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Journal of Craniovertebral Junction and Spine
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EDITORIAL
Year : 2021  |  Volume : 12  |  Issue : 4  |  Page : 327-328  

Basilar invagination, spinal “degeneration,” and “lumbosacral” spondylolisthesis: Instability is the cause and stabilization is the treatment


Department of Neurosurgery, Lilavati Hospital and Research Center; Department of Neurosurgery, R N Cooper Hospital and Medical College; Department of Neurosurgery, Bombay Hospital Institute of Medical Sciences, Mumbai, Maharashtra, India

Date of Submission06-Nov-2021
Date of Acceptance06-Nov-2021
Date of Web Publication11-Dec-2021

Correspondence Address:
Atul Goel
Department of Neurosurgery, Lilavati Hospital and Research Center, Bandra, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcvjs.jcvjs_140_21

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How to cite this article:
Goel A. Basilar invagination, spinal “degeneration,” and “lumbosacral” spondylolisthesis: Instability is the cause and stabilization is the treatment. J Craniovert Jun Spine 2021;12:327-8

How to cite this URL:
Goel A. Basilar invagination, spinal “degeneration,” and “lumbosacral” spondylolisthesis: Instability is the cause and stabilization is the treatment. J Craniovert Jun Spine [serial online] 2021 [cited 2022 Jan 25];12:327-8. Available from: https://www.jcvjs.com/text.asp?2021/12/4/327/332217



In the year 1998, we identified atlantoaxial facetal listhesis as the initial point of pathogenesis of basilar invagination.[1],[2],[3] Subaxial spinal “degeneration” was also identified to have its origin in facetal listhesis. Standing human position and “lifelong” stress on muscles facilitating this posture form the basis of facetal listhesis. Muscle abuse, disuse, and injury propel “vertical” spinal instability that manifests initially in the form of reduction in the interfacetal space and subsequently listhesis.[4]

Telescoping of the spinal segments as a result of muscle weakness forms the basis of basilar invagination in the craniovertebral junction and spinal degeneration in the subaxial spine. The atlantoaxial instability is more often chronic or long standing. Our articles refer to a number of natural protective maneuvers in the face of chronic atlantoaxial instability that lead to musculoskeletal and neural alterations.[5],[6],[7],[8],[9],[10],[11],[12],[13],[14] These alterations include short neck, short head, short spine, torticollis, dorsal kyphoscoliosis, Klippel-Feil alteration, C2–3 fusion, assimilation of atlas, bifid arches of atlas and axis, platybasia, Chiari formation, and syringomyelia.[5],[6],[7],[8],[9],[10],[11],[12],[13],[14] Despite the fact that all the mentioned secondary manifestations appear to be compressing or deforming the neural structures, our analysis suggests that they are all secondary to vertical spinal instability, are protective natural events, and are reversible following atlantoaxial stabilization.[15] Essentially, the clinical issue in basilar invagination is spinal instability and stabilization is the treatment.[16] It is not neural deformation or compression that is the cause of symptoms, but it is muscle weakness-related spinal instability that initiates, propels, and establishes secondary manifestations and results in clinical symptoms.[17],[18],[19] Restoration or realignment of the musculoskeletal and neural structures can eventually happen, either in the early or delayed postoperative period. It has to be clearly understood that the aim of surgery is spinal segmental stabilization and not any direct surgical action against any of the secondary manifestations.[16] Secondary manifestations and neural compression that might persist after stabilization need only observation and no direct surgical action. Even when the realignment is incomplete and there is persistent radiological evidence of “compression,” there may not be any need for “decompression” of the neural structures. Resection of bone in an unstable spinal segment for “decompression” may actually be harmful in the long run as the bone available for arthrodesis is consequently reduced.

In degenerative spinal disease, all the known so-called “pathological” entities such as osteophyte formation, ligamentum flavum buckling, disc space reduction, and disc bulging into spinal canal and several similar issues that ultimately result in reduction in neural foramina and spinal canal are related to primary issue of vertical spinal instability.[4] Instability at the facets is related to compromise of the strength or turgor of the muscles that facilitate the movements and standing human posture. Despite the fact that all the secondary events have been incriminated to be the cause of clinical symptoms, our observations suggest that symptoms are related more to instability and its secondary effects. As in the craniovertebral junction, all the secondary manifestations have a naturally protective role and are reversible following stabilization. “Only stabilization” of the affected spinal segment/s is the treatment.

Lumbosacral (and other spinal segment) spondylolisthesis is a result of incompetence of the muscles and related spinal instability. Spondylolisthesis is actually a manifestation of more “severe” form of spinal segmental instability or spinal degeneration. The fracture of pars interarticularis in cases with lumbosacral listhesis simulates the fracture of pedicle of C2 in cases of Hangman's fracture. The clinical symptoms are related to spinal instability and not neural deformation or compression as is observed on radiological imaging. Like in basilar invagination, wherein there is a need to stabilize the atlantoaxial joint and any form of bone decompression can be avoided, in lumbosacral spondylolisthesis, it is essential to firmly stabilize the affected spinal segment with the aim of arthrodesis or fusion and avoid any form of bone decompression. Moreover, although preferable, it is unnecessary to directly aim at realignment. This concept suggests that any form of laminectomy, discoidectomy, or distraction–realignment for decompression and realignment can be avoided in cases of lumbosacral spondylolisthesis.



 
   References Top

1.
Kothari M, Goel A. Transatlantic odonto-occipital listhesis: The so-called basilar invagination. Neurol India 2007;55:6-7.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Goel A, Bhatjiwale M, Desai K. Basilar invagination: A study based on 190 surgically treated patients. J Neurosurg 1998;88:962-8.  Back to cited text no. 2
    
3.
Goel A. Treatment of basilar invagination by atlantoaxial joint distraction and direct lateral mass fixation. J Neurosurg Spine 2004;1:281-6.  Back to cited text no. 3
    
4.
Goel A. Vertical facetal instability: Is it the point of genesis of spinal spondylotic disease? J Craniovertebr Junction Spine 2015;6:47-8.  Back to cited text no. 4
    
5.
Goel A, Shah A. Reversal of longstanding musculoskeletal changes in basilar invagination after surgical decompression and stabilization. J Neurosurg Spine 2009;10:220-7.  Back to cited text no. 5
    
6.
Goel A, Jain S, Shah A. Radiological evaluation of 510 cases of basilar invagination with evidence of atlantoaxial instability (Group A Basilar Invagination). World Neurosurg 2018;110:533-43.  Back to cited text no. 6
    
7.
Goel A, Nadkarni T, Shah A, Sathe P, Patil M. Radiologic evaluation of basilar invagination without obvious atlantoaxial instability (Group B Basilar Invagination): Analysis based on a study of 75 patients. World Neurosurg 2016;95:375-82.  Back to cited text no. 7
    
8.
Goel A, Sathe P, Shah A. Atlantoaxial fixation for basilar invagination without obvious atlantoaxial instability (Group B Basilar Invagination): Outcome analysis of 63 surgically treated cases. World Neurosurg 2017;99:164-70.  Back to cited text no. 8
    
9.
Goel A, Patil A, Shah A, Dandpat S, Rai S, Ranjan S. Os odontoideum: Analysis of 190 surgically treated cases. World Neurosurg 2020;134:e512-23.  Back to cited text no. 9
    
10.
Goel A. Short neck, short head, short spine, and short body height – Hallmarks of basilar invagination. J Craniovertebr Junction Spine 2017;8:165-7.  Back to cited text no. 10
    
11.
Goel A, Vutha R, Shah A, Dharurkar P, Jadhav N, Jadhav D. Spinal kyphoscoliosis associated with Chiari formation and syringomyelia 'recovery' following atlantoaxial fixation: A preliminary report and early results based on experience with 11 surgically treated cases. World Neurosurg 2019;125:e937-46.  Back to cited text no. 11
    
12.
Goel A. Is atlantoaxial instability the cause of Chiari malformation? Outcome analysis of 65 patients treated by atlantoaxial fixation. J Neurosurg Spine 2015;22:116-27.  Back to cited text no. 12
    
13.
Shah A, Sathe P, Patil M, Goel A. Treatment of “idiopathic” syrinx by atlantoaxial fixation: Report of an experience with nine cases. J Craniovertebr Junction Spine 2017;8:15-21.  Back to cited text no. 13
    
14.
Goel A, Nadkarni T, Shah A, Ramdasi R, Patni N. Bifid anterior and posterior arches of atlas: Surgical implication and analysis of 70 cases. Neurosurgery 2015;77:296-305.  Back to cited text no. 14
    
15.
Goel A, Shah A, Rajan S. Vertical mobile and reducible atlantoaxial dislocation. Clinical article. J Neurosurg Spine 2009;11:9-14.  Back to cited text no. 15
    
16.
Goel A. Basilar invagination: Instability is the cause and stabilization is the treatment. Neurospine 2020;17:585-7.  Back to cited text no. 16
    
17.
Goel A. Not neural deformation or compression but instability is the cause of symptoms in degenerative spinal disease. J Craniovertebr Junction Spine 2014;5:141-2.  Back to cited text no. 17
    
18.
Goel A, Dandpat S, Shah A, Rai S, Vutha R. Muscle weakness-related spinal instability is the cause of cervical spinal degeneration and spinal stabilization is the treatment: An experience with 215 cases surgically treated over 7 years. World Neurosurg 2020;140:614-21.  Back to cited text no. 18
    
19.
Goel A, Grasso G, Shah A, Rai S, Dandpat S, Vaja T, et al. “Only spinal fixation” as surgical treatment of cervical myelopathy related to ossified posterior longitudinal ligament: Review of 52 cases. World Neurosurg 2020;140:556-63.  Back to cited text no. 19
    




 

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