The mechanisms for detrusor overactivity following suprapontine damage are, however, different from those following spinal cord injury (SCI). Damage to central inhibitory pathways or sensitization of peripheral afferent terminals in the bladder can unmask primitive voiding reflexes and be expressed as spontaneous involuntary contractions of the detrusor. Patients report varying degrees of storage symptoms such as urinary urgency, frequency, nocturia, and incontinence (collectively known as “overactive bladder symptoms”). (DO) is the most common cause for urinary incontinence following neurological disease. Neurogenic Lower Urinary Tract DysfunctionĪ neurourological classification of neurological disorders is useful to understand that different patterns of LUT dysfunction can arise following neurological disease ( When deemed appropriate to void, the pontine micturition center (PMC) is released from the tonic inhibition of higher cortical centers, and parasympathetic-mediated detrusor contraction accompanied by relaxation of the pelvic floor and external and internal urethral sphincters results in effective bladder emptying. This results in low pressure filling and continence. During bladder filling, sympathetic and pudendal nerves mediate contraction of the smooth (internal) and striated (external) urethral sphincter, whereas sympathetic-mediated inhibition of the detrusor prevents contractions. This phasic pattern of activity, as well as degree of voluntary control and dependence on learned behavior, is unique to the LUT compared with other autonomically innervated structures such as the cardiovascular system.Ĭonnections between the pons and the sacral spinal cord, as well as the peripheral innervation that originates from the caudal spinal cord, need to be intact to effect storage and voiding. Switching from the storage to the voiding phase is initiated by a conscious decision, which is influenced by the perceived state of bladder fullness and an assessment of the social appropriateness of voiding. The frequency of micturition in a person with a bladder capacity of 400 to 600 mL is once every 3 to 4 hours, and the bladder is in a storage phase more than 99% of the time. This results in low-pressure filling and periodic voluntary emptying. Neurological Control of Lower Urinary Tract Functions in HealthĪ complex neural network acts as a switching circuit to maintain a reciprocal relationship between the reservoir function of the bladder and sphincter function of the urethra. An individualized, patient-tailored approach is required for the management of lower urinary tract dysfunction in this special population. In select patients, reconstructive urological surgery may become necessary. Neuromodulation offers promise for managing both storage and voiding dysfunction. Intra-detrusor injections of onabotulinumtoxinA have revolutionized the management of neurogenic detrusor overactivity. Incomplete bladder emptying is most often managed by intermittent catheterization, and storage dysfunction is managed by antimuscarinic medications. The preliminary evaluation consists of history taking, and a bladder diary and may be supplemented by tests such as uroflowmetry, post-void residual measurement, renal ultrasound, (video-)urodynamics, neurophysiology, and urethrocystoscopy, depending on the clinical indications. This acknowledged difference in morbidity is considered when developing appropriate management algorithms. The risk for developing upper urinary tract damage and renal failure is considerably lower in patients with slowly progressive nontraumatic neurological disorders, compared with those with spinal cord injury or spina bifida. The site of the neurological lesion and its nature influence the pattern of dysfunction. Lower urinary tract dysfunction is a common sequel of neurological disease resulting in symptoms that significantly impacts quality of life.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |