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EDITORIAL
Year : 2023 | Volume
: 14
| Issue : 1 | Page : 1-3
Joint “release” and joint “realignment:” Are they necessary for the treatment of basilar invagination?
Atul Goel
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; Department of Neurosurgery, K. J. Somaiya Medical College, Hospital and Research Center, Mumbai, Maharashtra, India
Correspondence Address:
Atul Goel
Department of Neurosurgery, Lilavati Hospital and Research Center, Bandra, Mumbai - 400 050, Maharashtra
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/jcvjs.jcvjs_14_23
For several decades, basilar invagination was identified to be a congenital anomaly and an outcome of primary structural malformation. Various speculations regarding the possible causes of embryonic dysgenesis have been analyzed.[1],[2],[3] Several landmark contributions on the subject find a place in the literature. A number of radiological parameters that help in identifying the presence of basilar invagination and quantifying its extent have been popularly used. Instability of the craniovertebral junction was essentially not considered to be of primary significance in the management and none of the major articles on the subject focused or even dwelled on this subject. “Compression” of the neural structures was identified to be the pathological issue and accordingly, “decompression” was the surgical treatment. Transoral surgical route was a popular mode of decompression for Group A basilar invagination and foramen magnum decompression was identified to be a simple and safe form of treatment for Group B basilar invagination.[4] Some authors observed that the procedure of decompression that involved the removal of bone and soft tissues had the potential of resulting in immediate or delayed postoperative instability of the craniovertebral junction. Accordingly, some authors modified their technique of decompression by transoral route[5] or by posterior foramen magnum decompression.[6] Few authors recommended primary stabilization of the craniovertebral junction in addition to decompression.[4]
In the year 2004, we identified that instability is the primary issue and the nodal point of pathogenesis in Group A basilar invagination.[7] We suggested a modification of our technique of lateral mass plate and screw fixation[8],[9] for the treatment of Group A basilar invagination. The technique involved the opening of the atlantoaxial joint, denuding of the articular cartilage, “distraction” of the facets, impaction of Goel facet spacer and bone graft into the articular cavity, and subsequent plate and screw fixation.[7] The technique resulted in the stabilization of the atlantoaxial joint, reduced basilar invagination, and realigned the craniovertebral junction. The terms instability in pathogenesis and “reduction-realignment” as treatment were introduced for the first time in the literature for Group A basilar invagination.[7] This concept of the possibility of manipulation of facets, reduction, and realignment has revolutionized the field of craniovertebral junction in general and of treatment of basilar invagination in particular.[10] During this time period, we observed that there is fixed atlantoaxial instability in cases with Group B basilar invagination, and recommended foramen magnum decompression as treatment.
As our experience in the field matured, we identified the clinical entity of central or axial atlantoaxial instability or dislocation (CAAD).[11],[12],[13] CAAD can be present even when dynamic imaging does not depict any abnormal bone movements, any alteration in the atlantodental interval, or any evidence of neural or dural compression. Such a form of instability is usually present in chronically unstable atlantoaxial joints. Several so-called pathological clinical entities such as Chiari formation, syringomyelia, basilar invagination, platybasia, Klippel–Feil abnormality, assimilation of atlas, C2-3 fusion, bifid arch of atlas, and os odontoideum are secondary clinical events that are naturally protective or adaptive, indicative of atlantoaxial instability and are reversible following atlantoaxial stabilization.[14],[15],[16],[17],[18],[19],[20],[21],[22],[23] We observed that these clinical events have a protective role, and preferred to label them as craniovertebral “alterations” rather than craniovertebral junction “anomalies.”[24] We preferred the term Chiari “formation” to Chiari “malformation.”[25] Direct surgical treatment for these secondary events is unnecessary and counter-effective.
The exact timing and cause of instability of the atlantoaxial articulation that will eventually result in basilar invagination can only be speculated. Our articles observe that birth trauma related to poor child delivery practices can be a cause of such injury.[4],[7] Unsafe child handling in the first few months of birth when head holding is incomplete can also be a cause. Protein–calorie malnutrition can propel clinical consequences. It also remains unclear as to how patients manifest differently despite the fact that the primary event is atlantoaxial instability.
Essentially, we observed that atlantoaxial instability is the primary point of genesis of both Group A and Group B basilar invagination.[10],[14],[15] Chronic or long-standing atlantoaxial instability is primary and basilar invagination is a secondary event that is naturally protective or adaptive. Our articles discuss that it is not neural deformation or neural compression that is the issue in craniovertebral junction and subaxial spine surgery, but it is the instability of the affected spinal segment. Instability is the nodal point of the pathogenesis of basilar invagination and the basis of presenting clinical symptoms.[26],[27]
Muscle weakness that leads to the incompetence of the facets is the cause of basilar invagination. It is not muscle hyperactivity, spasm, hypertrophy, or stretch that results in basilar invagination. Instability is the cause, and firm stabilization is the treatment.[27] Any kind of muscle/ligament section in the vicinity of the atlantoaxial articulation in an effort to “release” the “tension bands” and to achieve realignment is an unnecessary surgical exercise. Direct opening of the unstable articulation and its distraction is sufficient to release the malalignment. The “telescoped” facets need a distraction for realignment. Some surgeons prefer two-stage surgery. The first surgery involves transoral “release” of muscles, sectioning of the articular cartilage, sectioning of apical and/or alar ligaments, and removal of articular adhesions to achieve realignment.[28] Second-stage surgery involves posterior craniovertebral junction stabilization. Our opinion is that the first stage of transoral “release” of joint is an unnecessary and avoidable surgical procedure.
More than realignment, firm stabilization of the atlantoaxial joint is necessary in the treatment of basilar invagination. Atlantoaxial instability is the cause of basilar invagination, and atlantoaxial stabilization is the treatment. Although preferable and desired, realignment is not mandatory. Although we first described intra-articular spacers to achieve distraction and reduction of basilar invagination, our current strategy is to distract the facets and impact only bone graft in the articulation.[29],[30] Bone graft impaction provides additional space for bone fusion. In general, metal implants or spacers in the articular cavity are avoided and are used only when it is felt that additional stabilization of the articulation is necessary. More than realignment or reduction of basilar invagination, solid and firm stabilization of the atlantoaxial articulation is mandatory. Incomplete reduction following surgery is not an indication of decompression if the stabilization is satisfactory and leads to arthrodesis of the articulation and there is improvement or stabilization of neurological symptoms.
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