scholarly journals Alteration of the lysophosphatidic acid and its precursor lysophosphatidylcholine levels in spinal cord stenosis: A study using a rat cauda equina compression model

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Baasanjav Uranbileg ◽  
Nobuko Ito ◽  
Makoto Kurano ◽  
Daisuke Saigusa ◽  
Ritsumi Saito ◽  
...  

Abstract Cauda equina compression (CEC) is a major cause of neurogenic claudication and progresses to neuropathic pain (NP). A lipid mediator, lysophosphatidic acid (LPA), is known to induce NP via the LPA1 receptor. To know a possible mechanism of LPA production in neurogenic claudication, we determined the levels of LPA, lysophosphatidylcholine (LPC) and LPA-producing enzyme autotaxin (ATX), in the cerebrospinal fluid (CSF) and spinal cord (SC) using a CEC as a possible model of neurogenic claudication. Using silicon blocks within the lumbar epidural space, we developed a CEC model in rats with motor dysfunction. LPC and LPA levels in the CSF were significantly increased from day 1. Importantly, specific LPA species (16:0, 18:2, 20:4) were upregulated, which have been shown to produce by ATX detected in the CSF, without changes on its level. In SC, the LPC and LPA levels did not change, but mass spectrometry imaging analysis revealed that LPC was present in a region where the silicon blocks were inserted. These results propose a model for LPA production in SC and CSF upon neurogenic claudication that LPC produced locally by tissue damages is converted to LPA by ATX, which then leak out into the CSF.

1976 ◽  
Vol 44 (5) ◽  
pp. 613-616 ◽  
Author(s):  
Glen S. Merry ◽  
D. Barry Appleton

✓ A case is reported of spinal aneurysm in a child with a family history of hereditary hemorrhagic telangiectasia causing spinal cord and cauda equina compression. The operative approach is discussed.


2017 ◽  
Vol 12 (11) ◽  
pp. S2325
Author(s):  
H. Neji ◽  
M.A. Haouari ◽  
M. Attia ◽  
M. Affes ◽  
I. Baccouche ◽  
...  

2011 ◽  
Vol 02 (01) ◽  
pp. 017-022 ◽  
Author(s):  
Tarek A Aly

ABSTRACT Introduction: Patients with spinal injuries have been treated in the past by laminectomy in an attempt to decompress the spinal cord. The results have shown insignificant improvement or even a worsening of neurologic function and decreased stability without effectively removing the anterior bone and disc fragments compressing the spinal cord. The primary indication for anterior decompression and grafting is narrowing of the spinal canal with neurologic deficits that cannot be resolved by any other approach. One must think of subsequent surgical intervention for increased stability and compressive posterior fusion with short-armed internal fi xators. Aim: To analyze the results and efficacy of spinal shortening combined with interbody fusion technique for the management of dorsal and lumbar unstable injuries. Materials and Methods: Twenty-three patients with traumatic fractures and or fracture-dislocation of dorsolumbar spine with neurologic deficit are presented. All had radiologic evidence of spinal cord or cauda equina compression, with either paraplegia or paraparesis. Patients underwent recapping laminoplasty in the thoracic or lumbar spine for decompression of spinal cord. The T-saw was used for division of the posterior elements. After decompression of the cord and removal of the extruded bone fragments and disc material, the excised laminae were replaced exactly in situ to their original anatomic position. Then application of a compression force via monosegmental transpedicular fixation was done, allowing vertebral end-plate compression and interbody fusion. Results: Lateral Cobb angle (T10–L2) was reduced from 26 to 4 degrees after surgery. The shortened vertebral body united and no or minimal loss of correction was seen. The preoperative vertebral kyphosis averaged +17 degrees and was corrected to +7 degrees at follow-up with the sagittal index improving from 0.59 to 0.86. The segmental local kyphosis was reduced from +15 degrees to −3 degrees. Radiography demonstrated anatomically correct reconstruction in all patients, as well as solid fusion. Conclusion: This technique permits circumferential decompression of the spinal cord through a posterior approach and posterior interbody fusion.


2020 ◽  
Vol 11 ◽  
pp. 175
Author(s):  
Shawn Singh Rai ◽  
Carlos Rodrigo Goulart ◽  
Sepehr Lalezari ◽  
Michael Anthony Galgano ◽  
Satish Krishnamurthy

Background: Dorsal migration of an intervertebral lumbar disc fragment is exceedingly rare and may result in spinal cord or cauda equina compression. Radiologically, these lesions may be misdiagnosed as extradural masses or epidural hematomas. Case Description: We present three cases involving dorsal migration of sequestered lumbar disc fragments resulting in cauda equina syndromes. A 31-year-old male, 79-year-old female, and 47-year-old female presented with cauda equina syndromes attributed to the migration of dorsal sequestered lumbar disc fragments. Prompt surgical decompression resulted in adequate outcomes. Here, we review the three cases and the current literature for such lesions. Conclusion: Dorsal migration of sequestered lumbar disc fragments is exceedingly rare, and these lesions are frequently misdiagnosed as extradural masses of other origin or epidural hematomas. Here and in the literature, prompt epidural decompression both confirmed the correct diagnosis and resulted in excellent outcomes.


Neurosurgery ◽  
1986 ◽  
Vol 19 (3) ◽  
pp. 415-420 ◽  
Author(s):  
Terrell D. Kjerulf ◽  
Daniel W. Terry ◽  
Richard J. Boubelik

Abstract Most reports regarding synovial cysts of the spinal canal have been presentations identifying an unusual pathological entity that is to be included in the differential diagnosis of cauda equina compression syndromes. Most of the 26 cases reported represent isolated examples of this pathological process. We present five cases of lumbar synovial cysts encountered in our practice in the past 8 years. Patients with lumbar synovial cysts do not demonstrate any predictable clinical picture. They may present with a unilateral sciatica or neurogenic claudication. Lumbar extension is usually restricted, whereas flexion is full. Mechanical signs of nerve root entrapment or lumbosacral plexus irritation are unimpressive. Neurological deficits are usually mild, if present. Radiological findings include degenerative spondylosis, spondylolisthesis, and a rounded posterolateral extradural mass of low attenuation value adjacent to a facet shown on computed tomographic scan. The etiology of lumbar synovial cysts is not known. Histological findings of myxoid degeneration, microcystic change, calcification, and hemosiderin deposits suggest that chronic microtrauma with occasional focal hemorrhage may play a major role in the etiology of the cysts. With resection of the cyst, the postoperative course is usually uneventful. Recurrences have not yet been encountered in our patients.


2003 ◽  
Vol 14 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Sanjay N. Misra ◽  
Howard W. Morgan

The authors review the management of thoracolumbar kyphotic deformity in cases of achondroplasia. The presence of angular thoracolumbar kyphosis in achondroplasia is well recognized. In children this is initially a nonfixed deformity that persists, however, in more than 10% of individuals and becomes a fixed thoracolumbar kyphotic deformity. Additionally, with the coexistent spinal canal stenosis, neurological damage can occur and manifest as spinal cord or cauda equina compression. The nature of this condition, the natural history, and management options are discussed. Anatomical and biomechanical factors relevant to the condition are specifically highlighted. Avoidance of pitfalls in the management of these patients is discussed for both pediatric and adult patients.


Sign in / Sign up

Export Citation Format

Share Document