The spinal cord-bladder relationship
Whenever I’m seeing a patient in the emergency room with new acute or rapidly progressive lower extremity paraparesis, the first thing that comes to my mind is, “Does the patient have a spinal cord problem or a peripheral nerve problem?” The second thing that comes to my mind is, “Jesus I hope they don’t have a spinal cord problem…” But what if it is a spinal cord problem? What are the pathways involved in urination and voluntary retention? And how are these pathways compromised? This week, the physiology and pathophysiology of urinary dysfunction from spinal cord disease, and why as a neurologist or emergency medicine physician you just can’t avoid it.
Get it, aVOID it?
So the reason I decided to produce an episode on this theme stemmed from an experience I had as a senior resident getting called from a junior resident about a patient in the emergency room. The patient who was being evaluated went from normal standing, walking, talking, to being unable to stand unsupported and now they could barely flex their hips. As you may have predicted from the title of this week’s episode, one of my questions had to do with the patient’s bladder function. But what does that even matter?
The answer begins with the two basic functions of bladder control: emptying and retention. Briefly, bladder emptying, or voiding is mediated by spontaneous, involuntary relaxation of the internal urinary sphincter once the bladder has filled. But there is a backup system in place that is under voluntary control to maintain urinary continence, and this relies on somatic innervation of the external urinary sphincter. Some have said this pathway permits you a sort of “social” control to your continence. There also must be involuntary contraction of the bladder detrusor muscles in order to void, and you need both of these functions to coordinate their activity simultaneously, or else the bladder will fail to empty. So as you might expect, the failure of these sympathetic, parasympathetic and somatic signals will result in urinary retention.
Now, how does this happen in the normal individual? At small bladder volumes, urinary retention is a normal process and takes place unconsciously. We think this level of control relies on a subcortical network, which is probably impaired in conditions like normal pressure hydrocephalus. When the bladder fills with urine, the visceral afferent fibers signal a desire to void that gradually increases in intensity. This signal is received by the insular cortex, which is basically the autonomic homunculus of the brain and is responsible to some degree for things like blood pressure and heart rate as well as urination. Now, despite the increasing sensation as your bladder fills, in normal individuals, the voiding reflex does not occur unless it would be emotionally safe and socially appropriate. So the nervous system requires more somatic or voluntary control of bladder and urethral function in order to prevent spontaneous urination. Collectively, these autonomic and somatic pathways converge as what’s known as the “guarding reflex.” Guarding you from an embarrassing consequence of drinking too much coffee. And, it shouldn’t surprise you that there is a delay in the maturation of these higher pontine and suprapontine centers for voluntary control of urination. It takes toddlers several years before they can master this task.
Back to the patient I was hearing about from the junior resident… (Remember, the one who I suspected may have had a cord injury?) When there is a cord injury rostral to the lumbosacral level, technically an upper motor neuron lesion, there is loss of voluntary and involuntary supraspinal control of urination (mediated by the supplementary and primary motor cortices, pontine micturition center, and others). This essentially leads to an areflexic, acontractile bladder. Early on this means urinary retention. And you should know that historically, acute urinary retention and post-renal azotemia were the leading causes of death following acute spinal cord injury even throughout the most recent world wars. This period of spinal shock typically lasts 6-12 weeks, however cases up to 12 months of spinal shock have been reported.
After this period, the lumbosacral sympathetic and parasympathetic pathways take over full control of bladder function, resulting in bladder overactivity. Meaning a purely reflexic bladder. Urodynamic studies can be used to confirm this. Following hydration, the bladder distends with urine, the lumbosacral cord recognizes there is a full bladder, a critical threshold is reached, and [urination sound effect] there you have it. Spontaneous and uncontrollable bladder emptying. Anticholinergics like oxybutynin and tolterodine can often be used for symptomatic management in suprasacral cord injuries, but are not often effective. Furthermore, and even more problematic for these patients, when voiding occurs, it is often incomplete given that there is simultaneous activation of the urethral sphincter and bladder detrusor muscles—both of which are under autonomic control. You could say it takes a bit of voluntary muscle contraction to squeeze out those last few drops. This phenomenon is titled “detrusor sphincter dyssynergia,” and it underscores why patients with spinal cord injury and urinary incontinence develop frequent urinary tract infections. What I learned here is that it may not be the frequent catheterizations that account for UTIs, but actually the chronic overdistension of the bladder. Studies have shown that bladder overdistension results in bladder wall ischemia leading to muscle breakdown. So, it follows that as long as you maintain the bladder at normal volumes with frequent intermittent catheterization, you should be able to prevent UTIs.
And that’s why you ask about urinary control in suspected spinal cord injury! Acutely, there can be urinary retention due to bladder areflexia. And chronically, the loss of voluntary signaling results in a purely reflexive bladder with spontaneous voiding.
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- Seth JH, Panicker JN, Fowler CJ. The neurological organization of micturition. Handbook of clinical neurology. 2013;117:111-117
- Samson G, Cardenas DD. Neurogenic bladder in spinal cord injury. Phys Med Rehabil Clin N Am. 2007;18:255-274, vi
- de Groat WC, Griffiths D, Yoshimura N. Neural control of the lower urinary tract. Compr Physiol. 2015;5:327-396