The intervertebral disc is a complex complicated structure, consisting of annulus, nucleus proper, and vertebral endplates (Figure 1; SDC Figure 2, http://links.lww.com/BRS/B105). The undefined interior portion of the disc is a composite of nucleus proper and disc matrix, consisting of proteoglycans, cells, and metabolites. The annulus fibrosus comprises numerous lamellae buckling outward and becoming increasingly tenuous as they fan out in many directions. The darker outer annulus (a different type of collagen) is believed to be the strongest ligament in the spine (SDC Figure 3, http://links.lww.com/BRS/B105). This capsule anchors the strongest fiber into the bone. Endplates consist of an apophyseal ring of specialized strong woven bone and an inner spongy, innervated, elastic portion that shows minimal resistance to subsidence of spinal implants.
Endplates consist of many vascular components, which provide vital nutrients for bone growth and regeneration. Subarticular collecting veins underlying the cancellous bony portion of the endplates branch and communicate and terminate in glomeruloid buds, which are highly vasoactive. Contrast magnetic resonance imaging shows transgression of nutrients and transport of metabolites and waste products through this system—not through the annulus. Improving the supply of nutrients and blood to the disc, even if it is slightly degenerating or painful, provides better support and protection for the patient and remains the best treatment option.
A clear understanding of spinal anatomy facilitates diagnosis and treatment of degenerative disc disorder (DDD), spinal stenosis, and other degenerative pathologies. For the cascade of DDD, the classification system developed by Pfirrmann et al1 indicates that at early stages, magnetic resonance imaging reveals no nucleus (the first structure to disappear) and shows an anatomically featureless disc. The outermost part of the disc remains intact. Later stages of DDD show increased loss of disc height, with the disc disintegrating into lumps of tissue resembling crabmeat. Loss of 50% of disc height leads to severe subluxation of joints, which are no longer congruent. With disc rupture, ingrowth of blood vessels occurs as granulation tissue from the epidural space—cells, blood vessels, and, proprioceptive nerves. When the segment is collapsing completely, conflict of posterior elements is inevitable—kissing spines (bone grinding on bone)—causing sclerosis. The ligamentum flavum, once straight and stretched, now becomes redundant and buckling. This is a highly painful condition that can be surgically alleviated. When the disc is completely resorbed, vertebra is grinding on vertebra and sclerosis ensues, with shutdown of the vascular supply, even more subluxation, facet joint arthrosis, osteophyte formation, and synovitis, resulting in a “pinhole stenosis” of the foramen.
In addition to adjacent segment instability caused by overuse and overstress, segments adjacent to the stiffened part of the spine can become unstable when spinal implants are inserted. When implants are placed in the conventional way, the multifidus muscle may be damaged or destroyed, affecting both strength and fine-tuning of muscles, thus reducing muscular control in the adjacent segment. To minimize damage, the surgeon should leave the multifidus in place, along with the lumbodorsal aponeurosis (fascia). An intermuscular approach ensures a clear view of small vessels and nerves, while completely sparing individual muscles.
Anatomy textbooks provide one rendition of the spine but cannot ascertain interindividual variability. Cerebrospinal fluid is needed to transport nutrients to the cauda equina roots and toxic metabolites from the roots (Figure 1). An individual born with short pedicles will inevitably have a small thecal sac and may develop prestenosis (Figure 2). Stenosis typically occurs not at the bony ring but at the mobile portion of the segment (disc and joints). A dynamic component causes extension of the spine and narrowing of the canal. When the spine is extended, the canal becomes narrower through buckling of the ligamentum flavum, thecal sac, and roots. When one stoops forward, the spine straightens out and buckling is alleviated.
Two-level degeneration of the disc is characterized by low disc height and disc bulging (Figure 3). Blood is pumped into the compartment, but venous blood can no longer drain. Accumulating metabolic waste products lead to the type of compartment syndrome that is alleviated when you bend forward or sit down. Recognition of this event is important for surgeons who wish to treat stenosis at early stages. The continuum of spinal stenosis starts with congestion/stasis and progresses to obstruction of the arteries and structural changes. Only at the final stage does neurocompression occur. “Neurogenic claudication” was first described by Henk Verbiest, who established the relationship between lumbar spondylosis and neurogenic signs and symptoms in the legs. As a result of his work, most spinal surgeons now point to neurogenic claudication as spinal stenosis.2
Late stages of hypertrophy and degenerative stenosis are painful. Liberating the root, especially the ganglion, renders it more mobile. Many surgeons successfully work from the contralateral side in an orthograde fashion to follow the root out of the canal. Typically, the vertebrae, not the bodies, are collapsing. One should consider the stabilizing qualities of posterior elements before performing surgery to achieve stabilization.
1. Pfirrmann CWA, Metzdorf A, Zanetti M, et al. Magnetic resonance classification of lumbar intervertebral disc degeneration. Spine (Phila Pa 1976)
2. Babhulkar S, Pawar S. Ramani PS. Clinical presentation of lumbar disc herniation. Jaypee Brothers Medical Publishers, Textbook of Surgical Management of Lumbar Disc Herniation
. Daryaganj, New Delhi, India: 2013.