scholarly journals Cauda equina compression due to tabetic arthropathy of the spine

1973 ◽  
Vol 36 (2) ◽  
pp. 260-264 ◽  
Author(s):  
P. S. Ramani ◽  
R. P. Sengupta
Keyword(s):  
Cauda Equina ◽  
Cauda Equina Compression

scholarly journals FUNCTIONAL OUTCOME AFTER EXPERIMENTAL CAUDA EQUINA COMPRESSION

1997 ◽  
Vol 79-B (4) ◽  
pp. 670-674 ◽  
Author(s):  
F. E. Sayegh ◽  
G. A. Kapetanos ◽  
P. P. Symeonides ◽  
G. Anogiannakis ◽  
M. Madentzidis
Keyword(s):  
Functional Outcome ◽  
Cauda Equina ◽  
Cauda Equina Compression

A prospective study of the role of bladder scanning and post-void residual volume measurement in improving diagnostic accuracy of cauda equina syndrome

2020 ◽  
Vol 102-B (6) ◽  
pp. 677-682
Author(s):  
Galateia Katzouraki ◽  
Akbar Jaleel Zubairi ◽  
Oded Hershkovich ◽  
Michael P. Grevitt
Keyword(s):  
Risk Stratification ◽  
Prospective Study ◽  
Clinical Assessment ◽  
Predictive Value ◽  
Cauda Equina Syndrome ◽  
Cauda Equina ◽  
Cost Savings ◽  
Volume Measurement ◽  
Cauda Equina Compression ◽  
Mri Scans

Aims Diagnosis of cauda equina syndrome (CES) remains difficult; clinical assessment has low accuracy in reliably predicting MRI compression of the cauda equina (CE). This prospective study tests the usefulness of ultrasound bladder scans as an adjunct for diagnosing CES. Methods A total of 260 patients with suspected CES were referred to a tertiary spinal unit over a 16-month period. All were assessed by Board-eligible spinal surgeons and had transabdominal ultrasound bladder scans for pre- and post-voiding residual (PVR) volume measurements before lumbosacral MRI. Results The study confirms the low predictive value of ‘red flag’ symptoms and signs. Of note ‘bilateral sciatica’ had a sensitivity of 32.4%, and a positive predictive value (PPV) of only 17.2%, and negative predictive value (NPV) 88.3%. Use of a PVR volume of ≥ 200 ml was a demonstrably more accurate test for predicting cauda equina compression on subsequent MRI (p < 0.001). The PVR sensitivity was 94.1%, specificity 66.8%, PPV 29.9% and NPV 98.7%. The PVR allowed risk-stratification with 13% patients deemed ‘low-risk’ of CES. They had non-urgent MRI scans. None of the latter scans showed any cauda equina compression (p < 0.006) or individuals developed subsequent CES in the intervening period. There were considerable cost-savings associated with the above strategy. Conclusion This is the largest reported prospective evaluation of suspected CES. Use of the PVR volume ≥ 200 ml was considerably more accurate in predicting CES. It is a useful adjunct to conventional clinical assessment and allows risk-stratification in managing suspected CES. If adopted widely it is less likely incomplete CES would be missed. Cite this article: Bone Joint J 2020;102-B(6):677–682.

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 ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Lysophosphatidic Acid ◽  
Mass Spectrometry Imaging ◽  
Cauda Equina ◽  
Motor Dysfunction ◽  
Lipid Mediator ◽  
Neurogenic Claudication ◽  
Imaging Analysis ◽  
Cauda Equina Compression ◽  
Tissue Damages

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.

The Neurological Compromised Spine Due to Ewing Sarcoma. What First

Neurosurgery ◽  
2015 ◽  
Vol 77 (5) ◽  
pp. 718-725 ◽  
Author(s):  
Lida Mirzaei ◽  
Suzanne E.J. Kaal ◽  
Hendrik W.B. Schreuder ◽  
Ronald H.M.A. Bartels
Keyword(s):  
Ewing Sarcoma ◽  
Neurological Deficit ◽  
Multidisciplinary Approach ◽  
Cauda Equina ◽  
Case Series ◽  
Decompressive Laminectomy ◽  
Cauda Equina Compression ◽  
Before And After ◽  
Frankel Grade

Abstract BACKGROUND: The vertebral column is an infrequent site of primary involvement in Ewing sarcoma. Yet when Ewing sarcoma is found in the spine, the urge for decompression is high because of the often symptomatic compression of neural structures. It is unclear in alleviating a neurological deficit whether chemotherapy is preferred over decompressive laminectomy. OBJECTIVE: To underline, in this case series, the efficiency of initial chemotherapy before upfront surgery in the setting of high-grade spinal cord or cauda equina compression of primary Ewing sarcoma. METHODS: Fifteen patients with Ewing sarcoma primarily located in the spine were treated at our institution between 1983 and 2015. Localization, neurological deficit expressed as Frankel grade, and outcome expressed as Rankin scale before and after initial chemotherapy, the recurrence rate, and overall survival were evaluated. The multidisciplinary approach of 1 case will be discussed in detail. RESULTS: Nine patients (60%) were female. The age at presentation was 15.0 ± 5.5 years (range: 0.9–22.8 years). Ten patients (67%) were initially treated with chemotherapy, and 1 patient (7%) was treated primarily with radiotherapy followed by chemotherapy. The remaining 4 patients (27%) were initially treated with decompressive surgery. All patients treated primarily nonsurgically improved neurologically at follow-up, showing the importance of chemotherapy as an effective initial treatment option. CONCLUSION: Adequate and quick decompression of neural structures with similar results can be achieved by chemotherapy and radiotherapy, avoiding the local spill of malignant cells.

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