Degenerative Cervical Myelopathy: Degeneration versus Adaptation

By Tom Jesson, with thanks to John Drummond

With the work of the RECODE-DCM and myelopathy.org campaigns, degenerative cervical myelopathy has taken its place as one of the most important serious pathologies in MSK practice. It’s a good time then to pause and try to truly understand this condition - beyond the red flags.

What does ‘degenerative’ mean?

Degenerative changes don’t just mean wearing away, but also growth. Osteoarthritic knobbly knees are a good, visible example of this apparent paradox. How does it happen in the cervical spine?

The first step: just as skin dehydrates and sags with age, intervertebral discs dehydrate and flatten (1–3). As a disc flattens, the vertebrae above and below it press into each other more. "Settling like a pile of dishes", as the great physiotherapist Gregory Grieve put it (4). Consequently, the bony surfaces of the vertebrae bear more and more load.

In response, the bony surfaces of our vertebrae thicken, much like skin forms calluses when overused. This new bone has a “brittle, sugary consistency”, as the surgeon K. Lewer Allen described in one of the earliest descriptions of Degenerative Cervical Myelopathy (DCM) (5). The bone forms on facet joints, uncovertebral joints, and extends into spurs on the posterior lips of vertebrae. These bony extensions help support the spine against thinning discs, but they also crowd the spinal cord. Allen observes that "At operation, when the dura is opened, the cord is found kinked and displaced backwards" (5).

Meanwhile, as discs flatten, the spine shortens. This shortening causes the already thickened ligamentum flavum to slacken and buckle outwards, further crowding the spinal cord (2). Add to this the fact that narrowing discs also tend to bulge outwards, and there are three kinds of structures - bone, ligament and disc - encroaching upon the spinal cord. 

Mechanical stress on the cord

We tend to think of bone, ligament and disc encroachment as compressing the cord. But the cord experiences more than compression; it faces tension, shear force, and even torsion stress too (6). For example, a bone spur pressing into the cord might cause myelopathy not where the cord is compressed, but on the opposite side where the cord stretches (7).

Neck movement adds dynamic stress. When you flex your neck, the cord stretches over vertebrae and those degenerative changes (7). When you extend your neck, the cord gets pinched by those same changes. Bone spurs create “deep grooves” in the cord's anterior surface, says Alf Breig, forming “humps” on the posterior side (7). 

This variety of cord stresses helps to explain why DCM presents so differently. It varies between individuals, can fluctuate week to week in early stages, and differs between limbs in the same person. These variations partly explain why no single test reliably detects DCM (8).

What happens to the cord?

Firstly, mechanical stress squeezes blood vessels, which stops blood from flowing (2,8). The first surgeons to document DCM described how the cord blanched under stress points (5,9). “On flexing the neck there was posterior displacement of the cord, producing pallor” (5), wrote one.