The normal voiding activity is participated by the spinal reflex center and sympathetic, parasympathetic, and somatic nerves. Damage to the central nervous system or peripheral nerves that control voiding function and cause vesicourethral dysfunction is called neurogenic bladder. There are two categories according to the function of the detrusor muscle: (i) hyperreflexia of the detrusor muscle; and (ii) absence of reflexes of the detrusor muscle. Neurogenic vesicourethral dysfunction is a group of dysfunctional disorders of the bladder and/or urethra caused by neuropathy or damage, often accompanied by a coordinated malfunction of the vesicourethra. Neurogenic vesicourethral dysfunction produces complex voiding symptoms, with dyspareunia or urinary retention being one of the most common symptoms. The resulting induced urinary complications are a major cause of death in patients. How can structural and functional damage to the upper urinary tract be effectively prevented? The treatment of neurogenic bladder is mainly to protect the function of the upper urinary tract to prevent pyelonephritis and hydronephrosis leading to chronic renal failure; secondly, to improve the symptoms of voiding disorders in order to alleviate the patient’s pain in life. The specific measures of treatment are to use various non-surgical or surgical methods to reduce the amount of residual urine, which can reduce urinary tract complications after the amount of residual urine is eliminated or reduced to very little (<50mL). (1) Non-surgical treatment (1) Catheterization: Whether for the purpose of promoting urine storage or voiding, intermittent catheterization can effectively treat neuromuscular voiding dysfunction, eliminate the pain of long-term catheterization or even suprapubic cystostomy, and create conditions for further treatment (bladder enlargement, controlled urinary flow diversion). (2) Adjunctive treatment: (1) regular bladder emptying; (2) pelvic floor muscle training; (3) training of "trigger point" urination; (4) use of external urinary collection devices for men. (3) Medication: ①Medication for overactivity of the detrusor muscle, such as M-blockers. (2) Drugs to treat contractile weakness of the detrusor muscle, M receptor agonists. ③Drugs to reduce bladder outlet resistance, such as alpha-blockers. ④Drugs that increase bladder outlet resistance: alpha agonists. ⑤Drugs that reduce urine production, such as desmopressin. (6) Other drugs. (4) Acupuncture therapy: acupuncture has a good effect in treating sensory paralysis of the bladder due to diabetes mellitus, and is particularly effective for early lesions. (5) Closure therapy: This method is suitable for upper motor neuron lesions (hyperreflexia of the forced urinary muscles), and those with good results after closure, the residual urine volume is significantly reduced, and the symptoms of urinary disorders are significantly improved. In a small number of patients, the effect can be maintained for several months to a year after 1 closure. These patients require only periodic closure and do not need to resort to surgery. (6) Bladder training and dilatation: This method can be used to treat patients with severe symptoms of urinary frequency and urgency and no residual urine or very little residual volume. Ask the patient to drink water regularly during the day, 200mL per hour. extend the interval between urination as much as possible, so that the bladder can be easily and gradually expanded. 2.Surgical treatment Its effect is to improve bladder compliance and capacity and change bladder outlet resistance. It needs to be proven ineffective by non-surgical treatment and performed after the neuropathy is stabilized. Patients with mechanical obstruction of the lower urinary tract should consider removing the obstructing factor first. Surgical approaches are divided into four major categories: procedures to treat urinary storage dysfunction, procedures to treat voiding dysfunction, procedures to treat both urinary storage and voiding dysfunction, and urinary flow diversion procedures.