Neurogenic urinary bladder

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Hyper-reflexic Neurogenic Urinary bladder with DSD Presenter: Dr. Md. Monowarul Islam rtn24@yahoo.com 8801818169894 Dhaka,Bangladesh Topic:

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Author: Dr.Md.Monowarul Islam MBBS, FCPS(Surgery) National institute of kidney diseases and urology Dhaka, Bangladesh Email: rtn24@yahoo.com www.zorpia.com/rtn24

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Afferent Efferent Micturition Reflex : When urine fills the bladder, an excitatory signal  sacral cord  spinal reflex center  efferent  involuntary detrusor contractions with coordinated voiding ( Primitive voiding )

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Micturition is controlled via: Frontal lobe Pons Spinal cord Splanchnic Pudendal nerve Sympathetic T11 –L2 Parasympathetic S2,3,4 S2,3,4 Rule of 3

1.Cortical micturation center:

1.Cortical micturation center Location: Frontal lobe Function: Inhibitory to PMC Inhibition: Urge to urinate disappears Inhibition withdraw: When urination appropriate, allow voiding The brain’s control of the PMC is part of the social training that children experience at age 2 - 4 years

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Paracentral lobule in the medial aspect of the frontal-parietal junction,

2.PMC (Pontine Micturition Center):

2.PMC ( Pontine Micturition Center) The relay center between the brain and the bladder Location: Reticular formation Nature: Excitatory Function: Co-ordination

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3.Sacral spinal cord Somatic: Onuf's nucleus Sacral parasympathetic nucleus (SPN) : Intermediolateral cell column of second, third, and fourth sacral cord : pelvic splanchnic nerves (nervi erigentes) Sacral reflex center Primitive voiding center

Peripheral Nervous System:

Peripheral Nervous System Somatic (S2-S4) Pudendal nerves Excitatory to external sphincter Parasympathetic (S2-S4) Pelvic nerves Excitatory to bladder, relaxes sphincter Sympathetic (T11-L2) Inhibitory to bladder body, excitatory to bladder base/urethra -

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Virtual tour of pelvic nerve

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The right and left components of the pelvic plexus communicate behind the rectum and anterior and posterior to the vesical neck. Division of these vessels (the so-called lateral pedicles of the bladder and prostate) risks injury to the pelvic plexus with attendant postoperative impotence (Walsh and Donker, 1982; Walsh et al, 1983).

Neurogenic bladder types:

Neurogenic bladder types Cerebral Neuron – uninhibited bladder; urge incontinence Pontine Neuron- Reflex/Automatic bladder DSD/DESD/Autonomic dysreflexia Sacral & peripheral N. – Affarent: Atonic / Areflexic bladder; overflow incontinence Affrarent + Effarent: Autonomus bladder( Small hypertrophied)

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A small number of persons will have a “mixed” bladder when there has been only partial damage to the spinal nerves.

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Spastic Neurogenic bladder: A small (150 cc ), trabeculated bladder with "Christmas tree" appearance. Fir/Christmas tree Bladder changes

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DSD/DESD/PSD Detrusor sphincter dyssynergia, unless specified otherwise, refers to dyssynergia of the striated sphincter and is sometimes abbreviated DSD or DESD. –campbell 9th True DESD should exist only in patients who have an abnormality in pathways between the sacral spinal cord and the pontine micturition center The term smooth sphincter dyssynergia or proximal sphincter dyssynergia is occur in an individual with autonomic hyperreflexia /dysreflexia ( Spinal cord injury above T6 level ). Chapter 59

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Dysfunctional Voiding This syndrome, also described by various authors as non-neurogenic neurogenic bladder, learned voiding dysfunction presents with a history of unexplained lower urinary tract dysfunction ap pears urodynamically to be involuntary obstruction at the striated sphincter level, existing in the absence of demonstrable neurologic disease

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Voiding pattern in DESD

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Causes

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Spinal injury: Spinal shock ( retention ) , few weeks later Injury between pons to sacral center : Hyper-reflexic bladder with DESD Injury above T6 : Autonomic dysreflexia with DSD Sacral center and nerves : Areflexic / flaccid bladder

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Summary

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On-off switch Relay center Primitive voiding Cerebral PMC SMC

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Stroke, MS, Dementia, Parkinsonism, Head injury Stroke, MS, Head injury Spinal injury, T. myelitis Spinal injury, Radical Pelvic surgery Cerebral PMC SMC

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UMNL - Spastic UMNL - Spastic LMNL Flaccid / atonic/ areflexic Cerebral PMC SMC

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DESD - NO DESD – Yes DSD – above T6 No Neural activity Cerebral PMC SMC

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Hyper-reflex voiding Hyper-reflex voiding Voiding by Straining Cerebral PMC SMC

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Diagnosis

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Strictly DSD/DESD can only be diagnosed from an EMG trace or x-ray findings, but the the pressure and flow only can suspect.

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Effects If left untreated, DESD can result in: UTI VUR Hydronephrosis Renal insufficiency Kidney stones Occur when the urine has a high level of minerals that form stones

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Management

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Goals of Management Adequate storage at low intravesical pressure Adequate emptying at low intravesical pressure Absence or control of infection No catheter or stoma Upper urinary tract preservation or improvement Social acceptability and adaptability

Treatment Options:

Treatment Options The results of treatment of voiding dysfunction are rarely perfect Current treatment options aim to minimize intravesical pressure and its detrimental effect on the upper urinary tract. These includes: 1-Chronic indwelling catheterization. 2-CISC. 3-Pharmacological therapy. 4-Bladder augmentation Urinary diversion. 5-External sphincterotomy. 6- Urolume stent. 7-Botulinum toxin inj. 8-Intrathecal continous baclofen infusion. 9-Balloon dilatation. 10-Laser sphincter ablation.

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Drugs: Anticholinergics: 1.Oxybutynine 2.5-5mg BID/TID 2. Tolterodoline – highly effective 3. Capsaicin – single intravesical instillation provide relief for several months

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Figure 5 Injection sites using the minimally invasive outpatient technique

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UroLume Urethral Stent

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The UroLume® Urethral Stent Features It has the potential to expand to a diameter of 14 mm (42F) Allows for a full range of endoscopic procedures It is available in lengths of 1.5 cm, 2.0 cm, 2.5, 3.5 and 4.0 Potentially reversible; the external sphincter remains intact Allows normal ejaculatory function Less costly and less invasive than surgery Becomes fully incorporated within the body Fully compatible with MRI

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Urological Adventure Thanks

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The terms unstable bladder/detrusor instability and detrusor hyperreflexia were introduced 30 years ago. Their introduction has an interesting history: at that time the English-speaking world had adopted Patrick Bates' term unstable bladder to describe involuntary detrusor contractions seen during urodynamic studies, as the bladder was filled. At the same time the other major protagonists and innovators in urodynamics, the Scandinavians, were using the term detrusor hyperreflexia. How was this confusing situation to be resolved? The answer, a political one, was given by the International Continence Society's standardization committee under its first chairman, Tage Hald ( Bates et al, 1980 ). The solution was to designate the term unstable bladder for involuntary detrusor contractions seen in patients with no obvious cause for the contractions and to use the term detrusor hyperreflexia for patients whose involuntary contractions had a neurologic cause, for example, multiple sclerosis. The overactive bladder (OAB) is defined as urgency, with or without urge incontinence, usually with frequency and nocturia.

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Little, too, is known about the natural course of development or maturation of the structure as well as function of the sphincter mechanism. Literature suggests that immature detrusor-sphincter coordination, manifested as detrusor hypercontractility and interrupted voiding, commonly occurs in the first 1 to 2 years of life causing some degree of functional bladder outflow obstruction ( Sillen et al, 1992 ; Yeung et al, 1998 ). In a postmortem study of the ontogeny of the external urinary sphincter in human fetuses, infants, and young children, Kokoua and colleagues (1992) found significant age-related differences in the histologic structure of the sphincter as compared with that in adults. Striated muscle fibers of the sphincter first appeared at around 20 weeks of gestation, then became arranged in a concentric pattern as a closed ring, fused posteriorly to form a tail-like structure that was directed to the perineal body. Posterior splitting of the striated sphincter, starting first caudally and progressively in a cephalad manner then occurred during the first year of life, coinciding in parallel with gradual resorption of the “tail,” to eventually giving way to a mature omega-shaped structure. Because a complete closed ring of striated sphincteric muscle was present up to 1 year of age in over 40% of cases, it may well be conjectured that this could be related to the high intravesical pressures and interrupted voiding that are commonly observed during urodynamic studies in infants ( Sillen et al, 1992 ; Yeung et al, 1995a, 1998 [119] [120]).

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