System Nerve Changes after SCI
Voluntary control of urination
requires spinal communication between the lower urinary tract and the brain. After
a spinal cord injury (SCI), this communication is disrupted. The brain is no longer
able to use the spinal cord to communicate with organs below the level of injury.
Therefore, the normal signals to empty the bladder, or to inhibit the bladder
from emptying, are not properly sent or received. Without input from the brain,
the bladder becomes "neurogenic" or "neuropathic."
Reflexes often remain intact
below the level of injury. Over time, some reflexes even become hyperactive
when the inhibitory effects of the higher neuro function is lost.
Though there are many possible
effects of SCI on the urinary system, they all involve some combination of changes
in muscle activity or sensation. The muscles involved can be the detrusor muscle
of the bladder, the striated muscle of the sphincter, and/or the smooth muscle
of the internal sphincter or urethra. The changes in sensation can involve the
bladder and/or the urethra.
We can classify spinal cord
injuries according to location of the lesion. Then, we can make some generalizations
about the SCI's effect on the urinary system.
- supraspinal lesions:
Though these are not strictly "spinal cord injuries", we include
this category for completeness and comparison. They include all cerebral diseases
such as cerebral hemorrhage and thrombosis, dementia, tumors, arteriosclerosis
and Parkinson's disease.
- Commonly results
in bladder overactivity or hyperreflexia, (AKA "reflex",
or "spastic" bladder). When the bladder fills, there
is an automatic trigger for the bladder to empty. The
receptors continue to receive stimulation, and a "reflex arc"
continues to send the message out to the spinal cord to initiate voiding.
- The bladder hyperactivity
is due to the absence of cerebral inhibition of the micturition reflex.
If the only the cerebrum is damaged, the intact pons ensures that the
external sphincter still functions in a coordinated manner with the detrusor
- The patient commonly
experiences urinary frequency and incontinence. If the cerebrum is unable
to process ascending sensory stimulation, urinary retention and overflow
bladder that is hyperreflexic is overactive. It tends to empty "automatically".
- suprasacral lesions:
All spinal cord lesions above the sacrum. Suprasacral trauma is the most common
cause of SCI-related voiding dysfunction.
- Immediately following
SCI, the result is usually detrusor areflexia, or the inability
of the bladder to contract. This generally causes some degree of urinary
retention. This "spinal shock" can last from several
months up to 2 years.
- When reflex activity
returns, the bladder is able to contract, and pass urine again. The bladder
stretch receptors are stimulated by bladder filling; this produces frequent
spontaneous contractions of the detrusor muscle. The result is a small,
hyperactive bladder, where voiding is interrupted, involuntary or incomplete.
- In addition, in 70
- 100% of suprasacral lesions, there is also Dyssynergia or Detrusor
Sphincter Dyssynergia (DSD). Here, coordination between the detrusor
muscle and the bladder sphincter is affected. Instead of the sphincter relaxing,
followed by detrusor contraction, the bladder may contract against the closed
sphincter. Urine is prevented from leaving the bladder, resulting in intermittent
voiding, urinary retention, bladder distention and reflux.
- Vesicoureteral reflux
commonly occurs with suprasacral injuries. The bladder becomes less "stretchable",
therefore is sometimes called "high pressure," or has "low
vesicle compliance." The functioning bladder sphincters won't allow
the urine to exit, leading to reflux into the ureters and kidney. Upper
urinary tract problems due to backpressure can ultimately lead to renal
- infrasacral lesions:
All lesions inside or outside the spinal canal, involving the sacral cord
- Results in an atonic
(AKA non-reflex or flaccid) bladder. Here the autonomic
reflex is weak or absent. In this case it's impossible to know when (or
if) the urine will be removed from the body. There is no longer any way
to know if the bladder is full, and no urge to urinate. The flaccid bladder
is the result of injury to the micturition center of the sacral cord, the
cauda equina, or the sacral roots that supply the bladder.
- With infrasacral lesions,
the atonic detrusor muscle is easily overstretched, leading to overdistention
- With sacral injuries,
bladder management doesn't change much from the acute to long term stage,
because bladder function doesn't significantly improve .
Suprasacral lesions (lesions above the sacrum) often are associated
with detrusor sphincter dyssynergia.