Overactive bladder (OAB) is a frequent complication of stroke and vascular dementia. It is a complex syndrome manifesting in the impaired analysis of afferent impulses and the impaired efferent signals generation in the cortex and subcortical brain zones involved in urination regulation. Disruption between urination brain centers and spinal structures leads to impaired cholinergic (urge incontinence), indirect sympathetic (pollakiuria) and non-cholinergic impulse transmission. Nocturia and polyuria are caused by melatoninergic and vasopressinergic transmission impairment respectively. Urge incontinence (UI) is the most common symptom of brain disease. OAB early diagnosis and treatment are still to be improved. A great part of experimental research of the last decades disregarded the psychological aspect of AOB and thus could not describe psychologically-mediated reflexes. Still such symptoms as compelling urge to urinate and loss of urethral sensitivity can not be well described by experimental research. In order to reveal them patient history and complaints should be assessed in their combination with the neurological symptoms, process localization (Barrington’s nucleus, etc.) as well as its clinical characteristics (progression speed and cyclic character, rehabilitation prognosis). We think that the assessment of reflexes involved in lower urinary tract (LUT) complex function plays a key role in AOB patient assessment. The main 12 urination LUT reflexes have been described by F. J. F. Barrington, M. Kuru and D. T. Mahony. Studying the changes of these reflexes in various neurologic conditions is an important task of neurourology.

The article presents a new concept of formation of the syndrome of hyperactive bladder on the basis of violations of the implementation of the 4 reflexes of urination, which provides the normal retention of urine and are responsible for the accumulation function of the bladder. First we analyzed the main point of application of drugs of anticholinergic and sympathomimetic actions in the reflexes of urination and mechanisms of restoration of function of the lower urinary tract in patients with acute and chronic vascular diseases of the brain.
Study was provided in Scientific center of Neurology (Moscow). 140 patients were included in study, 50 patients after ischemic stroke and 70 patients with discirculatory encephalopathy. In comparison group were 20 patients with DE and Benign hyperplasia prostate. There were 3 stages of trial: 1.research of clinical aspects of overactive bladder in all patients groups. Also comparative diagnostic evaluation was performed. 2. Clinical examination of all patients. 3. Pharmacological analysis of cholinergic and adrenergic regulation lower urinary tracts.
Methods of research: Neurological examination, assessment of mental condition urological evaluation: anamnesis of life, assessment of complaints, voiding dairy, IPSS, rectal evaluation, bacteriological evaluation of urine samples, ultrasound diagnostic, urodynamic study. Also ultrasound of vessels of the head and neck was provided. Method of neurovisualisation: MRI, CT.

Cerebral representations of the bladder and its sphincters include dominant center (right insular cortex - правый островок Рейля?) and paired zones. Paired zones lesion leads to reversible urination disorders. Ischemic lesion of functionally unpaired lower frontal cortex results in irreversible diurnal pollakiuria.
Changes in the central nervous system zones involved in urination regulation can be caused by acute and chronic ischemia as well as other pathological process. Reflex assessment is recommended to analyze such changes.
Clinical manifestations of UI include 4 symptoms: compelling urge to urinate, urge incontinence per se and less often (in the lack of frontal control due to ischemia) pollakiuria and inability to stop urination once it began. In post-stroke UI patients we identified 4 reflexes that if impaired result in a full range of UI clinical symptoms: detrusor inhibiting reflex, perineodetrusorinhibitory reflex, urethrosphincteric guarding reflex, detrusourethral inhibitory reflex.
Thus the following three mechanisms underlie UI in post-stroke patients.

first UI mechanism takes place at urine accumulation phase. Dysfunction of urethral sphincter охраняющего (protective?) reflex results in reduction of mean effective bladder volume. Much lower urine volume in the bladder is perceived by the brain as normal due to the decrease of lower frontal cortex perception threshold.
Second UI mechanism takes place during an urge to urinate. Impairment of detrusor inhibiting sympathetic reflex causes limbic system overreaction and manifests in compelling urge to urinate. In the first case patients complain of frequent urination with a small amount of urine at each micturition. This can be easily traced by using a bladder diary. In the second case patients complain of compelling urge to urinate that can arise suddenly at any time. Spinal part of the sympathetic nervous system also plays an indirect role in this condition by regulating bladder filling with urine.
Third UI mechanism takes place at the urination start. Impairment of perineal detrusor inhibiting reflex and detrusor reflex that inhibits urethral contraction leads to inability to prevent urination start (first reflex) and to stop urination once it began (second reflex). Detrusor inhibiting perineal reflex is provided by pyramidal system and indirectly involves n-cholinergic system in urine continence. Thus the voluntary control of pelvic floor muscles contraction is lost. Detrusor reflex that inhibits urethral contraction is an involuntary parasympathetic reflex that causes initial detrusor contraction at urination start.

Urination impairment is a clinical symptom of stroke. Its clinical presentation depends on the localization of brain ischemic lesion. Single symptom manifestation results from a local brain lesion, polysymptomatic condition is accounted for by multiple brain lesions. Consequence of urologic signs and symptoms in patients with brain vascular disease reflects the dynamics of pathological process in the brain. Sudden appearance of symptoms is characteristic of lacunar and hemisphere infarction, a gradual symptom development is typical for leucoaraiosis. Functional reorganization of brain neuronal networks following a stroke account for symptoms regression whereas the increasing neuronal degeneration in chronic brain ischemia leads to symptoms progression. Bladder diary and urodynamic testing help to differentiate sensory, motor and sphincter neurogenic urination disorders in post-stroke patients.

Barrington F. J. F. The effect of lesions of the hind- and mid-brain on micturition in the cat. Q. J. Exp. Physiol. 1925; 15: 81–102.
Mahony DT, Laferte RO, Blais DJ. Intergral storage and voiding reflexes. Neuro- physiologic concept of continence and micturition. Urology. 1977; 9 (1): 95–107.
Goldfarb RA, Pisansky A, Fleck J, Hoversten P, Cotter KJ, Katorski J, et al. Neuro- genic Lower Urinary Tract Dysfunction in Adults with Cerebral Palsy: Outcomes fol- lowing a Conservative Management Approach. J Urol. 2016 Apr;195 (4 Pt 1):1009–13. DOI: 10.1016/j.juro.2015.10.085