuclei involved in urinary control, such as the basal ganglia, cerebellum, globus pallidus, corpus striatum, thalamus, etc. When these neural pathways or nuclei are damaged, patients may have urinary dysfunction in addition to specific cognitive, sensory-motor dysfunction, and clinical manifestations of the primary disease. The types of urinary dysfunction vary depending on the site of the lesion.

　　(2) Parkinson's Disease: A chronic progressive central nervous system dysfunction characterized by limb tremors, slow body movements, unsteady gait, and齿轮样rigidity of the limbs during examination. 25% to 75% of patients have bladder dysfunction, mainly manifested as difficulty initiating urination, urgency, or urge incontinence.

　　(3) Brain Tumor: When a tumor involves the frontal lobe, basal ganglia, or midbrain, urinary dysfunction may occur, thus this symptom has certain implications for localization diagnosis. The main symptoms are frequent urination, urgency, and urge incontinence. In a few cases, difficulty urinating and urinary retention may occur.

　　(4) Multiple Sclerosis: A chronic progressive central nervous system disease characterized by scattered demyelinating plaques in the brain and spinal cord, causing a variety of different neurological symptoms or signs. Early in the disease, about 5% of patients may have bladder dysfunction, while in the later stages, this can reach 90%. Symptoms may include frequent urination, urgency, urge incontinence, and occasionally urinary retention.

　　(5) Senile dementia: Urinary incontinence is the most common symptom of the urinary system, mostly urgent urinary incontinence and loss of consciousness control over micturition. The main mechanism is that the cerebral cortex loses control over the spinal cord detrusor center.

　　2. Spinal cord lesions

　　(1) Trauma: Spinal cord injury is divided into direct injury, indirect injury, and high-speed projectile injury, among which indirect injury is the most common, such as vertebral fracture, dislocation, or semi-dislocation. The early stage of spinal cord injury is the spinal cord shock period, during which the spinal cord below the injury level loses control over all tissues and organs it支配. Spinal cord shock usually lasts for 2 to 3 weeks, and some may last for more than 2 years. In the late stage of injury, fibrosis and scar formation occur at the injury site, and spinal meningeal adhesion may occur. The neurons at the injury site are replaced by astrocytes, and spinal cord gliosis occurs.

　　(2) Spinal cord diseases: Such as spinal tuberculosis, intervertebral disc herniation, metastatic tumors, cervical spondylosis, etc.

　　(3) Vascular diseases: Spinal artery embolism can cause damage to the corresponding part of the spinal cord.

　　(4) Neural tube defects: The lumbar and sacral regions are most common. Large defects can cause spinal cord and meningeal herniation, and are often accompanied by spinal maldevelopment.

　　(5) Others: Cysticercosis, poliomyelitis, transverse myelitis, and multiple sclerosis can all lead to bladder and urethral dysfunction.

　　3. Peripheral nerve lesions

　　(1) Diabetes: Long-term diabetes mellitus patients due to sugar metabolism disorder, causing increased vascular resistance in the endoneurium, leading to ischemia and hypoxia, causing degeneration and atrophy of nerve cells, nerve axon degeneration, and demyelination of nerve fibers. The density of neurons in the bladder wall becomes sparse, axons have degenerative changes and nerve fragments, and the conduction of impulses of the传入 and传出 fibers of the bladder is impaired, leading to dysuria. Bladder dysfunction is one of the common complications of diabetes patients, with an incidence rate as high as 43% to 87% in type 1 diabetes patients.

　　(2) Postoperative removal of pelvic organs: Such as radical resection of rectal cancer, radical resection of uterine cancer, etc., postoperative urinary abnormalities often occur, with an incidence rate of 7.7% to 68%. It has now been confirmed that this is due to the injury of the parasympathetic nerves, sympathetic nerves, pelvic ganglia, and pudendal nerves in the pelvis caused by surgery.

　　(3) Herpes zoster: The latent herpes zoster virus is located in the posterior horn cells of the spinal cord and spreads along the nerve sheath, damaging the nerves. Urinary frequency and urinary retention may occur when the lumbar or sacral nerves are involved.

　　Disease Mechanism

　　Neurogenic bladder is pathophysiologicaly divided into detrusor hyperreflexia and detrusor areflexia. Detrusor instability (DI), detrusor hyperreflexia (DHR), and reduced bladder compliance are the three main types of detrusor hyperactivity, while the sphincter can show normal coordination, external sphincter dyssynergia, or internal sphincter dyssynergia. Detrusor areflexia (DVA) is common in patients with neurological diseases, while bladder outlet obstruction (BOO) caused by hyperactivity of the sphincter during micturition is also very common, and it is difficult to differentiate the comprehensive symptoms of male DVA patients from those of BOO patients. This is because DVA can be accompanied by normal sphincter coordination, external sphincter spasm, denervation of the external sphincter, and internal sphincter spasm.

　　There are many methods for classifying neurogenic bladder and urethral dysfunction.

　　1, Hald-Bradley Classification Method:Reflecting functional changes based on the site of the lesion:

　　(1) Lesions above the spinal cord in the detrusor contraction and urethral sphincter relaxation are coordinated, with most cases having detrusor reflex hyperactivity and normal sensory function.

　　(2) Lesions above the sacrum in most cases have detrusor reflex hyperactivity, and the activity of the detrusor and urethral sphincter is not coordinated. The degree of sensory function is related to the extent of nerve damage, which may be partial or complete loss.

　　(3) Lesions below the sacrum include the sensory and motor nerve lesions of the sacrum. Due to the damage to the detrusor motor nerve, detrusor areflexia can occur, and sensory nerve damage can lead to the loss of sensory function.

　　(4) Peripheral autonomic neuropathy is most commonly seen in diabetic patients, characterized by incomplete bladder sensory function, increased residual urine volume, and finally decompensation, with weak detrusor contraction.

　　(5) Muscle lesions can include detrusor muscle itself, smooth muscle sphincter, and all or part of striated muscle sphincter. Detrusor dysfunction is the most common, often secondary to decompensation after long-term bladder outlet obstruction.

　　2, Lapides Classification Method:Classification according to changes in sensory and motor functions after nerve damage:

　　(1) Sensory Impairment Neurobladder: Caused by the obstruction of sensory fibers between the bladder and spinal cord or between the spinal cord and the brain. It is relatively common in diabetes, dysmetria, and aplastic anemia. Urodynamic changes include a large bladder capacity, high compliance, and low-pressure filling curve, which may result in a large amount of residual urine.

　　(2) Paralytic Neurobladder: Caused by damage to the parasympathetic motor nerve of the bladder. Common causes include pelvic surgery or injury. Early symptoms include difficulty in urination, painful urinary retention, and other symptoms. Bladder pressure measurement shows that the bladder can be normally filled, but it is difficult to initiate voluntary bladder contraction when the bladder reaches its maximum capacity. In the later stage, there are changes in bladder sensory function and a large amount of residual urine. Bladder pressure measurement shows that the bladder capacity increases, with a high compliance bladder, and cannot initiate detrusor contraction.

　　(3) Inhibitory Neurobladder: Caused by the destruction of the central nervous system or nerve conduction fibers that can inhibit the sacral urinary center, resulting in the loss of inhibitory effect on the sacral urinary center. It is common in cerebrovascular diseases, brain or spinal cord tumors, Parkinson's disease, demyelinating diseases, and other conditions. Most cases are characterized by frequent urination, urgency, and urge incontinence. On urodynamic examination, the bladder contracts involuntarily during the storage phase, can initiate detrusor contraction to urinate voluntarily, and generally has no difficulty in urination and no residual urine.

　　(4) Reflex neurogenic bladder: Originating from complete sensory and motor pathway damage between the sacral cord and brainstem. It is most common in traumatic spinal cord injury and transverse myelitis, and can also occur in demyelinating diseases, as well as any process that may cause significant spinal cord injury. Typical manifestations include the loss of bladder sensation and the loss of the ability to autonomously initiate contraction, but spontaneous detrusor contractions may occur during bladder filling, with coordination disorders between the detrusor and sphincter muscles.

　　(5) Autonomous neurogenic bladder: Caused by damage to the sacral cord, sacral nerve roots, or pelvic nerves, resulting in complete separation of sensory and motor functions of the bladder. Patients cannot initiate micturition autonomously and have no bladder reflex activity. Bladder pressure measurement shows no autonomous or spontaneous detrusor contractions, with low bladder pressure and increased capacity.

　　3. Krane-Siroky classification method:Classify according to the abnormalities shown by urodynamic examination:

　　(1) Detrusor overactivity: The spontaneous or induced contraction of the detrusor muscle during the storage phase is called detrusor instability. If it is accompanied by abnormality of the central nervous system, it is called detrusor overactivity. The diagnostic criteria are the spontaneous detrusor contractions with an amplitude exceeding 1.47 kPa (15 cmH2O) during the storage phase. It is divided into the following subtypes: ① Coordination of the sphincter is normal: Refers to the coordinated relaxation of the urethral sphincter during detrusor contraction and micturition. ② Coordination of the external sphincter is abnormal: Refers to the external sphincter remaining in a state of contraction during detrusor contraction and micturition, leading to incomplete opening of the urethra. ③ Coordination of the internal sphincter is abnormal: Refers to the internal sphincter not relaxing during detrusor contraction and micturition.

　　(2) Absence of detrusor reflex: Refers to the inability or weakness of the detrusor muscle to contract during micturition. It can be further divided into the following subtypes:

　　① Coordination of the sphincter is normal: Refers to the coordinated relaxation of the urethral sphincter during urination.

　　② Sphincter spasm or dyskinesia: Manifested as the external sphincter remaining in a state of continuous contraction during urination.

　　③ Sphincter spasm or dyskinesia: Manifested as the non-opening of the urethral orifice during urination.

　　④ Denervation of the external sphincter: Refers to the atrophy and relaxation of the urethral external sphincter and pelvic floor muscles after losing neural control, causing the bladder and urethra to descend and the urethra to angle, resulting in difficulty in urination.

　　Urinary tract infection is the most common complication of neurogenic bladder, with 10% to 15% of patients developing urinary tract stones. Vesicoureteral reflux occurs in 10% to 40% of neurogenic bladder cases and is usually reversible. There is a possibility of spontaneous improvement when the micturition condition improves, residual urine decreases, and bladder pressure decreases. Other complications may include pyelonephritis, renal failure, hydronephrosis, and decreased renal function.

　　1. Symptoms

　　1. The symptoms of detrusor overactivity are caused by uninhibited contractions, mainly including frequent urination, urgency, and urge incontinence. Some patients may present with stress incontinence or enuresis.

　　2. Patients with detrusor areflexia cannot open or insufficiently open the bladder neck during urination, which is often manifested as difficulties in urination, urinary retention, and overflow incontinence, etc.

　　3. In addition to urinary symptoms, there may be symptoms such as constipation, fecal incontinence, decreased or lost perineal sensation, limb paralysis, etc.

　　Two, physical examination

　　1. Anal sphincter tone test:The relaxation of the anal sphincter indicates the inactivity or decreased activity of the spinal cord center. Over-contraction of the anal sphincter indicates hyperactivity of the spinal cord center reflex.

　　2. Anal reflex test:Stimulating the skin around the anus, if the anus contracts, it indicates the existence of spinal cord activity.

　　3. Bulbocavernosus reflex test:Stimulating the glans penis or clitoris can cause anal sphincter contraction, indicating the existence of spinal cord activity.

　　The diagnosis of neurogenic bladder and urethral dysfunction mainly includes three major aspects: the diagnosis of nervous system lesions, such as the nature, location, degree, and scope of the lesions; the diagnosis of bladder and urethral dysfunction, such as the type, degree, upper urinary tract condition, and urinary system complications; the diagnosis of dysfunction of other related systems and organs.

　　Three, whether the urinary dysfunction is caused by a neurologic lesion

　　1. Medical history

　　(1) Patients with urinary dysfunction accompanied by defecation dysfunction (such as constipation, fecal incontinence, etc.) may have a neurogenic bladder with possible nerve lesions.

　　(2) Pay attention to whether there is a history of trauma, surgery, diabetes, poliomyelitis, or a history of drug use.

　　(3) Pay attention to whether there is a decrease or loss of the sensation of urinary urgency, bladder distension, etc. If the sensation of the bladder is significantly decreased or lost, it can be diagnosed as a neurogenic bladder.

　　2. Examination

　　(1) When there is a decrease in perineal sensation, a decrease or increase in anal sphincter tone, it can be diagnosed as a neurogenic bladder. However, the lack of these signs does not exclude the possibility of a neurogenic bladder.

　　(2) Pay attention to whether there are malformations such as spina bifida, meningocele, and sacral hypoplasia.

　　(3) There is residual urine, but there is no mechanical obstruction in the lower urinary tract.

　　(4) Electrostimulation of the spinal cord reflex test, this method mainly tests whether the spinal cord reflex arc of the bladder and urethra is intact (i.e., whether there is a lesion in the lower motor neuron) and whether there is a lesion in the neurons from the cerebral cortex to the pudendal nerve nucleus (spinal cord center) (whether there is a lesion in the upper motor neuron). Therefore, this test can diagnose whether it is a neurogenic bladder, and also distinguish between lower motor neuron lesions (detrusor areflexia) and upper motor neuron lesions (detrusor reflex hyperactivity).

　　Four, methods to differentiate between two types of neurogenic bladder

　　1. When measuring bladder pressure, observe whether there is an uninhibited contraction; it is necessary to use standing position pressure measurement, coughing, and catheter traction as stimulation methods.If there is an uninhibited contraction, it belongs to the category of detrusor reflex hyperactivity. Otherwise, it belongs to the category of detrusor areflexia.

　　This test is one of the main criteria for classification, but:

　　(1) Inflammation, stones, tumors, and lower urinary tract obstruction (such as benign prostatic hyperplasia) can also cause uninhibited contractions in patients with non-neurogenic bladder.

　　(2) In patients with detrusor reflex hyperactivity, some patients need to be stimulated before the appearance of inhibitory contraction during pressure measurement in the supine position.

　　2. Ice water test:After emptying the bladder with a F16 catheter, rapidly inject 60ml of 14℃ ice water. If the bladder is a detrusor reflex hyperactivity bladder, the ice water (including the catheter) will be ejected from the urethra within a few seconds; if the bladder is a detrusor reflex bladder, the ice water will slowly flow out of the catheter.

　　3. Anal sphincter tension:Patients with anal sphincter relaxation belong to the category of detrusor areflexia.

　　4. Urethral closure pressure graph:Maximum urethral closure pressure is normal or higher than normal in patients with detrusor reflex hyperactivity, and lower than normal in patients with detrusor areflexia.

　　5. Urethral resistance measurement:The normal urethral resistance is 10.6 kPa (80 mmHg). The urethra of a detrusor areflexia patient is lower than normal.

　　Among the above examinations, observing whether there is an inhibitory contraction is relatively accurate, while other almost checks have more opportunities for error. The cause of the error may be a 'mixed' lesion type (Bors classification) of neurogenic bladder, that is, the neural lesion of the detrusor is not at the same level as the neural lesion of the external urethral sphincter.

　　In addition to the history, physical examination, and related auxiliary examinations, neuroelectrophysiological examination has become an important part of the diagnosis of neurological disorders.

　　In addition to the history, signs, and other routine examinations, urodynamic examination plays an extremely important role in the diagnosis of bladder and urethral dysfunction. It not only shows various manifestations of bladder and urethral dysfunction but also reveals the pathogenesis of the disorder, providing important evidence for etiological analysis and treatment.

　　Neurogenic bladder patients should control their fluid intake appropriately, avoid excessive intake of large amounts of water and fluids every day, urinate promptly, and do not hold urine. Pay attention to personal hygiene, change underwear frequently. Women should wipe from front to back with clean toilet paper after urination. Both partners should clean the local area thoroughly before and after sexual intercourse, and immediately empty the bladder of urine before and after sexual intercourse.

　　A series of imaging examinations, such as intravenous urography (excretory urography), ultrasound, cystography, and urethrogram, are helpful to evaluate the secondary damage and disease progression of neurogenic bladder, and can also show urinary tract stones. Cystoscopy can determine the degree of outflow obstruction of the bladder. A series of bladder pressure tracings can be performed during the recovery period of hypotonic bladder to provide the detrusor function index, indicating the prospects for recovery. Urodynamic measurements of voiding flow rates, electromyography of the sphincter to check the urethral pressure, are all helpful for diagnosis.

　　Urine examination in patients with urinary tract infections may show red blood cells, white blood cells, and positive urine culture.

　　1. Ice water test:If there is an injury above the spinal cord center, after injecting ice water into the bladder, the ice water will be forcefully ejected within a few seconds; if there is an injury below the spinal cord center, there will be no such reaction.

　　2. Urodynamic examination:Reflects detrusor reflex hyperactivity or detrusor areflexia and urethral sphincter function.

　　3. Voiding cystourethrography:It can be seen that there are small trabeculae formation, diverticula, and typical 'Christmas tree' shaped bladder. Dynamic observation shows abnormal contraction of the detrusor muscle, abnormal coordination between detrusor muscle contraction and urethral internal and external sphincters, and increased residual urine.

　　In terms of daily diet and precautions for neurogenic bladder, in terms of diet, caffeine can cause bladder neck contraction and lead to spasmodic pain in the bladder, so one should drink less coffee. Eat more watermelons, grapes, pineapples, pears, etc. Drink more water, maintaining a daily urine output of at least 1500 milliliters or more. Clams, corn, and mung beans can help relieve symptoms such as frequent urination, urgency, and dysuria. Avoid eating sour and spicy刺激性 food, such as strong alcohol, balsamic vinegar, sour fruits, etc. During the treatment of cystitis, it is strictly forbidden to drink alcohol, chili, chicken, fish, beef, shrimp, seafood pickles, as poor dietary control in patients may extend the treatment time.

　　1. Eat more diuretic foods, such as watermelons, grapes, pineapples, celery, pears, etc.

　　2. Clams, corn, mung beans, and scallion whites can help relieve symptoms such as frequent urination, urgency, and dysuria.

　　3. Increase water intake, maintaining a daily urine output of at least 1500 milliliters or more.

　　4. Avoid eating sour and spicy刺激性 food, such as strong alcohol, chili, balsamic vinegar, sour fruits, etc.

　　5. Avoid eating citrus fruits because they can cause alkaline urine, which is conducive to bacterial growth.

　　6. Caffeine can cause bladder neck contraction and lead to spasmodic pain in the bladder, so one should drink less coffee.

　　The main treatment for neurogenic bladder is to protect kidney function, prevent pyelonephritis, hydronephrosis leading to chronic renal failure; the next is to improve urination symptoms to alleviate the pain in daily life. Specific measures are to adopt various non-surgical or surgical methods to reduce residual urine volume, and after the residual urine volume is eliminated or reduced to a very low level (less than 50ml), urinary tract complications can be reduced. However, it must be noted that a few patients, even with very little or no residual volume, may still experience complications such as pyelonephrosis, pyelonephritis, and renal function decline. These patients have strong detrusor contraction during urination, and the intravesical pressure can reach above 19.72kPa (200cmH2O) (normal should be below 6.9kPa, i.e., 7cmH2O). These patients should receive treatment early to relieve lower urinary tract obstruction.

　　1. Non-surgical treatment

　　1. Catheterization:Whether for the purpose of promoting storage or urination, intermittent catheterization can effectively treat neuro-muscular urinary dysfunction, alleviating the pain of long-term catheter use or suprapubic cystostomy, and creating conditions for further treatment (cystoplasty, controllable urinary diversion). Years of clinical observation have proven its safety and effectiveness in long-term use. Initially, the patient can be instructed to catheterize every 4 hours, and the specific interval time can be self-managed thereafter, following the principle of not causing urinary incontinence and not overfilling the bladder. Practice has shown that symptomatic infection is not common. Indwelling catheterization or cystostomy is generally used for a short period of time, but for some patients, regular replacement of catheters for long-term bladder drainage is the only feasible method.

　　2. Adjuvant therapy

　　(1) Timed bladder emptying, especially for patients with detrusor reflex hyperactivity. Instruct patients to urinate every 3 to 4 hours, regardless of urgency. Drug therapy is often used in conjunction with timed urination.

　　(2) Pelvic floor muscle training, perineal area electrical stimulation is often used as an adjuvant treatment for female stress urinary incontinence to increase bladder outlet resistance.

　　(3) Training for trigger point urination, using Crede technique for urination can increase intravesical pressure and contraction, promoting bladder emptying, but for some low compliance bladder with reflux cases, the Crede technique may exacerbate renal function damage.

　　(4) For some male cases, external urinary collection devices such as penile clamps or condom catheters can be used.

　　3. Drug therapy

　　(1) Medications to inhibit bladder contraction: Clinically, more than one drug with different pharmacological mechanisms is commonly used to treat detrusor involuntary contractions. A. Anticholinergic drugs: propantheline, 15 to 30mg per dose for adults, once every 6 hours, taken on an empty stomach, the most commonly used in clinical practice; atropine has 'tolerance', and can only partially inhibit detrusor contraction. These drugs can cause dry mouth, tachycardia, blurred vision, reduced intestinal peristalsis, and with high doses, can cause hypotension and erectile dysfunction. Contraindicated in patients with severe bladder outlet obstruction and glaucoma. B. Smooth muscle relaxants: the most commonly used is flavoxate (Niaojingling), 0.1 to 0.2g per dose for adults, 3 times a day, effective for patients with urgency, incontinence, and detrusor reflex hyperactivity, with few side effects. C. Calcium channel blockers: such as nifedipine, 10mg per dose, 3 times a day. Some tricyclic antidepressants, beta-adrenergic agonists, etc., are also used in clinical practice.

　　(2) Medications to promote bladder urination: A. Parasympathomimetic drugs: carbamylmethylcholine, 7.5mg per dose, once every 4 to 6 hours, administered subcutaneously, with good clinical efficacy for treating high compliance bladder; when combined with manual urination, the effect is even better. B. Alpha-adrenergic antagonists: such as tamsulosin, terazosin, etc., which can reduce bladder outlet resistance.

　　(3) Medications to increase bladder outlet resistance: A. Alpha-adrenergic drugs: such as ephedrine, 25mg per dose, 4 times a day; amitriptyline 25mg per dose, once at night, with definite efficacy. Contraindicated in patients with hyperthyroidism, and should be used with caution in patients with cardiovascular diseases. B. Alpha-adrenergic antagonists: such as propranolol 10mg per dose, 4 times a day, effective for some patients, but contraindicated in asthmatic patients. C. For postmenopausal women, estrogens can increase urethral resistance, such as 1mg of尼尔雌醇 tablets per dose, once every 2 weeks.

　　(4) Medications to reduce bladder outlet resistance: commonly used highly selective α1 receptor blockers such as terazosin, tamsulosin, etc. Prazosin is an α1 receptor blocker, and α1 receptors can be divided into high-affinity α1H receptors and low-affinity α1L receptors. α1H receptors can be further divided into α1A, α1B, α1C, and α1D four subtypes. Terazosin (2mg/time, 1 time/night) belongs to the type mainly based on α1H receptor blockers, and tamsulosin (0.2mg/time, 1 time/night) is an α1A receptor blocker. Clinical experience shows that the efficacy and symptom relief effect of the former are better than those of the latter, but the latter rarely has side effects such as orthostatic hypotension, also known as 'first-dose phenomenon'.

　　4. Acupuncture therapy:Acupuncture treatment has a good effect on the sensory atypical bladder caused by diabetes, and is particularly effective for early lesions.

　　5. Sealing therapy:This method was advocated by Bors and is suitable for upper motor neuron lesions (detrusor reflex hyperactivity). It is not very effective for lower motor neuron lesions (detrusor areflexia). After sealing, good results can be achieved, with a significant reduction in residual urine volume and明显 improvement in urinary symptoms. A few patients can maintain the effect for several months to a year after the first sealing. These patients only need regular treatment and do not need surgery.

　　The sealing therapy is carried out in the following order:

　　(1) Mucosal sealing: empty the bladder with a catheter, inject 90ml of 0.25% Pantocaine solution, and expel it after 10 to 20 minutes.

　　(2) Bilateral pudendal nerve block.

　　(3) Selective sacral nerve block: block a pair of sacral nerves from S2 to S4 each time. If there is no effect, S2 and S4 can be combined with S4 block.

　　6. Bladder training and dilation:This method can be used for the treatment of severe symptoms of urinary frequency and urgency with little or no residual urine. Instruct patients to drink water at regular intervals during the day, 200ml per hour. Try to extend the interval between urination to make the bladder easily expand gradually.

　　2. Surgical treatment

　　Its function is to improve bladder compliance and capacity, and change the resistance of the bladder outlet. It requires proof of inefficiency through non-surgical treatment and should be performed after the stabilization of the neurological lesion. For patients with lower urinary tract mechanical obstruction, it should be considered to remove the obstructive factors first.

　　1. Surgery to reduce bladder outlet resistance

　　(1) Transurethral bladder neck incision or partial resection is the most common surgical method for treating bladder neck obstruction and functional abnormalities of the bladder and urethra, applicable to patients with sufficient bladder capacity and good detrusor contraction, and where the proximal urethral pressure distribution shows a sphincter pressure ≥ detrusor pressure. The key point of the surgery is to incise the range near the acropodium. For refractory cases with multiple surgeries and ineffective results, it is generally necessary to wear an external urine collection device after the incision of the external sphincter.

　　(2) Cysto-urethral Y-V plasty is suitable for detrusor overactivity, significant residual urine, ineffective closed treatment, or the need to treat bladder lesions simultaneously.

　　(3) For female patients, over-urethral extension (F40～F50) is effective, this method is simple to perform, can be repeated, and has good urinary control.

　　(4) Botulinum toxin A injection into the external sphincter has certain practical value and can be effective for over a month.

　　(5) Other surgical methods, such as pudendal nerve section, sacral root section, or even urinary diversion, are now rarely used due to severe and numerous complications; similarly, incision of the external sphincter should be avoided, and intermittent self-catheterization should be preferred.

　　2, Surgery to Increase Bladder Outlet Resistance

　　(1) Intraurethral injection around the urethra, although less effective for male urinary incontinence than for female, is the preferred method for treating urinary incontinence due to its simplicity, safety, and few complications.

　　(2) Cysto-urethral suspension surgery, as a classic method to increase bladder outlet resistance, has many surgical methods, is effective, and is often used to treat female stress urinary incontinence.

　　(3) Fascial suspension surgery, which uses the anterior sheath of the rectus abdominis and perineal muscles to compress the bulbous urethra or surround the posterior urethra, is suitable for incomplete sphincter function or severe female stress urinary incontinence.

　　(4) Other surgical methods, such as bladder outlet reconstruction, are mainly used to treat urinary incontinence caused by incomplete bladder outlet closure; inflatable artificial urinary sphincters are used less clinically due to many complications and high cost.

　　3, Surgical Methods to Increase Bladder Compliance and Nutrition:The most commonly used procedure is bladder augmentation, with an efficacy rate of over 80%. It plays an important role in treating refractory voiding dysfunction and reconstructing the lower urinary tract function. Intermittent catheterization or short-term indwelling catheterization can significantly alleviate certain degrees of bladder emptying obstruction in some patients.

　　Three, Treatment of Complications:The main complications of neurogenic bladder include urinary tract infections, stones, urethral diverticula, vesicoureteral reflux, and others. They can be treated separately with anti-infection, extracorporeal shock wave lithotripsy, or surgical incision for stone removal, and various forms of anti-reflux surgery.