Urinary bladder clinical anatomy, neurophysiology, approach to bladder dysfunction and management.

1. Bladder Neurology
Speaker : Dr. Reshma
Moderator : Dr Enna Sondhi

2. Clinical Anatomy

3. Detrusor muscle
• Sympthetic (T11 - L2) [Hypogastric nerve] -Via β3-
adrenergic receptors - inhibition and relaxation of the
detrusor muscle
• Parasympathetic (S2,S3,S4) [Pelvic splanchnic nerve] - via
M2/M3 cholinergic receptors (NT - Ach) - contraction of the
detrusor muscle.

4. Internal Sphincter
• Smooth muscle
• Involuntary control
• Sympthetic (T11 - L2) [Hypogastric nerve] -Through alpha-1
receptors causes Contraction of internal sphincter

5. External Sphincter
• Skeletal muscle
• Voluntary control
• Innervated by Somatic nervous system (S2,S3,S4)
[Pudendal nerve] -Through Nicotinic receptors (NT - Ach)

6. Bradley’s Neurology in Clinical Practice, 7th edition, page no. - 606

7. Neuronal control

8. Parasympathetic
• CENTRE: S2-S4 in intermediolateral column
• SUPPLY THROUGH: Pelvic splanchnic nerves
• NEUROTRANSMITTER : ACh via M3
• Bladder detrusor contraction
• Internal sphincter relaxation

9. Sympathetic
• CENTRE: T11-L2 intermediolateral column
• SUPPLY THROUGH: Hypogastric Nerve
• β3- receptors -inhibition and relaxation of the detrusor
muscle.
• Alpha-1 receptors - Contraction of internal sphincter
• Facilitate bladder storage and continence

10. Somatic
• CENTRE: ONUF’S Nucleus in the Ventral horn of S2-S4
• SUPPLY THROUGH: Pudendal Nerve
• NT : Ach, Nicotinic Receptors
• FUNCTION : Controls The External Sphincter

11. Spinal Reflex Arc
• AFFERENT ARC :- Stretching of bladder wall - through the
Pelvic nerve (Parasympathetic ) to the spinal micturition
Center.
• DETRUSOR CENTER :- Sacral segments S2-S4 of the spinal
cord.
• EFFERENT ARC :-Travels through the Pelvic nerve -
contraction of detrusor muscle and relaxation of internal
urethral sphincter.

12. Pontine Micturition Center
• BARRINGTON'S NUCLEUS
• From the pontomesencephalic micturition center, efferents
to the spinal cord descend by way of the reticulospinal
tracts ( located medially and anteriorly in the anterior
funiculus) to the detrusor motor neurons in the
intermediolateral cell columns of the sacral gray matter (S2–
S4).
• Pontine output is excitatory for voiding reflex.

13. Higher Center
• Situated in Prefrontal lobe, Paracentral lobule, Cingulate
gyrus, •Insula.
• Efferents from the cortical and subcortical micturition
centers descend by way of the pyramidal tracts to the
pudendal nuclei (Onuf’s nucleus) in the sacral spinal
cord (S2–S4).
• Cortical input is inhibitory on micturition reflexes.
CORTICAL CENTERS:

14. SUBCORTICAL CENTERS :
Thalamic nuclei, Limbic system, Red nucleus, Substantia
nigra, Hypothalamus, Subthalamic nucleus.
CEREBELLUM :
Anterior vermis of the cerebellum, fastigial nucleus are
concerned with micturition.
Higher Center

15. Gaurding Reflex
First impulse comes at 150ml :- signal from spinal cord via
posterior
column -> PAG -> L region of PONS activates
sympathetic and pudendal nerve, leads to relaxation of
detrusor, constriction of internal urethral sphincter and
constriction of external urethral sphincter.

16. Voiding Reflex
Intense bladder (~450ml) afferent firing in the pelvic nerve
activates spinobulbospinal reflex pathways that pass through
the pontine micturition centre (BARRINGTON'S NUCLEUS)
which is under continuous cortical inhibition.

17. Voiding Reflex
If :-
1.afferent signals from the bladder are sufficiently strong
2. voiding is safe
3. voiding socially appropriate
Then cortical inhibition decreases.

18. Voiding Reflex
• Stimulates the parasympathetic outflow to the bladder and to
the urethral smooth muscle.
• Inhibits pudendaloutflow to the urethral outlet.
• Inhibits the sympathetic outflow to urethral outlet.
And leads to voiding.
This -

19. Neurogenic Bladder
Classification

20. Hald and Bradley
• Supraspinal lesion
• Suprasacral spinal lesion
• Infrasacral lesion
• Peripheral autonomic neuropathy
• Muscular lesion
On the basis of Neuroanatomy

21. Lancet Neurology Vol 14 July 2015

22. Lapides Classification

23. • 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
Uninhibited Bladder

24. Reflex Neurogenic
Bladder
• 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

25. 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.
• Increased bladder capacity and residual urine.
• Overflow incontinence, no urgency.
• Voiding possible only by maneuver.
• Causes: Cauda equina syndrome,Conus medullaris.

26. 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 like DM,
Amyloidosis

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

29. History
• Patients with storage dysfunction complain of frequency for micturition, nocturia, urgency and
urgency incontinence. Urgency, frequency and nocturia, with or without incontinence, is
called the overactive bladder syndrome, urge syndrome or urgency-frequency syndrome
• Patients experiencing voiding dysfunction report hesitancy for micturition, a slow and
interrupted urinary stream, the need to strain to pass urine, and double voiding. Patients may
be in complete urinary retention
• Drug history
• Bladder diary-The bladder diary supplements the history taking and records the frequency for
micturition, volumes voided, episodes of incontinence, and fluid intake over the course of a
few days

30. Bradley’s Neurology in Clinical Practice, 7th edition, page no. - 612

31. I
Investigations-
• Screening for Urinary Tract Infections-urine sample should be sent off to the lab for culture.
• Bladder Scan- It is pertinent to estimate the post void residual urine by ultrasonography.
• It evaluates for evidence of damage such as upper urinary tract dilatation or renal scarring.
• Urodynamic Studies-measurements of urine flow rate and residual volume, cystometry during
both filling and voiding, videocystometry, and urethral pressure profilometry
• Investigations Requiring Catheterization-Cystometry evaluates the pressure-volume
relationship during nonphysiological filling of the bladder and during voiding. The detrusor
pressure is derived by subtraction of the abdominal pressure (measured using a catheter in
the rectum) from the intravesical pressure (measured using a catheter in the bladder).

32. Bradley’s Neurology in Clinical Practice, 7th edition, page no. - 608

33. Management-
Bradley’s Neurology in Clinical Practice, 7th edition, page no. - 617

34. Treatment approach
to neurogenic
bladder dysfunction
Bradley’s Neurology in Clinical Practice, 7th edition, page no. - 620

35. Thank You