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Adjacent-Segment Disease


Adjacent-segment pathology (ASP) is a common complication of spinal surgery. This chapter focuses on the causes, common clinical scenarios, and treatment options to avoid or treat ASP. Surgery changes the anatomy, physiology, kinematics, and biomechanics of the operated and contiguous elements of the spine. Nowhere are the influences of these factors more important than at the segments immediately above or below a surgical fusion. Short-term gratification from surgery can be tempered by long-term dissatisfaction when progressive degeneration causes symptoms to recur. Predicting the long-term outcome and assessing the risk/benefit ratio of surgery depends on accurate knowledge of the natural history of the patient and changes to the natural history from surgery. The dramatic increase in spinal fusion rates over the last 2 decades makes additional surgery for ASP much more common. Expert treatment is guided by a thorough knowledge of the natural history, potential problems, complications, and treatment options for ASP.

Definition

ASP is an all-encompassing phrase describing abnormal changes to the spinal structures bordering an operative segment. ASP becomes important only when the pathology influences the clinical natural history. ASP can be thus be subdivided into radiographically detectable adjacent-segment degeneration (ASDeg) versus clinically relevant adjacent-segment disease (ASDis). The mere presence of radiographically detectable change to the spine does not equate to clinical relevance. Considerable research focuses on how surgery affects ASP with the ultimate goal of preventing, managing, or treating clinically relevant ASDis.

Natural History

Asymptomatic degenerative disc disease is common and parallels the normal spine aging process. The degenerative process is dynamic and progresses throughout life. Boden et al. evaluated lumbar spine MRI scans of asymptomatic volunteers. Degeneration or bulging discs were present in 35% of subjects 20 to 39 years old. Degenerative changes, including disc herniations and spinal stenosis, increased to 57% of individuals over age 60 years. In a separate study, Boden et al. reported similar findings in the cervical spine. Elfering et al. also showed that degenerative radiographic findings progress with age. They prospectively reviewed MRI scans of asymptomatic volunteers over a 5-year timeline. A total of 41% of individuals showed advancement of degenerative changes without clinical symptoms. Clearly, progressive, asymptomatic degenerative changes to the spine are a normal part of the aging process.

The influence of surgery on the normal, expected degenerative process remains a subject of debate. Surgical interventions are associated with ASDis, but whether these interventions significantly accelerate or cause the degeneration is debated. Without randomized, controlled studies comparing surgical to nonsurgical patients, the significance of surgery on the degenerative process must be analyzed by less direct studies. Furthermore, the radiographic acceleration may not be clinically relevant. Radiographic adjacent-segment degeneration does not correlate well with symptomatic disease. In a study of postsurgical degenerative changes, Mannion et al. concluded that spinal fusion was associated with increased ASDeg but without influence on ASDis.

Biomechanical and clinical outcome studies implicate surgery as an accelerating factor to ASDeg. Biomechanical studies demonstrate changes in adjacent-level intradiscal pressure and alterations of spine kinematics after a one-level fusion. Other studies implicate excessive motion at adjacent spine segments. Torsional stresses due to spinopelvic imbalance alter disc stresses and physiology. All of these changes could theoretically alter the natural history of the adjacent disc.

Clinical outcome studies also implicate surgery as a contributing factor to ASP. The rate and severity of adjacent-level disc degeneration is not uniform after a fusion. Several independent studies show that the rate of ASDis varies depending on the type of surgery. Laminectomy above the fusion, length of the fusion, type of fusion, instrumentation, and other factors change the rate of ASDis. The influence of surgical type on rate of ASDis links surgery to the degenerative process.

Although the causes may be debatable, ASDeg and ASDis are realities of spinal practice. In a meta-analysis of the literature, Park et al. found that the incidence of symptomatic ASDis after spinal fusion ranged from 5.2% to 18.5% ( Fig. 101.1 ). The authors concluded that the biomechanical alteration of the levels adjacent to the fusion accelerated the natural history of ASDeg.

FIG. 101.1, Spinal stenosis at level above a fusion. (A) Lateral radiograph showing preexisting L4–L5 fusion. (B) Axial computed tomography/myelogram showing adjacent level stenosis at L3–L4.

The normal spine starts to degenerate at an early adult age, then progresses throughout life. Most degenerative disease is asymptomatic, but for those who have symptoms, surgery may be necessary. Surgery alters the anatomy, physiology, biomechanics, and kinematics of the spine. Although debated, surgery likely accelerates ASDeg and ASDis, possibly leading to subsequent revision surgery.

Types of Adjacent-Level Degeneration

Box 101.1 lists the types of adjacent-level degenerative changes complicating patient management. The changes can occur alone or in combination. Management can range from observation to complex spinal reconstruction.

Box 101.1
Types of Adjacent-Level Degeneration

  • Disc degeneration

  • Disc herniation

  • Spinal stenosis

  • Spondylolisthesis

  • Retrolisthesis

  • Lateral listhesis

  • Scoliosis

  • Kyphosis

  • Proximal junctional failure

  • Proximal junctional fracture

  • Sagittal imbalance

  • Instability

  • Facet degeneration

  • Spondylolysis

Etiology

The etiology of ASDeg is divided into several broad categories to help organize and stratify risk factors.

Biomechanical

Changes in motion, stress, strain, and stability influence the durability and strength of spinal structures. Surgical resection of posterior supporting elements—such as interspinous ligaments, facets, and paraspinous muscles—change the balance of forces aligning the spine. Malakoutian et al. reviewed published literature on kinematic changes at levels adjacent to a fusion. They found that range of motion was affected more at the rostral end of the fusion than the caudal end. Range of motion increased 10% to 30% at the rostral end of a fusion. The findings are consistent with clinical prevalence of degenerative changes at the rostral segment in 70% to 100% of patients. They concluded that muscle damage from spine surgery may play a key role in ASDeg.

Fusions also alter the location of forces within the spine. The center of rotation of adjacent levels changes according to the type of fusion. A posterior fusion displaces the center of rotation cephalad and posterior, increasing the stress on the facets. An anterior fusion displaces the center of rotation cephalad and anterior, increasing the shear and compressive stresses on the disc. A bilateral posterolateral fusion causes only slight increase in the facet joint stresses and had the least effect on the adjacent levels.

Other alterations in biomechanics include a change in disc pressure. Fusions and spinal malalignment in the sagittal and frontal planes alter disc kinematics and accelerate degenerative changes.

Genetic

The response of an intervertebral disc to similar mechanical factors is not uniform from patient to patient. Just as there is a spectrum of radiographic degenerative changes in asymptomatic individuals, there is also a spectrum of adjacent-segment changes after the same type of fusion. Monozygotic twin studies comparing patients with dissimilar occupations attribute 26% to 72% of the difference in degenerative changes to genetic factors rather than environmental differences. Gene expression response to mechanical loading is variable and can alter cellular metabolism of the disc.

Physiology

Cell metabolism may be altered in adjacent discs as a response to immobilization. Cole et al. found in a canine study that disc metabolism was markedly altered adjacent to a fusion. Similar changes were not observed in a control group.

Risk Factors

See Box 101.2 for a comprehensive list of risk factors implicated in the degenerative process.

Box 101.2
Risk Factors for Adjacent-Level Degeneration

  • Age

  • Preexisting adjacent level disc degeneration

  • Adjacent-level facet degeneration

  • Ending fusion at L5

  • Length of fusion

  • Gender

  • Excessive distraction after posterior lumbar interbody fusion

  • Laminectomy adjacent to a fusion

  • Type of fusion

  • Sagittal imbalance

  • Body mass index

  • Instrumentation

  • Pelvic incidence/lumbar lordosis mismatch

  • Facet trophism and sagittal alignment

  • Osteoporosis

  • Iatrogenic muscle damage

Clinical Scenarios

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