Fairly uncommon problem, considering the scope of lumbar disc herniations.
Results from the combination of a small canal or a large herniated disc fragment compressing the entire thecal sac against the posterior wall of the neurocanal.
Can present acutely or more insidiously:
Back pain radiating into both legs. Sensory changes bilaterally.
Loss of rectal sphincter tone.
Bilateral motor weakness.
Decreased perineal sensation.
Ultimately, the primary concern in cauda equina syndrome is the potential for long term bowel/bladder and sexual function.
Treatment – Urgent decompression – classically, less than 6 hours.
So what is the prognosis of bladder dysfunction in the setting cauda equina syndrome caused by massive disc herniation?
Kostuik J.P. et al., Cauda Equina Syndrome and Lumbar Disc Herniation, JBJS-A, 68-3: 386-391, March 1986
Retrospectively reviewed 31 patients with cauda equina secondary to a central lumbar disc, 10 who presented with acute, sudden onset of severe symptoms, and 21 with slower, intermittent and gradual symptoms. Average time to decompression ranged from 1.1 days for the acute patients to 3.3 days for the less acute patients. No patient was decompressed within 6 hours. All 31 had bladder dysfunction preoperatively (urinary retention). 23 of 30 patients regained normal voiding patterns three to fourteen days after decompression. 7 of 30 had partial recovery with incomplete emptying (6 had persistent perianal numbness as well). 5 of these 7 were from the acute presentation group. There was no correlation of time to surgery and return of function, but the recommendation was that decompression be done as soon as possible to minimize scar formation.
What about bladder dysfunction in the typical lumbar disc?
Bartolin, Z. Et al, Bladder Function in Patients with Lumbar Intervertebral Disk Protrusion, Journal of Urology, Vol 159, 969-971, March 1998
Prospectively studied 114 patients with lumbar disc herniations, none of whom had the classic features of cauda equina syndrome clinically. They found that 27% had detrusor areflexia on urodynamic testing. All of these patients, however, reported some difficulty voiding with straining.
A Review of Bladder Function
Detrusor muscle – smooth muscle of the bladder; contraction results in emptying
Internal sphincter – not really an anatomic entity, but rather the confluence of detrusor muscle fibers around the origin of the urethra. Closes off the urethral origin in the resting state, maintaining continence.
External sphincter – well defined ring of strong striated skeletal muscle surrounding the urethra as it passes through the pelvic floor. Provides voluntary control.
Nervous System Factors
Sympathetic – arise from T11-L2 segments, innervating the detrusor muscle and the internal sphincter via the hypogastric plexus. Allows the bladder to FILL – relaxes detrusor muscle while stimulating the tonic contraction and closure of the internal sphincter.
Parasympathetic – arise from S2-S4, innervating the detrusor muscle via pelvic nerves. Stimulates bladder EMPTYING – contracts detrusor muscle.
Somatic – arise also from S2-S4, innervating the external sphincter via pudendal nerves (which also carry sensory fibers back to the S2-4), allowing voluntary motor control.
The Reflex Voiding Center – S2-S4
A sensation of filling first occurs when the bladder contains 175 to 250 cc of urine. The urge to void occurs between 350-400 cc.
Sensory neurons from the bladder to the cord carry signal through the pudendal nerves that the bladder is filling.
This filling stimulates a coordinated parasympathetically mediated contraction of the bladder through pelvic nerves, and a relaxation of the external sphincter.
This reflex response is inhibited in adults pathways that connect to higher centers (undeveloped in infants).
A Review of Bladder Function
So What Happens