Possible causes of overactive bladder syndrome include bladder detrusor instability, abnormal urethral and pelvic floor muscle function, neurological abnormalities and hormonal abnormalities, anxiety and tension, and poor voiding habits.
1. Instability of bladder detrusor: For example, chronic inflammatory infections of the urinary system or non-neurogenic factors may cause abnormal contraction of the detrusor muscle during the storage phase, leading to symptoms such as urgency and frequency of urination.
2. Abnormal function of the urethra and pelvic floor muscles: due to the overlap of the bladder adjacent tissues and organs with the bladder’s controlling nerves, or bladder adjacent tissues and organs of the bladder’s diseases directly stimulate the bladder, resulting in abnormal bladder function, or recent urological or laparoscopic surgeries, which damages the urethra and the pelvic floor muscles, the above symptoms may also occur.
3. Nerve abnormalities and hormone secretion abnormalities: the nerve center transmits inhibitory or excitatory signals to the bladder to make the bladder start urinating at the appropriate urine volume. If the inhibitory signals sent by the nerve center are weakened or the excitatory signals are increased, overactive bladder syndrome will result.
4. Anxiety and tension and poor urination habits: emotional tension, anxiety, fear of incontinence, fear of painful urination, etc., tend to make the patient form self-suggestion, intentionally or unintentionally reminding themselves to urinate, and ultimately form poor urination habits and psychology.
If overactive bladder syndrome is suspected, early medical treatment is recommended. Behavioral treatment is the mainstay for patients with mild symptoms, including bladder training, pelvic floor muscle training, maintaining a healthy body weight, and consuming the right amount of fluids; for severe symptoms, behavioral treatment should be accompanied by medication; and surgical treatment may be an option if the treatment plan is ineffective.