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Thread: Question for Dr. Young about Cauda Equina Syndrome

  1. #1
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    Question for Dr. Young about Cauda Equina Syndrome

    Dr. Young

    Has there been any new treatments to reverse the effects of Cauda Equina Syndrome?

    Thank you in advance for your input.

    Tim

  2. #2
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    Is the Cauda Equina a part of the actual spinal cord, or is it the branching of the peripheral nerves? My SCI was around the Conus, but I feel burning and a sticking feeling at the Cauda Equina.

    sherman brayton

  3. #3
    lots of info on cauda if you use a search with just that word.
    i have it CES, it hurts a lot, i think Dr young had mentioned that a doctor in Florida was the expert in it, i wish there was one in the NY area

  4. #4
    sped, I am not sure what would be new for you. Here are some abstracts that might be of interest.

    Lang, et al. (2004) from Freiburg Germany reported that many patients with traumatic lumbosacral plexus injuries also have cauda equina injuries and that reconstruction of spinal nerves with repair of ventral roots resulted in recovery of leg function including walking and standing. This is of interest because it suggests that German centers or at least this particular German center is quite optimistic about the beneficial effects of reconstructive surgery for lumbosacral plexus and cauda equina injuries.

    Quinones-Hinjjosa, et al., used neurophysiological monitoring during surgical untethering of the cauda equina. In 15 patients, they assessed the stimulation threshold for tethered roots and suggest that monitoring prevented loss of function that often happen after such surgeries.

    Thongtrangan, et al. at Stanford reported the results of 17 cauda equina cases. They had good results in 14 out of 17 cases but concluded that the results were not influenced by the timing of surgery but rather depended on the severity of injury.

    Myckatyn, et al. mentioned the possible use of stem cell therapies for cauda equina.

    Sekiguchi, et al. studied an experimental cauda equina model in rats and found that cauda equina syndromes or injuries of spinal roots between the dorsal root ganglia and the spinal cord do not produce mechanical allodynia.

    There have not been any new treatments reported this year.

    Wise.


    • Lang EM, Borges J and Carlstedt T (2004). Surgical treatment of lumbosacral plexus injuries. J Neurosurg Spine. 1: 64-71. Department of Plastic and Hand Surgery, Albert-Ludwig Universitat, Freiburg, Germany. OBJECT: The purpose of this study was to analyze therapeutic possibilities and clinical outcomes in patients with lumbosacral plexus injuries to develop surgical concepts of treatment. METHODS: In a retrospective investigation 10 patients with injuries to the lumbosacral plexus were evaluated after surgery. The patients were assessed clinically, electrophysiologically, and based on the results of magnetic resonance imaging and computerized tomography myelography. In most patients a traction injury had occurred due to severe trauma that also caused pelvic fractures. In most cases the roots of the cauda equina of the lumbosacral plexus had ruptured. In cases of spinal root ruptures repair with nerve grafts were performed. In cases in which proximal stumps of the plexus could not be retrieved palliative nerve transfers by using lower intercostals nerves or fascicles from the femoral nerve were performed. CONCLUSIONS: Lesions of the proximal spinal nerves and cauda equina occur in the most serious lumbosacral plexus injuries. Patients with such injuries subjected to reconstruction of spinal nerves, repair of ventral roots in the cauda equina, and nerve transfers recovered basic lower-extremity functions such as unsupported standing and walking.

    • Quinones-Hinojosa A, Gadkary CA, Gulati M, von Koch CS, Lyon R, Weinstein PR and Yingling CD (2004). Neurophysiological monitoring for safe surgical tethered cord syndrome release in adults. Surg Neurol. 62: 127-33; discussion 133-5. Department of Neurological Surgery, University of California-San Francisco, 505 Parnassus Avenue, Moffitt Hospital Room M779, Box 112, San Francisco, CA 94143-0112, USA. BACKGROUND: Release of tethered spinal cord by sectioning of the filum terminale carries a significant risk of injury to the neighboring motor and sensory nerve roots. Intraoperative neurophysiological monitoring techniques can help to minimize these adverse neurologic outcomes. METHODS: We performed a retrospective review of 67 consecutive patients undergoing tethered cord release. We excluded 52 pediatric patients which limited our study to 15 adult patients treated during a four year period, including patients with a thick filum, low lying conus, myelomeningocele, filum tumor, spinal cord malformation, and/or lipoma. Clinical outcomes were determined from postoperative follow-up visits. Two patients were lost to follow up and were excluded from the clinical outcome analysis. Electrical stimulation of the filum terminale and lumbo-sacral nerve roots in conjunction with electromyogram (EMG) recording was performed intraoperatively. RESULTS: The mean electrical threshold for EMG response during stimulation of the filum terminale was 37.1 volts (V), range 15 to 100 V. In comparison, the lowest threshold obtained by direct stimulation of the ventral nerve roots was a mean of 1.46 V, with a range of 0.1 to 7 V. More than 70% of the patients studied demonstrated a filum to motor root threshold ratio of 100:1 or greater. No patient developed new neurologic symptoms or signs postoperatively. Bowel and bladder function improved in 46% of patients, back pain in 39% and motor function in 31%. Eight percent reported decline in bladder control and worsening back pain postoperatively. CONCLUSIONS: The often dramatic difference in the threshold of the filum terminale and adjacent motor nerve roots (100:1) helps to identify, isolate, and safely section the filum terminale. Tethered cord release using intraoperative neurophysiological monitoring is safe and in the majority of cases leads to improvement or at least, stabilization of neurologic function. Monitoring prevented intraoperative nerve root injury that might have resulted in immediate onset of new neurologic deficits caused by the surgical procedure.

    • Thongtrangan I, Le H, Park J and Kim DH (2004). Cauda equina syndrome in patients with low lumbar fractures. Neurosurg Focus. 16: e6. Department of Neurosurgery, Stanford University Medical Center, Stanford, California 94305-5327, USA. OBJECT: Symptoms of cauda equina syndrome (CES) can include low-back pain, sciatica, lower-extremity weakness, sensory deficit, perineal hypesthesia or anesthesia, and loss of bowel or bladder function. Several causes of the syndrome are recognized, but its optimal treatment remains controversial and has been broadly based on data gathered from series involving herniated discs. Information on the treatment of CES caused by low lumbar traumatic injuries has not been well documented. METHODS: Between January 2000 and December 2003, 17 consecutive cases of CES caused by low lumbar traumatic injuries at L2-5 were identified. The traumatic injuries consisted of gun shot wound in two cases, motor vehicle accident in 11, and a fall from height in four. Conus medullaris injuries causing CES were excluded from this review. Presenting symptoms, mechanisms of injury, radiographic images, timing of surgery, surgical approaches, and neurological status at the final follow up were documented. All patients underwent follow up of at least 12 months. Fourteen of 17 patients had satisfactory outcomes. Despite undergoing surgery within the first 24 hours postinjury, three patients had what was classified as a poor outcome given their residual deficits and included two cases with gunshot injuries. Recovery of leg weakness occurred within 4 months, whereas bladder and bowel function recovered within 3 months. All patients in this series underwent decompression within less than 48 hours after syndrome onset. Overall, the authors found no difference regarding timing of surgery between patients in the satisfactory outcome group and those in the poor outcome group. CONCLUSIONS: Based on the evidence in this study, the severity of a patient's condition on initial presentation is the most crucial factor in predicting outcome following CES due to low lumbar injuries. Although the matter of the timing of surgery remains controversial, the authors of this study recommend that surgery be performed within 48 hours of syndrome onset.

    • Myckatyn TM, Mackinnon SE and McDonald JW (2004). Stem cell transplantation and other novel techniques for promoting recovery from spinal cord injury. Transpl Immunol. 12: 343-58. Division of Plastic and Reconstructive Surgery, Washington University School of Medicine, 4444 Forest Park Boulevard, St. Louis, MO 63108, USA. A number of potential approaches aim to optimize functional recovery after spinal cord injury. They include minimizing the progression of secondary injury, manipulating the neuroinhibitory environment of the spinal cord, replacing lost tissue with transplanted cells or peripheral nerve grafts, remyelinating denuded axons, and maximizing the intrinsic regenerative potential of endogenous progenitor cells. We review the application of stem cell transplantation to the spinal cord, emphasizing the use of embryonic stem cells for remyelinating damaged axons. We speculate that harnessing the potential of endogenously born stem cells already present in the spinal cord represents an important therapeutic target. We also discuss the potential application of peripheral nervous system reconstruction to recovery from spinal cord injury. The principles of peripheral nerve regeneration and concepts of nerve grafting are reviewed. Particular attention is given to peripheral nerve allotransplantation for repairing extensively injured tissue when autologous donor nerve material is scarce. The potential role of nerve transfers for reconstructing the injured spinal cord, particularly the cauda equina and lumbosacral plexus, are also described.

    • Sekiguchi M, Kikuchi S and Myers RR (2004). Experimental spinal stenosis: relationship between degree of cauda equina compression, neuropathology, and pain. Spine. 29: 1105-11. Department of Orthopaedic Surgery, Fukushima Medical University, School of Medicine, Fukushima City, Japan. miho-s@fmu.ac.jp. STUDY DESIGN: An analysis of pathologic changes after different degrees of cauda equina compression. OBJECTIVES: To explore the association between the degree of the cauda equina compression and the extent of pathologic change, expression of tumor necrosis factor (TNF-alpha), and neuropathic pain. To compare with distal nerve compression injury. SUMMARY OF BACKGROUND DATA: Compression of the cauda equina reduces blood flow in compressed nerve roots and causes TNF-alpha expression and neuropathological change. In peripheral nerve, expression of TNF-alpha in Schwann cells is associated with primary demyelination without pain while TNF-alpha expression by macrophages is associated with axonal (Wallerian) degeneration and pain. METHODS: Two square-shaped pieces of silicon were placed into the fourth and sixth epidural space in rats. Various sized silicon was used in each group (mild, moderate, and strong compression groups), while no silicon was used in the sham-operated group. Mechanical allodynia was determined by the von Frey test. Comparisons of the number of TNF-alpha- and apoptosis-positive cells were made using immunohistochemistry. RESULTS: There was no significant mechanical allodynia observed in any group. Some nerve roots showed demyelination following mild cauda equina compression. Axonal degeneration was observed in the moderate and strong cauda equina compression groups. TNF-alpha-immunoreactive cells were increased in all compression groups. Apoptosis of dorsal root ganglion cells was less than apoptosis in the spinal cord. CONCLUSION: Mild cauda equina compression induces TNF-alpha expression and demyelination. Moderate and strong cauda equina compression induces TNF-alpha expression and degeneration associated with macrophage invasion. Neither demyelination nor degeneration in the cauda equina induced mechanical allodynia. Nerve lesions proximal to the dorsal root ganglion do not produce significant mechanical allodynia. Dorsal root ganglion apoptosis may be important for pain.

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