DJD of Spine Flashcards
cartilaginous endplaye
serves as the growth plate for vertebral bodies (like epi plate) frm max thickness at infancy down to 1mm thick avascular layer of hyaline cartilage in adultsq
3 main structures of IV disk
cartilaginous endplates
central nucleus pulposus
peripheral annulus fibrosus
nucleous pulposus
conists of proteoglycan (aggrecan w/ chondroitin sulfate side chains) and h20 matrix held by a network of collagen II and elastin fibers
annulus fibrosis
made of 20 rings (lamellae) of highly organized collagen I fibers that run parallel within the same lamella but perpendicular to the adjacent rings for max tensile strength
annulus fibrosus fux
helps the nucleus pulposus recover its original shape when pressure is removed
what supplies blood to the inner edge of the annulus
2 capillary plexuses–> O2 and nutrients must diffuse ~8mm frm there to the nucleus, making the IVD hypoxic and thus dependent on anaerobic metabolism–>produce lactate–>diffuse to opposite sides of nutrients
innervation of annulus fibrosis
only the outer 1-2mm of annulus are innervated, while the inner annulus and disc are aneural and avascular
what happens in natural aging
decreased water content and decreased proteoglycan content–> disc becomes smaller and less flexible–>increased collagen I content (replacing collagen II)–>nucleus becomes stiffer and less translucent with age
annulus in natural aging
recives more pressure because nucleus is less shock-absorptive–> increased collagen, stiffness–> weaker
two factors involved in natural aging
idiopathic loss of endplate blood supply
non-enzymatic glycation–>formation of AGEs–>make disc glycans more sticky and brittle and increase lamellar collagen fiber crosslinking–> decrease tensile strength, and discal tissue begins to have a distinct shade of brown
when eventually the disc collapses (in natural aging)
compressed unevenly by bone–> “stone in shoe deformity”
deformity in natural aging classified from
1 (normal with strong water signal) to 5 (no water signal)
degeneration
mimics natural aging but at an accelerated rate and usualy with more symptoms
–proposed that premature degeneration begins with injury and micrfx to the endplate, rupture of inner annulus and other genetic and environmental factors
DDD
disc degenerationt hat produces symptomatic pain associated with neovascularization and aforementioned ingrowth of sensory nerves
because disc pressure is weaker (they can grow without compression–>increase nociception from the disc)
the degenerative cascade
internal disc disruption–>disc herniation–>disc generation–>spinal stenosis–>degenerative spondyloisthesis–>degenerative scholiosis
- can skip some steps*
disc herniation
usually fromt hinner postero-lateral corner of the disc during bending with rotation of the spine
when does disc herniation occur
with sudden violent trauma (sports) or (more commonly) with less severe trauma (lifting, bending)
herniated pprtion of the disc may..(3)
- be covered with thin layer of peripheral annulus (protrusion)
- rupture through the full thickness of the annulus and lie under the posterior longitudinal ligament or in directly under the dural sac or nerve root (extrusion)
- lose contact with the original disc; moving away (sequestration)
location of herniation is proportional to
affected nerve root
posterolateral disc herniation usually affects the
traversing (exits one segment below) nerve root ex ) C4-C5,C5
far lateral or foraminal disc herniation usually affects
nerve root above
L4,5–>L4
clinical presentation of disc herniation
radiculal pain (pain along the affected nerve root) patients usually come to clinical leaning to one side (sciatic scoliosis) to avoid pain
cauda equina syndrome
disc compresses S2-S4 on both sides affecting bowel/bladder emergency
symptoms in disc herniation + resolution
usually resolve over 6-8 weeks in 80% of cases
if they fail to resolve or begin to cause weakness or numbness–>surgery (discetomy)
