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Neurogenic Bladder

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Neurogenic Bladder

  2. 2. OUTLINE • Introduction • Applied anatomy and physiology • Neuraxis and circuitry • Common symptoms of neurogenic bladder • Levels of bladder dysfunction • Investigations • Treatment available
  3. 3. 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 . • Non Neurogenic bladder refers to dysfunction of the urinary bladder due to dynamic disturbance of genitourinary system. • Complaints about bladder function are >common in patients with neurological disease • 98% of lifetime bladder is in storage phase
  4. 4. ANATOMY • The UB is a smooth muscle chamber • Composed of two main parts: (1) BODY (2) NECK • Bladder Muscle is Detrusor muscle- Smooth muscle. • Trigone : Small triangular area ,Immediately above the bladder neck. • The bladder neck is 2 to 3 cm long, and its wall is composed of detrusor muscle interlaced with a large amount of elastic tissue. Muscle in this area is called Internal sphincter. Its natural tone normally keeps the bladder neck and posterior urethra empty of urine • Posterior urethra- lower part of the bladder neck ( because of its relation to the urethra) • External urethral sphincter :- Voluntary skeletal muscle ( Other entirely smooth muscle). The external sphincter muscle is under voluntary control of the nervous system and can be used to consciously prevent urination even when involuntary controls are attempting to empty the bladder. • Capacity:- Is about 300 ml with a maximum capacity of 500 ml
  5. 5. Efferent innervation NERVE ACTION FUNCTION Parasympathetic S2,3,4 Pelvic nerve(nervi erigentes) – hypogastric plexus Detrusor muscle contraction Internal sphincter relaxation Voiding Sympathetic T11-L2 Hpogastric nerves ---inferior hypogastric ganglion Detrusor muscle relaxation Internal sphincter Contraction Storage Somatic :FROM AHC- S-2,3,4 Pudendal nerve (ventral rami) Voluntary innervations initiate or inhibits micturition through cortical control Voluntary control Afferent innervation Parasympathetic S= 2,3,4 Pudendal nerve –enter through posterior rami and terminate in anterolateral column Sensation of pain and distension conveyed from bladder wall and internal capsule Carried normal sensation Sympathetic (T9 L2) Hypogastric plexus:enter through posterior rami and terminate in anteromediolateral column T9-L2 Sensation of painful distension conveyed from bladder wall Carried painful sensation
  6. 6. INNERVATION Afferent innervation :- • PNS(S 2,3,4) --Pudendal nerve –enter through posterior rami and terminate in anterolateral column • Sympathetic (T10- L2)-- Hypogastric plexus:enter through posterior rami and terminate in anteromediolateral coulmn Efferent innervation:- Parasympathetic: S2-S4 ––> pelvic plexus (Pelvic nerve=nervi erigentes) ––> cholinergic postganglionic fi bers ––> bladder + sphincter • Sympathetic: T10-L2 ––> hypogastric/ pelvic plexus ––> noradrenergic postganglionic fibers ––> smooth muscle of bladder base, internal sphincter, proximal urethra • Somatic: (AHC S2,S3,4) ––> pudendal nerve (ventral rami)––> external sphincter
  7. 7. RECEPTORS & INNERVATION • Detrusor - intermediolateral gray column of S2,3,4 parasympathetic – pelvic n (M2 receptors) • External urethral sphincter - innervated by somatomotor S2,3,4 nucleus (Onuf’s Nucleus)-pudendal n (Nicotinic receptor) • Trigone and internal sphincter innervated by Sympathetic T10,11,12 (less important) • SNS acts through B2 and A1 receptors Afferent Pathways • Sensations of pain, temp, urgency is follows the anterolateral 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
  8. 8. NEURAXIS • Frontal lobe- Sends inhibitory signals • Pons (Pontine Micturition Center=PMC) – Major relay/excitatory center – Coordinates urinary sphincters and the bladder – Affected by emotions • Spinal cord (S2-4)-Intermediary between upper and lower control • Peripheral nervous system- Parasympathetic (S2-S4)-Pelvic nerves Excitatory to bladder, relaxes sphincter Somatic (S2-S4)-Pudendal nerves -Excitatory to external sphincter Sympathetic (T10-L2) – Hypogastric nerves to pelvic ganglia – Inhibitory to bladder body, excitatory to bladder base/urethra
  9. 9. Central neural control PET studies Blok et al . Brain 1998 1.CORTEX – increased blood flow • During storage During micturition Mid cingulate gyrus Rt Inferior frontal gyrus Lat bilateral frontal lobes Rt. Anterior cingulate gyrus Periaqueductal gray matter (PAG) 2.PONS • 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 ventrolateral pontine tegmentum was activated (L region)
  10. 10. Innervations Afferent • Somatic: pudendal nerve • Visceral: sympathetic and parasympathetic fibers (sensation of fullness) Efferent • Parasympathetic: S2-S4 ––> pelvic plexus ––> cholinergic postganglionic fibers ––> bladder + sphincter • Sympathetic: T10-L2 ––> hypogastric/ pelvic plexus ––> noradrenergic postganglionic fibers ––> smooth muscle of bladder base, internal sphincter, proximal urethra • Somatic: S2-S3 ––> pudendal nerve ––> external sphincter
  11. 11. Central neural controlPET studies Blok et al . Brain 1998 • Successful voiders–Rt Inferior frontal gyrus Rt Ant cingulate gyrus • Pontinemicturition center- M region • Unableto void – Mid cingulate gyrus Lat bilateral frontal lobes • Pontinestoragecenter - L region PAG
  12. 12. Peripheral Nervous System • Parasympathetic (S2-S4) – Pelvic nerves • Excitatory to bladder, relaxes sphincter • Somatic (S2-S4) – Pudendal nerves • Excitatory to external sphincter • Sympathetic (T10-L2) – Hypogastric nerves to pelvic ganglia – Inhibitory to bladder body, excitatory to bladder base/urethra • Afferents through Pelvic, pudendal, hypogastric by A-delta fibers – Micturition reflex, stretch and fullness sensation C-fibers – Noxious sensation
  13. 13. FUNCTION OF BLADDER Function Balance between suprasacral modulating pathways, sacral cord and the pelvic floor Emptying phase: “Voiding Reflex” Series of coordinated eventsSeries of coordinated events involving outlet relaxation,involving outlet relaxation, detrusor contractiondetrusor contraction Storage phase: “Guarding reflexes” constant afferent input to maintain continence
  14. 14. Normal Voiding Normal Voiding • SNS primarily controls bladder and the IUS – Bladder increases capacity but not pressure – Internal urinary sphincter to remain tightly closed – Parasympathetic stimulation inhibited • PNS:-Immediately prior to PNS stimulation, SNS is suppressed Stimulates detrusor to contract Pudendal nerve is inhibited →external sphincter opens → facilitation of voluntary urination • Somatics (pudendal N) regulate EUS,Pelvic diaphragm Delaying voiding or voluntary voiding: • When an individual cannot find a bathroom nearby, the brain inhibit PMC to prevent detrusor contractions & actively contract the levator muscles to keep the external sphincter closed • Thus , voiding process requires coordination of both the ANS and somatic nervous system, which are in turn controlled by the PMC located in the brainstem.
  15. 15. DEVELOPMENT IN ADULT • In child Controlled by • Sacral spinal cord reflex • Newborns void 20 x/day with only a slight decrease during the 1st year of life • Bladder capacity increases & voiding frequency decrease with growth Bladder capacity in Ounces (30ml) = Age (yrs) +2 • 1-2 yrs: conscious sensation of bladder fullness develops • 2-3 yrs: Ability to initiate or inhibit voiding voluntarily develops • 2-4 yrs: Voiding comes under reliable voluntary control • By age 4 Micturition spinal reflex fully modulated by CNS micturition center via a spinobulbospinal tact • Initially child has better control over external sphincter than bladder Cortical Diencephalic Mechanism PMC Spinal tract NeuronSpinal efferent Mechanism Ganglia BLADDER A afferentC afferent COLD Perineal stimulation
  16. 16. MICTURITION(VOIDING) REFLEX Sensation of bladder fullness via pelvic and pudendal nerves to S 2,3,4 Frontal lobe decides social appropriateness Periaqueductal gray matter RECIPROCAL ACTIVITY BETWEEN SPHINCTER & DETRUSSOR Medial Pontine micturition center Onuf’s nucleus to pudendal nervesDetrussor center (S 2,3,4) to pelvic nerves Micturition
  17. 17. STORAGE REFLEXES Passive low level phenomena mediated by a spinal reflex
  18. 18. Description of Terminology Storage - At low pressure until such time as it is convenient and socially acceptable to void Voiding - Initiated by inhibition of the striated sphincter and pelvic floor, followed some seconds later by a contraction of the detrusor muscle. • Storage Problem: Failure to Store normal volumes of urine at low pressure & without leakage – Non compliant bladder -Irritable bladder – Inadequate sphincter tone during filling • Emptying Problem: Failure to empty completely, on command, efficiently at low pressures – Failure of neurological control of bladder -Bladder muscle failure – Failure of sphincter relaxation during voiding • Voiding symptoms: Storage symptoms Hesitency Frequency Slow stream Urgency Straining to void Urge incontinence Terminal dribbling Nocturia Feeling of incomplete emptying.
  19. 19. Description of Terminology • Hesitency: Difficulty to initiate micturition • 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.) • Urgency: extreme desire to void • Urinary incontinence: Involuntary loss of urine that is objectively demonstrable & is a social or hygenic problem (Abraham P et al 2002) • Nocturia : Interruption of sleep by urge to void • Outflow obstruction: BPH, urethral stricture, prostate cancer
  20. 20. Description of Terminology • Overflow incontinence: Involuntary passage of urine at a greater than normal bladder capacity. Due to impaired detrusor contractility OR A frequent dribble of urine as a result of inefficient bladder emptying : drugs, peripheral nerve injury, old age, myogenic injury • Stress incontinence: Incontinence because of increase in intra abdominal pressure Causes: trauma after birth, pelvic surgery, vaginal wall hypermobility,irradiation , meningomyelocele , epispadias • DETRUSOR HYPEREFLEXIA(DH): OAB ;involuantary detrusor contraction symptoms due to a suprapontine neurologic disorder. The detrusor & sphincter function incoordination. • DETRUSOR SPHINCTER DYSSYNERGIA(DSD)-: 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 injury) • AUTONOMIC DYSREFLEXIA: Is an exaggerated sympathetic response to any stimuli below the level of the lesion
  22. 22. Reflexic –Spastic /uninhibited/UMN Areflexic - autonomous/flaccid/LMN Sensory characteristics No inhibitions influence time & place of voiding Bladder empties in response to stretching of bladder wall characteristics Bladder acts as if there were paralysis of all motor functions characteristics lack of sensation of need to urinate clinical manifestations -Incontinence -frequency -urgency -voiding is unpredictable and incomplete clinical manifestations Fills without emptying Retention Dribbling incontinence Clinical manifestations Poor bladder sensation , Infrequent voiding of large residual volume causes :- corticospinal tract lesion observed in SCI/stroke/multiple sclerosis/brain tumor/brain trauma causes:- lower motor neuron lesion cuased by trauma involving S2-S4 lesions of cauda equina/pelvic nerves causes:- damage to sensory limb of bladder spinal reflex arc seen in multiple sclerosis/diabetes mellitus
  23. 23. Type of Urinary Incontinence 1.Stress-Urine loss during activities such as coughing, sneezing, laughing or lifting. 2.Urge-A sudden need to urinate, occasionally with large volume urine loss. Can also exist without incontinence (Urgency). 3.Overflow- A frequent dribble of urine as a result of inefficient bladder emptying symptoms are similar to stress incontinence. 4.Mixed- stress + urge forms. 5.Functional- Urine loss not associated with any pathology or problem in the urinary system.
  24. 24. TYPE OF BLADDER + + + + + + + + + + + + 0 + 0 0 + + + + 0+ + + DSD DI/OI DA
  25. 25. 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, PD, Demyelinating disease
  26. 26. 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
  27. 27. 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 maneuver • Cystometrogram shows low pressure and no emptying contraction • Causes: Cauda equina syndrome,Conus medullaris Spinal shock
  28. 28. 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 over distension of bladder • Bulbocavernosus & anal reflexes absent • Causes: Tabes dorsalis Neuropathies mainly small fibers: DM, Amyloidosis
  29. 29. 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 
  30. 30. CORTICAL LESION • Intracranial tumors, damage after rupture of an aneurysm, penetrating brain wounds, and prefrontal lobotomy subjects (Andrew and nathan 1964). patients with right frontal lobe disorders who had urinary retention and in whom there was restoration of voiding when the frontal lobe disorder was treated successfully (Fowler 1999). • DH with coordinated urethral sphincter is MC • c/ o urinary frequency, urgency, and urge incontinence • First-line treatment for detrusor hyperreflexia includes anticholinergic medication
  31. 31. STROKE • 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)
  32. 32. DEMENTIA: • 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 muscle change and central is secondary to loss of cortical inhibition of primitive bladder reflex contractions • Detrussor overactivity found in 58% (AD), 90% (VAD) and 50% (both) (Mori et al 1999) • Del-Ser et al (1996) found that the onset of urinary incontinence was significantly earlier in patients with DLB (3.2 years after dementia onset) than in patients with Alzheimer’s disease (6.5 years after dementia onset )
  33. 33. 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 ventricles which anatomically includes sacral motor fibers that innervate legs and bladder, thus explaining abnormal gait and incontinence • Urodynamic 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.
  34. 34. Parkinson disease: • Voiding dysfunction in 35 to 70% of patients • Urinary symptoms began approximately 5 years after onset of motor symptoms (wing et al 2006). • MC Hypothesis is basal ganglia have an inhibitory effect on 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) Pseudodysnergia may occur d/t delay in ext sphinter relaxation. Bladder sensation preserved. • Bladder symptoms are correlated 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 subthalamic nucleus (STN-DBS) improved voiding dysfunction in PD patients .( Herzog J et al. Brain2006)
  35. 35. MSA • 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 frequency in 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 Neurosurg Psychiatry 2000; 68: 65–9 .) • Pathophysiology : Affects several location in CNS- • 1. BO is caused by neuronal loss in pons • 2. Incomplete bladder emptying is caused by loss of parasympathetic innervation due to neuronal degeneration in the Inter Medio Lateral (IML) column of spinal cord • 3. AHC loss in onuf’s nucleus results in denervation of the EUS • 4.Sympathetic nerve atrophy causes non-functional bladder and an open bladder neck
  36. 36. 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 mechano sensitivity 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 mid thoracic (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
  37. 37. Multiple sclerosis: • Interruption of the reticulospinal pathways between the pontine 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). • 1.MC is DH,( 50-90% of patients with MS). • 2.Upto 50% of patients have DSD-DH • 3.Detrusor areflexia occurs in 20-30% of cases Multiple sclerosis
  38. 38. 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 • Rx-CIC, long-term indwelling catheterization, or urinary diversion. BJU Int 2005; 95: 733–8 .
  39. 39. Herniated disc: • Slow and progressive herniation of the lumbar disc may cause irritation of the sacral Nn. and cause DH • Acute compression of the sacral roots associated with deceleration trauma will prevent nerve conduction and result in detrusor areflexia • Urodynamics – Depends on nerve injury • DA with intact bladder sensation may occur • Internal sphincter denervation may occur • If the peripheral sympathetic nerves are damaged, the IUS will be open and nonfunctional • Striated sphincter, however, is preserved
  40. 40. Herpes zoster • Herpes virus lies dormant in the dorsal root ganglia or the sacral nerves • Sacral nerve involvement leads to impairment of detrusor function • Early stages of herpes infection are a/w frequency, urgency, and urge incontinence • Later stages include decreased bladder sensation, increased residual urine, and urinary retention • Urinary retention is self-limited and will resolve spontaneously with clearing of the herpes infection.
  41. 41. Clinical evaluation - History: • Urinary symptoms: 1.Onset: Etiology help 2.Sense of bladder filling: Motor/Sensory/Cortical 3.Can they feel urine passing: Afferent Neuraxis 4.Can they stop urine passing in midstream at will: Efferent Neuraxis 5.Does bladder leak continually or suddenly pass large volume: OI/DSD/Sensory 6.Frequency: NON NEUROGENIC/NEUROGENIC 7.Stream: NON NEUROGENIC/NEUROGENIC 8.Initiation: CORTEX/OUTLET 9.Termination : CORTEX/OUTLET 10.Ablity to stop on command : CORTEX 11.Volume of urine passed : LMN/UMN 12.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
  42. 42. 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
  43. 43. ASSESMENT OF LOWER URINARY TRACT : • Urodynamic studies are necessary to document type of bladder dysfunction • Measurement of urine flow rate • Measurement of post-void residual(PVR) volume • Cystometry during filling and voiding • Video-cystometry • Urethral pressure profile measurement • Assessment of pelvic floor neurophysiology
  44. 44. INVESTIGATIONS • Noninvasive bladder investigations – Post void residual volume – In out catheterization, – Ultrasound ( N is <100ml) – Uroflowmetry : Voided volume ( >100ml) Maximal flow, maximal and average flow rate (M > 20ml/sec F > 15ml/sec) • Cystometry * Measure detrusor pressure (Intravesical presure – Rectal pressure) * Bladder infused till 400 to 600ml – Pressure should not rise to >15cm water (Stable bladder) * Neurogenic detrusor overactivity – Involutary detrusor contraction during filling phase * Voiding phase – Detrusor pressure M < 50cm water F < 30cm water • Sphincter EMG – Reinnervation with prolonged duration of MUAPs • Neuroimaging – Cauda equina & conus lesions, spinal, supra pontine and pontine lesions
  45. 45. INVESTIGATIONS • 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 • 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
  46. 46. TREATMENT: • Non-invasive conservative treatment – Electrical stimulation – Drugs • Minimal invasive treatment – Catheterization – Botulinum toxin injections in the bladder – Sphincterotomy • Surgical treatment – Detrusor myectomy – Sacral rhizotomy with Sacral ant root stimulation – Sacral neuromodulation – Sphincterotomy
  47. 47. Non-invasive conservative treatment • 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 : Stress incontinence, as well as urge and mixed incontinence • Stimulation for a minimum of 4 weeks Decreasing bladder outlet resistance • Alpha-blockers (non-selective and selective) have been partially successful for decreasing bladder outlet resistance, residual urine and autonomic dysreflexia.
  48. 48. Drugs for detrusor overactivity • Anticholinergic are the most useful medications available for neurogenic detrusor overactivity. • 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 ). • GENERIC NAME DOSE (mg) FREQUENCY • Oxybutynin 2.5-5 tds • Tolterodine ( selective) 2 bd • Trospium chloride 20 bd • propiverin 25-150 tds
  49. 49. 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).
  50. 50. Catheters: • 3 types – Indwelling urethral catheters – Suprapubic catheters – Intermittent catheterization Catheterization usually used for • Atonic bladder with overflow incontinence • Overactive bladder with detrusor sphincter dyssynergia
  51. 51. 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
  52. 52. GUIDELINES FOR CATHETERIZATION • 1. Intermittent catheterization is the standard treatment for patients who are unable to empty their bladder • 2. Patients should be well instructed in the technique and risks of IC. • 3. Aseptic IC is the method of choice • 4. The catheter size should be 12-14 Fr • 5. The frequency of IC is 4-6 times per day • 6. The bladder volume should remain below 400 mL • 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.
  53. 53. TREATMENT • Botulinum toxin injections in the bladder most effective minimally invasive treatment to reduce neurogenic detrusor overactivity • Repeated injections seem to be possible without loss of efficacy • 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
  54. 54. TAKE MY MESSAGE • 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

Editor's Notes

  • The bladder is composed of bands of interlaced smooth muscle (detrusor). The innervation of the body of the bladder is different from that of the bladder neck. The body is rich in beta adrenergic receptors. These receptors are stimulated by the sympathetic component of the autonomic nervous system (ANS). Beta stimulation, via fibers of the hypogastric nerve, suppress contraction of the detrusor. Conversely, parasympathetic stimulation, by fibers in the pelvic nerve, cause the detrusor to contract. Sympathetic stimulation is predominant during bladder filling, and the parasympathetic causes emptying.
    Two sphincters control the bladder outlet. The internal sphincter is composed of smooth muscle like the detrusor and extends into the bladder neck. Like the detrusor, the internal sphincter is controlled by the ANS and is normally closed. The primary receptors in the bladder neck are alpha-adrenergic. Sympathetic stimulation of these alpha receptors, via fibers in the hypogastric nerve, contributes to urinary continence.
    The external sphincter is histologically different from the detrusor and internal sphincter. It is striated muscle. Like skeletal muscle, it&amp;apos;s under voluntary control. It receives its innervation from the pudendal nerve, arising from the ventral horns of the sacral cord. During micturition, supraspinal centers block stimulation by the hypogastric and pudendal nerves. This relaxes the internal and external sphincters and removes the sympathetic inhibition of the parasympathetic receptors. The result is unobstructed passage of urine when the detrusor contracts.
    The ureters pass between the layers of the detrusor and enter the bladder through the trigone. The ureters propel urine into the bladder. The bladder passively expands to accept urine. As the bladder expands and intravesicular pressure increases, the ureters are compressed between the layers of muscle, creating a valve mechanism. This valve mechanism limits the backflow of urine.
    The normal adult bladder can hold about 500 cc of urine. After emptying, the bladder may still retain about 50 cc residual volume. At about 150 cc of volume, stretch receptors in the detrusor begin signaling the CNS via afferent nerves; at 400 cc we are &amp;quot;seeking&amp;quot; an appropriate toilet
    Summary: Normally, we are able to control where and when we void. This is largely because the cerebrum is able to suppress the sacral micturition reflex. If the sacral reflex is unrestrained, parasympathetic stimulation via the pelvic nerve causes detrusor contraction. Detrusor contraction is suppressed by alpha and beta sympathetic stimulation via the hypogastric nerve. In response to afferent stimulation, the cerebrum becomes aware of the need to void. If it is appropriate, the cerebrum relaxes the external sphincter, blocks sympathetic inhibition, the bladder contracts and urine is expelled
  • Typical obstructive symptoms are:
    difficulty in starting to urinate despite pushing and straininga weak stream of urine; several interruptions in the stream
    dribbling at the end of urination
    Bladder changes cause:
    a sudden strong desire to urinate (urgency)
    frequent urination
    the sensation that the bladder is not empty after urination is completed
    frequent awakening at night to urinate (nocturia)
  • The principal nerve supply of the bladder is by way of the pelvic nerves, which connect with the spinal cord through the sacral plexus, mainly connecting with cord segments S-2 and S-4. Coursing through the pelvic nerves are both sensory nerve fibers and motor nerve fibers. The sensory fibers detect the degree of stretch in the bladder wall. Stretch signals from the posterior urethra are especially strong and are mainly responsible for initiating the reflexes that cause bladder emptying.
    Innervation of the urinary bladder and its sphincters : 
    The motor nerves transmitted in the pelvic nerves are parasympathetic fibers. These terminate on ganglion cells located in the wall of the bladder. Short postganglionic nerves then innervate the detrusor muscle. In addition to the pelvic nerves, two other types of innervation are important in bladder function. Most important are the skeletal motor fibers transmitted through the pudendal nerve to the external urethral sphincter. These are somatic nerve fibers that innervate and control the voluntary skeletal muscle of the sphincter.
    Also, the bladder receives sympathetic innervations from the sympathetic chain through the hypogastric nerves, connecting mainly with the L-2 segment of the spinal cord. These sympathetic fibers stimulate mainly the blood vessels and have little to do with bladder contraction. Some sensory nerve fibers also pass by way of the sympathetic nerves and may be important in the sensation of fullness and, in some instances, pain.
    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
    Innervation of male 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)
    Afferent sensation through pelvic n and pudendal n, hypogastric n (Ad and C fibers) to Periaqueductal gray matter pontine micturition center S 2,3,4
    S 2,3,4
    Innervation of male lower urinary tract
  • Periaqueductal gray matter Medial Pontine micturition center Frontal lobe decides social appropriateness Onuf’s nucleus to pudendal nerves Detrussor center (S 2,3,4) to pelvic nerves RECIPROCAL ACTIVITY BETWEEN SPHINCTER &amp; DETRUSSOR Micturition
  • Spinal Cord Lesions:
    Detrusor areflexia at initial insult but progress to hyperreflexic state over time Spinal cord lesions (above T6) DSD –DH and smooth sphincter dyssynergia. A/w autonomic dysreflexia. Autonomic dysreflexia is an exaggerated sympathetic response to any stimuli(instrumentation of bladder /rectum below the level of the lesion(mc cervical ) Rx decompress the rectum or bladder, parenteral ganglionic or adrenergic blocker as chlorpromazine, may be used. Spinal Cord Lesions
    Slide 65:
    Spinal cord lesions (below T6) Detrusor hyperreflexia, striated sphincter dyssynergia, and smooth sphincter dyssynergia but no autonomic dysreflexia. C/o incomplete bladder emptying secondary to dsd, or loss of facilitatory input from higher centers Treatment involves cic and anticholinergic medication
  • 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&amp;apos;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