Urinary bladder clinical anatomy, neurophysiology, approach to bladder dysfunction and management.
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Added: May 07, 2024
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Bladder Neurology Speaker : Dr. Reshma Moderator : Dr Enna Sondhi
Clinical Anatomy
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.
Internal Sphincter Smooth muscle Involuntary control Sympthetic (T11 - L2) [Hypogastric nerve] - Through alpha-1 receptors causes Contraction of internal sphincter
External Sphincter Skeletal muscle Voluntary control Innervated by Somatic nervous system (S2,S3,S4) [Pudendal nerve] - Through Nicotinic receptors (NT - Ach)
Parasympathetic CENTRE: S2-S4 in intermediolateral column SUPPLY THROUGH: Pelvic splanchnic nerves NEUROTRANSMITTER : ACh via M3 Bladder detrusor contraction Internal sphincter relaxation
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
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
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.
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.
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:
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
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.
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.
Voiding Reflex If :- 1.afferent signals from the bladder are sufficiently strong 2. voiding is safe 3. voiding socially appropriate Then cortical inhibition decreases.
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 -
Neurogenic Bladder Classification
Hald and Bradley Supraspinal lesion Suprasacral spinal lesion Infrasacral lesion Peripheral autonomic neuropathy Muscular lesion On the basis of Neuroanatomy
Lancet Neurology Vol 14 July 2015
Lapides Classification
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
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
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.
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
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
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
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).