Chapter Clinical Summary
Academic synthesis, diagnostic methodology, and surgical recommendationsAdult scoliosis (AS) encompasses coronal spinal deformities in the skeletally mature spine and may arise from progressive de novo degeneration of a previously straight spine, progression of pre-existing adolescent idiopathic scoliosis into adulthood, or secondary etiologies. With global population aging, its clinical significance is expanding rapidly, primarily because the deformity frequently associates with chronic back pain, radiculopathy, neurogenic claudication, loss of global trunk balance, and profound functional disability. In degenerative de novo scoliosis, the process initiates through asymmetric disc and facet joint degeneration, driving vertebral rotatory subluxation, laterolisthesis, and spinal canal stenosis. In adult idiopathic scoliosis, age-related degeneration superimposes on pre-existing structural curves, typically inducing loss of lumbar lordosis. Rather than focusing solely on the coronal Cobb angle, the chapter highlights that sagittal spinopelvic alignment is the dominant determinant of pain, disability, and reconstructive strategy.
To present the foundational principles for recognizing, classifying, and managing adult scoliosis. The reader will differentiate degenerative de novo from adult idiopathic and secondary deformities, correlate symptoms with coronal, sagittal, and neural pathologies, perform comprehensive full-spine spinopelvic assessments, utilize the Aebi and SRS-Schwab classifications, and understand the core principles governing conservative therapy, surgical indications, multiplanar realignment, neural decompression, and complication prevention.
Degenerative de novo scoliosis develops in patients without a prior history of scoliosis. Asymmetric disc collapse alters segmental stability and transfers uneven loads across facet joints, inducing rotatory subluxation, lateral listhesis, and foraminal stenosis. Adult idiopathic scoliosis represents the progression of pre-existing adolescent curves into maturity, where superimposed degenerative changes exacerbate structural deformities and flatten lumbar lordosis. Aebi's etiological classification organizes these curves into primary degenerative, progressive idiopathic, and secondary forms.
Axial back pain is the most frequent symptom, related to muscle fatigue and facet arthrosis. Radiculopathy and neurogenic claudication stem from degenerative stenosis and neuroforaminal compromise. The chapter underscores that sagittal malalignment correlates much more strongly with pain and disability than coronal asymmetry. Positive sagittal imbalance forces substantial muscular compensation and increases energy expenditure during standing and walking. Figure 35.1 illustrates the clinical assessment of trunk imbalance and compensatory mechanisms.
Full-spine standing radiographs are essential, evaluating the spine and pelvis as an integrated kinetic chain. Beyond coronal curve magnitude, regional curves and sagittal parameters are systematically quantified. Figure 35.3 details core spinopelvic parameters: pelvic incidence (PI), pelvic tilt (PT), sacral slope (SS), lumbar lordosis (LL), and sagittal vertical axis (SVA). The SRS-Schwab classification (Figure 35.4) combines coronal curve patterns with three validated sagittal modifiers (PI-LL mismatch, pelvic tilt, and SVA), providing a standardized framework linked directly to health-related quality of life.
Initial therapy incorporates physical rehabilitation, core stabilization, low-impact exercise, multimodal pharmacotherapy, and targeted image-guided spinal injections. The efficacy of bracing remains limited in adult deformity. Conservative management aims to control pain and optimize function, recognizing that it does not reverse structural bony deformity.
Surgical indication is highly individualized and warranted for intractable disabling pain, progressive neurological deficits, incapacitating claudication, or severe global malalignment. Unlike adolescent surgery, adult reconstructive goals are functional: decompressing neural structures, relieving mechanical pain, and restoring an age-appropriate spinopelvic alignment. Reconstructions range from targeted focal decompression to extensive multi-level fusions with corrective osteotomies (Figures 35.5 and 35.6).
In clinical practice, evaluation must begin with identifying the primary symptom driving disability: axial mechanical pain, radicular pain, neurogenic claudication, or postural fatigue while standing. Clinical examination in bipedal stance evaluates global posture, pelvic retroversion, knee flexion, and detailed neurological function. Full-spine standing radiographs must encompass hips and femoral heads. The SRS-Schwab classification structures this analysis, highlighting the degree of sagittal compensation (PI-LL mismatch and pelvic tilt). Conservative care is the first-line approach for most patients. When surgery is considered, surgical goals must balance structural correction against physiological risk. Patient age, comorbidities, bone mineral density (DEXA and Hounsfield unit assessment), nutritional status, and smoking history dictate feasibility. Untreated osteoporosis substantially increases hardware pullout and proximal junctional kyphosis (PJK/PJF). Reconstructive alignment targets should be age-adjusted, avoiding overcorrection in elderly patients while providing adequate lordosis and horizontal gaze. In medically frail patients with predominantly radicular symptoms, focal decompression or limited MIS interbody fusion may achieve clinical goals without the high morbidity of extensive deformity fusions.