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Basilar invagination was for long considered to be a radiological curiosity rather than a surgically treatable clinical entity. Subsequently, for several years, including in our article dedicated to the subject in 1998, basilar invagination was associated with ‘fixed’ or ‘irreducible’ atlantoaxial joint and decompression was considered to be the treatment.1 Depending on the direction of neural compression, anterior transoral odontoidectomy (group 1 basilar invagination) or posterior foramen magnum bone and/or dural decompression (group 2 basilar invagination) were the modalities of surgical treatment.1 In 2004, the possibility of reducing basilar invagination by atlantoaxial facetal distraction and achieving craniovertebral junction realignment revolutionized the treatment for basilar invagination.2 The concept was that basilar invagination (group A) is a result of ‘vertical’ spinal instability and the atlantoaxial facetal listhesis that eventually results in basilar invagination mimics lumbosacral listhesis.3 It was observed that in the entity of ‘fixed’ or ‘irreducible’ atlantoaxial dislocation, atlantoaxial joint is actually not stable or fused but is an unstable spinal segment and the joint in such cases is not only mobile but is pathologically hypermobile and can be reduced by manual distraction of the facets. Since the introduction of this concept, a number of authors have resorted to attempts at reducing atlantoaxial instability and realigning craniovertebral junction and the authors recommending ‘decompression’ as a primary modality of surgical treatment is gradually but definitely reducing all over the world. Our studies identify muscle weakness related to disuse or injury as a nodal point of genesis of atlantoaxial instability and subsequent development of basilar invagination. Ligamentous ‘stretch’ has not been identified to have a role in the pathogenesis of atlantoaxial instability or of basilar invagination and anterior and/or posterior ‘release’ of ‘tension bands’ ligaments or muscle groups by sectioning has not been identified to have a place in the surgical treatment. Since 1988, our technique of atlantoaxial fixation involves opening of the atlantoaxial joint, denuding the articular cartilage and introduction of bone graft within the articular cavity prior to lateral mass instrumentation.4,5 All these principle surgical steps are essential in achieving strong atlantoaxial arthrodesis. In 2004, we introduced intra-articular metal spacers to facilitate and sustain facetal distraction in cases with basilar invagination, rotatory dislocation, and irreducible and even reducible atlantoaxial dislocation.2,6-8 As the experience has increased, it is now realized that distraction of the facets of atlas and axis and packing of bone graft in the articular cavity can lay a ground for solid bone arthrodesis and the reliance on intra-articular facetal implant can be reduced if not entirely avoided. Whilst the metal implants provides for stability, bone graft provides for fusion of the facets and also sustains stability-immobility and distraction.9 As the experience in surgically managing Neurospine

Basilar Invagination: Instability Is the Cause and Stabilization Is the Treatment