1) The document discusses the nerve supply, reflexes, and evaluation and management of adult neurogenic bladder. It describes the sympathetic, parasympathetic, and somatic innervation of the bladder and how different types of lesions can result in overactive or underactive bladder. 2) Evaluation involves a neurological exam, bladder diary, lab tests, imaging like ultrasound, and urodynamic studies to characterize the type of neurogenic bladder and rule out complications. 3) Management depends on the type of neurogenic bladder and aims to protect the upper urinary tract while achieving continence and quality of life. It may involve conservative measures, medications, procedures like botulinum toxin injection, or surgeries like augmentation cyst

1. ADULT NEUROGENIC BLADDER
Dr.Roshan V Shetty
Senior Resident
Department of Urology
AJIMS&RC
Mangaluru

4. NERVE SUPPLY
SensoryMotor
• Sympathetic Parasympathetic
T11, T12, L1, L2 Most
Filling of Bladder
• Parasympathetic Sympathetic
S2, S3, S4(nerve erigentes) Few
Emptying of Bladder
• Somatic
Pudendal nerve
Voluntary control of micturition

5. Peripheral Afferent(Sensory)
Pelvic nerve afferents consist of the following 2 fibers:
• Myelinated A-delta fibers:
* Mediating normal micturition sensitive to gradual distention of the urinary
bladder
• Unmyelinated C-fibers:
*Under normal conditions: do not respond to bladder distention.
*Various pathological conditions including
– SCI: Chemoreceptors and mechano-sensitive nociceptors from the bladder and urethra
become hyperactive and can cause hyper-reflexic bladder and urinary incontinence.

7. Peripheral efferent innervation(motor)
• Sympathetic pathways:-
– Originate from the T11-L2
– Travel through inferior-mesenteric / hypogastric plexus and
hypogastric nerve to reach the Pelvic plexus
– Inhibit the bladder body and excite the bladder base and proximal
urethral sphincter
• Parasympathetic nerves:
– Emerge from the S2-4
– Pass via pelvic nerves to the pelvic plexus
– Excite the bladder and relax the urethral sphincter
• Sacral somatic pathways:
– Emerge from the S2-4 (Onuf’s nucleus)
– Form pudendal nerve
– Efferent fibres of which excite the distal striated urethral sphincter
causing its contraction.

8. REFLEXES
STORAGE REFLEXES
SYMPATHETIC STORAGE REFLEX SOMATIC STORAGE REFLEX
(Bladder afferent loop reflex) (Guarding reflex)

9. -Urine storage mechanism.
-Reflex activation triggered by afferent
activity induced by distention of
the urinary bladder.
stimulating α1 adrenergic receptors
in the urethral smooth muscle
: -> promotes closure of the
urethral outlet
stimulating β3 adrenergic receptors
in the detrusor smooth muscle
: -> inhibits neurally mediated
contractions of the bladder
SYMPATHETIC STORAGE REFLEX (Bladder afferent loop reflex)

10. • SOMATIC STORAGE REFLEX (Guarding
reflex)
During normal urine storage this pathway is tonically
active.
-A more rapid somatic storage reflex: during sudden
unexpected increase in bladder pressure like
coughing , sneezing or straining, it becomes
dynamically active to contract the rhabdosphincter.
-Alterations in these mechanisms may develop in
neurogenic bladder dysfunction.
-Direct activation of these reflexes by electrical
stimulation of the sacral spinal nerve roots (sacral
neuromodulation) forms the basis of treatment.

11. • SOMATIC MICTURITION REFLEX -
(urethra to bladder reflex)
To aid normal unhindered voiding-
In response to urethral fluid flow,
sensory nerves in the wall of the
urethra send afferent inputs
through the pudendal nerve to
the sacral spinal cord.
This aids voiding by –
-initiating bladder contractions in
the quiescent bladder
-augmenting bladder contractions
already underway
-suppressing sphincter activity

13. Central Nervous System
Periaqueductal Grey
Afferent information regarding fullness
of bladder
Pontine Micturition Centre
Lateral Region- Storage
Medial region - Evacuation
Frontal Lobe
Inhibition of Micturition Until its socially feasible

15. International Continence Society

16. Classification of Neurogenic Bladder
1)Lesions above PMC (e.g. stroke or brain tumor)
producing uninhibited bladder
2)Lesions between PMC & Sacral spinal cord (e.g., traumatic SCI or MS involving
cervicothoracic spinal cord)
producing an UMN bladder
3)Sacral cord lesions that damage detrusor nucleus but spare pud;N
producing a mixed type A bladder (detrusor areflexia)
4)Sacral cord lesions that spare detrusor nucleus but damage pud;N
producing mixed type B bladder (Flaccid sphincter)
5) Sacral cord or Sacral nerve root injuries
producing an LMN bladder
UMNL
LMNL

18. Suprapontine
Suprasacral
Sacral
ALZHEIMER’S
PARKINSON’S
CVA/STROKE
BRAIN TUMOUR
MYELOMENINGOCOELE
SPINAL CORD INJURY
SPINAL STENOSIS
MULTIPLE SCLEROSIS
DIABETES
PELVIC SURGERY
PELVIC CRUSH INJURY
HERPES ZOSTER

19. Suprapontine
-Detrusor Overactivity
-Reduced sensation.
-Low capacity bladder.
(due to reduction of inhibition of PMC by cortical &
subcortical structure damage)
-Co-ordinated sphincter.
-Risk of UUT damage is less.

20. Suprasacral
Detrusor Over-activity
DESD
Risk of renal damage is High
Sensation Normal  Increased
If higher than T6 – Autonomic Dysreflexia

21. Sacral
Detrusor Areflexia/Flaccid sphincter
Poor Bladder Compliance
Smooth Sphincter fixed, Non relaxing
Striated sphincter fixed
Sensation can be normal  increased
Mixed Type A Mixed Type B Sacral Nerve
root injuries

22. Neurogenic bladder can lead to…
• N-LUTS
• Lower urinary tract infections
• Urinary retention/Urinary tract obstructions
• Upper urinary tract infections
• Serious systemic illnesses including septicemia & ARF
• NDO may cause incontinence, which not only leads to
embarrassment, depression & social isolation but also may lead to
skin decubiti, urethral erosions & upper urinary tract damage.

23. Symptoms URGENCY/FREQUENCY/UI HESITANCY, DIFFICULTY TO
PASS URINE, RETENTION,
OI
Signs Bladder -Normal Bladder -Distended
Muscle tone LL Spastic Hypotonic
DTR Exaggerated Sluggish/Absent
Plantar Extensor Flexor
Lesion Above Sacral cord Sacral Cord/ Cauda equina
UMN LMN

24. Neuro-urological Evaluation
Dorsher PT, et al. Advances in Urology. Volume 2012, Article ID 816274, 16 pages.
QOL

27. Neuro-urological Evaluation
• Voiding diary with voiding pattern, fluid intake & voiding issues
• Neurological examination
– Mental status,
– Reflexes,
– Strength & Sensation (including sacral dermatomes)
to determine if there are neurologic conditions present that may contribute to
voiding dysfunction

29. Neuro-urological Evaluation
• Mechanical causes such as prostate enlargement or bladder prolapse can be found on urologic exam
that may impact voiding function
• Issues with
– cognition,
– hand strength & coordination,
– joint contractures, mobility,
– sexuality, social/medical support
other factors may impact type of bladder rehabilitation that is feasible for a given patient
• For SCI patients:
– Motor level of spinal lesion,
– Whether injury is complete or incomplete,
– Extremity tone, rectal sensation/tone, presence/absence of voluntary rectal tone
– Bulbocavernosus reflex should be determined

31. In Spinal Cord Injury patients
Spinal Shock
• Bladder becomes Atonic
• Some form of Bladder drainage has to be initiated- IDC/SPC/CISC
• As peripheral reflex excitability gradually returns, urodynamic evaluation should
be performed
• A cystogram is needed to rule out reflux.
• The UDS should be repeated every 3 months as long as spasticity is improving
and then annually to check for complications of the upper urinary tract.
• A fluid intake of at least 2–3 L/day should be maintained (100–200 mL/h) to
avoid infection.
• Ambulate patient, elevate head end.

32. Lab Evaluation
• Urinalysis
• Urine culture & sensitivity
• Serum BUN/creatinine
• Creatinine clearance

33. Ultrasound
• Non-invasive means of determining urine post-void residual
volumes, especially if precise measurement is not required
• Bladder wall thickness
• Changes in renal Parenchyma
• Prostatomegaly +/-
• Congenital anomalies

34. Post-void residual (PVR) urine
• PVR urine volume involves transurethral catheterization to measure residual urine
volume in bladder immediately after voiding to determine ability of the bladder to
empty completely
• PVR determination should always be performed after discontinuing Foley
catheterization or before instituting intermittent catheterization as part of a bladder
retraining program

35. Post-void residual (PVR) urine
• PVRs are necessary to prevent overdistension of bladder & determine frequency of
catheterization that is needed to keep residual urinary volumes under approximately
100 cc
• Abnormal residual volumes have been defined by volumes greater than 100 cc or
greater than 20% of voided volume & residual urine volumes under 100 cc are
associated with reduced risk of development of bacterial cystitis.

36. UFR evaluation
• Non-invasive way to quantify urinary flow, defined as volume of urine voided per
unit of time
• Urine flow is dependent on force of detrusor contraction as well as urethral
resistance
• Urine flow rate patterns are not diagnostic, but high flow rates are often seen with
neurogenic detrusor overactivity & poor flow rates may reflect weak detrusor
pressure and/or urinary outlet obstruction

37. Urodynamic evaluation
• Urodynamic evaluation should be completed to assess urinary
function, including:
1. Uroflowmetry
2. Bladder cystometrogram/electromyogram (CMG/EMG)
3. DLPP measurement
4. Urethral pressure profile (UPP)
5. Video UDS/Ambulatory UDS

38. Robert C. McDonough. Hospital Physician. 2007; 14 Part1.
Urodynamic study demonstrating detrusor instability

39. Robert C. McDonough. Hospital Physician. 2007; 14 Part1.
Urodynamic study: Detrusor–external sphincter dyssynergia

41. Differential Diagnosis
• Cystitis
• Chronic Urethritis
• Vesical Irritation Secondary to Psychic Disturbance
• Interstitial Cystitis
• Cystocele
• Bladder Outlet Obstruction

42. Management
• The primary aims for treatment of neuro-urological symptoms,
and their priorities, are
– protection of the UUT
– achievement (or maintenance) of urinary continence
– restoration of LUT function
– improvement of the patient’s QoL.
Other considerations are the patient’s disability, cost-effectiveness,
technical complexity and possible complications.

43. Treatment
Non-invasive conservative
Minimally invasive
Surgical
Neuro-Urological rehabilitation
Drug treatment
Assisted Bladder emptying Bladder Neck and urethral procedures
Denervation, deafferntiation, Sacral
neuromodulation
Bladder covering by striated muscle
Bladder Augmentation
Urinary Diversion

44. After evaluation
• Neurogenic Overactive Bladder
• Neurogenic Areflexic Bladder

45. Neurogenic Overactive Bladder
Reasonable Bladder Capacity
• Rehabilitate the bladder to a functional state
• Being able to go 2–3 hours between voiding and be continent during this interval.
• Voiding is initiated using trigger techniques
-tapping the abdomen suprapubically;
-tugging on the pubic hair;
-squeezing the penis;
-scratching the skin of the lower abdomen, genitalia, or thighs.
• Some patients in this category can empty the bladder completely but are incontinent due to
inconvenient triggering of the voiding reflex.
• They may be helped by low-dose anticholinergic medication or by neural stimulation.

46. Markedly Diminished functional Vesical Capacity <100 mL
• Involuntary voiding can occur as often as every 15 minutes.
• Satisfactory training of the bladder cannot be achieved, and alternative measures must be taken.
• Rule out reduced FBC is not due to a large residual volume of urine.
• One of the following treatment regimens can then be administered
– A permanent indwelling catheter +/-anticholinergic medication.
– A condom catheter and a leg bag in males if residual urine volumes are small and the patient does not have
bladder pressures >40 cm of water on UDS .
– Performance of a sphincterotomy in males( Last resort)
– Conversion of the spastic bladder to a flaccid bladder through sacral rhizotomy.
– Neurostimulation of the sacral nerve roots to accomplish bladder evacuation.
– Urinary diversion for irreversible, progressive upper urinary tract deterioration.

47. Muscarinic receptor antagonists/ B3 agonists
• First Line for N-Detrusor overactivity blocking the muscarininc receptors in the
bladder
• Long term use unfavaourable due to adverse effects
– Tolteridine
– Oxybutyinin
– Probanthine
– Darifenacin/Solifenacin
– Mirabegron

48. Intravesical Instillation of Medications
• Capsaicin and resiniferatoxin
• C-fiber afferent neurotoxins
• Clinical use Limited
Neurostimulation (Bladder Pacemaker)

49. Botulinum-A Toxin
• Injecting of 100–300 units of botulinum-A toxin into 30–40 sites in the bladder in adults who have
detrusor hyperreflexia.
• Intravesical injection of botulinum toxin resulted in improvement in medication refractory overactive
bladder symptoms.
• Risk of increased PVRU and symptomatic urinary retention was significant.
• ICS recommends in patients resistant to Anitmuscarinic agents

50. Neurogenic Areflexic Bladder
• If the neurologic lesion completely destroys the micturition center, volitional voiding
cannot be accomplished without manual suprapubic pressure.
• Bladder evacuation can be accomplished by straining, using the abdominal and
diaphragmatic muscles to raise intraabdominal pressures.
• Partial injuries to the lower spinal cord (T10–11) result in a spastic bladder and a
weak or weakly spastic sphincter. Incontinence can then result from spontaneous
detrusor contraction

51. Bladder Training and Care
In partial lower motor neuron injury, voiding should be tried every 2 hours by the clock to avoid
embarrassing leakage.
This helps protect the bladder from overdistention due to a buildup of residual urine.
Intermittent Catheterization
Extremely satisfactory solution to the problems of the flaccid neuropathic bladder
Surgery
TUR - Hypertrophy of the bladder neck or an enlarged prostate,
-To weaken the outlet resitance
Complete urinary incontinence due to sphincter incompetence can be managed by
– implanting an artificial sphincter
– Bladder neck and posterior urethral reconstruction also may be considered as a way to increase
outlet resistance
Parasympathomimetic Drugs
• Symptomatic treatment of the milder types of flaccid neuropathic bladder if proven on UDS

52. COMPLICATIONS OF NEUROGENIC BLADDER
• Infection
• Hydronephrosis
• Calculus
• Renal Amyloidosis
• Sexual Dysfunction
• Autonomic Dysreflexia
• Malignancy

53. Follow up
• The UUT should be checked by ultrasonography at regular
intervals in high-risk patients X once every 6 months
• Physical examination and urine laboratory X every year
• A UDS should be performed as a diagnostic baseline, and
repeated yearly.
• The increased prevalence MIBC in neuro-urological patients
also warrants longterm follow-up.

54. Conclusions
• Neuro-urological disorders have a multi-faceted pathology.
• Extensive Workup and specific diagnosis
• Treatment individualized to Medical, Physical condition and
patients future expectations
• Close surveillance Life Long
Golden rule: as effective as needed, as non-invasive as possible.

55. References
• EAU guidelines 2020
• Smith & Tanagho General Urology 18th edition
• Campbell Textbook of Urology 11th edition
• Dorsher PT, et al. Advances in Urology. Volume 2012

56. Thank You