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Discogenic pain is pain which originates in the intervertebral discs
of the spine. It is thought to be the cause of up to 40% of chronic
low back pain.
Anatomy:
The intervertebral discs (IVD) are located between the vertebral
bodies and serve as both a shock absorber and a hinge to allow
movement of the spine. There are several parts to the IVD: the
thick annulus fibrosis on the outside of the disc which is composed
of 11-20 layers of thick membranes, the nucleus pulposis (NP)
which is in the center of the discs, and the endplate which is a
cartilage plate between the rest of the disc and the bone of the
vertebral bodies. Normally there are no blood vessels in the disc
and no nerves in the disc. The body's weight is carried on the
spine with the vertebral body above pressing down on the disc
with an oscillation occuring during each step while walking. With
each oscillation, the nucleus pulposis which is normally soft,
squishes down and out against the annulus fibrosis on the sides.
The pressure is then transferred to the annulus fibrosis which
bulges out slightly with each step, then rebounds to an
uncompressed state like a spring.

Pathology:
                                            As a person ages, the intervertebral disc
has less moisture inside and develops cracks around the outside edge of the
annulus. Most disc degeneration is gradual and does not result in significant
amounts of pain. Up to 50% of the population may have MRI and x-ray
evidence of significant degenerative disc disease yet have little reported pain.
However, there are conditions which are part degenerative and part trauma
(such as repeated lifting over years, heavy lifting, automobile accidents, etc)
which can lead to a painful disc. Normally a disc does not have pain reception
inside the disc except for the center of the endplate under which lie nerves
that transmit pain. When a disc becomes degenerative and loses moisture in
the nucleus and annulus, several things happen which may lead to pain.
First, there begins to occur on MRI the development of "black discs" which
are discs without sufficient moisture in the nucleus pulposis (see the pic).
Either associated with lack of moisture or due to trauma to the disc, cracks
develop in the disc, initially around the outer edge of the annulus fibrosis.
These cracks are seen on MRI and called "high intensity zones (HIZ)" or "rim
lesions", and are also called circumferential annular fissures. These cracks
leak potent enzymes from the disc onto the surrounding nerves of the spine
and onto the sensitive ligaments behind the disc. The annular tears ultimately
extend into the middle of the disc as "radial tears". Secondly, there may
develop fractures of the endplate due to abnormal weight load distribution
within the disc. This occurs due to hardened demoisturized areas of the disc
placing focal pressure on the area of the endplate above and below the
hardened area. Endplate fractures directly activate the pain signals from the
endplates. Thirdly, there develops cavitation within the nucleus where there
are large areas of the nucleus that begin to collapse. This worsens the
weight load distribution on the endplates. Fourthly, there is ingrowth of
nerves and blood vessels from outside the annulus to the inside of the
annulus and into the nucleus. These nerves travel in the fissures or tears
through the annulus and are directly compressed by twisting and bending of
the annulus. Fifthly, the endplates develop calcium deposits over the
cannaliculi which are the openings from the vertebral body bone that provide
nutrients to the disc and building blocks to make the moisture absorbing
proteoglycans. When there are calcium deposits over these openings, the
nutrient supply stops and the disc fails to produce proteoglycans in the
nucleus resulting in more moisture loss and collapse of the structures inside
the nucleus. The nucleus fails to provide support to the vertebral body
weight that results in a transfer of that weight to the annulus fibrosis.
Ultimately, the annulus begins to buckle and collapse since the annular fibers
are oriented up and down, and are designed to contain pressure from the
nucleus, not from the endplates. This buckling causes more cracks in the
annulus with increasing leakage of enzymes being produced by the disc.
Sixthly, once the disc space collapse begins to occur due to lack of internal
disc support, weight begins to be transferred from the buckling annulus to
the facet joints. Normally the facet joints hold about 15% of the weight of
the spine, but when the disc space collapses, this may increase to 60%. Such
increased weight on the facets causes the cartilage of the facets to
degenerate and fragment, and ultimately the body tries to reinforce the facet
joints by creating more bone around the joints. This increased bone
produces bone spurs around the facet joints which result in facet arthritis in
the back of the joint and in the most severe cases, results in a constriction of
the spinal canal itself in front of the facets joints. This is called spinal
stenosis. Seventh, the annulus begins to bulge outward into the spinal canal
when the disc space collapses resulting in pressure placed on the sensitive
posterior longitudinal ligament and ultimately may compress the spinal canal
or spinal nerves. The combination of the bulges of the annulus, folding of
the ligaments due to disc space collapse, facet joint enlargement lead to
central spinal stenosis which results in thigh and leg pain when walking.
Eighth, the edges of the vertebral bodies begin to approach one another
when the disc space collapses and this results in the body attempting to
strengthen these areas by building up more bone. This results in more bone
spurs, this time on the vertebral bodies. This condition is known as
spondylosis or arthritis of the spine and is characterized by xray findings of
the vertebral bodies becoming very wide at the bottom and top, giving an
hourglass appearance to the vertebral bodies. The increased bone formation
is called spondylotic lipping and may result in a bone on bone grinding during
movement of the spine.
So there are several areas within the disc which may lead to pain including
annular tears (chemical leakage and nerve ingrowth), endplate fractures,
abnormal weight distribution, and arthritis of the spine.
and there is further There are several pain sensitive areas inside the disc

TESTING FOR DISC DISEASE:
At this time, we can test for annular tears with discography, for endplate
fractures with discography combined with CT afterwards, and arthritis via
facet or pseudoarthrosis injections. MRI, CT, bone scans, and plain film
x-rays do not predictably nor reliably demonstrate the source of pain from
the discs. Only discography when used at low pressures (measured
pressures) in patients without significant psychiatric disease can demonstrate
the pathology of the disc.

TREATMENTS FOR DISCOGENIC DISEASE:
Conservative therapies include physical therapy, epidural steroid injections,
VAX-D, inversion table traction, massage, PT.
Minimally invasive therapies include intradiscal glucose therapy, IDET,
selective endoscopic discectomy with annuloplasty. More aggressive
therapies include Dynesis, artificial disc implantation, and spinal fusion
surgery.