It is only through the understanding of lumbar spine pathophysiology and its clinical correlates that specific rational treatment for patients becomes possible. Rational therapy requires making a specific diagnosis first.
The elucidation of the “degenerative cascade” and its meaning for patient care has reflected significant personal effort on the part of a number of pioneers concerned with this challenge.
Prominence in this small group have been William Kirkaldy-Willis, Harry Farfan, and Henk Verbiest. It was Kirkaldy-Willis who first conceptualized and published his theories regarding the “Degenerative Cascade.” This was the first unification of multiple theories regarding the normal progression of lumbar spine degeneration. The figure below is from the textbook “Managing Low Back Pain” published in 1983 by Churchill Livingstone. Kirkaldy-Willis’ original work still remains the single most brilliant correlation of pathophysiologic observations. This work created a format by which these observations could be related to clinical diagnosis and subsequent rational patient therapy. Failure to understand this schema has clearly been the single most cause of the “failed back surgery syndrome” as well as much well intentioned, but ineffective or destructive spine therapy.
With the modern recognition of genomic spine disorders and the ability, through non-invasive high-resolution MRI imaging, to monitor change throughout an individual’s lifetime we are now able to validate the observations of those who have tried to show us the way.
Normal Spinal Anatomy
This section, on the Clinical Cascade, begins with a depiction of the basic elements of a spinal segment. A segment includes adjacent vertebrae and the intervertebral disc between them. Shown, to the left, is such a segment. Red Dot- Intervertebral Disc
Green Dot- Dorsal Nerve Root Ganglion (shown separating into primary and secondary rami). Blue Dot- The facet (or zygoapophyseal joint). Black Dot- The dural sac containing the pia and arachnoid layers, the nerve roots of the cauda equina and the exiting nerve roots.
Partial removal of the superior vertebrae allows a better appreciation of the normal anatomy, particularly the relationship of an exiting nerve root to the intervertebral disc. Note that the interior of the disc(nucleus pulposus) is distinct from it enveloping tough collagenous layered capsule (annulus fibrosis).
When “disc” is spelled with a “k” it is a misnomer. The term disc is a biologic term. The term disk is a technical term as in “computer disk.”
The anatomically correct spelling for “annulus” is with one “n.” Common medical usage has, however, prevailed in this regard and dictated the spelling “annulus”.
The Degenerative Cascade
In 1980 Harry Farfan pointed out, on the basis of his research, that: “Disc and facet joint degeneration leads to dynamic spinal instability.”
The typical initiating event in the “Degenerative Cascade” is the loss of internal disc integrity. This can be on a congenital (genomic) basis as well as a result of the process of aging as well as acquired insult and injury (i.e. certain stressful occupations).
In genomic situations (i.e. Juvenile Discogenic Disease) disc nutrition may be poor because of the existing endplate abnormalities and premature disc collagen deterioration. On the other hand the collagen itself may have not formed normally at birth due to congenital enzymatic deficiencies. Even when the collagen is well formed and receives good local nutrition it can be progressively destroyed by acquired insult and/ or injury. The entire process can (and is) adversely affected by factors such as cigarette smoking, environmental pollutants and lack of exercise. The net result of adverse influence is that instead of there being a tough, gristle-like, disc the collagen (and disc) then become incompetent to do the job of segmental support. This process bears great similarity to that which occurs when tough steak is “tenderized” by pounding it with a mallet.
With this loss of segmental loss of support is the development of segmental dysfunction. This can progress to the point of true segmental instability. The result is similar to a automobile body developing “shimmy” also reflecting acquired insult and injury.
In this illustration disruption of the posterior annulus of the disc has occurred. In this example radial tears are seen in the posterior annulus. When such tears contain inflammatory fluid they appear on MRI scan as an area of high intensity and are referred to as a “HIZ” tear. HIZ tears have been directly correlated with low back pain.
Progressive degeneration and tearing of the disc initiates the cascade: This process basically causes loss of segmental stability. The tears can coalesce and form a channel through which the annular material can protrude causing a “herniated disc.” The process itself can produce a “discogenic” pain syndrome.
In the degenerative cascade disc degeneration leads to segmental dysfunction and stress is then directed to the facet joints. Facet degeneration then occurs in association with facet enlargement (hypertrophy) with subsequent erosion of the articular surfaces leading to other pathologic changes.
Shown above to the left is a drawing of “normal” by artist Frank Netter. To the right is an actual specimen provided by Harry Farfan demonstrating the beginning of degenerative changes.
From left-to-right the figures above (provided by William Kirkaldy-Willis) show the results of progressive degeneration. To the left the arrow points to eroded articular surface, in the center a CT scan demonstrating the same change, and, finally, as a result of continuing erosion a degenerative spondylolisthesis is created (spondylo-vertebrae; listhesis- slip) where the facets have lost their ability to help support the associated vertebrae (they have become anatomically “incompetent”).
The facets are markedly degenerated, mechanically incompetent, eroded and contain fluid (effusion). This situation is a “pain generator” as the sensory nerves from the dorsal root ganglia are continually stimulated by the abnormal movement of the segment.
This type of low back pain is referred to as a “facet syndrome” as opposed to a “discogenic pain syndrome.” Often, in the early stages of this process, disc injections, blocks, and related procedures can be performed as well as facet injections and blocksas relatively simple, minimally invasive, means of relieving patient pain and disability. Facet problems are much more amenable to simple treatment than discogenic pain problems. They can also become complex as shown in the series of images below:
This is a case of a 52 year old female with underlying genomic spine disease. A degenerative spondylolisthesis has developed at L4-5. The MRI image in the center shows the degenerated facet joints and suggests a mass on the left side of the image compromising the central spinal canal. Lesions such as this are often synovial cysts or chondromas from the degenerated facet. In this case, as shown on the right CT image the mass is a calcified chondroma. This mass has been chronically compressing and distorting the dural sac.
Iatrogenically Produced Facet Problems
Low back pain secondary to facet degeneration is a common phenomenon. Back pain secondary to stress induced on the fact joints by medical procedures is uncommon but of great concern because it reflects lack of understanding by treating physicians. Classic examples are:Post-chemonucleolysis collapse of the disc interspace.
Post-artificial disc surgery rotational instability. It is unfortunate that primary care physicians, who are the “gatekeepers” of patient care know little regarding the nature of back pain or its effective therapy. Because of this physicians either refer all back patients or turn to “shotgun”, non-specific, and sometimes ill-advised procedures such as blind epidural steroid injections rather than therapies specific to the needs of the patient based on a specific understanding of the problem.
“There is no such thing as non-specific back pain, but there are non specific doctors”