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