Spondylosis Spin13 Spondylosis



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Spondylosis Spin13 ()

Spondylosis

Last updated: September 5, 2017



Etiopathophysiology 2

Mechanisms of damage / irritation to neural structures 6



Epidemiology 7

Cervical Spondylosis 8



Clinical Features 8

Cervical Spondylosis 8

Lumbar Spondylosis 13

Diagnosis 14

Plain X-ray 14

Cervical Spondylosis 15

Lumbar Spondylosis 15

MRI 16

Cervical Spondylosis 16



Lumbar Spondylosis 22

CT myelography 22

Cervical Spondylosis 22

Lumbar Spondylosis 24



Differential Diagnosis 25

Conservative Treatment 26

Surgical Treatment – Cervical Spondylosis 26

Surgical Treatment – Lumbar Spondylosis 27

Prognosis 28

Cervical Spondylosis 28



Special Entities 28

Diffuse idiopathic skeletal hyperostosis (s. diffuse idiopathic skeletal hyperostosis, Forestier disease) 28

ossification of posterior longitudinal ligament (OPLL) 28


Spondylosis:

  1. ankylosis of vertebra

  2. any degenerative spinal lesion.

  3. progressive degeneration of intervertebral discs, leading to proliferative changes of surrounding structures

CSM – cervical spondylotic myelopathy.

Etiopathophysiology



Degenerative changes of spine universally accompany aging!

see p. Spin11 >>



Most are sequelae of intervertebral disc degeneration - loss of disc height causes:

  1. narrowed intervertebral foramina.

  2. increased load on vertebral bodies → reactive vertebral changes → osteophytes.

    • most osteophytes are anterior or lateral in projection.

    • osteophytes reduce range of movement and may result in spontaneous fusion.

  3. increased load on facet & uncovertebral (Luschka) jointshypertrophic osteoarthritic changes.

    • remodelling of articular surfaces → instability → forward slippage of upper on lower vertebra.

    • synovial cysts are frequently solid (cartilaginous or myxomatous) - can be confused with migratory disc fragments or intraspinal tumor; attachment to joint space is characteristic.

  4. bulging of disc annulus; osteophytes converge on protruded annulus, and may convert it into bony ridge (transverse bar) that protrudes posteriorly (compromising spinal canal); protrusion laterally compromises foramina.

  5. laxity of ligaments + increased load / traction on ligamentsinfolding (hypertrophy) of ligamentum flavum, ossification of posterior longitudinal ligament (see below)

These changes narrow spinal canal* & intervertebral foramina

*acquired spinal stenosis - may form subarachnoid block (with CSF protein content↑ below block).



N.B. patients with congenitally narrow spinal canal are at increased risk!

Central canal stenosis can cause myelopathy (cervical) or cauda equina syndrome (lumbar)

Lateral recess stenosis can cause radiculopathy.

Intervertebral foramen stenosis can cause radiculopathy.



Sources of osteophytes compromising intervertebral foramen:

  1. edges of vertebral bodies.

  2. facet (interpedicular, zygapophyseal) joints

  3. uncovertebral (Luschka) joints (only in cervical vertebrae).

    • on sagittal MRI or reformatted CT, foramina appear as comma-shaped, fat-filled spaces just above disc level; roots exit via bulbous upper portion (just below pedicles) - early degeneration of disc and facet joints effaces only fat inferior to nerve roots.





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