Saturday, May 20, 2017

Introduction to Neurogenic bladder

Also known as neuromuscular dysfunction of the lower urinary tract, neurologic bladder dysfunction, and neuropathic bladder, neurogenic bladder refers to all types of bladder dysfunction caused by an interruption of normal bladder innervation. Subsequent complications include urinary incontinence, residual urine retention, urinary tract infection, calculi formation, and renal failure. A neurogenic bladder can be spastic (hypertonic, reflex, or automatic), flaccid (hypotonic, atonic, nonreflex, or autonomous), or uncoordinated (dyssynergic).

At one time, neurogenic bladder was thought to result primarily from spinal cord injury; now, it appears to stem from a host of underlying conditions:
  • cerebral disorders, such as cerebrovascular accident, brain tumor (meningioma and glioma), Parkinson’s disease, multiple sclerosis, and dementia
  • spinal cord disease or trauma, such as spinal stenosis (causing cord compression) or arachnoiditis (causing adhesions between the membranes covering the cord), cervical spondylosis, myelopathies from hereditary or nutritional deficiencies and, rarely, tabes dorsalis
  • disorders of peripheral innervation, including autonomic neuropathies resulting from endocrine disturbances such as diabetes mellitus (most common)
  • metabolic disturbances, such as hypothyroidism, porphyria, or uremia (infrequent)
  • acute infectious diseases such as Guillain-BarrĂ© syndrome
  • heavy metal toxicity
  • chronic alcoholism
  • collagen diseases such as systemic lupus erythematosus
  • vascular diseases such as atherosclerosis
  • distant effects of cancer such as primary oat cell carcinoma of the lung
  • herpes zoster
  • sacral agenesis.
An upper motor neuron lesion (above S2 to S4) causes spastic neurogenic bladder, with spontaneous contractions of the detrusor muscles, elevated intravesical voiding pressure, bladder wall hypertrophy with trabeculation, and urinary sphincter spasms.

A lower motor neuron lesion (below S2 to S4) causes flaccid neurogenic bladder, with decreased intravesical pressure, increased bladder capacity and large residual urine retention, and poor detrusor contraction.
Signs and symptoms
Neurogenic bladder produces a wide range of symptoms, depending on the underlying cause and its effect on the structural integrity of the bladder. Usually, this disorder causes some degree of incontinence, changes in initiation or interruption of micturition, and an inability to completely empty the bladder. Other signs and symptoms of neurogenic bladder include vesicoureteral reflux, deterioration or infection in the upper urinary tract, and hydroureteral nephrosis.

Spastic neurogenic bladder
Depending on the site and extent of the spinal cord lesion, spastic neurogenic bladder may produce involuntary or frequent scanty urination without a feeling of bladder fullness and possibly spontaneous spasms of the arms and legs. Anal sphincter tone may be increased.
Tactile stimulation of the abdomen, thighs, or genitalia may precipitate voiding and spontaneous contractions of the arms and legs. With cord lesions in the upper thoracic (cervical) level, bladder distention can trigger hyperactive autonomic reflexes, resulting in severe hypertension, bradycardia, and headaches.

Flaccid neurogenic bladder
Features of flaccid neurogenic bladder include overflow incontinence, diminished anal sphincter tone, and a greatly distended bladder (this is evident on percussion or palpation), but without the accompanying feeling of bladder fullness because of sensory impairment.

The patient’s history may include a condition or disorder that can cause neurogenic bladder, incontinence, and disruptions of micturition patterns. The following tests will help evaluate the patient’s bladder function:
  • Voiding cystourethrography evaluates bladder neck function, vesicoureteral reflux, and continence.
  • Urodynamic studies help evaluate how urine is stored in the bladder, how well the bladder empties, and the rate of movement of urine out of the bladder during voiding. These studies consist of four components:
  • Urine flow study (uroflow) shows diminished or impaired urine flow.
  • Cystometry evaluates bladder nerve supply, detrusor muscle tone, and intravesical pressures during bladder filling and contraction.
  • Urethral pressure profile determines urethral function with respect to the length of the urethra and the outlet pressure resistance.
  • Sphincter electromyelography correlates the neuromuscular function of the external sphincter with bladder muscle function during bladder filling and contraction. This evaluates how well the bladder and urinary sphincter muscles work together.
  • Retrograde urethrography reveals the presence of strictures and diverticula. This test may not be performed on a routine basis.


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