Neuropathic bladder disorders

U.B is probably the only visceral smooth muscle organ that is under complete voluntary control from the cerebral cortex. Its smooth muscle arrange in different direction intermingled with each other near the internal meatus they arrange in 3 layers, inner longitudinal, middle circular & outer longitudinal.

The circular muscle end in the bladder neck forming the internal sphincter the others reach the prostatic urethra in male & the distal end of urethra in female The external sphincter is a true sphincter in the prostatic urethra in male & in the mid urethra in female they are supplied by pudendal nerve, when bladder contract to push urine the external sphincter relax voluntarily

The bladder supply by both sensory & motor, the sensory pass to the S2,3&4 segments of spinal cord, the efferent nerves from S2,3,&4 to the bladder through pelvic nerve that initiate muscle contraction. In the bladder sensation of fullness (300-400ml) pass to the spinal cord through sensory impulse which lead to contraction of detrusor through efferent nerves.

to control act of micturition there is inhibitory reflex from cerebral cortex through the spinal cord to inhibit the contraction of smooth muscle of bladder so act of micturition not started until favorable place & time are to start. micturition usually assisted by abdominal muscle contraction.

The micturition reflex Intact reflex pathways via the spinal cord & the pons are required for normal micturition. Afferents from the bladder are essential for activation of the sacral center, which then cause detrusor contraction, bladder neck opening, & sphincteric relaxation. The pontine center through its connection with sacral center, may send either excitatory or inhibitory impulses to regulate the micturition reflex.

Electrical or chemical stimulation of medial pontine micturition center generate contraction of detrusor & relaxation of the external sphincter. Disruption of pontine control, as in upper spinal cord injury, leads to contraction of detrusor without sphincteric relaxation (detrusor – sphincter dyssynergia).

Urodynamic studies Techniques used to obtain graphic recording of the activity of urinary bladder. Uroflowmetry is the study of flow of urine from the urethra. The normal peak flow rate for male 20-25 ml/s & for female 25-30 ml/s. lower flow rate suggest bladder outlet obstruction or weak detrusor.

Cystometry the urodynamic evaluation of the reservoir of urinary bladder normal bladder capacity is 400-500 ml. the 1st desire to void is felt when volume reach 150-200 ml. but the detrusor filling pressure should remain unchanged until there is definite sense of fullness 350-400 ml. the true capacity of bladder.

Detrusor contraction before this point are considered abnormal & the result of hyperreflexic or uninhibited bladder. Normal voiding pressure in the bladder shouldn’t raise above 30 ml of water, with normal voiding there shouldn’t be any residual urine & voiding accomplished without straining. The interference with normal conduction of nerves of the bladder called neurogenic bladder.

Classification of neurogenic bladder according to the level of injury

1-Spastic neuropathic bladder due to lesion above the sacral micturition center Most lesion in the cerebral cortex or spinal cord above the micturition center (S2,3 &4 spinal segment) will cause bladder spasticity. Sacral reflux arcs remain intact but loss of inhibition from higher center.

Common lesions above the brain stem affect voiding include dementia, CVA, multiple sclerosis, tumors, & inflammatory disorders such as encephalitis & meningitis. These lesions can produce urge, frequency, residual urine, retention, recurrent UTI & gross incontinence. In lesion above the pontine micturition center detrusor—sphincter dyssynergia doesn’t occur & leakage may occur because the need to void cannot be felt.

Spinal cord lesion can be result from trauma, herniated intervertebral disc, vascular lesion, multiple sclerosis, syringomyelia or myelitis. May cause sever genitourinary dysfunction. detruso—sphincter dyssynergia may cause detrusor hypertrophy & with time renal function may become compromised.

Clinical finding the severity of symptoms depend on the site & extent of the lesion as well as the length of time from injury symptoms include involuntary urination, which is often frequent spontaneous, scant, & triggered by spasms in lower extremities, A true sensation of fullness is lacking, although vague lower abdominal pain due to stretching of the overlying peritoneum may be felt. The sensory level of injury need to be established, followed by assessment of anal, blbocavernosal, knee, ankle, & toe reflexes.

2-Flaccid (atonic) neuropathic bladder due to lesion at or below the sacral Affect either motor or sensory fibers or both. Injury to the detrusor motor nucleus The most common cause of flaccid neuropathic bladder is injury to the spinal cord at the micturition center, S2-4.

Other causes of anterior horn cell damage include infection due to poliovirus or herpes zoster & iatrogenic factors such as radiation or surgery External sphincter & perineal muscle tone are diminished. Because pressure in the bladder is low, little outlet resistant is needed to provide continence. Evacuation of bladder may be accomplished by straining but with variable success.

Injury to the afferent feedback pathways Flaccid neuropathic bladder also result from variety of neuropathies, include -DM, -tabes dorsalis, -pernicious anemia, & -posterior spinal cord lesion which lead to loss of sensory input to the detrusor nucleus or change in motor behavior due to loss of neurotransmission.

The end result loss of perception of bladder filling permits overstretching of the detrusor. Atony of the detrusor result in weak, inefficient contractility. Capacity is increase & residual urine is significant.

Clinical finding pt experience flaccid paralysis & loss of sensation affecting the muscles & dermatomes below the level of injury. The principle urinary symptom is retention with overflow incontinence. male pt lose their erections. Storage pressure within the bladder remain below the outlet resistance, therefore neither bowel nor urinary incontinence is a major factor.

Neurological changes are typically lower motor neuron. Extremity reflexes are hypotonic or absent. -Perineal sensation at level of S2 & 3 -anal tone S2. -out side of the foot S2 & sole S2&3.

D.Dx of neuropathic bladder 1-Cystitis Symptom disappear after definitive antibiotic therapy & the urodynamic behavior reverts to normal. 2-Chronic urethritis Chronic inflammation of urethra not necessarily associated with infection may presented with frequency, nocturia, & burning on urination. 3-Psychological disturbance May present with long history of bouts of frequency perineal or pelvic pain. Due to excessive pelvic muscle tension.

4-Interstitial cystitis The typical pt is woman above 40 yr with frequency, nocturia, & suprapubic pain of unknown cause. The symptoms are brought on by bladder distention. Capacity is limited (often <100 ml), urinalysis is normal & there is no residual urine. Distention of bladder with cystoscope produce bleeding from petechial hemorrhages & fissuring in the mucosa.

5-Cystocele Herniation of the bladder & or the urethra through the anterior vaginal wall also may present with frequency, nocturia, & stress incontinence. 6- Bladder outlet obstruction Urethral stricture, BPH, CAP, may simulate the presentation of neuropathic bladder.

Diagnosis In addition to history &clinical finding GUE may show infection. Renal function test may be normal or impaired. X-ray finding U/S, plain film, MRI. Cystoscope & urodynamic studies.

Treatment The aim of treatment is to preserve the renal function by low intravesical pressure. 1-Spinal shock During this stage with atonic bladder, intermittent catheterization using strict aseptic technique has proved to be the best form of management. This avoid UTI, as well as complication of indwelling catheter (eg, urethral stricture, abscess, erosion, stones)

-encourage fluid intake & ambulation in a wheelchair as soon as possible. -Urodynamic studies to be repeated every 3 months as long as spasticity is improving & then annually to check for complication of upper urinary tract.

2-specifc types of neuropathic bladder A-Spastic neuropathic bladder If reasonable bladder capacity & the pt able to go 2-3 hr between voiding with continent during this period, voiding is initiated using trigger techniques (tapping the abdomen suprapubically, or scratching the skin of lower abdomen genitalia & thighs.) But if markedly diminished functional vesical capacity( <100 ml) involuntary voiding every 15 min. one of the following regimen can be used.

1-permanent indwelling catheter with or without anticholinergic medication. commonly used drug oxybutynin chloride (ditropan) 5mg 2-3 times /day.& propanthelin bromide. 2-condom catheter in male if residual urine is small & intravesical pressure <40 cm of water (eg no risk of reflex). 3- performance of sphincterotomy by surgically eliminating all outlet resistant in male (contraindicated in female), turn the bladder into urinary conduit.

4-conversion of spastic bladder to flaccid through sacral rhizotomy. 5-Nuerostimulation of sacral nerve root (bladder pacemaker). 6-urinary diversion for irreversible, progressive upper urinary tract deterioration.

B-Flaccid bladder Bladder evacuation can be achieved by straining using the abdominal & diaphragmatic muscle. Or Crede maneuver, manual suprapubic pressure to raise intra-abdominal pressure. Any pt with adequate bladder capacity can benefit from regular clean intermittent catheterization (CIC) every 3-6 hr.