Not neural deformation or compression but instability is the cause of symptoms in degenerative spinal disease.

The spinal cord and brain have remarkable resilience, tolerance, and plasticity. Unless the compression is “acute,” the neural function can be retained even when the brain or the spinal cord is severely compressed and compromised. Such a state is clearly appreciated in cases where there is severe and longstanding hydrocephalus and the brain is reduced to thin filament, its functioning may be only marginally affected. Similarly, in cases with syringomyelia, the cord substance is reduced to a membrane but the neurological function may remain remarkably and astonishingly well-preserved. In longstanding benign tumors and cysts, the neural function can remain preserved despite the gross anatomical neural tissue loss.

In degenerative disease of spine, spinal compression is usually a chronic phenomenon. The neural compromise is seldom acute. The cord or dural tube compression is obvious on magnetic resonance imaging (MRI) and computed tomography (CT) scan imaging. The more prominently seen anatomical structures on imaging are vertebral bodies, discs, osteophytes and ligaments, and the neural structures. The compromise or compression of the neural structures can be clearly visualized. The extent of compression of the neural structures and the reduction in the disc spaces and neural foramina can suggest the nature of disease and the need to relieve the cord of its compression and deformation.

However, it seems that subtle and persistent abnormal movements in the spine that lead to repeated minor or micro injuries are the more important cause of its functional loss. More important than restoring the shape of the neural structures, it is crucial to stop the abnormal movements. In the spine, the facets are the only true joints. Instability in the joints is difficult to appreciate on conventional imaging. The oblique profile, lateral location, and relatively small size make identification of any abnormality or abnormal movement difficult. Essentially, the images show the effect of the pathology and not the pathology itself. However, direct handling of the facets and observation during surgery can clearly demonstrate its unstable character and suggest the need for surgical stabilization. The instability of the facets can even be seen when images do not show any abnormality of the soft tissues in the spinal segment.

The instability in the facets is not antero-posterior instability that can be appreciated in the vertebral bodies or even in the facets of atlas and axis due to their transverse location. The instability in the facets is “vertical” instability and the superior facets slips over the adjoining inferior facets in the form of retrolisthesis. Weakness of the muscles of the nape of the neck due to disuse or abuse is the cause of vertical facetal instability. Facetal instability leads to reduction in size of the neural foramina, spinal canal, and the intervertebral body space. Eventually, the height of the individual spinal segment reduces with the increasing age and progressive instability. Buckling of the ligamentumflavum and the posterior longitudinal ligaments that ultimately lead to formation of osteophytes are also secondary events to primary facetal instability. Degeneration of the disc is not the primary cause of reduction of the disc space but the facetal instability is the cause.[12] In effect, disc degeneration is not the primary point of beginning of degenerative activity in the spine. As hypothesized by Goel earlier,[12] it is facetal instability and its secondary effects on bone, ligaments, and disc that form the complex of degenerative spinal disease.

In the craniovertebral junction, instability is the major factor than the more obvious radiological features of neural compression. The deformation of the cord related to the odontoid process can frequently appear remarkable and the cause of neurological deficit. However, it is the instability at the atlantoaxial facets that is the major issue. The atlantoaxial axial joint was considered to be fixed or stable in cases with basilar invagination and in “irreducible” dislocations. However, the identification of the fact that the dislocation in such cases is not fixed and the joint is not fused but is abnormally mobile has revolutionized the treatment of these anomalies.[34] Goel proposed distraction of facets and fixation of the joint and craniovertebral junction realignment as the treatment for basilar invagination and irreducible dislocation. However, for resolution of symptoms, fixation of the joint is more crucially important than reduction of basilar invagination.

Similar to these concepts, stabilization of the subaxialfacets, and their fixation is more crucially important than distraction and realignment of the facets. On the basis of these concepts, Goel proposed “only fixation” as an ideal form of treatment for both lumbar and cervical degenerative disease.[56] However, Goel facet spacer technique that distracts, reduces, and stabilizes the joint seems to be safest and is an optimum form of stabilization technique.[78]

Essentially, it means that “decompression” of the neural structures by removal of bone, osteophyte, ligaments, or disc can be avoided if it is understood that instability is the cause of problem. Even in craniovertebral junction, anterior transoral or posterior foramen magnum bone decompression can be avoided if surgery focuses on stabilization of the facets that is the site of normal movement and the site of abnormal movement. The focus of treatment can be toward stabilization or the pathology rather than decompression of or resection of the effects of the pathology.