Introduction

The degenerative cascade can occur in a variety of ways. When the disc degenerates and loses its height, shortening of the anterior spinal column occurs. In most cases, the collapse of the disc space occurs symmetrically, leading to loss of lumbar lordosis and accentuation of thoracic kyphosis. However, the disc may collapse asymmetrically, which in turn can lead to a lateral bending of the spine. When this occurs over multiple segments, a degenerative scoliosis may develop, causing imbalance in posture, often in both the coronal and the sagittal planes.¹

The anatomic characteristics of degenerative scoliosis and idiopathic adolescent scoliosis differ significantly. Whereas scoliosis that develops in childhood is marked by significant rotation of the vertebral bodies, little rotation is appreciated in most adult degenerative scoliosis patterns. Furthermore, there is a propensity for the adult scoliosis curve to develop in the lumbar rather than the thoracic spine. This is likely due to the greater mobility of the lumbar spine, which undergoes a more clinically evident degeneration of the disc.

The treatment of scoliosis in the aging spine differs markedly from scoliosis treatment of the growing spine. The key differences are the lack of mobility of the adult spine, the presence of osteopenia and osteoporosis, the location of the curve, the curve magnitude, the need for decompression, and the frailty of older patients with their associated comorbidities. The goals of treatment differ as well. In adolescent idiopathic scoliosis, there is more concern with deformity and less with pain. In adult degenerative scoliosis symptoms are related more to pain (both back pain and nerve pain) than deformity.

As our population increases in age, the prevalence of symptomatic degenerative scoliosis will increase concomitantly. The incidence of complications is high for this type of surgery.² The risk of these complications increases with advanced age and other medical comorbidities. The goal of minimally invasive surgery is to decrease the soft tissue trauma associated with large midline posterior and thoracoabdominal approaches, which require take-down of the diaphragm. This chapter addresses the key indications for surgical treatment, minimally invasive strategies for scoliosis treatment, contraindications to minimally invasive surgery, and potential pitfalls of MIS treatment.

Basic Science of Minimally Invasive Spine Surgery

The posterior paraspinal muscles provide dynamic stability to the spinal column.³ Numerous studies have investigated the anatomic, histologic, and radiographic properties of many of these muscles with the goal of understanding pathologic changes associated with spinal abnormalities such as chronic low back pain, disc herniation, scoliosis, and degenerative lumbar kyphosis. Paradoxically, some operations designed to treat these various spinal disorders actually disrupt these muscles and, in turn, may lead to substantial functional deficits, various pain syndromes, or both. Minimally invasive spine surgery techniques strive to minimize surgical trauma to these muscles, thereby preserving their function. Architectural studies show that the multifidus muscle stands out among all other lumbar muscles, and indeed many extremity muscles, as a most extreme example of a muscle designed to stabilize the lumbar spine against flexion. This functional design was elucidated by means of intraoperative laser diffraction and quantitative architecture measurements that demonstrated (1) an extremely large physiologic cross-sectional area, greater than that of any other lumbar spine muscle, and (2) a sarcomere length range exclusively on the ascending portion of the length–tension curve.⁴ The large physiologic cross-sectional area and relatively short fibers indicate that the multifidus muscle is architecturally designed to produce large forces over a narrow range of lengths. This design allows the multifidus muscle to function more to stabilize the spine and less to provide motion of the spine. As a stabilizer, it acts to maintain optimal joint forces throughout the spine as the body assumes various positions requiring prolonged flexion (such as assembly-line work) or extension (such as standing).

Clinical Practice Guidelines

The main reason for surgical treatment of adults with scoliosis is pain. Pain can occur in several ways. First, the pain of neurogenic claudication develops with the degenerative cascade. This is exacerbated by spinal malalignment. Both lateral listhesis and anterolisthesis reduce the area of the canal. The resulting stenosis is more severe than the corresponding degree of degeneration in a well-aligned spine. If there is severe asymmetric disc collapse, the neuroforamina will close down on the side of the concavity, which in turn can cause radiculopathy.

Pain also occurs because of the degenerative arthritis that develops within the disc and facet joints. Bone-on-bone movement between motion segments can cause pain in a manner analogous to degenerative joint disease in the knee and hip. Furthermore, a malalignment will create focal areas of increased stress. Finally, postural imbalance can lead to fatigue-related muscle pain. Much as in flat back syndrome, early muscle fatigue and pain can develop as the patient tries to compensate for coronal and/or sagittal imbalance. In contrast to adolescent scoliosis, the concern for curve progression is relatively low. The pain associated with stenosis, radiculopathy, and early muscle fatigue drives surgical decision-making. It is rare to perform surgical correction of deformity in the absence of pain in adults with degenerative scoliosis.

Endoscopic Transforaminal Decompression for Unilateral Radiculopathy

Occasionally, a patient with degenerative scoliosis will complain mainly of leg pain, with only minor back pain. In most cases, the pain is due to neuroforaminal stenosis. Traditionally, this has been treated with hemilaminectomy and foraminotomy. However, there is risk of worsening deformity due to loss of stability when excessive bony resection is necessary and when the activity of the multifidus muscle is disrupted. An extraforaminal approach has been used with good success via a Wiltse-type paramedian approach. A minimally invasive modification of this technique utilizes tubular retractors that dilate the soft tissue and minimize retraction pressures. Although this is still performed with the patient under general anesthesia, the accessibility of the neuroforamen is sufficient. However, it is technically challenging to use the operating microscope because of the angle of the approach.

The endoscopic technique provides another avenue of treatment and it can be performed using local anesthesia.⁵ This is advantageous for patients with significant medical comorbidities that make general anesthesia risky. Furthermore, the endoscopic technique allows a more lateral trajectory to the spine, facilitating deeper entry into the neuroforamen (Figure 60-1).

FIGURE 60-1 Endoscopic Transforaminal Decompression. A 7-mm endoscopic cannula is placed at the extraforaminal opening of the affected level. A combination of bipolar probes (Ellman International, Inc., Oceanside, N.Y.), holmium side-firing lasers (Trimedyne, Inc., Irvine, Calif.), and mechanical trephines (Joimax, Inc., Campbell, Calif.) are used to release the neuroforaminal ligament, superior edge of the facet joint capsule, and lateral edge of the ligamentum flavum as it becomes confluent with the facet joint capsule. Mechanical trephines are used under fluoroscopic guidance to remove the superior edge of the superior articular process. A combination of ligamentous release with a small amount of bony resection decompresses the exiting nerve root. The angled bipolar probe is passed into the spinal canal to manually confirm adequate decompression. A, AP radiograph showing asymmetric disc collapse with narrowing of the left L4 and L5 neuroforamina. B, Left parasagittal T1-weighted MR image showing narrowing of the left L4 and L5 neuroforamina. (open arrows) C, Endoscopic view of the facet joint capsule. D, Endoscopic view of the semicircular removal of superior articular process using trephines. The rough cancellous bone can be seen as a superior dome in the field of view. E, Intraoperative AP C-arm image showing the endoscopic cannula docked at the extraforaminal opening of the left L4 neuroforamen. F, Intraoperative lateral C-arm image showing the endoscopic cannula docked at the extraforaminal opening of the left L4 neuroforamen. Intraoperative AP image showing the endoscopic angled probe passing through the superior (G), middle (H), and inferior (I) aspects of the neuroforamen. The ability to pass the probe through the neuroforamen without resistance confirms an adequate decompression.

Deformity Correction via Direct Lateral Anterior Interbody Fusion

A powerful method of deformity correction is the direct lateral interbody fusion (DLIF) technique (Figures 60-2 through 60-5). This technique was best described by Ozgur and colleagues⁶ using the XLIF system (Nuvasive, San Diego, Calif.). The key feature of the technique is the ability to rest the interbody spacer along the strongest portion of the vertebra endplate, namely, the cortical rim or apophyseal ring. The annulus inserts at this location and the cortex of the vertebral body acts as a vertical support. Because the interbody spacer is placed from the lateral position, the implant may overhang past the edge of the disc space, ensuring that the implant fully rests on the strongest portion of the endplate. If placed from an anterior or anterolateral position, the interbody spacer would enter the canal or the neuroforamen. In addition, the DLIF technique preserves the anterior longitudinal ligament. It is presumed that by keeping the integrity of this structure, the spine maintains a pivot point from which to correct an asymmetrically collapsed disc.