Neurol India Home 

Year : 2016  |  Volume : 64  |  Issue : 4  |  Page : 839--840

Author's reply

Vedantam Rajshekhar 
 Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632 004, Tamil Nadu, India

Correspondence Address:
Vedantam Rajshekhar
Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632 004, Tamil Nadu

How to cite this article:
Rajshekhar V. Author's reply.Neurol India 2016;64:839-840

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Rajshekhar V. Author's reply. Neurol India [serial online] 2016 [cited 2022 Aug 13 ];64:839-840
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Full Text

I thank Dr. Goel for his interest in our article on 3-level corpectomy in patients with cervical spondylotic myelopathy (CSM) and ossified posterior longitudinal ligament (OPLL) published recently in the Journal.[1]

Dr. Goel's hypothesis on the pathogenesis of spondylotic disease and OPLL rests exclusively on “instability” due to degenerative changes in the facet joints. Hence, his proposed management strategy involves stabilizing the cervical spine using spacers placed in the facet joints without any decompression. He cannot, however, deny that the disc and the ligaments such as the posterior longitudinal ligament (PLL) also participate in the degenerative process and contribute to cord compression. Therefore, the two main points of contention with respect to the pathogenesis of CSM are whether the degenerative process started in the facet joints or the discs and PLL, and whether instability alone (dynamic compression) or both static and dynamic compression play a role.

The first argument is more of “chicken or egg” situation and it is almost impossible to prove whether the degeneration starts initially in the facet joints or the discs and subsequently involves the other. The second argument, to my mind, is a settled issue. Dynamic compression due to instability as a cause of CSM has a long history. As far back as 1954, Pallis et al.,[2] documented the contribution of instability, recognized on plain radiographs as “subluxation” of the bodies, to the causation of CSM. Nurick,[3] in his landmark article in 1972, corroborated their findings by reporting that the proportion of patients with subluxation was higher in the poorer grades than in those in the better grades. In other words, dynamic compression was recognized by these early workers to be an important component for the pathogenesis of CSM.

Flowing from these early observations of “instability” in patients with CSM and experimental evidence,[4] “stabilization” of the cervical spine was suggested as a necessary component of the surgical management, although, almost always with decompression of the neural elements.[5],[6],[7] In the case of conservative therapy, however, immobilization of the neck alone in a cervical orthosis is a valid option and has been shown to be associated with improvement.[8] I do not agree that fusion following decompression surgeries such as central corpectomy is only done because of the destabilizing effects of the corpectomy; it is also done as a method for addressing any existing instability in the spine caused by the spondylotic process. In recent years, even proponents of a posterior decompression surgery such as a laminectomy have incorporated fusion into the procedure.

The management of CSM or OPLL is generally accepted to consist of both decompression and stabilization. It would not be prudent to ignore the obvious “static” compression seen on imaging and rely solely on immobilization of the spine to achieve good outcomes. The good outcomes reported with ventral decompression and fusion reported by different surgeons from across the world over the last five decades stands as testimony to its efficacy.[7],[9] Currently, I believe, as do most neurosurgeons, that some form of decompressive surgery is the standard of care for patients with significant myelopathy due to CSM or OPLL.

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1Gupta A, Rajshekhar V. Functional and radiological outcome in patients undergoing three-level corpectomy for multilevel cervical spondylotic myelopathy and ossified posterior longitudinal ligament. Neurol India 2016;64:90-6.
2Pallis C, Jones AM, Spillane JD. Cervical spondylosis. Brain 1954;77:274-89.
3Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain 1972;95:87-100.
4Cusick JF, Steiner RE, Berns T. Total stabilization of the cervical spine in patients with cervical spondylotic myelopathy. Neurosurgery 1986;18:491-5.
5Ducker TB. Experimental injury of the spinal cord, in Vinken PJ, Bryun GW (eds): Handbook of Clinical Neurology. Injuries of the spine and spinal cord and column. Amsterdam: North Holland, 1976, Vol 25, pp 9-26.
6Bohlman HH. Cervical spondylosis with moderate to severe myelopathy. A report of seventeen cases treated with Robinson anterior cervical discectomy and fusion. Spine 2:151-162, 1977.
7Saunders RL, Bernini PM, Shirreffs Jr TG, Reeves AG. Central corpectomy for cervical spondylotic myelopathy: A consecutive series with long-term follow-up evaluation. J Neurosurg 1991;74:163-70.
8Roberts AH. Myelopathy due to cervical spondylosis treated with collar immobilization. Neurology 1966;16:951-4.
9Rajshekhar V, Kumar GSS. Functional outcome after central corpectomy in poor-grade patients with cervical spondylotic myelopathy or ossified posterior longitudinal ligament. Neurosurgery 2005;56:1279-85.