Overactive bladder: causes and pathogenesis

It is well established that the causes of the hyperactive bladder are a consequence of neurogenic and non-neurogenic lesions. Neurogenic disorders occur at the level of the supraspinal centers of the nervous system and the conducting pathways of the spinal cord, and not the neurogenic disorders - a consequence of the age-related changes in detrusor, IVO, and anatomical changes in the position of the urethra and bladder.

Some morphological changes in the detrusor are known with hyperactivity. Thus, in most patients with a hyperactive bladder, a decrease in the density of the cholinergic nerve fibers that have a hypersensitivity to acetylcholine is detected. These changes are called "post-synaptic cholinergic denervation of detrusor." In addition, with the help of electron microscopy, it was possible to establish violations of normal intercellular connections in the detrusor of the hyperactive bladder in the form of protrusion of intercellular connections and protrusion of the cell membrane of one myocyte into another with the approach of intercellular boundaries - the "tight connection of two parallel planes of adjacent myocytes". Based on these morphological changes characteristic of the hyperactive bladder, Brading and Turner (1994) proposed a theory of the pathogenesis of the development of detrusor hyperactivity, based on the increased excitability of myocytes, which are closely related to each other at the sites of denervation.

It is believed that the cause of denervation, in addition to nerve disorders, may be detrusor hypoxia due to age-related ischemic changes or due to IVO. In the latter case, this is confirmed by the presence of a hyper-reactive bladder in 40-60% of men with prostate adenoma. Thus, the primary cause of detrusor hyperactivity in a hyperreactive bladder is hypoxia, which develops in the detrusor due to age-related arteriolosclerosis or as a result of IVO, and leads to detrusor denervation (revealed in detrusor biopsies in all types of detrusor hyperactivity). In response to the deficit of nervous regulation in myonites, compensatory structural changes occur in the form of close contacts between neighboring cells with increased nervous excitability and conductivity. And then any contraction of individual myocytes (spontaneous or provoked by stretching the wall of the bladder during the accumulation of urine) leads to involuntary contractions according to the principle of "chain reaction" of the entire detrusor. This theory of the development of detrusor hyperactivity in a hyperreactive urinary bladder is now considered to be the most correct.

[1], [2], [3], [4], [5]

Epidemiology of the hyperactive bladder

According to the International Society for Urine Retention, a hyperactive bladder is observed in about 100 million people in the world. In the US, the diagnosis of a hyperactive bladder is more common than diabetes mellitus, peptic ulcer diseases of the stomach and duodenum, and is included in the 10 most common diseases. There are reasons to believe that the symptoms of a hyperactive bladder are in 17% of the adult population in Europe. Empressive urination occurs in 16% of women in Ukraine.

Despite the fact that the hyperactive bladder is more often diagnosed in the elderly, its symptoms are also found in other age groups. The greatest number of patients was noted at the age of more than 40 years. While in men over the age of 60 there is a clear tendency to increase the incidence, and in women, on the contrary. - to decrease. Thus, the hyperactive bladder is a fairly common clinical syndrome that occurs in different age groups and leads to physical and social disadaptation.

[6], [7], [8], [9], [10], [11], [12], [13]