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Multiple Sclerosis, Transverse Myelitis, Tropical Spastic Paraparesis, Progressive Multifocal Leukoencephalopathy, Lyme Disease
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Michele Fascelli, Howard B. Goldman
Intracranial plaques develop in the periventricular zone of approximately 60%–80% of cases, resulting in loss of voluntary control of initiation or prevention of voiding, as the perception of fullness and ability to inhibit bladder contraction depend on alert and normally functioning sensorium.9 Micturition reflex and the bladder-urethral sphincter synergy remain intact.
Anatomy and Physiology of the Autonomic Nervous System
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
The simplest form of reflex occurs at the spinal level, without the need for central connections. These reflexes include those for emptying the bladder and rectum. Filling of these organs causes stimulation of stretch receptors in the walls, resulting in an increase in traffic of afferent impulses to the sacral spinal cord. On reaching a specific intensity, there is reflex contraction of the detrusor muscle of the bladder and increased peristalsis of the descending colon. The rectum and sigmoid colon contract vigorously, the internal anal sphincter (smooth muscle) relaxes and defaecation occurs. Normally, ascending pathways to the medulla transmit this information on fullness of the rectum and a voluntary decision can be made to inhibit defaecation. This is achieved by contraction of the external anal sphincter (skeletal muscle) and relaxation of the rectum and sigmoid colon which reduces the pressure and thus stimulation of stretch receptors. This may continue until the rectum is distended to the point where defaecation is unavoidable. In very young children this voluntary control of defaecation does not occur because the necessary nerve pathways have yet to reach full maturity. Similarly, in adults whose spinal cord is severed at or above the sacral level (paraplegics), voluntary control is lost and the reflex is purely spinal. The micturition reflex of the bladder operates in a similar fashion.
Urinary Incontinence in Older Adults
Published in K. Rao Poduri, Geriatric Rehabilitation, 2017
Nicole Strong, Sara Z. Salim, Jean L. Nickels, K. Rao Poduri
A number of neurologic conditions can result in UI. Neurogenic bladder is a dysfunction in voiding due to neurologic injury and can affect urine storage and coordinated voluntary voiding. The micturition reflex involves detrusor contraction and urethral sphincter relaxation, the coordination of which allows for normal voiding. This is regulated by the PMC.
Physiotherapeutic assessment and management of overactive bladder syndrome: a case report
Published in Physiotherapy Theory and Practice, 2023
Bartlomiej Burzynski, Tomasz Jurys, Karolina Kwiatkowska, Katarzyna Cempa, Andrzej Paradysz
Gormley, Lightner, Faraday, and Vasavada (2015) observed that patients suffering from OAB are very often treated using the second and third tiers of treatments, while they are almost never treated using behavioral therapy or more conservative treatments. This may result from a lack of knowledge of conservative methods of OAB treatment and so demonstrates the need for wider education on this matter. Similar conclusions are presented by Kasman, Stave, and Elliott (2019) who claimed that conservative treatment is often insufficiently used and poorly understood by physicians. Physiotherapeutic treatment is becoming an integral part of urology and represents one possible conservative treatment option. Previous studies have perceived the physiotherapeutic treatment of OAB through the prism of pelvic floor muscle training (Bø et al., 2020; Olivera et al., 2016; White and Iglesia, 2016). Justification for the efficacy of pelvic floor muscle training is based on the fact that the increase in muscle tension leads to increased pressure in the urethra, then decrease in tension of the musculus detrusor vesicae, and thus inhibition of the micturition reflex. Therefore, patients have more time to reach toilet facilities and avoid urine leakage. Moreover, pelvic floor muscle training leads to permanent changes in the morphology of pelvic structures, which may stabilize neurogenic activity and pressure in the urethra.
Are We missing out the role of oxytocin in overactive bladder syndrome?
Published in The Aging Male, 2020
Prostaglandins (PGs) are hormones that are produced, released, and effective locally; such agents are called autocoids. One of the earliest recognized effects of PGs was the stimulation of myometrial contractions. Besides stimulating uterine myometrial contraction, OT causes the release of PGs from different organs including bladder [35]. PGs are locally synthesized in the bladder muscle and mucosa [36]. This synthesis is initiated by stretch of the detrusor muscle, bladder nerve stimulation, bladder mucosa damage, and inflammation mediators. PGs are released from the bladder into the general circulation in response to distension. In regard to PG related changes in the micturition reflex, it was envisaged that they might act directly on the afferent nerves to modulate firing and so, trigger micturition at lower bladder volumes [34].
Pharmacological treatments available for the management of underactive bladder in neurological conditions
Published in Expert Review of Clinical Pharmacology, 2018
Seyedeh-Sanam Ladi-Seyedian, Behnam Nabavizadeh, Lida Sharifi-Rad, Abdol-Mohammad Kajbafzadeh
In the normal situation, micturition reflex initiates after maximal filling of bladder and consequent stretch in bladder wall. Afterwards, afferent nerves, brain circuits, and efferent nerves conduct the impulse, respectively, which leads to an effective and sustainable detrusor contraction. Sacral parasympathetic nucleus and pontine micturition center (PMC) facilitate this reflex [13]. PMC is normally inhibited by limbic system and in turn receives inputs from higher cortical centers. During the storage phase, afferent fibers are responsible for bladder volume monitoring. Intact bladder sensation is fundamental to initiate micturition reflex and efferent system action [21]. Magnitude of detrusor contraction during voiding is also regulated by afferent system [22]. Efferent pathway provides contraction of bladder detrusor and adjusts speed, magnitude, and duration of contraction [21]. It is intuitive that interruption of signaling in aforementioned pathways and regulatory centers could result in diminished, absent, or ineffective detrusor contractility. Therefore, a variety of neurogenic diseases and injuries could result in UAB. Among them brain strokes, multiple sclerosis, Parkinson’s disease, diabetes mellitus, and spinal cord injuries are the well-known neurogenic causes of UAB. There is also evidence that diminution of response occurs in brain regions (responsible for interpretation of sensory inputs from the bladder) as age increases [18].