الفهرس 
Anatomy and Neurophysiology of Lower urinary tractOnly 14 pages are availabe for public view
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Abstract
Filling of the bladder and voiding involve a complex pattern of afferent and efferent signaling in parasympathetic (pelvic nerves), sympathetic (hypogastric nerves), and somatic (pudendal nerves) pathways. These pathways constitute reflexes, which either keep the bladder in a relaxed state, enabling urine storage at low intravesical pressure, or initiate bladder emptying by relaxing the outflow region and contracting detrusor.
Many systems have been developed to classify various voiding and storage problems. This includes: Bors-Comarr Classification, Hald-Bradley Classification, Bradley Classification, Lapides Classification, Urodynamic Classification, The Krane and Siroky classification, International Continence Society Classification, and the Functional Classification System.
Urodynamic tests, including uroflowmetry, cystometry, pressure-flow studies, urethral pressure profiles, and electromyography (EMG), were provides useful clinical information about the function of the urinary bladder, the sphincteric mechanism, and the voiding pattern itself.
Management of Neurogenic Bladder
For ease classify treatments for neurogenic voiding dysfunction under the broad categories of whether they facilitate filling/storage and emptying/voiding.
Self-intermittent catheterization is still the mainstay of therapy to provide sufficient emptying in patients with hand function. Common pharmacologic treatments to reduce bladder contractility include: Relatively Pure Muscarinic Agents (e.g. Tolterodine Tartrate, Darifenacin and Solifenacin), Anticholinergic Agents with “Mixed” Actions (e.g.Oxybutynin Chloride and Flavoxate Hydrochloride), Tricyclic Antidepressants, Desmopressin, and Intravesical injection therapy (e.g. Intravesical oxybutynin and Intravesical peppers).
Oral pharmacotherapy is rarely successful for treatment of functional obstruction although alpha-adrenergic blockers have been used in spinal cord injury patients.
Cholinergic drugs help to increase bladder muscle tone and contractility in cases of neurogenic detrusor underactivity.
Recent advances in management of neurogenic bladder
Intravesical injection of botulinum toxin A; acts by inhibiting acetylcholine release at the presynaptic cholinergic junction resulting in regionally decreased muscle contractility and muscle atrophy at the site of injection. BTX- A has a good result in treating detrusor-sphincter dyssynergia, urine retention and detrusor overactivity due to neurogenic causes.
Brindley and his colleagues developed an implantable device to empty the bladder and control the sphincters. The prosthesis uses sacral anterior root stimulation (Finetech–Brindley SARS) through Posterior sacral rhizotomy for roots of S2 to S5 followed by intradural electrode placement on the sacral anterior root supplying the bladder.
Sacral root Neuromodulation is indicated for the management of refractory urge incontinence, refractory frequency/urgency syndromes, and urinary retention in the absence of obstruction; by PNE using an insulated foramen needle placed in S3 foramen, when the desired responses to stimulation are recorded a permenant quadripolar electrode lead is inserted and connecting to IPG.
Tissue engineering is used as an alternative to free tissue grafts for bladder augmentation by harvesting autologous cells from the diseased organ, expanding these cells in vitro, and seeding them onto a matrix, which is then implanted into the donor organ. Three factors are known to influence the organ regeneration process: the biomaterial, which should replicate the effects of the extracellular matrix (ECM); the source of the cells that are seeded onto the biomaterial; and the environmental conditions during regeneration, which influence the development of the blood vessel and nerve supply to the construct.
NGF gene therapy using herpes simplex virus was used to treat overflow incontinence caused by diabetic neurogenic bladder dysfunction by injecting HSV carrying the NGF gene into the bladder wall.