Episodic cauda equina compression from an intradural lumbar herniated disc: a case of ‘floppy disc’

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.

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Does a history of lumbar spine surgery predict radiological cauda equina compression in patients undergoing MRI for suspected cauda equina syndrome?

British Journal of Neurosurgery ◽

10.1080/02688697.2019.1687845 ◽

2019 ◽

Vol 34 (1) ◽

pp. 76-79

Author(s):

Savva Pronin ◽

Julie Woodfield ◽

Ingrid Hoeritzauer ◽

Alan Carson ◽

Jon Stone ◽

...

Keyword(s):

Lumbar Spine ◽

Spine Surgery ◽

Cauda Equina Syndrome ◽

Cauda Equina ◽

Lumbar Spine Surgery ◽

Cauda Equina Compression ◽

History Of

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

Scientific Reports ◽

10.1038/s41598-019-52999-5 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 4

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.

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