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Chapter Summary
• Context: Degenerative cervical myelopathy (DCM) represents the leading cause of progressive nontraumatic spinal cord dysfunction in adults worldwide. Disc degeneration, spondylotic osteophytosis, facet arthrosis, ligamentum flavum buckling, dynamic hypermobility, and ossification of the posterior longitudinal ligament (OPLL) progressively narrow the cervical canal reserve. The pathophysiology combines static compressive forces, dynamic injury during flexion-extension, and secondary ischemic microvascular and histopathological cord damage. Clinical diagnosis is frequently delayed because early symptoms—subtle loss of hand dexterity, buttoning difficulty, mild paresthesias, or discreet gait imbalance—are easily misattributed to normal aging or peripheral neuropathies. Magnetic resonance imaging (MRI) is essential to detect cord compression and intramedullary signal changes; however, radiographic stenosis is also prevalent in asymptomatic individuals, making comprehensive neurological examination mandatory. Functional scoring systems (mJOA, Nurick) standardize severity assessment. Management depends on myelopathy severity, progression rate, number of stenotic levels, sagittal alignment (lordosis vs kyphosis), compression location (anterior vs posterior), and, in OPLL, specific morphology and dural ossification.
• Chapter Objective: To elucidate the pathophysiology and clinical presentation of DCM, achieve early recognition of compressive cervical myelopathy, apply validated clinical scoring scales (mJOA, Nurick) and multi-modality imaging, understand the classification and surgical implications of OPLL (K-line), and select anterior, posterior, or combined surgical approaches based on compression geometry, level span, and sagittal alignment.
• Static compression, dynamic strain, and neural ischemiaThe chapter structures DCM pathophysiology into three interacting pillars: static structural stenosis, repetitive dynamic flexion-extension strain, and secondary spinal cord ischemia. This multi-hit model explains why resting static MRI alone does not reflect the total physiological burden on the cord.
• Clinical diagnosis begins with manual and gait functionLoss of fine motor dexterity, clumsiness when buttoning shirts, handwriting changes, gait unsteadiness, hyperreflexia, clonus, Hoffmann's sign, and Babinski responses are cardinal findings. The modified Japanese Orthopaedic Association (mJOA) and Nurick scoring scales (Tables 48.1 and 48.2) document severity and monitor progression. Figure 48.4 details key neurological exam maneuvers.
• Ossification of the Posterior Longitudinal Ligament (OPLL)OPLL presents distinct continuous, segmental, mixed, and focal morphological types (Figure 48.1) and frequently associates with dural ossification ('double-layer sign', Figure 48.2). The K-line concept (Figure 48.3) integrates sagittal alignment and ossification prominence to predict whether posterior decompression alone can achieve sufficient indirect cord drift.
• Diagnostic imagingPlain radiographs assess cervical lordosis and mobility. CT excels at mapping ossified masses in OPLL and canal geometry. MRI evaluates cord effacement and intramedullary T2/T1 signal alterations. Dynamic flexion-extension MRI (Figure 48.10) can unmask position-dependent cord compression missed on neutral scans.
• Surgical strategy tailored to alignment and anatomyModerate-to-severe myelopathy (mJOA < 15) and progressive clinical decline mandate surgical decompression. Mild cases may be monitored under close surveillance in select patients. Anterior approaches (ACDF, ACCF), posterior laminectomy with fusion, expansive laminoplasty, and circumferential reconstructions each offer distinct profiles. Multi-level involvement, anterior versus posterior compression, sagittal lordosis vs kyphosis, and K-line status dictate the optimal corridor.
• Clinical Application: In clinical practice, any patient presenting with dropped objects, deteriorating handwriting, difficulty fastening buttons, or unexplained gait stiffness warrants immediate evaluation for DCM, even if neck pain is completely absent. A normal sensory exam or concurrent polyneuropathy does not rule out spinal cord compression. MRI demonstrates cord effacement and T2 hyperintensity; high-resolution CT is mandatory if OPLL is suspected to map dural ossification and prevent catastrophic CSF fistulas. When deciding between anterior and posterior surgery, spinal alignment is decisive: posterior laminoplasty or laminectomy with fusion relies on posterior cord drift, which requires preserved cervical lordosis and a K-line positive configuration. In cervical kyphosis or K-line negative OPLL, the cord remains tented over anterior compressive masses after posterior decompression, necessitating anterior corpectomy (ACCF), anterior controllable antedisplacement and fusion (ACAF), or circumferential reconstruction.
