Neuro Urology and The Neurogenic Bladder

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Neuro Urology and The Neurogenic Bladder

1. 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 . 
2. Non Neurogenic bladder refers to dysfunction of the urinary bladder due to dynamic disturbance of genitourinary system. 
Micturition Pathway
3. detrusor muscle of the bladder is innervated by parasympathetic neurons located in the S2-S4  column
4. internal uretheral sphincter at the neck of the bladder receives its innervation from the intermediolateral column at the T12–L1 level, via the sympathetic prevertebral plexus and the hypogastric nerve.
5. In response to stretch, afferent impulses are carried to the sacral spinal cord. 
6. Sacral cord projections to the PAG (Periaqueductal grey) are relayed to the pontine micturition center (Barrington’s nucleus) in the dorsomedial pontine tegmentum, near the locus caeruleus, which sends descending fibers to the preganglionic parasympathetic motoneurons in the sacral cord innervating the bladder. 
7. The pontine micturition center is under the control of centers in the forebrain
8. Descending impulses activate the efferent centers in the sacral cord, causing contraction of the detrusor muscle and relaxation of the internal sphincter.
9. Forebrain lesions may cause loss of voluntary bladder control but do not affect the spinobulbo-spinal reflex mechanisms. 
10. Disruption of the bulbospinal pathway from the pontine micturition center to the sacral cord, and lesions affecting the afferent and efferent connections between the bladder and the conus medullaris, may cause severe disturbances in bladder function.
11. Symptoms of bladder dysfunction 
○ Frequency, urgency, precipitate micturition, massive or dribbling incontinence, difficulty in initiating urination, urinary retention, and loss of bladder sensation may occur.
12. Type and Localization of Bladder Dysfunction 
 ○ Loss of supraspinal control – uninhibited bladder 
 ○ spinal cord lesion above sacral level reflex neurogenic bladder – automatic bladder 
 ○ spinal cord lesion involving sacral level – autonomous bladder 
 ○ lesion involving afferent sensory neurons -sensory neurogenic bladder 
 ○ lesion involving efferent motor neurons -motor paralytic bladder 
13. Loss of Supraspinal Control –Uninhibited neurogenic bladder
• there is a loss of the cortical inhibition of reflex voiding 
• Lesions of CNS involving area above pons 
• bladder tone remains normal
• Bladder distention causes contraction in response to the stretch reflex. 
• Micturition is usually precipitous and complete 
• There is frequency, urgency, and incontinence that are not associated with dysuria. 
• 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
14. Spinal Cord Lesion Above Sacral Level – Reflex neurogenic bladder
○ occurs with severe myelopathy or extensive brain lesions causing interruption of both the descending autonomic tracts to the bladder and the ascending sensory pathways above the sacral segments of the cord. 
○ 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
○ bladder capacity is small, and micturition is reflex and involuntary. 
15. Spinal Cord Lesion Involving Sacral Level- Autonomic neurogenic bladder 
• one without external innervation. 
• 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 
• It is caused by neoplastic, traumatic, inflammatory, and other lesions of the sacral spinal cord, conus medullaris or cauda equina and with congenital anomalies such as spina bifida, spinal shock
• There is destruction of the parasympathetic supply. 
• contractions occur as the result of stimulation of the intrinsic neural plexuses within the bladder wall.
• The amount of residual urine is large, but the bladder capacity is not greatly increased
16. Lesion Involving Afferent Sensory Neurons- Sensory paralytic bladder
• found with lesions that involve the posterior roots or posterior root ganglia of the sacral nerves, or the posterior columns of the spinal cord. 
• Sensation is absent, and there is no desire to void. 
• There may be distention, dribbling, and difficulty both in initiating micturition and in emptying the bladder. 
• 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
• There is a large amount of residual urine.
17. Lesion Involving Efferent Motor Neurons –Motor paralytic bladder 
• develops when the motor nerve supply to the bladder is interrupted. 
• 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 
• The bladder distends and decompensated, but sensation is normal. 
18. Receptors and Innervation of Bladder
• 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
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 
Urgency: extreme desire to void 
Urinary incontinence: Involuntary loss of urine that is objectively demonstrable & is a social or hygenic problem 
Nocturia : Interruption of sleep by urge to void  
Outflow obstruction: BPH, urethral stricture, prostate cancer
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 Hyperreflexia(DH): involuntary detrusor contraction symptoms due to a suprapontine neurologic disorder. 
Detrusor Sphincter Dysynergia (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
20. Type of Urinary Incontinence 
Stress-Urine loss during activities such as coughing, sneezing, laughing or lifting. 
Urge-A sudden need to urinate, occasionally with large volume urine loss. Can also exist without incontinence (Urgency)
Overflow– A frequent dribble of urine as a result of inefficient bladder emptying symptoms are similar to stress incontinence. 
Mixed– stress + urge forms. 
Functional– Urine loss not associated with any pathology or problem in the urinary system
Bladder Involvement in specific conditions 

21. Bladder function in Cortical Lesions
• Intracranial tumors, damage after rupture of an aneurysm, penetrating brain wounds, and prefrontal lobotomy subjects
• 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
22. Bladder function in 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 
• Urodynamics: detrusor overactivity (MC). 
• Detrusor areflexia can also be seen,esp in acute cerebral shock.
• 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 
23. Bladder function in 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)   
• 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 )
24. Bladder function in 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.
• Improvement in urodynamic function has been demonstrated within hours of lumbar puncture in patients with NPH
25. Bladder function in Parkinson disease: 
• Voiding dysfunction in 35 to 70% of patients 
• Urinary symptoms began approximately 5 years after onset of motor symptoms 
• 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
• Moderate doses of levodopa alleviated detrusor overactivity but high doses aggravated it.
• Recently, DBS of the subthalamic nucleus (STN-DBS) improved voiding dysfunction in PD patients 
26. Bladder function in 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
27. Bladder function in 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 :
○ 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
28. Bladder function in 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
29. Clinical evaluation of Bladder function
• History: 
○ Urinary symptoms: 
○ Onset: Etiology 
○ Sense of bladder filling: Motor/Sensory/Cortical 
○ Can they feel urine passing: Afferent Neuraxis 
○ Can they stop urine passing in midstream at will: Efferent Neuraxis 
○ Does bladder leak continually or suddenly pass large volume: OI/DSD/Sensory 
○ Initiation: CORTEX/OUTLET 
○ Termination : CORTEX/OUTLET 
○ Ablity to stop on command : CORTEX 
○ Volume of urine passed : LMN/UMN 
○ H/O of spinal injury or surgery and meningomyelocele, Low backache, lower limb paresis, sensory sympt. 
○  Drugs: anticholinergics and αadrenergics Sexual and bowel dysfunction & Other autonomic symptoms 
○ Genitourinary symp: UTI, reflux, stones,surgery Obstetric history: no. of deliveries, prolapse uterus
30. 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
31. Drugs for detrusor overactivity 
• Anticholinergic 
• Muscarinic receptor antagonists. 
• Propiverine has both anticholinergic and calcium channel blocking properties & it is better tolerated than oxybutynin 
32. Drugs for detrusor underactivity 
• Cholinergic drugs, such as bethanechol chloride and distigmine bromide , 
•  There is no drug with evidence of efficacy for underactive detrusor(LOE 2a, Gr of recom B).
33. Catheters: 
• Indwelling urethral catheters 
• Suprapubic catheters
• Intermittent catheterization 
• Catheterization usually used for 
○ Atonic bladder with overflow incontinence  
○ Overactive bladder with detrusor sphincter dyssynergia
• Intermittent catheterization is the standard treatment for patients who are unable to empty their bladder 
• Aseptic IC is the method of choice 
• frequency of IC is 4-6 times per day 
• bladder volume should remain below 400 mL 
• 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.

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