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 Table of Contents  
CASE REPORT
Year : 2018  |  Volume : 2  |  Issue : 1  |  Page : 5-8

A rare presentation of cauda equina syndrome due to compression by vertebral endplate masquerading as intervertebral disc extrusion


Department of Orthopaedics, JSS Medical College and Hospital, JSS University, Mysore, Karnataka, India

Date of Web Publication25-Sep-2018

Correspondence Address:
Supreeth Nekkanti
Department of Orthopaedics, JSS Medical College and Hospital, JSS University, Mysore, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/EJSS.EJSS_2_18

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  Abstract 

Cauda equina syndrome (CES) is an orthopedic emergency. The common causes of CES are intervertebral disc prolapse and traumatic injuries of the spine. We report an unusual case of vertebral endplate erosion into the spinal canal leading to CES. We report a 37-year-old male patient who had a history of low back pain radiating to both the legs for 1 month. He was receiving treatment at a local hospital. He presented to our emergency department with the inability to stand, walk, or void for 1 day. Radiographs and magnetic resonance imaging confirmed CES due to intervertebral disc prolapse. Our patient's diagnosis of vertebral endplate extrusion was made intraoperatively when the extruded material was found to be hard in consistency, and histopathological analysis confirmed the diagnosis. A diagnosis of vertebral endplate causing CES has been reported only in adolescents but never in adults. Preoperative computed tomography scans can help in easy diagnosis.

Keywords: Cauda equina syndrome, laminectomy, vertebral endplate extrusion


How to cite this article:
Balan G, Moogali AS, Nekkanti S, Mruthyunjaya M. A rare presentation of cauda equina syndrome due to compression by vertebral endplate masquerading as intervertebral disc extrusion. J Spinal Stud Surg 2018;2:5-8

How to cite this URL:
Balan G, Moogali AS, Nekkanti S, Mruthyunjaya M. A rare presentation of cauda equina syndrome due to compression by vertebral endplate masquerading as intervertebral disc extrusion. J Spinal Stud Surg [serial online] 2018 [cited 2018 Dec 14];2:5-8. Available from: http://www.jsss-journal.com/text.asp?2018/2/1/5/242153


  Introduction Top


Cauda equina syndrome (CES) is a serious neurological condition in which neurological dysfunction affects the lumbar and sacral nerve roots within the vertebral canal. The most common cause is central disc protrusion at L5–S1 level.[1] Various other less common causes have been reported. The causes are outlined below[1] [Figure 1].
Figure 1: Table of list of causes of cauda eauina syndrome

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One of the rarest causes reported in the literature is an erosion of the vertebral endplate where the fragment protrudes into the spinal canal; the symptoms may mimic extruded lumbar intervertebral disc.[2] We report an extremely rare case of CES which was caused by mechanical compression of eroded endplate in the spinal canal in a 37-year-old patient. There has been no previous such report in an adult patient in our review of the literature.


  Case Report Top


A 37-year-old male patient who is a daily wage laborer by occupation with a history of a low backache radiating to bilateral lower limb for 1 month, who was diagnosed to have prolapsed disc at a local hospital where he was advised to take rest and analgesics. He presented to us in the emergency department with complaints of inability to stand, walk, and void since 1 day. On examination, he was found to have perianal anesthesia and loss of rectal tone. Moreover, power in his bilateral hip and knee joint was found to be 4/5 and ankle, extensor hallucis longus, extensor digitorum longus, flexor hallucis longus muscle, and flexor digitorum longus was found to be 3/5. About 600 ml of urine was collected on catheterization.

X-ray showed decreased L5–S1 disc space with the erosion of the lower L5 and upper S1 end plates with spondylotic changes [Figure 2]. Magnetic resonance imaging (MRI) was done which showed prolapsed intervertebral disc at L5–S1, obliteration of the spinal canal at the level of S1 and change in the signal intensity of the material compared to that of disc material. Lesions were seen in L1 and L3 suggestive of hemangioma [Figure 3]a and [Figure 3]b.
Figure 2: Preoperative radiograph

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Figure 3: (a and b) Preoperative magnetic resonance imaging

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The patient was taken up for emergency laminectomy, decompression of the canal, and discectomy using posterior midline approach. The material which was found in the canal was shiny, smooth and hard, unlike the routine extruded disc [Figure 4]. Histological examination showed fibrocartilagenous material with abundant blood vessels in between which was suggestive of a vertebral endplate [Figure 5]. Postoperative period was uneventful.
Figure 4: Intraoperative photograph of end plate material removed

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Figure 5: Histopathological photograph of the end plate material

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The patient was encouraged active straight leg raise test, knee and ankle range of motion exercises, and walking with the support of walker from the day 1 after the surgery. Suture removal was done on the post operative day 10. The patient had gradual improvement of his neurological deficit. At 1-year follow-up, the patient has regained his normal neurological functions (lower limb power 5/5 and normal sensation) except for difficulty in the erection of penis [Figure 6]a,[Figure 6]b,[Figure 6]c,[Figure 6]d,[Figure 6]e.
Figure 6: (a-e) Follow up photos showing the good function of lower limbs at 1 year

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  Discussion Top


Very little has been published about vertebral endplates protruding into the spinal canal causing neurological complications. Mahaisavariya and Wittayakom[2] published a similar case of the end plate displacing into the spinal canal in a 15-year-old in 1993. His patient suffered a sudden weakness involving the L5, S1 1 day after trying to carry a heavy weight which subsequently progressed to complete loss of motor and sensation over the foot and ankle. Techakapuch in 1981[3] also reported a similar case in 1981, but the exact details of the cause and treatment were not found. There have been a few articles of slipped vertebra apophysis into the spinal canal in adolescents.[2],[3],[4],[5],[6],[7],[8],[9],[10] There have been no previous reports published of a similar pathology in an adult.

In our patient, a 37-year-old male heavy manual laborer had persisting low back pain with numbness over a month, following which it progressed to complete loss of rectal tone, inability to void and to stand up on his feet.

The most common cause of CES is a lumbar disc prolapsed with an incidence of 2%–6%.[1] Vertebral endplate fragments causing CES have been reported only in two cases.

Fraser et al.[11] studied 105 patients with CES to define a set of criteria to help orthopedicians to provide a diagnosis of CES. He published that one or more of the following must be present: (1). Bladder and bowel dysfunction, (2). Reduced sensation in the saddle area, and (3). Sexual dysfunction, with a possible neurologic deficit in the lower limb (motor/sensory loss and reflex change).

He explained that the psychosocial aspects of the back pain and inability or dysfunction micturition might cause the patient to withhold information about lack of erection. Saddle anesthesia and urinary retention more than 500 ml are the best positive predictors of CES.[1],[12],[13] Micturition dysfunction is usually required to diagnose CES.[14]

Tandon and Sankaran, in 1967[15] described three clinical scenarios for CES as follows: (1). Rapid onset without a previous history of back problems. (2). Acute bladder dysfunction with a history of low back pain and sciatica, and (3). Chronic backache and sciatica with gradually progressing CES often with canal stenosis. Our patient seems to best fit in the third clinical scenario.

In 2002, Gleave and Macfarlane[1],[16] proposed the description of CES into two stages. CESI-When the syndrome is incomplete the patient has urinary difficulties of neurogenic origin including altered urinary sensation, loss of desire to void, poor urinary stream, and the need to strain to micturate.

CESR-the complete syndrome is characterized by painless urinary retention and overflow incontinence when the bladder is no longer under executive control. There is usually extensive or complete saddle and genital sensory deficit with deficient trigone sensation. Our patient falls under the CESR category with significant urinary problems.

MRI is the gold standard for diagnosis of CES as it clearly depicts the soft-tissue pathology and delineates the level of nerve root compression.[1] Poor patient tolerance, pacemakers, claustrophobia are possible contraindications to MRI. In such patients, myelography or computed tomography (CT) myelography may be preferred.[1],[17] Inflammatory markers and cerebrospinal fluid studies should be performed when inflammatory or infective pathology is considered. In our patient, an MRI was done, and a diagnosis of disc extrusion at L5–S1 was made.

Immediate surgical decompression is the mainstay of treatment of CES. The stabilization of the spine may be required in cases of extensive decompression or instability following decompression. There is limited evidence to suggest the best approach for decompression.[1]

Our patient was operated, and the extruded material was removed completely thus relieving the compression of the nerve roots. The extruded material was hard in consistency which raised a doubt about the diagnosis of vertebral endplate extrusion. The extruded material was sent for histopathological analysis which confirmed the suspicion of vertebral endplate extrusion into the lumbar spinal canal causing CES.

Histopathological analysis of the vertebral endplate usually shows a thick cartilaginous endplate with only a few chondrocytes. This layer is stained pink with areas of light blue, and seems to contain calcified fibrocartilage based on gross morphology, although immunostaining for Type I and Type II collagen is needed to confirm this.[18]

Second, there is a bony endplate that serves as the transition from the cartilaginous layer and the vertebral body. The bony endplate only contains relatively fewer blood vessels. There are 1–3 layers of tidemark-like structures identified between the calcified cartilage and bony endplate.[18],[19] Similar features were seen in our patient's histopathological photographs.

The patient recovered symptomatically. He regained 5/5 motor function of his lower limbs, and he has no sensory deficit. The patient still cannot induce an erection of his penis.

The limitation of this case file is that we did not conduct a CT scan of the spine to evaluate the extruded material. The CT scan could help us confirm that the material was a vertebral endplate and not a disc. Mahaisavariya and Wittayakom[2] did a CT scan in his patient after they found evidence of a bone fragment in the spinal canal in the plain radiographs. The absence of such evidence in the plain radiograph made it diagnostically challenging for the authors, and he was treated as a patient with intervertebral disc extrusion. The authors feel that this could be the diagnostic learning point from this study.


  Conclusion Top


Vertebral endplate fragments causing cauda equina syndrome is extremely rare and has never been reported in adults. A strong index of suspicion followed by a CT scan of the spine is essential to make the diagnosis. Histopathology of the biopsied material usually confirms the radiological diagnosis. The mainstay of treatment of CES is early adequate decompression and stabilization when needed.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Dhokia R, Eames N. Cauda Equina Syndrome: A review of the current position. Hard Tissue 2014;3:7.  Back to cited text no. 1
    
2.
Mahaisavariya B, Wittayakom T. Lumbar vertebral growth plate displaced into the spinal canal. A case report of a 15-year-old boy. Acta Orthop Scand 1993;64:103-4.  Back to cited text no. 2
    
3.
Techakapuch S. Rupture of the lumbar cartilage plate into the spinal canal in an adolescent. A case report. J Bone Joint Surg Am 1981;63:481-2.  Back to cited text no. 3
    
4.
Farrokhi MR, Masoudi MS. Slipped vertebral epiphysis (report of 2 cases). J Res Med Sci 2009;14:63-6.  Back to cited text no. 4
    
5.
Swärd L, Hellström M, Jacobsson B, Karlsson L. Vertebral ring apophysis injury in athletes. Is the etiology different in the thoracic and lumbar spine? Am J Sports Med 1993;21:841-5.  Back to cited text no. 5
    
6.
Chang CH, Lee ZL, Chen WJ, Tan CF, Chen LH. Clinical significance of ring apophysis fracture in adolescent lumbar disc herniation. Spine 2008;33:1750-4.  Back to cited text no. 6
    
7.
Kadam G, Narsinghpura K, Deshmukh S, Desai S. Traumatic lumbar vertebral ring apophysis fracture with disk herniation in an adolescent. Radiol Case Rep 2017;12:427-30.  Back to cited text no. 7
    
8.
Handel SF, Twiford TW, Reigel DH, Kaufman HH. Posterior lumbar apophyseal fractures. Radiology 1979;130:629-33.  Back to cited text no. 8
    
9.
Ehni G, Schneider SJ. Posterior lumbar vertebral rim fracture and associated disc protrusion in adolescence. J Neurosurg 1988;68:912-6.  Back to cited text no. 9
    
10.
Lowrey JJ. Dislocated lumbar vertebral epiphysis in adolescent children. Report of three cases. J Neurosurg 1973;38:232-4.  Back to cited text no. 10
    
11.
Fraser S, Roberts L, Murphy E. cauda equina syndrome: A literature review of its definition and clinical presentation. Arch Phys Med Rehabil 2009;90:1964-8.  Back to cited text no. 11
    
12.
Balasubramanian K, Kalsi P, Greenough CG, Kuskoor Seetharam MP. Reliability of clinical assessment in diagnosing cauda equina syndrome. Br J Neurosurg 2010;24:383-6.  Back to cited text no. 12
    
13.
Yan L, Liu Y, He B, Liu J, Luo Z, Hao D. Clinical case-series report of traumatic cauda equina herniation: A pathological phenomena occurring with thoracolumbar and lumbar burst fractures. Medicine 2017;96:e6446.  Back to cited text no. 13
    
14.
Korse NS, Jacobs WC, Elzevier HW, Vleggeert-Lankamp CL. Complaints of micturition, defecation and sexual function in cauda equina syndrome due to lumbar disk herniation: A systematic review. Eur Spine J 2013;22:1019-29.  Back to cited text no. 14
    
15.
Tandon PN, Sankaran B. Cauda equina syndrome due to lumbar disc prolapse. Indian J Orthop 1967;1:112.  Back to cited text no. 15
    
16.
Gleave JRW, Macfarlane R. Cauda equina syndrome: what is the relationship between timing of surgery and outcome? Br J Neurosurg 2002;16:325-8  Back to cited text no. 16
    
17.
Shinbane JS, Colletti PM, Shellock FG. Magnetic resonance imaging in patients with cardiac pacemakers: Era of “MR conditional” designs. J Cardiovasc Magn Reson 2011;13:63.  Back to cited text no. 17
    
18.
Zhang Y, Lenart BA, Lee JK, Chen D, Shi P, Ren J, et al. Histological features of endplates of the Mammalian spine: From mice to men. Spine 2014;39:E312-7.  Back to cited text no. 18
    
19.
Zhang Y, Drapeau S, An HS, Markova D, Lenart BA, Anderson DG, et al. Histological features of the degenerating intervertebral disc in a goat disc-injury model. Spine 2011;36:1519-27.  Back to cited text no. 19
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]



 

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