Worsening Leg Weakness and a Negative Lumbar MRI
The patient is a 52-year-old male whose health is generally very good. He has no back pain but presents with acute pain, numbness and tingling sensations in both legs; right is greater than the left. He presents in our office for a second opinion.
Previously, he was evaluated by his primary care physician and treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and chiropractic care. However, his lower extremity numbness, tingling and weakness worsened. There is no saddle anesthesia or bowel/bladder incontinence. His symptoms continued to worsen to the point where he was falling.
Then he was referred to a physical medicine specialist who ordered electrodiagnostic testing (EMG/NCV) and MRI of the lumbar spine (Fig. 1), which revealed a small facet cyst on the right side of L4-L5 (Fig. 2). Following aspiration of the synovial cyst, no improvement in symptoms was noted. Physical therapy for strengthening was prescribed, but the patient was unable to participate given his profound weakness and gait problems.
Figure 1. Sagittal MRI
Figure 2. Axial MRI, facet cyst at L4-L5 circle in red
The patient takes no daily medications and has no known allergies.
- Blood pressure: 131/91
- Pulse: 81
- Height: 75 inches
- Weight: 225 pounds
- BMI: 28.1
- Pain: 6/10 in the lower extremities
He ambulates with the assistance of a quad cane. His gait is very unsteady and cadence is interrupted. He is very wobbly, and falls or nearly falls with use of the quad cane. He is unable to heel-toe walk without assistance.
- Rotation of the hip does not reproduce any of his pain
- No muscle fasciculation in the thigh or the calf
- No atrophy of the major muscle groups in the lower extremities
- NSAIDs did not improve symptoms
- Chiropractic care did not improve symptoms
- Oral prednisone mild decreased numbness for a few days
- No substantial improvement following aspiration of the right L4-L5 facet cyst
- Physical therapy was not helpful
Figure 3. Lateral X-ray
Figure 4. Anteroposterior X-ray
Figure 5. Sagittal MRI; myelomalacia changes from severe stenosis
Figure 6. Axial MRI; severe cord compression from degenerative changes and soft disc
Severe spinal stenosis with cord compression and myelomalacia changes at T11-T12
Suggest TreatmentIndicate how you would treat this patient by completing the following brief survey. Your response will be added to our survey results below.
We performed a trans-thoracic minimally invasive discectomy, decompression of the conus medullaris and extreme lateral interbody fusion with a PEEK cage.
Figure 7. PEEK cage placement
Figure 8. Implanted PEEK cage
The patient was hospitalized for 3 days. He required a chest tube for 48 hours. Otherwise, his immediate post-operative course was uneventful.
- Two weeks post-op the patient was off all narcotics.
- At post-op week 4, he returned to sit down duty at work, and working 40 hours.
- At post-op week 8, his strength was essentially normal and his gait was significantly improved without the use of assisted devices.
- He did and continues to have some degree of lower extremity paresthesias, which is being treated with gabapentin only.
This is an interesting case history, with what appears to have had a very favorable outcome. As it is somewhat rare, it is worth presenting and highlighting. I would agree with the initial work-up, starting with a lumbar MRI scan. The L4-L5, small, facet cyst, did not correlate with this patient's advancing symptoms. The cyst would affect, primarily, the exiting L4 or possibly the traversing L5 root on the right side, but would not lead to more proximal or bilateral weakness. Since it appears that both legs were involved in their entirety, looking proximal was the right thing to do. To save time, perhaps a cervical and thoracic MRI could have been obtained; though in this case, as demonstrated, that is an academic discussion, as the findings were clear in the thoracic spine. I would note, however, in addition to the T11-T12 high-grade stenosis and myelomalacia, there appears to be cord atrophy extending to T9-10. Due to the marked weakness, I would have considered extending the posterior decompression to that level. Nonoperative options were tried, but in this case there was some urgency in proceeding with surgery, which is the most definitive treatment for this advancing paraparesis.
The author chose a lateral approach to the T11-T12 disc. The disc is somewhat off center to the left and that should, coupled with the distraction of the disc space by the cages allow for direct and indirect decompression. I would, however, be concerned about just a one-level procedure and a one-level interbody cage without any fixation. As noted above, it appears he has cord atrophy extending proximally two levels, and I would have performed a two-level laminectomy to more assuredly decompress the cord at all levels involved (T9-T12). I am also "concerned" about the lack of rigid fixation. Perhaps it is "rigid" since the facets and posterior elements are intact and the disc space is "maximally" distracted. However, we have seen many instances of stand-alone cages develop pseudoarthrosis along with instability/motion. This cord cannot afford that. Assuming the decompression at T11-T12 is enough, I would either have added a plate and screws into the vertebral bodies laterally at T11-T12, or perform a limited posterior decompression with pedicle screw fixation T11-T12 (though as noted I would have extended the decompression and, therefore, the fusion two levels more proximally). The alternative to what was done, and/or what I offered, would be a more extensive, open transthoracic approach, though this may necessitate taking down part of the diaphragm, and is not needed if one is familiar with the far lateral tubular approach. An alternative would be a posterior lateral costotransversectomy with decompression and interbody fusion, coupled with posterior instrumentation and fusion since the incision would be more posterior. An isolated laminectomy would not be adequate. A posterior laminectomy with taking down part of the rib and a pedicle may gain access to the disc, but I do not feel it would give enough lateral access to decompress this completely. With all the above in mind, it appears, at the two-month follow-up, the patient is doing well, which is the goal. The important message is to continue to look further, if the obvious starting point (in this case lumbosacral MRI) does not explain the clinical symptoms and signs.
Authors' Response to Case Discussion
First, we would like to thank Dr. Garfin for his sagacious points illustrated by this case. The cord atrophy discussed is most likely due to imaging and not true atrophy when axial images are reviewed. With this in mind, extending the surgical field to include T9 was felt to be more destructive than necessary. The area of pathology was felt to be isolated to T11-T12 in light of the stenosis, as well as the myelomalacial changes on the MRI.
It has been the experience of our practice that, in the absence of gross instability of the posterior column, a one level standalone interbody cage in the thoracic spine will generally do well. This is in part to bracing that is supported by the ribs, anterior and posterior longitudinal ligaments, and posterior dynamic and static stabilizers. It would seem more likely that additional surgery in the posterior column may provide support with pedicle fixation, but would also increase the morbidity of surgery and increase the likelihood of adjacent segment disease in an area already consumed with degenerative changes.
In closing, this patient presented with acute weakness not supported by the previous workup. We extended our workup to reveal the genesis of this patient's pathology. We opted to treat the patient and not the MRI.