10 Cervical Disk Disease
10.1 Background
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Disk disease is often described as a result of two pathologies:
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Disk herniation characterized by herniated nucleus pulposus (HNP).
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Degenerative disk disease (DDD).
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These conditions are common and commonly asymptomatic:
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10% of asymptomatic individuals younger than 40 years have HNP on magnetic resonance imaging (MRI).
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25% of asymptomatic individuals younger than 40 years have DDD on MRI.
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The progression of a pathologic intervertebral disk may result in compression of adjacent neural structures including the spinal cord and neural roots.
10.2 Etiology and Pathophysiology
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HNP:
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Secondary to stress on annulus of disk:
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Most often posterolateral as the supportive posterior longitudinal ligament (PLL) is weakest here.
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Increased risk for herniation from aging and disk degeneration:
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Decreased water content and proteoglycan content of nucleus pulposus.
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Characteristics of herniation:
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Protrusion:
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Base (neck) wider than head of herniation.
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Herniation of nuclear pulposus penetrates through annular fibers but remains within the annular margin.
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Extrusion:
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Base narrower than head of herniation.
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Herniation tears through annular margin.
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Can displace (migrate) cranially or caudally.
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Sequestration:
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Free disk fragment separated from original herniation.
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DDD (spondylosis):
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Aging of disk results in biochemical component changes ( Fig. 10.1 ):
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Decreased cross-linking of collagen, decreased water content.
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Decreased blood supply to outer annulus:
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Lactate increases with resultant acidic changes, further degenerating disk.
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Decreased strength from degenerative changes leads to chronic tears throughout annulus.
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Degenerative cycle includes the following:
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Disk degeneration (disk bulging, decreased disk space).
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Joint degeneration (facet arthrosis and uncinate spurring).
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Ligamentous alterations (ligamentum flavum thickening due to loss of disk height).
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Spinal deformity (kyphosis, following the loss of disk height and transfer of load to the uncovertebral and facet joints).
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10.3 Symptoms and Clinical findings
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Both DDD and HNP result in tearing of disks with eventual impingement of nearby neural elements including spinal cord.
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Axial neck pain:
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Unclear etiology.
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Peripheral disk contains nociceptors and PLL:
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Annular tears and herniation potentially activates these receptors.
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Radiculopathy:
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Radiating pain in a pattern consistent with the nerve root involved:
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With or without neurologic symptoms (lower motor neuron symptoms).
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Occurs from direct impingement of nerve roots exiting the spinal cord and vertebral column ( Fig. 10.2 ):
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Lateral HNP or osteophytes can compress exiting nerve root near neural foramen:
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Known as neuroforaminal stenosis.
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Cervical nerve root travels above the similar-named pedicle (i.e., the C5 nerve root travels above the C5 pedicle).
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DDD osteophytes or narrowing of neural foramen, compressing nerve root.
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Inflammation from tears results in chemical radiculitis, furthering radicular symptoms.
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Myelopathy:
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Upper motor neuron symptoms:
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Patients may present with classic findings:
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Gait instability.
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Weakness and clumsiness in manual dexterity.
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Axial neck pain and stiffness.
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Diffuse numbness/tingling not isolated to single dermatome.
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Occurs from central compression of spinal cord:
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Herniation or osteophytic spurs causing narrowing of cervical spinal cord canal ( Fig. 10.2 ):
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Known as central stenosis.
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Torg–Pavlov ratio: ratio of width of cervical canal to cervical body diameter:
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<0.8 = central stenosis.
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Normal is 1.0.
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Microtrauma from neck flexion/extension along with vascular injury furthers injury to spinal cord.
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