Bladder, Micturition,Neurological control and disturbances, management

1. Dr Ashwin Lathiya
SR neurology
GMC Kota
Neurological control of Micturition Order
and Disorder

2. OUTLINE OF THE PRESENTATION
 Anatomy & Physiology of micturition
 Terminology
 Classification of neurogenic bladder
 Various disease and bladder
 Diagnosis
 Management
 Take home

3. ANATOMY OF URINARY BLADDER
 Bladder divides into two parts:
[1] body and [2] base
 Body of the bladder is composed of
smooth muscle k/a detrusor muscle
 Base of the bladder is comprised of
Trigone, a triangular area at posterior
wall of bladder
Bladder neck ,which opens into
urethra.

4. Internal sphincter:
• Involuntary smooth muscle at bladder neck
• Absent in females
External sphincter:
• Skeletal muscle, voluntary control
• In urogenital diaphragm
 Superior and Inferior vesical artieries branches of ant. trunk of internal
iliac
 Internal iliac veincommon iliacIVC
 External iliac nodes

6. Nerve Detrusor Internal
sphincter
External
sphincter
Final effect
Parasympathetic
(Pelvic n= Nervi
Erigentis)
Contraction Relaxation Not supplied Emptying of
bladder
Sympathetic
(Hypogastric n)
Relaxation Contraction Not supplied Filling of bladder
Somatic
(Pudendal n)
Not supplied Not supplied Contraction Voluntary
control
of micturition

7.  Sensations of pain, temp, urgency 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.  Block et al. --PET studies
 1. PMC/Berrington’s nucleus/M region--in rostral pontine tegmentum;
voiding of urine.
 2. Pontine storage centre/L region--located ventrolateral to PMC;
inhibits micturition.
 3. PAG
 4.Anterior and caudal hypothalamus
 5.Insula
 6.Anterior cingulate cortex
 7.Locus ceruleus
 8.Medial frontal cortex(right inferior frontal gyrus)-seat of attention and
response selection; selects socially appropriate place for micturition.

11. PHYSIOLOGY
 Function --to store and expel urine in a coordinated, controlled
fashion, regulated by the central and peripheral nervous systems.
 Bladder capacity changes throughout person's life.
 In children, bladder volume: (years of age + 2) x 30mL
 Wall pressure of 5 to 15 mmHg--sensation of bladder fullness
 >30 mmHg-- painful

12. Amount of Urine
<50 ml Residual volume
250 ml First desire
>400 ml Urgency
>600 ml Painful urgency
800-900 ml Physiological capacity
1000 ml Anatomical capacity

13.  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.

14. STORAGE SYMPTOMS
 Increased daytime frequency--if he voids too often by day. =Pollakisuria
 Nocturia--if has to wake at night one or more times to void.
 Urgency--sudden compelling desire to pass urine which is difficult to defer.
 Urinary incontinence--any involuntary leakage of urine.
 Stress urinary incontinence--involuntary leakage on effort or exertion, or
on sneezing or coughing.
 Urge urinary incontinence--involuntary leakage accompanied by or
immediately preceded by urgency.
 Mixed urinary incontinence--involuntary leakage associated with urgency
and also with exertion, effort, sneezing or coughing.

15. VOIDING SYMPTOMS
 Slow stream--perception of reduced urine flow, usually compared to
previous performance.
 Intermittent stream (Intermittency)--when flow stops and starts, on one or
more occasions, during micturition.
 Hesitancy--difficulty in initiating micturition resulting in delay in the onset
of voiding after pt is ready to pass urine.
 Straining to void--muscular effort used to either initiate, maintain or improve
the urinary stream.
 Terminal dribble--prolonged final part of micturition, when the flow has
slowed to a trickle/ dribble.

16. POST MICTURITION SYMPTOMS
 Feeling of incomplete emptying
 Post micturition dribble--involuntary loss of urine immediately after he
has finished passing urine, usually after leaving the toilet.

17.  Detrusor hypereflexia=OAB: Involuntary detrusor contraction
symptoms due to a suprapontine neurologic disorder. The
detrusor & sphincter function in coordination.
• Detrusor sphincter dyssynergia: is defined as detrusor
contraction concurrent with involuntary contraction of the
urethral and/or periurethral striated muscle.
• Detrusor areflexia:Is complete inability of the detrusor to
empty due to lower motor neuron lesion ( eg , sacral cord or
peripheral nerves injury)

18. CLASSIFICATION

19. LAPIDES CLASSIFICATION
Level of lesion Bladder
1.Loss of supraspinal control Uninhibited bladder
2.Spinal cord lesion above sacral level Automatic
3.Spinal cord lesion involving sacral level Autonomous
4.Lesion involving afferent neurons Sensory neurogenic bladder
5.Lesion involving efferent neurons Motor paralytic bladder

20. UNINHIBITED BLADDER
LOSS OF SUPRASPINAL CONTROL
 Results from injury to corticoregulatory tract exerting
inhibitory control on PMC
 Lesions above pons.
 Frequency, urgency & urge incontinence.
 Micturition is usually precipitous and complete.
 Low or absent residual volume
 Bladder behaves like infants  urine voided anytime
anywhere without control
 Causes: CVA, frontal tumors, parasagittal meningioma, ACA
aneurysm, NPH, PD, Demyelinating disease

21. REFLEX NEUROGENIC BLADDER(AUTOMATIC)
SPINAL CORD LESION ABOVE SACRAL LEVEL
 Post–spinal shock second stage of recovery.
 Hyperactive micturition reflex with loss of voluntary
control  small amount of urine collected in the bladder
elicits the micturition reflex
 Bladder tone increased, capacity reduced
 No residual urine
 Causes: spine cord injury, compressive myelopathy,
myeilitis, syringomyelia

22. AUTONOMOUS BLADDER
SPINAL CORD LESION INVOLVING SACRAL LEVEL
 Spinal cord injury that causes complete motor and sensory
impairment of the bladder from the sacral cord.
 Bladder tone flaccid, sensation absent.
 Inability to initiate micturition.
  bladder capacity and residual urine.
 Overflow incontinence, no urgency.
 Voiding possible only by maneuver.
 Causes: Cauda equina syndrome,Conus medullaris.

23. SENSORY NEUROGENIC BLADDER
LESION INVOLVING AFFERENT SENSORY NEURONS
 Selectively interrupt the sensory fibers from the bladder to
spinal cord or from the afferent tract to the brain
 Impaired bladder sensation painless distention
 Initiation of micturition is possible.
 If bladder not voided at timely basis l/t over distension of
bladder
 Bulbocavernosus & anal reflexes absent
 Causes: Tabes dorsalis
Neuropathies mainly small fibers: DM, Amyloidosis

24. MOTOR PARALYTIC BLADDER
LESION INVOLVING EFFERENT MOTOR NEURONS
 Disease processes that affect parasympathetic motor
innervation of the bladder.
 Inability to initiate or maintain micturition.
 Bladder sensations intact.
 c/o Painful retention of urine or impaired bladder
emptying.
  Bladder capacity, residual urine, infection.
 Bulbocavernosus & anal reflexes absent
 Causes: Lumbosacral meningomyelocele,
Extensive pelvic surgery or trauma ,
Lumber spinal stenosis
Herpes zoster

25. STROKE
 Acute presentation: Urinary retention; mecha. not clear but pheno
termed “cerebral shock’’
 Chronic presentation: Freq, Urg, Incontinence
 Incontinence after stroke is frequently transitory and upto 80%
recover and being continent at 6 months
 Frontal lobe and internal capsule lesion: Detrusor overactivity and
increased rate of uninhibited sphincter relaxation
 Brainstem stroke: Obstructive voiding symptom and retention.
 Urodynamics: Detrusor overactivity (MC). Detrusor areflexia can
also be seen, esp in cerebellar lesion or in acute phase related to
cerebral shock.

26. DEMENTIA
 Cause of incontinence is multifactorial.
 Functional incontinence not derived from abnormality in the
lower urinary tract or its innervation, but from immobility, gait
disorder, cognitive disability, decreased motivation, rigidity,
spasticity.
 Onset of urinary incontinence significantly earlier in DLB (3.2
years after dementia onset) than in AD (6.5 years after dementia
onset ) Del-Ser et al (1996)
 Detrussor overactivity found in 58% (AD), 90% (VAD) (Mori et al 1999)

27. NORMAL PRESSURE HYDROCEPHALUS
 Incontinence is late feature.
 Mechanism: Failure of CSF to flow into the parasagittal
subarachnoid space (where most fluid resorption occurs).
 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: detrusor overactivity in 95% pts.
 Improvement in urodynamic function has been demonstrated
within hours of lumbar puncture in patients with NPH.

28. PARKINSON DISEASE
 Prevalence -38% and 71%
 LUTS- most common nonmotor symptom (Martinez et al 2007)
 Urinary symptoms began approximately 5 years after onset of motor
symptoms (wing et al 2006).
 MC Hypothesis is basal ganglia have inhibitory effect on the
micturition reflex, and with neuronal loss in the substantia nigra,
detrusor hyper-reflexia develops
 MC symptoms freq, nocturia, urgency, and urge incontinence
 Urodynamics: detrusor overactivity in filling phase.
 Bladder symptoms are correlated with extent of dopamine depletion,
neurologic disability and with stage of disease.
 DBS of the subthalamic nucleus improved voiding dysfunction.

29. MSA
 Urinary dysfunction is a prominent autonomic feature (more than
90%)and may precede overt neurological involvement by 4-5 years
 Difficulty voiding (79%)
 Nocturnal urinary frequency (74%),
 Urgency, Urg incontinence(63%),
 Nocturnal enuresis (19%)
 Urinary retention (8%)
 Pathophysiology : Affects several location in CNS-
1. BO--by neuronal loss in pons
2. Incomplete bladder emptying--by loss of parasympathetic innervation
due to neuronal degeneration in the intermediolateral 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 open
bladder neck

30. SPINAL CORD LESIONS
 Detrusor areflexia ( spinal shock) at initial insult but progress to
hyperreflexic and DSD over few weeks
 c/o urgency, frequency, incomplete bladder emptying , difficulty
in initiating micturition.
 In neurologic mid thoracic (above T6 or higher) lesion--
autonomic dysreflexia occur secondary to loss of supraspinal
inhibitory control of thoracolumbar sympathetic outflow l/t
massive discharge of the sympathetic system.
 Autonomic dysreflexia is exaggerated sympathetic response to
any stimuli below the level of the lesion.

31. MULTIPLE SCLEROSIS
 32% to 96%
 Interruption of the reticulospinal pathways between the pontine
and sacral micturition centers cause DSD
 Plaques located in the spinal afferents and efferents of the sacral
reflex arc inhibit bladder contraction and result in impaired
emptying or urinary retention
 Intracranial plaques result in loss of voluntary control of
initiation or prevention of voiding
 Urodynamics :
1.MC is DH ( 50-90% of patients with MS).
2.Upto 50% of patients have DSD-DH
3.Detrusor areflexia in 20-30% of cases

32. DIABETIC CYSTOPATHY
 10 or more years after the onset of DM
 D/t autonomic and peripheral neuropathy
 Most patients have other long-term diabetic complications.
 C/f –Initially loss of sensation of bladder filling followed by loss
of motor function
• Urodynamics-- bladder sensation,  residual urine, impaired
detrusor contractility, and later detrusor areflexia
• Rx-CIC.

33. HERNIATED DISC
 Slow and progressive herniation of the lumbar disc-- nerve
irritation and DH
 Acute compression of the sacral roots d/t deceleration trauma --
prevent nerve conduction and result in detrusor areflexia
 Displaced disc material have direct neurotoxic and vascular
effects on spinal nerve roots, which is unrelated to compressive
effects.
 Unilateral and less severe sensory loss--more favorable
prognosis, while persistent sensory deficits suggest that bladder
contractility may not completely recover.

34. MICTURITION SYNCOPE
 Reflex syncope (neurally mediated syncope)
 Cardiovascular reflexes become intermittently inappropriate, in
response to trigger, resulting in vasodilatation and bradycardia
l/t fall in BP and global cerebral hypoperfusion.
 Middle-aged man using vasodilators or after drinking alcohol;
absent prodrome.
 Tilt table test.
 Recognition and avoidance of trigger.

35. HISTORY
Do you feel to pass urine urgently? With passing of
few drops en route to bathroom?
Urgency and urge
Incontinence
Do you feel to pass urine more frequently than
before?
Increased frequency
Do you wake up frequently in night to pass urine? Nocturia
Do you have problem in initiating urine? Hesitancy
Do you feel few drops of urine keep passing without
your knowledge?
Urinary dribbling
Do you feel you have not passed urine completely? Incomplete bladder
emptying
Have you started wearing pads? Incontinence
Is there a burning sensation while initiating
micturition?
Burning micturition
Is there small amount of passage of urine during
laughing, coughing, sneezing or any other physical
Stress incontinence

36.  H/o spinal injury or surgery or meningiomyelocele
 H/o Low back ache, lower limb paresis
 H/o CVA, PD, MS
 Sexual and bowel dysfunction & Other autonomic symptoms
 Obstetric history: No. of deliveries, Prolapse uterus
 Medicine H/o: antidepressants, diuretics, bronchodilators, and
antihistamines a/w LUTS

37. EXAMINATION
 Neurological exam-- mental status, bulk, tone, power, reflexes and
sensation (including sacral dermatomes)
 Spinal cord injury-- motor level of spinal lesion, extremity tone and
bulbocavernosus reflex
 Rectal exam to assess prostate size and consistency for a gross estimate
of the degree of BPH
 Abdominal exam after voiding to:
•Assess for palpable bladder- present with incomplete emptying
•Assess for abdominal mass- that cause pressure on the bladder

38. INVESTIGATIONS
 Urine- UTI can cause irritative voiding symptoms and urge
incontinence.
 Urine cytology- carcinoma-in-situ of the urinary bladder cause
frequency and urgency
 voiding diary-daily record of the patient's bladder activity; objective
documentation of the patient's voiding pattern, incontinent episodes,
and inciting events a/w incontinence.
 MRI spine and brain
 Radiological evaluation of upper urinary tract

39.  Diagnostic Procedures:
 PVR
 Uroflow rate
 Filling cystometrogram
 Voiding cystometrogram (pressure-flow study)
 EMG
 Cystoscopy
 Videourodynamics

42. ABRAHAMS-GRIFFITHS (AG) NOMOGRAM
AG no. (BOOI) =pdetQmax – 2Qmax
BJU International, Volume: 84, Issue: 1, Pages: 14-15, First published: 25 December 2001, DOI: (10.1046/j.1464-410x.1999.00121.x)

43. TYPICAL URINE VOIDING CURVES

44. TREATMENT
 Non-invasive conservative treatment
 Minimal invasive treatment
 Surgical treatment

45. MANAGING STORAGE DYSFUNCTION
1. Antimuscarinic agents,
2. β3- receptor agonists,
3. Desmopressin,
4. Botulinum toxin, and
5. Tibial neuromodulation

46.  ANTIMUSCARINIC AGENTS:
 first-line management for overactive bladder, including urge
incontinence.
 MOA: Competitive antagonist at muscarinic receptors l/t
detrusor relaxation and lower intravesical pressures.
 S/E:Dry mouth, blurred vision for near objects, constipation, and
tachycardia, alterations in cognition and consciousness
 Caution: Elderly, risk of fall (trospium chloride or darifenacin-
less impact on cognition)

48.  β3-RECEPTOR AGONISTS--Mirabegron
 FDA approved in 2012 for OAB
 25-50 mg daily
 S/E: Palpitations, raised blood pressure rarely, atrial fibrillation.
 Devoid of anticholinergic s/e

49.  DESMOPRESSIN
 MOA: synthetic analogue of arginine vasopressin, temporarily
reduces urine production by promoting fluid reabsorption at the
time of renal excretion.
 For the treatment of nocturia in MS, providing symptom relief
for up to 6 hours, as well as for managing nocturnal polyuria.
 S/E: hyponatremia or fluid overload.
 Caution: Older age, dependent leg edema.
 C/I:CrCl<50ml/min

50.  BOTULINUM TOXIN
 2nd line for neurogenic detrusor overactivity–related incontinence
 Approved dose: 200 units of onabotulinumtoxinA via flexible or rigid
cystoscopy as 20 to 30 injections into the bladder wall
 Effect lasts 8 to 11 months
 Caution: Risk of urinary retention; before undergoing treatment,
patients should be counseled about the possibility of requiring to use a
catheter.
 Age>65, dependent leg edema
 Contraindications:
 Absolute: active urinary tract infection and hypersensitivity to the
toxin or its components.
 Relative: Pregnancy, and concomitant use of drugs that affect the
neuromuscular junction (i.e.,aminoglycosides).

52.  TIBIAL NEUROMODULATION.
 Safe and effective treatment for mild-moderate OAB symptoms
 Percutaneous vs Transcutaneous
 Fixed-frequency electrical signal(200 msec pulses with a pulse
rate of 20 Hz) for 30-min outpatient treatment sessions once a
week for a period of 12 weeks.
 Advantage: Does not worsen voiding difficulties or increase the
postvoid residual, unlike other treatments such as antimuscarinic
agents or botulinum toxin.
 Effects are relatively short-lived

53. MANAGING VOIDING DYSFUNCTION
 PVR exacerbate overactive bladder symptoms and render
antimuscarinics and botulinum toxin less effective, Predispose to UTI
 Clean Intermittent self catheterization- 4 to 6 times per day
 Incidence of symptomatic UTI is low when intermittent catheterization
is performed regularly.
 Reflex voiding using trigger techniques and the Crede maneuver not
recommended
 Supra pubic vibration using a mechanical “buzzer” -MS with
incomplete bladder emptying and detrusor overactivity –effect is
limited
 Alpha-blockers relax internal urethral sphincter in men improve bladder
emptying and reduce PVR.
 Botulinum into the external urethral sphincter may improve bladder
emptying in patients with spinal cord injury who have significant
voiding dysfunction.

54. DRUGS FOR DETRUSOR UNDERACTIVITY
 CHOLINERGIC DRUGS: Bethanechol chloride and
Distigmine bromide;  detrusor contractility and promote
bladder emptying.
 Usual dose: 10 to 50 mg 3 to 4 times daily PO.
 Available studies do not support use because of possible serious
possible s/e
 Combination with cholinergic drug and alpha-blocker more
useful than monotherapy
 No drug with evidence of efficacy for underactive detrusor

55. DECREASING BLADDER OUTLET RESISTANCE
 ALPHA-BLOCKERS:for decreasing bladder outlet resistance,
residual urine and autonomic dysreflexia.
 MOA: Prostate smooth muscle relaxation l/t increased flow
 Used in men with retention d/t BPH
 DOXAZOSIN (1):  average PVR from 65 mL to 8 mL
 Dose:1 mg OD; titrate by doubling daily dose at 1- to 2-wk
intervals up to 8 mg OD based on response and tolerability (max:
8 mg/day)
 TAMSULOSIN:  incontinence episodes,  urine flow rate and
 post void residual volume
 Initial and Maintenance dose: 0.4 mg once daily.

57. SURGICAL TREATMENT
 Overactive Detrusor:
 Detrusor myectomy if conservative approaches failed
 Sacral rhizotomy with Sacral ant root stimulation in complete lesions
and sacral neuromodulation in incomplete lesions are effective Rx
 Bladder augmentation for severely thick or fibrotic bladder wall
 Underactive Detrusor
 SARS with rhizotomy and sacral neuromodulation are effective in
selected patients
 Overactive Urethra (DSD)
 Sphincterotomy is standard treatment for DSD
 Underactive urethra
 Placement of a urethral sling is established procedure.

60. TAKE HOME
 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.

61. REFERENCES
 Panicker J, DasGupta R. Bradly’s Neurology in clinical
practice.7th Ed. Elsevier 2016.Chapter 47: Neurourology. p 605-
621.
 Corcos J, Ginsberg V, Karsenty G. Textbook of Neurogenic
bladder (3rd Ed).
 Continuum (minneap minn) 2020;26(1, autonomic
disorders):178–199.
 International continence society guidlines.
 Abrams P, Cardozo L, Fall M, et al: The Standardisation of
Terminology of Lower Urinary Tract Function: Report from the
Standardisation Sub-committee of the International Continence
Society. Neurourol Urodyn 21: 167-178, 2002

62. THANK YOU