Initial sagittal MRI of the patient
Initial axial MRI of the patient
Second sagittal MRI of the patient following unsuccessful steroid treatment
Second axial MRI of the patient following unsuccessful steroid treatment
A 65-year-old man presents with right-sided sciatica that occasionally radiates down the posterior lateral thigh to the level of the ankle. Magnetic resonance imaging (MRI) is ordered, which shows right-sided foraminal stenosis at L4-L5 and L5-S1, with a small disc herniation at L4-L5. Congenitally short pedicles causing central stenosis are also noted.
The patient failed a trial of oral steroids but does improve following 2 courses of epidural steroid injections. His condition improved greatly until 24 hours later, when he began experiencing increased pain that radiated down both legs. Over the last 12 hours, he has experienced difficulty controlling his urination and has developed perianal numbness. An urgent MRI was ordered, and the second group of images reveals a large central disc herniation causing symptoms of cauda equina syndrome.
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The optimal time frame for surgical decompression after the onset of symptoms related to cauda equina syndrome is still open to debate. Most clinicians agree that surgery should be performed as soon as possible, to limit the progression of neurologic deficits.
However, no statistically significant postoperative improvements in neurologic deficits have been found in patients decompressed within 48 hours, compared with patients decompressed between 24 and 48 hrs. Improvements in neurologic outcomes have been found in patients treated within 48 hours, compared with those treated more than 48 hours after onset of symptoms. Therefore, surgical decompression is recommended within 48 hours after onset of symptoms to optimize postoperative outcomes.
Nerve regeneration depends on the length of time that the nerves have been affected and the extent of damage. Time is the only way to measure recovery, as nerve regeneration can take up to 2 years. Nerve injury can occur 1 of 3 ways:
- The nerve is compressed and “falls asleep.” Once the compression is relieved, the nerve function returns.
- The nerve axon is injured but the myelin sheath remains intact. The nerve axon regenerates along the myelin sheath at a rate of 1 mm per day or 1 inch per month. This explains why neurologic recovery can improve over a longer period.
- The myelin sheath is disrupted and so the axon cannot regenerate; therefore, no neurologic function will return.
In general, the severity of neurologic deficits preoperatively often predicts postoperative outcomes. Patients with profound loss of bowel and/or bladder function before surgery are much more likely to be incontinent and see less improvement postoperatively. Persistent neurologic deficits associated with cauda equina syndrome can also include saddle anesthesia, leg weakness, chronic pain, and sexual dysfunction.
Dagan Cloutier, MPAS, PA-C, practices in a multispecialty orthopedic group in the southern New Hampshire region and is editor in chief of the Journal of Orthopedics for Physician Assistants (JOPA).
- Qureshi A, Sell P. Cauda equina syndrome treated by surgical decompression: the influence of timing on surgical outcome. Eur Spine J. 2007;16(12): 2143-2151.
- Spector LR, Madigan L, Rhyne A, Darden II B, Kim D. Cauda equina syndrome. J Am Acad Orthop Surg. 2008; 16(8):471-479.