Cervical spondylosis

Cevic spondylosis

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Cervical spondylosis

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• Cervical spondylosis is the defined as “spinal canal and neural foraminal narrowing in cervical spine secondary to multifactorialdegenerative changes

• Approximately 25% of individuals younger than forty years of age, 50% of individuals over forty years of age, and 85% of individuals over sixty years of age have some degree of disc degeneration

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• The fibers of the annulus fibrosus that surround the nucleus pulposus lengthen, weaken, and fray with age and use, thereby allowing the disk to bulge posteriorly.

• this “soft-disk” herniation occurs mainly during the third and fourth decades of life when the nucleus is still gelatinous.

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• The disc loses height and bulges posteriorly into the canal.

• With this loss of height, the vertebral bodies drift toward one another.

• Posteriorly, there is infolding of the ligamentumflavum and facet joint capsule, causing a decrease in canal and foraminal dimensions.

• Osteophytes form around the disc margins and at the uncovertebral and facet joints.

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Radradiolgyclinics NA

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• A bulge involves more than half of the circumference of an intervertebral disc

• protrusion is distinguished from a disc bulge in that it involves less than half the circumference of the disc. Conversely it is distinguished from a disc extrusion in that its base is wider than its 'dome' and it does not extend above or below the disc level.

• disc extrusion has a broader dome than neck

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• The joints between the neural arches are the zygapophyseal joints or facet joints.

• The branches of the posterior primary ramiinnervate these joints.

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• endplates of the vertebral bodies progressively suffer mechanical stress with the consequent formation of osteophytes. These osteophytes are a natural trial to increase the load-bearing surface of the endplates in order to compensate for spine hypermobilitysecondary to disk degeneration.

• ossification of the posterior longitudinal ligament (OPLL), most commonly seen in the Asian population,

• osteophytes develop in the vertebral bodies, facet joints, and arches, and the ligamentum flavum thickens and ossifies

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Pathogenesis of Cervical Spondylosis

• intervertebral disc desiccation, which is associated with increase in the ratio of keratin sulfate to chondroitinsulfate

• the nucleus pulposus shrinks, loses elasticity, and becomes more fibrous due the loss of water, protein and mucopolysaccharides during the aging process

• Disc height is initially lost in the ventral portion of the disc, which results in a decrease in cervical lordosis

• These early changes ultimately lead to the main pathophysiological process of cervical spondylosis, a reduction in sagittal spinal canal diameter

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• these changes cause a transfer of axial load onto the facet joints, resulting in hypertrophy of those joints that further decreases the spinal canal’s diameter

• The annulus fibrosis is thinner dorsally, thus making it easier for the nucleus pulposus to dissect through and cause disc herniations into the spinal canal

• Preceding disc herniation, the peripheral fibers of the annulus fibrosis and Sharpey’s fibers dissect from the vertebral body edges

• posterior longitudinal ligament beginning to pull away from the vertebral bodies near the end plates

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• Where the PLL peels off the dorsal vertebral body, reactive bone formation begins forming spondylotic bone spurs

• These osteophytic growths may project into the intervertebral foramina

• increase in joint motion causes an acceleration of osteophyte growth, and this is most pronounced at C5- C6 and C6-C7

• --decrease in sagittal spinal canal diameter,

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Cervical Spine Posture

• upper cervical spine allows for varying degrees of motion in multiple directions

• lower parts of the cervical spine do not provide the same degree of motion. A significant feature of this part of the spine is the lordotic posture, and it is believed that this may play a role in preventing spinal cord injury.

• The facet joints are most effective in participating in axial load support when in extension

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axial view of cervical spinal stenosis with spinal cord impingement due to the combination of a congenitally narrow cervical spinal canal and superimposed cervical spondylosis.

Encroachment on the cervical spinal canal is caused by bulging disks often with osteophytic spurring, thickening of the posterior longitudinal ligament and ligamenta flava,

subluxation of one vertebra forward or backward on its neighbor, thickening of the posterior aspect of the uncovertebral joints, and osteoarthritis of the facet joints.

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Cervical spondylotic myelopathy

• long-tract signs resulting from a decrease in the space available for the cervical spinal cord

• Anteriorposterior diameter of the spinal canal,

• dynamic cord compression

• dynamic changes in the intrinsic morphology of the spinal cord

• the vascular supply of the spinal cord.

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Static Factors

• congenitally narrow cervical spinal canal• However, dynamic MRI studies of 295 patients with symptomatic CSM by

Morishita and colleagues showed increased segmental mobility in the cervical spine of patients with a congenitally narrow canal (<13 mm anteroposteriorly), suggesting that segmental instability may also contribute to accelerated sp

• Congenital anomalies of the cervical spine such as Klippel-Feil syndrome can lead to accelerated spondylosis.

• patients who have undergone surgical fusion of cervical vertebrae can have exaggerated spondylosis in adjacent segments.

• Both congenital and iatrogenic fusions likely result in excessive motion of adjacent unfused spinal levels, which leads to increased spondylosis. ondyl

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• normal cervical spinal canal sagittal diameter (posterior vertebral body to spinolaminar line) is 17 to 18 mm (C3–C7) in a white population

• patients with developmentally narrowed midcervical sagittal diameters smaller than 10 mm were often myelopathic, patients with canals of 10 to 13 mm were at risk for CSM, canals of 13 to 17 mm were seen in patients with symptomatic spondylosis but rarely myelopathy, and subjects with canals larger than 17 mm were not prone to develop spondylosis.

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• Acquired cervical central canal stenosis

• age-related spondylotic change (most common)

• OPLL, and ossification of the ligamentumflavum

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Dynamic Factors

• exacerbated by neck motion• The spinal cord stretches with flexion of the neck and it can be

compressed against osteophytic spurs and intervertebral disks protruding into the spinal canal.

• Hyperextension can pinch the spinal cord between the posterior margin of the vertebral body anteriorly and the laminae or ligamentum flavum posteriorly.

• Repetitive neck movements and trauma can also accelerate spondylosis.

• An animal study in which rabbits were exposed to repeated forcible neck extension and flexion movements showed early development of osteophytes. Similarly, rugby players and patients with dystoniccerebral palsy that included their cervical muscles developed accelerated spondylosis.

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• Penning et al.13 believed that symptoms of cord compression occurred when the transverse area of the cord was <60 mm2

• Houser et al. thought that the shape and degree of flattening of the spinal cord could be an indicator of neurologic deficit; 98% of their patients with severe stenosis and a banana-shaped spinal cord had clinicalevidence of myelopathy

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• Ono et al. Described an anterior-posterior cord compression ratio that was calculated by dividing the anterior-posterior diameter of the cord by the transverse diameter of the cord

• Patients with substantial flattening of the cord, suggested by an anterior-posterior ratio of <0.40 tended to have worse neurologic function. Oginoet al. Thought that an increase in this ratio to ≥0.40 or an increase in the transverse area to >40 mm2 was a strong predictor of recovery following surgery

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• Flexion and extension MRI images have shown that increased stenosis is two times more likely during extension than during flexion

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Loss of the ventral disc interspace height which occurswith the natural degenerative process results in loss of lordosis

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• Retrolisthesis of a vertebral body can result in pinching of the spinal cord between the inferior-posterior margin of a vertebral body and the superior edge of the lamina caudad to it .This compression may be aggravated in extension, and it may be relieved in flexion as the retrolisthesis tends to reduce.

• Forward slippage of a vertebral body may cause compression of the spinal cord between the superior-posterior margin of the vertebral body below and the lamina above. This is aggravated by flexion

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• spinal cord stretches with flexion of the cervical spine and shortens and thickens with extension

• Thickening of the cord in extension makes it more susceptible to pressure from the infolded ligamentum flavum or lamina

• In flexion, the stretched cord may be prone to higher intrinsic pressure if it is abutting against a disc or a vertebral body anteriorly

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• cervical spondylosis will typically result in stiffening of the spinal motion segments. It is not uncommon for the motion segments one or two levels above the stiff segments to become hypermobile. This is termed “compensatory subluxation”

• cervical kyphosis is not uncommon in patients with significant spondylotic changes. This deformity will aggravate the degree of compression in patients with cervical stenosis or disk herniations because the spinal cord will be stretched over the posterior aspect of the disks and vertebral bodies

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Kyphosis associated with cervical spondylosis causes neuralinjury, in part, by tethering the spinal cord over a ventral mass viathe “sagittal bowstring” effect (A). Dorsal decompression (i.e. via

laminectomy) may worsen deformation

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Ossification of the posterior longitudinal ligament (OPLL

• The ossification can be at one level, can involve skip-type lesions at multiple levels, or can be a continuous strip of bone

• The ossified ligament is often not a thin strip, but rather a bulbous mass that may be centrally or eccentrically located

• It can occur in conjunction with cervical spondylosisand often produces severe anterior compression of the spinal cord.

• Long-standing OPLL can ossify the adherent dura, which may create the problem of spinal fluid fistulae

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• degenerative elements compress blood vessels that supply the cervical spinal cord and proximal nerve roots.

• Ischemia may result from direct compression of larger vessels such as the anterior spinal artery and overall reduced flow in the pial plexus as well as in small penetrating arteries which supply the cord

• impairment of venous flow may lead to significant venous congestion and contribute to spinal cord ischemia

• the region of the spinal cord most affected by CSM (levels C5 to C7) is also the area with the most vulnerable vascular supply

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• Severe compression results in degenerative changes in the spinal cord.

• The central gray matter and the lateral columns show the most changes, with cystic cavitation, gliosis, and demyelination most prominent caudad to the site of compression. The posterior columns and posterolateral tracts show walleriandegeneration cephalad to the site of compression. These irreversible changes may explain why some patients do not recover following decompressive surgery.

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Cervical radiculopathy

• most common cause of cervical radiculopathy is a foraminal constriction of multifactorial origin including uncovertebral joint hypertrophy, facet arthropathy, and loss of disk space height.

• the herniated disk is located posterolaterally, compromising the nerve root at the entrance to the neural foramen; occasionally the herniated disk is centrally located and causes myelopathy. Cervical nerves exit in the inferior aspect of the foramen; hence the exiting, not the traversing, nerve is most likely to be impacted by a disk herniation or a disk–osteophytecomplex.

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Cervical Radiculopathy

• It is generally believed that only an inflamed or irritated nerve root can result in radicularpain on compression

• Chronic edema and fibrosis within the nerve root

• mechanical compression of the dorsal root ganglion

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• Ferguson and Caplan divided cervical spondyloticmyelopathy into four syndromes

• (1) medial syndrome, consisting primarily of long-tract symptoms;

• (2) lateral syndrome, consisting primarily of radicularsymptoms;

• 3) combined medial and lateral syndrome, which is the most common clinical presentation;

• (4) vascular syndrome, which presents with a rapidly progressive myelopathy and is thought to represent vascular insufficiency of the cervical spinal cord.


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Crandall and Batzdorf described five broad categories of cervical

spondylotic myelopathy• (1) transverse lesion syndrome, in which the corticospinal, spinothalamic,

and posterior cord tracts were involved with almost equal severity and which was associated with the longest duration of symptoms, suggesting that this categorymay be an end stage of the disease;

• (2) motor system syndrome, in which corticospinal tracts and anterior horn cells were involved, resulting in spasticity;

• (3) central cord syndrome, in which motor and sensory deficits affected the upper extremities more severely than thelower extremities

• (4) Brown-Séquard syndrome, which consisted of ipsilateral motor deficits with contralateral sensory deficits and which appeared to be theleastadvanced form of the disease, and

• (5) brachialgia and cord syndrome,which consisted of radicular pain in theupper extremity along with motor and/or sensory long-tract signs

J jneurosurg

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• Symptoms caused by cervical spondylosis can be categorized broadly into three clinical syndromes

• axial neck pain, cervical radiculopathy, and cervical myelopathy

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• Neck Pain• Degenerative changes at the cervical disc and facet

joints• The pain often stems from abnormalities in structures

innervated by the sinuvertebral nerve or branches of the posterior primary ramus.

• Among the structures that the sinuvertebral nerve innervates are the posterior longitudinal ligament, the epidural vasculature, and the spinal periosteum

• Less commonly, the pain can be attributed to the facet joints, which are innervated by the primary posterior ramus

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axial pain patternsproduced by injections into the facetjoints at the second through seventh

cervical level

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source of neck pain

• Anterior neck pain along the sternocleidomastoid muscle belly that is aggravated by rotation to the contralateral side is most often a result of muscular strain.

• Pain in the posterior neck muscles that is worsened by flexion of the head suggests a myofascial etiology.

• Pain in the posterior aspect of the neck that is aggravated by extension, especially with rotation of the head to one side, suggests the possibility of a discogenic component.

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Radicular pain

• symptoms are usually aggravated by extension or lateral rotation of the head to the side of the pain (the Spurling maneuver

• shoulder abduction sign.e., relief of severe radicular pain when the patient rests the hand on the top of the head

• decreasing tension within the nerve root, this position may lift the sensory root DRG directly cephalad or lateral to the source of compression, and decompression of epidural veins may contribute to pain relief

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• Upper cervical radiculopathies occasionally present as suboccipital pain with referral to the back of the ear.

• C4 radiculopathy can present as neck and shoulder pain with accompanying ipsilateraldiaphragmatic palsy

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Radiologic Evaluation

• Typical radiographic manifestations include disk-space narrowing, end-plate sclerosis, and osteophytic changes at the end-plates, uncovertebral joints, and facet joints.

• Plain radiographs remain an important part of the diagnostic workup, and anteroposterior (AP), lateral, and flexion-extension views of the cervical spine should be obtained in essentially all patients in this age group.

• Oblique views are useful for visualizing foraminalnarrowing, which is typically due to uncovertebral joint spurs; however,. The AP view allows identification of cervical ribs and scoliotic deformity. The lateral view is most important, as it demonstrates the degree of disk narrowing, the size of end-plate osteophytes, the size of the spinal canal, and sagittal alignment

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• In some cases, OPLL is visualized as a bar of bone running along the posterior aspect of the vertebral bodies.

• . Flexion-extension views are critical to diagnose instability, which may not be evident on a neutral lateral view.

• MR imaging provides optimal visualization of soft tissues, CT-myelography offers better definition of bone spurs and OPLL.

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• Sensory conduction studies are useful in the evaluation of a patient suspected ofradiculopathy because SNAPs are typically normal (because the lesion is rostral to the DRG in the intervertebral foramina) even in the face of clinical sensory loss, in contrast to the situation in plexopathy and peripheral nerve trunk lesions, where SNAPs are attenuated or absent.

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Needle EMG• A study is considered positive if abnormalities—especially acute

changes of denervation including fibrillation potentials and positive sharp waves—are present in two or more muscles that receive innervation from the same root, preferably via different peripheral nerves

• No abnormalities should be detected in muscles innervated by the affected root's rostral and caudal neighbors.

• Reduced motor unit potential (MUP) recruitment and MUP abnormalities of reinnervation (high-amplitude, increased duration, polyphasic MUPs) are also sought.

• in the later phases of nerve root compression, the only needle EMG changes indicative of radiculopathy might be chronic neurogenic changes of reduced recruitment and MUP remodeling.

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