neurogenic bladder


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NEUROGENIC BLADDER Prensented by Dr Arvind gupta Guide Dr M K Singh DM


Introduction Applied anatomy and physiology Pathophysiology Common symptoms of neurogenic bladder Levels of bladder dysfunction Investigations Treatment available Outline

Introduction : 

Introduction Neurogenic bladder refers to dysfunction of the urinary bladder due to disease of the central nervous system or peripheral nerves involved in the control of micturition . Complaints about bladder function are common in patients with neurological disease 98% of lifetime bladder is in storage phase To effect both storage and voiding, connections between the Pons and sacral spinal cord as well as peripheral innervations must be intact

Anatomy of bladder: 

Anatomy of bladder α receptors Detrusor β receptors M2 M3 muscarinic receptors N receptors

Innervation of lower urinary tract: 

Innervation of lower urinary tract Detrusor - innervated by S2,3,4 parasympathetic (muscarinic M2 receptors) intermediolateral gray column –pelvic n External urethral sphincter - innervated by somatomotor S2,3,4 nucleus (Onuf’s Nucleus)-pudendal n Trigone and internal sphincter innervated by Sympathetic T10,11,12 (less important) S 2,3,4

Peripheral nervous system: 

Peripheral nervous system Somatic (S2-S4) Pudendal nerves Excitatory to EUS Parasympathetic (S2-S4) Pelvic nerves Excitatory to bladder, relaxes sphincter Sympathetic (T10-L2) Hypogastric nerves to pelvic ganglia Inhibitory to bladder body, excitatory to bladder base/urethra Afferents Through pelvic, pudendal and hypogastric N.

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Spinal cord centers and nerves responsible for micturition .

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Central neural control: PET studies Micturition is being controlled by pontine micturition center (PMC) which is situated in mediodorsal Pons called as M region During storage phase PMC is inhibited by higher cortical control unless socially appropriate Blok et al asked to void the volunteers under scanner In successful voiders activity was shown in mediopost pons (M region) In subjects unable to void and storing urine a distinct region in the ventro -lat pontine tegmentum was activated (L region) Successful voiders Unable to void Pontine micturition center M region Pontine storage center L region Blok et al . Brain 1998

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Central neural control: FMRI study Increased blood flow During micturition Rt dorsomedial pontine tegmentum : PMC or M region Rt Inferior frontal gyrus Rt Ant cingulate gyrus During storage Periaqueductal grey PAG Mid cingulate gyrus Lat bilateral frontal lobes Ventrolateral pons : L region Kavia & Fowler, J Comp Neurol 2005; 493: 27-32

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Central neural control Textbook of neurogenic bladder 2 nd ed. 2008 . Jacques corcos, Eric Shick.

Afferent Pathways: 

Sensations of pain, temperature, urgency is found in the antero -lateral white columns. Conscious sensations (bladder distention,ongoing micturition, tactile pressure) follow the posterior columns A-delta fibers – Micturition reflex, stretch and fullness sensation C-fibers – Noxious sensation Afferent Pathways

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Neuroanatomic distribution of primary afferent and efferent components of storage and micturition reflexes within the sacral cord Pelvic n. Pudendal n. Pudendal n. Levator ani

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Passive phenomena mediated by a spinal reflex Bladder filling  low level visceral afferent Inhibits detrusor Activates IUS Inhibits parasympathetics Bladder distension  stimulates EUS (Guarding reflex) STORAGE REFLEXES

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VOIDING REFLEXES Involuntary Bladder fullness till micturition threshhold Visceral afferents Stimulates PMC Stim sacral parasymathetic Contracts detrusor Inhibit bladder outlet Inhib pudendal  relaxes EUS Inhib sympathetic Voluntary micturition Bladder fullness till micturition threshold Activation of cortical centers (socially appropriate condition forvoiding ) Stimulates PMC Stimulates sacral parasympathetics Hypogastric N. Bladder EUS Pudendal n. (-) (+) (-) (-)

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Levels of bladder dysfunction


LOSS OF SUPRASPINAL CONTROL (UNINHIBITED BLADDER) Lesions of CNS involving area above pons Micturition is usually precipitous and complete Frequency, urgency & urge incontinence Low or absent residual volume as there is no DSD Normal sensation of bladder filling Causes: CVA, frontal tumors,parasagittal meningioma,ACA aneurysm,NPH, Parkinsons disease, Demyelinating disease


SPINAL CORD LESION ABOVE SACRAL LEVEL REFLEX NEUROGENIC BLADDER (AUTOMATIC) Detrusor- sphincter dyssynergia is a rule Bladder sensation variably interrupted Bladder tone increased, capacity reduced Small residual urine Urgency, frequency and urge incontinence in incomplete lesions Inability to initiate voluntary micturition Cystometrogram shows uninhibited contractions of detrusor in response to small volume of fluid Causes: spine cord trauma, compressive myelopathy, myeilitis, syringomyelia


SPINAL CORD LESION INVOLVING SACRAL LEVEL AUTONOMOUS BLADDER Denervation of both afferent and efferent supply to bladder bladder tone flaccid, sensation absent, Inability to initiate micturition Increased bladder capacity and residual urine Overflow incontinence, no urgency No bladder reflex activity Infection risk high Voiding is possible only by crede maneuver Cystometrogram shows low pressure and no emptying contraction Causes: Cauda equina syndrom,Conus medullaris Spinal shock


LESION INVOLVING AFFERENT SENSORY NEURONS SENSORY NEUROGENIC BLADDER Impaired bladder sensation Initiation of micturition is possible c/o urinary retention or overflow incontinence Infection risk high If bladder not voided at timely basis  overdistension of bladder Bulbocavernosus & anal reflexes absent Causes: Tabes dorsalis Neuropathies mainly small fibers: DM, Amyloidosis


LESION INVOLVING EFFERENT MOTOR NEURONS MOTOR PARALYTIC BLADDER bladder tone flaccid, sensation intact c/o Painful retention of urine or impaired bladder emptying Inability to initiate or maintain micturition bladder capacity and residual urine markedly increased infection risk high Bulbocavernosus & anal reflexes absent Causes: Lumbosacral meningomyelocele, tethered cord syndrome Extensive pelvic surgery or trauma Lumber spinal stenosis

Nocturnal enuresis: 

Nocturnal enuresis Involuntary discharge of urine in night after the age at which bladder control should have been established Prevalence at 5 yr is 7% for male and 3% for female, at 10 yr 3% for male and 2% for female and at 18 yr 1% for male and rare for female Nocturnal enuresis is caused by three interacting pathogenetic mechanisms High arousal thresholds Nocturnal polyuria ( diuresis-dependent enuresis) Nocturnal detrusor over-activity ( detrusor dependent Enuresis) Diuresis-dependent enuresis is usually not combined with overt day-time bladder dysfunction In detrusor-dependency careful history-taking usually reveals the day-time incontinence, urgency symptoms.

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STROKE and voiding dysfunction 2 mechanisms: decreased sensation or awareness of bladder filling and inability to suppress bladder contraction Incontinence after stroke is frequently transitory and upto 80% recover and being continent at 6 months ( Brocklehurst JC et al 1985) Sakakibara R et al(1996) found that Urinary symptoms in 53% patients. Pts. with urinary symptoms had significantly more lesions located in the frontal lobe, Urodynamics: detrusor overactivity(MC). Detrusor areflexia can also be seen,esp in acute cerebral shock. (Burney Tl et al1996 Presence of post stroke incontinence within first wk is an indicator of a more severe CVA and independent risk factor for poor outcome at 3 months ( Patel M, et al J Am Geriatr Soc 2001; Petterson R et al . J Am Geriatr Soc 2006)


The cause of urinary incontinence in dementia probably is multifactorial. Functional incontinence is major cause. It refers to incontinence that is not derived from an abnormality in the lower urinary tract or its innervation, but from immobility, gait disorder, cognitive disability, and decreased motivation, overactive bladder (OAB)is a also major cause .two major etiologies for DO have been proposed: central and peripheral. Peripheral detrusor msl change and central This is secondary to loss of cortical inhibition of primitive bladder reflex contractions Detrussor overactivity found in 58% (AD), 91% (VAD) and 50% (both) (Mori et al 1999) Del-Ser et al (1996) found that the onsetof urinary incontinence was significantly earlier in patientswith DLB (3.2 years after dementia onset) than in patients with Alzheimer’s disease (6.5 years after dementia onset ) DEMENTIA

Normal pressure hydrocephalus: 

In NPH, Incontinence is late feature. Failure of CSF to flow into the parasagittal subarachnoid space (where most fluid resorption occurs) as the most likely mechanism Distortion of central portion of corona radiata and Periventricular white matter by distended ventricals which anatomically includes sacral motor fibers that innervate legs and bladder, thus explaining abn gait and incontinence urdynamic parameters consistent with detrusor overactivity in 95% pts.(Sakakibara et al 1996) Improvement in urodynamic function has been demonstrated within hours of lumbar puncture in patients with NPH. Normal pressure hydrocephalus

Parkinson disease: 

Voiding dysfunction in 35 to 70% of patients urinary sym began approx.5 years after onset of motor symptoms (wing et al 2006). MC Hypothesis is basal ganglia have an inhibitory effecton the micturition reflex, and with neuronal loss in the substantia nigra, detrusor hyper-reflexia develops. MC symptoms frequency,nocturia, urgency, and urge incontinence Urodynamics: detrusor overactivity in filling phase(MC), Pseudodyssnergia may occur d/t delay in ext sphinter relaxation. Bladder sensation preserved Bladder symptoms are correleted with extent of dopamine depletion, neurologic disability and with stage of disease(araki and kuno 2000) Moderate doses of levodopa alleviated detrusor overactivity but high doses aggravated it.(Benson et al 2001) Recently, DBS of the subthalamicnucleus (STN-DBS) improved voiding dysfunction in PD patients .( Herzog J et al. Brain2006) Parkinson disease


Urinary dysfunction is a prominent autonomic feature (more than 90%)and may precede overt neurological involvement by 4-5 years The most frequent urinary symptom was difficulty voiding in 79% of the patients, followed by nocturnal urinary frequencyin 74%., urgency incontinence in 63%, diurnal urinary frequency in 45%, nocturnal enuresis in 19%, and urinary retention in 8% ( Sakakibara R, et al J Neurol NeurosurgPsychiatry 2000; 68: 65–9 .) Pathophysiology : affects several location in CNS BO is caused by neuronal loss in pons Incomplete bladder emptying is caused by loss of parasympathetic innervation due to neuronal degeneration in the IML AHC loss in onuf’s nucleas results in denervation of the EUS Sympathetic nerve atrophy causes non -functional bladder and an open bladder neck Rx anticholinergics for urinary urgency and frequency,desmopressin for nocturnal polyuria , uroselective α- blockersand cholinergic stimulants for voiding difficulty, and CIC for large PVR. MSA

Spinal Cord Lesions: 

Detrusor areflexia( spinal shock) at initial insult but progress to hyperreflexic and DSD over few weeks C fiber emerge as major afferent mediate mechanosensitivity forming abnormal sacral segmental reflex resulting in automatic voiding c/o urgency frequency incomplete bladder emptying , interrupted stream, difficulty in initiating micturition In the patient with a neurologic midthoracic (usually with a lesion above T6) or higher spinal lesion, autonomic dysreflexia may occur secondary to loss of supraspinal inhibitory control of thoracolumbar sympathetic outflow and result from massive discharge of the sympathetic system Autonomic dysreflexia is an exaggerated sympathetic response to any stimuli below the level of the lesion Spinal Cord Lesions

Multiple sclerosis: 

Interruption of the reticulospinal pathways between thepontine and sacral micturition centers may cause DSD plaques located in the spinal afferents and efferents of the sacral reflex arc may inhibit bladder contraction and therefore result in impaired emptying or urinary retention Intracranial plaques may result in loss of voluntary control of initiation or prevention of voiding Urodynamics : ( Litwiller Seet al . J Urol 1999; 161: 743–57). MC is DH,( 50-90% of patients with MS). Upto 50% of patients have DSD-DH Detrusor areflexia occurs in 20-30% of cases Multiple sclerosis

Diabetic cystopathy: 

10 or more years after the onset of DM  D/t autonomic and peripheral neuropathy No exact data on the prevalence, incidence, and risk factors diabetic cystopathy are available Most patients with a diabetic neurogenic bladder show prominent signs of other long-term diabetic complications Bladder dysfunction appears to be related to the severity of diabetes, not to its duration( Buck AC 1988) C/f –initially loss of sensation of bladder filling followed by loss of motor function Urodynamics-elevated residual urine, decreased bladder sensation, impaired detrusor contractility, and, eventually, detrusor areflexia, +_DHIC also seen Rx-CIC, long-term indwelling catheterization, or urinary diversion. Yoshimura N et al .Recentadvances in understanding the biology of diabetes-associatedbladder complications and novel therapy. BJU Int 2005; 95: 733–8 . Diabetic cystopathy

Description of Terminology : 

Description of Terminology Voiding symptoms: hesitency , slow stream, straining to void, terminal dribbling & feeling of incomplete emptying. Storage symptoms: frequency, urgency, urge incontinence and nocturia Urinary retention: is the inability of the urinary bladder to empty. The cause may be neurologic or nonneurologic . Urinary frequency: voiding more than 7 times during day and more than once in night Am J Obstet Gynecol. 2009 May; 200(5): 552.e1–552.e7. Causes are excess fluid intake, detrusor overactivity , inadequate emptying, bladder hypersensitivity & psychogenic Urinary incontinence: involuntary loss of urine that is objectively demonstrable & is a social or hygenic problem (Abraham P et al 2002) Urgency: extreme desire to void Urge incontinence: incontinence associated with an urge to void

Description of Terminology : 

Description of Terminology Nocturia : interruption of sleep by urge to void Overflow incontinence: involuntary passage of urine at a greater than normal bladder capacity. Due to impaired detrusor contractility: drugs, peripheral n injury, old age, myogenic injury Outflow obstruction: BPH, urethral stricture, prostate cancer Stress incontinence: incontinence because of increase in intraabdominal pressure Causes: trauma after birth, pelvic surgery, vaginal wall hypermobility,irradiation , meningomyelocele , epispadias DH: OAB symptoms due to a suprapontine neurologic disorder. The detrusor & sphincter function in coordination. DSD-DH: overactive bladder symptoms due to neurologic UMN disorder of the suprasacral spinal cord. Paradoxically, the patient is in urinary retention; they are in dyssynergy (lack of coordination). Detrusor areflexia : is complete inability of the detrusor to empty due to a lower motor neuron lesion ( eg , sacral cord or peripheral nerves

Clinical evaluation - History: 

Clinical evaluation - History Urinary symptoms: onset, frequency, stream, initiation, termination, ablity to stop on command, vol of urine passed H/O of spinal injury or surgery and meningomyelocele Low backache, lower limb paresis, sensory sympt. PD, CVA, MS Drugs: anticholinergics and α adrenergics Sexual and bowel dysfunction & Other autonomic symptoms Genitourinary symp: UTI, reflux, stones,surgery Obstetric history: no. of deliveries, prolapse uterus Voiding diary: 3-5 day voiding diary is most helpful 24 hour urinary output, Number of voids, Voiding interval, Diurinal distribution, Timing and trigger of incontinence

Laboratory Studies: 

Urinalysis and urine culture- UTI can cause irritative voiding symptoms and urge incontinence. Urine cytology- carcinoma-in-situ of the urinary bladder causes symptoms of urinary frequency and urgency BUN and creatinine are checked if compromised renal function is suspected. MRI spine and brain Radiological evaluation of upper urinary tract Laboratory Studies


Urodynamic studies are necessary to document type of bladder dysfunction( grade of recommendation A) Measurement of urine flow rate Measurement of post-void residual volume Cystometry during filling and voiding Video-cystometry Urethral pressure profile measurement Assessment of pelvic floor neurophysiology ASSESMENT OF LOWER URINARY TRACT

Patient passes urine as naturally as possible in commode of flow-meter It produce a graphical print out with an analysis of max and average flow rate, time to reach max flow & voided vol. It should be combined with an USG measurement of post void residual vol. A significant neurogenic bladder disorder is unlikely if pt has good bladder capacity, N urine flow rate and empties to completion: 

Patient passes urine as naturally as possible in commode of flow-meter It produce a graphical print out with an analysis of max and average flow rate, time to reach max flow & voided vol. It should be combined with an USG measurement of post void residual vol. A significant neurogenic bladder disorder is unlikely if pt has good bladder capacity, N urine flow rate and empties to completion URINARY FLOWMETRY


UROFLOMETRY Normal values for uroflowmetry Gender Age Flow rate (ml/sec) Male  40  22 40-60  18  60  13 Female  50  25  50  18

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The bladder was filled (top trace) at 50 mL per minute (Vinfus) to a total of 300 mL. Detrusor pressure (Pdet) is derived by subtracting pr in the rectum (Pabd) from the measured intravesical pr (Pves). P det=Pabd- Pves First sensation of bladder filling at 100 ml Full capacity is 400-600 ml without an  in pr  15cm H2O (stable bladder) Detrusor overactivity is urodynamic observation characterized by involuntary detrusor contractions during the filling When bladder filling completes, pt voids into flowmeter Urine flow rate depends on both detrusor pr and outlet resistance Normal pr for men:  50cm H2O with flow rate  15ml/sec Normal pr for women:  30cm H2O with flow rate  20ml/sec Cystometry during bladder filling Cystometry

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EMG Ascertain the presence of coordinated or uncoordinated voiding. EMG of EUS may demonstrate DSD Cystoscopy Indicated for people complaining of persistent irritative voiding symptoms or hematuria It can diagnose obvious causes of bladder overactivity, such as cystitis, stone, and tumor, easily Determine etiology of the incontinence and may influence treatment decisions

Combined cystometrograms and sphincter EMG: 

Cystometrograms and sphincter EMG comparing reflex voiding responses in an infant (a) with a voluntary voiding response in an adult (b) and in a paraplegic patient (c) Upper line show bladder pr Lower tracing show sphincter EMG Combined cystometrograms and sphincter EMG

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Detrusor overactivity

Detrusor sphincter dyssynergia: 

Detrusor sphincter dyssynergia

Lower motor neuron bladder: 

Lower motor neuron bladder

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BLADDER OUTLET OBSTRUCTION Det pr >50 with flow rate <10 suggestive of obstruction Det pr >100 confirmed obstruction

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Videourodynamics When cystometry is carried out using a contrast filling medium and the procedure is visualized radiographically Useful to see Reflux into the ureters Thickening of the bladder wall and bladder diverticula. In detecting sphincter or bladder neck incompetence in genuine stress incontinence. Inspect the outflow tract during voiding in patients with suspected obstruction


TREATMENT Non-invasive conservative treatment Minimal invasive treatment Surgical treatment

Lower urinary tract rehabilitation: 

Kegel exercises ( De Ridder D, Acta Neurol Belg 1999 Mar;99(1):61 ,) Rehabilitation technique used to tighten and tone the pelvic floor muscles (ie, levator ani) eliminate urge incontinence.Contraction of the EUS induces reflex bladder relaxation. decrease the frequency of incontinence episodes. Improvement in 3-4 weeks in 56-95% Biofeedback ( McClurg D, et al Neurourol Urodyn 2006;25(4):337-48 .) If difficulty identifying levator ani muscle sensors is inserted in the patient's vagina or rectum and a second sensor is placed on her abdomen. These sensors detect electrical signals from the pelvic floor muscles When the exercises are performed properly, the electric signals from the pelvic floor muscles are registered on a computer screen combined with pelvic floor exercises show a 54-87% improvement Lower urinary tract rehabilitation

Electrical stimulation: 

Stimulation of levator ani muscles using painless electric shocks Electrical stimulation of pelvic floor muscles produces a contraction of the levator ani muscles and EUS while inhibiting bladder contraction. Depends on a preserved reflex arc through the intact sacral micturition center Can be used in conjunction with biofeedback or pelvic floor muscle exercises. Effective in treating female stress incontinence, as well as urge and mixed incontinenc Most beneficial when stress incontinence and very weak or damaged pelvic floor muscles coexist cured or improved patients ranged from 54-77% Stimulation for a minimum of 4 weeks Madersbacher H, Wyndaele JJ, Igawa Y, Chancellor M, Chartier-Kastler E, Kovindha A. Conservative management in neuropatic urinary incontinence. In: Incontinence, 2nd edn. Abrams P, Khoury S, Wein A, eds. Plymouth: Health Publication, 2002; pp. 697-754 . Electrical stimulation

Drugs for detrusor overactivity : 

Anticholinergic are the most useful medications available for neurogenic detrusor overactivity (Level of evidence:1, Grade of recommendation: A). Muscarinic receptor antagonists. Reduce DO and improve bladder compliance Propiverine has both anticholinergic and calcium channel blocking properties & it is better tolerated than oxybutynin (Madersbacher H et al ICS1997 ) Recently, darifenacin and solifenacin have been introduced , but no clinical experience with these drugs in neurogenic bladder overactivity has been published Additional treatment with desmopressin might improve the efficacy of the treatment (valiquette et al Arch Neurol 1996 Dec;53(12):1270-5 ). PDEI demonstrated significant effects upon detrusor overactivity in pilot studies and may become a future alternative or adjunct to anticholinergic treatment Drugs for detrusor overactivity GENERIC NAME DOSE (mg) FREQUENCY Oxybutynin 2.5-5 tds Tolterodine ( selective) 2 bd Trospium chloride 20 bd propiverin 25-150 tds

Drugs for detrusor underactivity : 

Cholinergic drugs, such as bethanechol chloride and distigmine bromide , have been considered to enhance detrusor contractility and promote bladder emptying. The available studies do not support the use of parasympathomimetics because of possible serious possible side effects Combination therapy with a cholinergic drug and an alpha-blocker appears to be more useful than monotherapy There is no drug with evidence of efficacy for underactive detrusor(LOE 2a, Gr of recom B). Drugs for detrusor underactivity

Decreasing bladder outlet resistance : 

Alpha-blockers (non-selective and selective) have been partially successful for decreasing bladder outlet resistance, residual urine and autonomic dysreflexia. (Levelof evidence: 2a, Grade of recommendation: B). Decreasing bladder outlet resistance

Minimal invasive treatment: 

Catheterization Botulinum toxin injections in the bladder Sphincterotomy: Minimal invasive treatment


3 types Indwelling urethral catheters Suprapubic catheters Intermittent catheterization Catheterization usually used for Atonic bladder with overflow incontinence Overactive bladder with detrusor sphincter dyssynergia Catheters

Intermittent catheterization: 

Intermittent self- or third-party catheterization is the gold standard for the Mx of neurogenic bladder, Performed using a short, rigid, plastic catheter Drain the bladder at timed intervals(eg,awakening, every 3-6 hours during the day, and before bed) or based on bladder vol The average adult empties the bladder 4-5 times a day. Thus, catheterization should occur 4-5 times a day Patients should wash their hands with soap and water. Sterile gloves are not necessary Intermittent catheterization

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Advantages Patient autonomy, freedom from indwelling catheter and bags Unimpeded sexual relations Lower rates of infection than the rates noted with indwelling catheters Studies show 1-4 episodes of bacteriuria occur per 100 days of intermittent catheterization performed 4 times a day No bladder contractur e Disadvantages: Urethral trauma Urethral inflammation, and stricture Intermittent catheterization

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GUIDELINES FOR CATHETERIZATION 1. Intermittent catheterization is the standard treatment for patients who are unable to empty their bladder (LOE: 2,Gr of recommendatn: A). 2. Patients should be well instructed in the technique and risks of IC. 3. Aseptic IC is the method of choice (LOE: 2, Gr recommendation: B). 4. The catheter size should be 12-14 Fr (Grade of recommendation: B). 5. The frequency of IC is 4-6 times per day (Gr of recommendation: B). 6. The bladder volume should remain below 400 mL (Gr of recommendation: B). 7. Indwelling transurethral and suprapubic catheterization should be used only exceptionally, under close control, and the catheter should be changed frequently. Silicone catheters are preferred and should be changed every 2-4 weeks, while (coated) latex catheters need to be changed every 1-2 weeks. (Grade of recommendation: A).

Botulinum toxin injections in the bladder : 

Botulinum toxin injections in the bladder most effective minimally invasive treatment to reduce neurogenic detrusor overactivity (Level of evidence: 1, Grade of recommendation: A). Repeated injections seem to be possible without loss of efficacy Del Popolo G, et al. Neurogenic detrusor overactivity treated with English Botulinum Toxin A: 8-year experience of one single centre. Eur Urol 2008 May;53(5):1013-19.

Sphincterotomy : 

Sphincterotomy is the standard treatment for DSD (level of evidence: 2, grade of recommendation A ) Bladder outlet resistance can be reduced without completely losing the closure function of the urethra The laser technique is advantageous Sphincterotomy

Surgical treatment : 

OveractiveDetrusor Detrusor myectomy is an acceptable, when more conservative approaches have failed (LOE: 2,Gr of rec: B). Sacral rhizotomy with Sacral ant root stimulation in complete lesions and sacral neuromodulation in incomplete lesions are effective Rx (GrB). Bladder augmentation is an acceptable option. For the treatment of a severely thick or fibrotic bladder wall, a bladder substitution might be considered ( Underactive Detrusor SARS with rhizotomy and sacral neuromodulation are effective in selected patients (LOE 2, Grade of recommendation: B).. Overactive Urethra (DSD) Sphincterotomy is the standard treatment for DSD (Level of evidence: 2, Grade of recommendation A). Underactive urethra The placement of a urethral sling is an established procedure(Level of evidence: 2, Grade of recommendation: B). Surgical treatment

Conclusions : 

Conclusions Complaints about bladder function are common in patients with neurological disease Neurological evaluation is important to diagnose type of neurogenic bladder Urodynamic studies are important to diagnose detrusor hyperreflexia (DH), detrusor sphincter dyssynergia (DSD), detrusor areflexia and organic outlet obstruction For DH, anticholinergics are primary T/t. For DSD, anticholinergics with α - blocker may be tried along with CIC For detrusor areflexia best therapy is CIC Long term use of indwelling catheters should be avoided