SPONDYLOSIS Spondylosis and spondylolisthesis Al had a vague ache in his low back.

It seemed a bit worse on the left side, and sometimes travelled to his buttock but never went down the leg. The pain worsened with bending over. Dr. Prager found no real abnormalities on Al's physical examination. Range of motion, pulses, reflexes, and strength was normal. An X-ray demonstrated some slippage in the lumbar region with mild to moderate osteoarthritic changes. The L4 vertebral body moved forward compared to the next lower one. Al was told to lose weight, given an abdominal muscle strengthening exercise program, and instructed to take up to eight Tylenol a day when the pain became uncomfortable. When he gar-dens, he uses a lumbar band for support. This form of back and neck pain usually produces localized discomfort or none at all. Diagnosed by X-rays of the spine, which show degenerative changes, spondylosis is the consequence of intersegmental instability due to a stress fracture of two small bones, resulting from shifts in compressive forces between facets and intervertebral discs (Figure 17). Pain may worsen with extension, but no neurologic deficits are present. Acetaminophen helps mild pain, and nonsteroidal antiinflammatory agents relieve mild to moderate symptoms. As spondylosis evolves, the vertebral body may become displaced or lean forward, resulting in a crooked spine, or spondylolisthesis. Degenerative spondylolisthesis is usually seen at the L4-L5 lumbar level and is associated with degenerative disc disease and disease of the facet joints, leading to segmental instability. A stress fracture of the pars intra-articularis is responsible for this. Low back pain is worse with standing and relieved by rest. Neurologic symptoms are absent, though fusion surgery may be required if the slippage becomes neurologically compromising. Degenerative Disc Disease: Spondylosis The integrity of the fnctional unit depends upon the adequacy of the intervertebml disc. In the anterior weight-bearing prion of the unit the hydroynamic proprties of the disc with its intadiscal pressure maintain the sepamtion of adjacent verebml bodies. This action elon-gates the spine, exers tension upon the longitudinal ligaments, and simultaneously separates the zygoapophyseal joints posteriorly. The foraminae are opned, the ligamentum Oavum is kept taut, and the interwined annular fbers are also placed under tension. Degenemtion of the disc apparently is an expected ocurrence pre-dictable in all humans. Puschel' claimed that by age 20, the disc has reached maximum development and degenerative changes appear. The sequence of degenemtive changes revealed that degenerative changes in the posterior articulations followed changes within the disc.' '

Changes in the interverebml disc have been noted very early in life. At first concentric tears can be noted in the annular fibers, indicating a failure of the matrix to maintain contact of the annular fibers with each other' (Fig. 114). Tears in the collagen fibers of the annulus appear early in the border between the nucleus and the cartilaginous plates and extend toward the center of the nucleus. This is contrary to the concept that rotator trauma in later life causes rupture of the outer annular fibers.' However, both probably occur: the former as a natuml evolution, the latter as suprimpsed trauma. Gradually the outward intradiscal pressure causes radial tears to occur in the disc (see Fig. 114). Thus the intradiscal pressure decreases and the vertebml bodies are prmitted to approximate (Fig. 115). As the annular fbers rupture in the periphery of the discs, there is a connective tissue reaction in which blood vessels grow in fom the long ligaments, gradually forming granular fbrous tissues. A CONCENTRIC I.DIAL FIGURE 114. Annular changes in the degenerating disc. A reveals concentric tears in the annulus that a first noted at age 15. They originat near the nucleus and are at first discrete. As the patient ages, they are found in geater number in the Quter margin and tend to merge into larger tears. B depicts mdial tears. These to begin centrally and proeed outward. They are more numerous in the posterior prtion of the disc. The pressure of the disc matrix pushes the tom fiber margins outward. When they reach the outer margin they "bulge" and deform the disc. In the newbor child the vertebral column is staight and the inter-vertebral discs are wide and rectangular. As the child becomes -bearing and erect, the lordotic lumbar curve forms. The discs assume a wedge shap with posterior narrowing. The lumbosacral disc is even more wedge-shapd due to the lumbosacral angle. Degenerative changes are most prominent in the posterior lateral quadrants where the tissues capable of producing pain and disability are present. Hereditary fctors must predispose to premature disc degeneration. Some patients in their sixth or seventh decade are remarkably free of degenerative changes and are asymptomatic. Others as young as 20 may have significant degenerative changes. There does not appar to be any significant diference due to sex or occupation.' The greatest degree of degeneration is noted at the lumbar (L ,) and the lumbosacral (L,-S,) intererebral spaces (75 prcent). This is pssibly due to the greatest angulation of the interverebral discs and the greatest propron of lumbar movement at these two interspaces. NO,MAL OUENEUHD , FICURE 115. Disc degeneration. Lft: Nonnal disc with intact nucleus and annular fibers. The spac is nonnal (N). Right: Degenerated disc with the nucleus outside its boundary and fgmented annular fbers and narrowed space (D). As the anterior weight-bearing porion of the functional unit compresses due to disc dehydration, the posterior joints also approximate. These posterior joints undergo degenerative changes (e.g., synovial and capsular thickening, degeneration of articular cartilage, adhesions, osteohondral factures, and even lose body formation). As there are fine sensory fbers that

tansmit pain and proprioeption located in the capsules,' the psterior joints can now become symptomatic. Gradual degenerative changes in all aspcts of the fnctional unit lead to the condition termed sponylosis (Fig. 116). SPONDYLOSIS The disease entity of degenerative arthritis of the spine is a sequela to interverebral disc degeneration. Degenerative arthritis, hypertrophic arthritis, discogenic degenerative disease, osteoarthropathy, and spondylosis are morbidly and mechanically similar, toward which disc de-generation is undoubtedly a predisposing factor. As the disc degenerates, the elastic fbers of the annulus decrease and are replaced by fbrous tissue. A loss of elasticity ensues, and flexibility of movement between two vertebrae is diminished. The intradiscal pressure that normally assists in keeping the vertebrae apar is decreased, and the verebrae approximate. Shok-absorbing ability is decreased. The fibrous capsule and its ligaments become slack, and anterior-posterior shearing movement, normally not possible, can now occur. Two pathologic conditions, capable of causing pain, result. The lig-"ments slacken when the vertebrae approximate, vertebral periosteal attachment of the ligaments weakens, and any pressure exerted on the ligament permits a dissection away from its periosteal attahment. Disc material usually confned within a taut ligamentous comparment cannow dissect the slack ligament from its previous site of attachment on the verebrae (Fig. 117). Furher extrusion of disc material is facilitated by the fagmentation of the annulus. The material extruded decreases the quantity of disc tissue between the verebrae and permits frher vertebral approximation, frher ligamentous laxity, more dissection of the ligamentous-periosteal at-tachment, and frher protrusion of nuclear material: the proess b-comes a vicious circle. The extruded material, since it is a foreign body, evokes an irritation reaction. This irritation may b removed by fibrousreplacement followed by calcifcaton. This calcifed extuded tissue becomes the "arthritc spur" seen on x-ray flm. Because of this the concept of spndylosis evolution appars feasible. With these changes in the mobile prtion of the lumbar spine, several conditons may result: 1. The usual symptoms of degeneratve arthritis, such as early moring stifess, constant aching, resticted range of motion, and limited duration of standing or sitting. 2. Nere root entrapment due to intervertebral foramen narrowing. 3. Pseudolaudication due to lumbar spine stenosis.