Bladder/bowel function in hemisection

[cbrons]

---

Members don't see this ad.

I recently went through a case in my textbook describing a 71 y/o woman with hemisection (Brown-Sequard) syndrome (just incase you happen to have it - it is somewhat older, it is Blumenfeld, Clinical Neuroanatomy Through Clinical Cases, 2e -- Case 7.4 Left Leg Weakness and Right Leg Numbness)

Anyway, these were the symptoms:

• Left leg weakness, increased tone, hyperreflexia, and Babinski’s sign
• Decreased vibration and joint position sense in the left foot and leg
• Decreased pinprick sensation on the right side below the umbilicus, with right leg numb, tingling paresthesias
• Left-sided thoracic back pain
• Stiff-legged, unsteady gait
• Impaired bowel and bladder function

They explained everything just fine, except the last one. All he said was, "The presence of bowel and bladder dysfunction suggests some bilateral involvement of the cord), as does the spastic gait, which sounds as if it may have involved both legs. The most likely clinical localization is left T9 or T10 hemicord lesion, with possible mild involvement of the right cord as well."
I was wondering if someone could be kind enough to explain prescisely why this patient would have impaired bowel and bladder function? Additionally, I thought the lesion would have to be lower than T9 or T10 to affect the various plexi involved in bladder function (i.e. pudendal nerve, pelvic splanchnic, hypogastric nerves, etc.).

 

[AlternateSome1]

OK, to state this somewhat simplistically - You have cortical input to these pathways, so a lesion above the lumbar region cuts out the efferent control of them leading to a spastic bladder. Injury to the the lower motor neurons or to the sensory input from the bladder leads to a flaccid bladder.

Think of this as analogous to spasticity/hyperreflexia with upper motor neuron lesions. Normally cortical input regulates the system that determines muscle tension. When this input is lost, the natural tendency is for the muscles to be tense, and any stretch of those muscles leads to resistance/clonus/hyperreflexia.

 

[cbrons]

OK, to state this somewhat simplistically - You have cortical input to these pathways, so a lesion above the lumbar region cuts out the efferent control of them leading to a spastic bladder. Injury to the the lower motor neurons or to the sensory input from the bladder leads to a flaccid bladder.

Think of this as analogous to spasticity/hyperreflexia with upper motor neuron lesions. Normally cortical input regulates the system that determines muscle tension. When this input is lost, the natural tendency is for the muscles to be tense, and any stretch of those muscles leads to resistance/clonus/hyperreflexia.

Thank you