There are six major categories for the causes of spinal pain (degenerative, deformity, trauma, infection, tumor, inflammatory). However, the most common by far is degenerative conditions of the spine. 80 percent of the adult population will have an episode of low back pain in their lifetime. Fortunately, 90 percent will obtain relief of pain within six to eight weeks and ninety five percent will be free of pain within six months. However, 70 to 90 percent will have a recurrence of their pain. Five percent of this population will go on to chronic pain and disability. Low back pain is the second most common reason for a physician visit. The common cold is first.
The best model to explain the changes responsible for spinal pain is called the degenerative cascade. It is based on the concept of the spinal motion segment. The spinal motion segment consists of the intervertebral disc, the vertebrae above and below the disc, the paired facet joints behind the disc, and the nerves within the spinal canal. The motion segment is highly resistant to loading forces during the first two decades of life. However, beginning in the third decade (twenties), the spine begins to age (degenerate) and continues to age progressively until death. As the spine degenerates, it is less able to resist loads (normal and abnormal) and is more susceptible to injury. Aging (degeneration), single injury, or multiple injuries lead to changes in the structural integrity of the disc, facet joints, and vertebral end plate cartilage.
The degenerative cascade is divided into three stages
depending on the amount of damage to the disc and facet joints at any point in
time. Stage I (dysfunction) starts at an early age (20-30) and is a reflection
of the first changes of degeneration. Stage II (instability) follows
dysfunction as degeneration progresses or abnormal loading is not corrected or
treated. It represents more severe tissue damage and usually occurs later in
life (late 30s- early 50s). Stage III (stabilization) is the end stage of the
degenerative cascade. It reflects the most severe tissue damage and attempts at
physiologic repair of the tissue. This stage occurs in the 60s and beyond.
Stage I Dysfunction
|
Facet Joint |
Disc |
|
Inflammation
(synovitis) |
Annular
strain |
|
Capsular
tear (minor) |
Annular
tear |
|
Meniscus
tear |
Vertebral
end plate injury |
|
Minor
cartilage injury |
|
Stage II Instability
|
Facet Joint |
Disc |
|
Capsular
tear (major) with laxity. Increasing rotational and sagittal
movement |
Increasing
annular tears and delamination |
|
Increasing
cartilage damage |
Annular
disruption with laxity. Increasing rotational and sagittal
movement. |
|
Increasing
inflammation |
Decreasing
nuclear proteoglycans and loss of water content.
Increase transfer of forces to annulus. Loss of disc height. Annular buckling
and tears. |
Stage III
Stabilization
|
Facet Joint |
Disc |
|
Severe
cartilage damage-loss of Joint surface. |
Increasing
annular tears and stiffness |
|
Joint
hypertrophy and bone spurs |
Increasing
nuclear degradation. Decreasing proteoglycans. Disc
resorption and loss of disc height. End plate irregularities. Bone spurs
(osteophytes) |
|
Spinal
stenosis-nerve compression |
Decreasing
nuclear proteoglycans and loss of water content.
Increase transfer of forces to annulus. Loss of disc height. Annular buckling
and tears. |
Clinical
Manifestations
Stage I Dysfunction
This stage usually presents as acute mechanical
low back pain. It is typically the patient's first episode of pain and is
usually short lived, self-limited, and improves with minimal intervention.
Extension and/or rotation usually produce pain from the facet joints at this
stage. Pain from the annulus/disc is usually limited to back pain worsened by
flexion or torsional movement, sitting, and bending.
Stage II Instability
This stage also presents as predominantly low
back pain. However, it is usually more severe and is not short lived,
self-limited, and requires significant intervention. It is often the patients
repeated episode of back pain. It is during this phase that recurrent annular
tears can lead to a disc rupture or herniation. The pain from a disc herniation
is more predominantly leg pain secondary to nerve root compression. Because of
the more severe tissue damage and incomplete healing of the tissues, the
episodes of back pain are more frequent, severe, and disabling.
Stage III
Stabilization
This stage can also present as back pain;
however, now leg pain is more prevalent. The hypertrophy and bone spurs of the
facet joint combined with the loss of disc height and bone spurs formed around
the rim of the disc produces spinal stenosis (narrowing of the spinal canal).
This can produce lateral recess and foraminal stenosis, which causes nerve root
pain. It can also cause central stenosis producing claudication
(leg pain worsened by walking relieved by sitting down in a flexed position).
The degenerative cascade is a very useful model. It describes the physiologic (normal) changes of aging in the spine. These changes may or may not be painful (which explains the high incidence of abnormal findings on imaging studies in asymptomatic or pain free individuals). It gives us an anatomic and physiologic basis for understanding where spine pain originates. When a patient presents with spine pain, we can identify what stage of the cascade their injury represents and what tissue is injured. We can then recommend treatment on a rational basis and predict the outcome of that treatment. We can also educate patients to recognize that their initial back pain is a warning sign of the negative potential of the degenerative cascade. With emphasis on education, life style changes, exercise, and body mechanics we can alter the long-term consequences.