Research Review by Dr. Shawn Thistle©


Feb. 2007

Study Title:

Pathophysiology of cervical myelopathy


Baptiste DC & Fehlings MG

Publication Information:

The Spine Journal 2006; 6: S190-S197.


Cervical myelopathy is the most common acquired case of spinal cord dysfunction in patients over 55. Cervical Spondylotic Myelopathy (CSM) is the diagnostic interpretation most familiar to manual therapists, while cervical myelopathy is a broad term encompassing a number of distinct pathologies in the cervical spine which lead to compression of the spinal cord. Clinically, these pathologies can be difficult to differentiate, often requiring advanced imaging to identify the exact cause.

Further, the signs and symptoms experienced by the patient can be extremely variable, depending on which specific area of the spinal cord is affected. Posterior, dorsolateral and ventrolateral columns, ventral horns, and the cervical nerve roots can all be involved, and patients often have more than one area of involvement. The specific pathophysiology of cervical myelopathy is still uncertain, however it is generally accepted that the disorder involves narrowing of the spinal canal secondary to anatomical degeneration of discs, facet joints, ligaments and connective tissue. This is often in conjunction with an already narrow spinal canal. As the canal space narrows, the risk of symptoms increases.

This disorder is influenced by static factors, referring to anatomical causes, and dynamic factors, referring to repetitive injury to the cervical cord related to movement abnormalities. The combination of these two factors can cause a cascade of inflammation, degeneration, and altered movement which leads to neuronal and glial injury, ischemia, exitotoxicity, and apoptosis (cell death).

The purpose of this review article was to summarize the pathophysiological processes associated with cervical myelopathy.

The authors reviewed human studies and relevant animal studies to create this review, which will be summarized below. Additional information regarding clinical presentation and examination was adapted from the additional paper referenced below.

  • the typical patient is male (by a ratio of 2.4:1) and over 50
  • C5-6 is the most frequently involved level, followed by C6-7 and C4-5 (see below why C3-4 is then the most common hypermobile segment)
  • typical symptoms include: pain, neck stiffness, upper limb paresthesia, weakness, clumsiness, gait disturbance, disequilibrium/dizziness, bladder dysfunction
  • typical signs include: decreased cervical ROM, sensory abnormality (touch, vibration, joint position sense etc.), weakness on manual muscle testing, muscle wasting, increased tendon reflexes below the level of compromise, spasticity, gait disturbance, coordination deficits, and long tract neurological signs (ex. Oppenheim’s and Babinski’s responses)
  • early presentation can be vague which often leads to delayed diagnosis
  • a full neurological examination should be completed, starting with cranial nerves and progressing to upper and lower limb examinations (including long tract tests)
  • include additional sensory tests – vibration, position sense etc., cerebellar function tests (ex. Rhomberg’s)
  • special signs can include: shoulder girdle wasting, fasciculations, atrophy of hand intrinsics, diminished grip/release test (patient smoothly opens and closes hand 20 times in 10 seconds), inability to perform heel-toe gait
  • IMAGING: x-ray studies should be ordered if significant neurological deficit is present, there is a history of trauma, or if the patient fails to respond to conservative care – CT or MRI can also be utilized
  • DIAGNOSTICS: somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) may assist in more specific neurological diagnosis

Spondylosis and Disc Degeneration (static/dynamic)
  • cervical discs are vulnerable to the same pathological processes as lumbar discs
  • with age, disc dehydration occurs accompanied by medial annular splitting and disappearance of the nucleus pulposis
  • this results in increased load on the uncovertebral processes, which become flattened, thus altering the load-bearing characteristics of the cervical motion segment
  • this process can result in an unstable motion segment secondary to disc degeneration
  • articular cartilage and endplates of the vertebral bodies respond to this by developing osteophytic spurs at the vertebral margins in an attempt to stabilize the adjacent segment
  • the intervertebral discs themselves can calcify to further stabilize the segment
  • diminished disc height and osteophytic overgrowth can lead to compression on the spinal cord, cervical nerve roots, or vertebral artery
  • C3-4 is thought to be the most common level of instability in the elderly, normally due to excessive degeneration and lack of motion at lower cervical segments
Ossification of the Posterior Longitudinal Ligament (OPLL) (static)
  • OPLL is a multifactorial disease, and is most prevalent in Japanese people (~2-4%) as well as other ethnic groups
  • involves ossification of the PLL which can span the entire length of the spine
  • normally presents as progressive myelopathy, and can even result in quadriparesis
  • thought to have a strong genetic component but the exact cause or mutation is not known
Ossifcation of the Ligamentum Flavum (OLF) (static)
  • OLF is most common in the thoracic and lumbar spines, but can occur in the neck
  • the most common symptoms associated with OLF are arm pain and weakness
  • as with OPLL, it tends to affect Japanese people most often, to the point where it is considered rare in other ethnic groups
  • the major diagnostic difference between OPLL and OLF is the anatomical location of the two structures
  • genetic similarities are thought to exist in the pathology of OPLL and OLF
Calcification of the Ligamentum Flavum (static)
  • another rare disorder primarily occurring in Japanese people
  • the most common presentation is subacute myelopathy in the absence of precipitating factors, sensory disturbance in the upper limb, clumsiness, difficulty walking, and urinary dysfunction
  • neck pain and low grade fever can also occur – thought to originate from inflammation at the calcified sites
  • some authors suggest that this condition could be due to an overlying calcium deposition disorder (such as calcium pyrophosphate deposition disease or pseudogout)
Congenital Canal Stenosis (static/dynamic)
  • the presence of canal stenosis (< 13mm sagittal) is highly correlated with later development of cervical myelopathy, however this relationship is not always consistent
  • normal canal diameter is thought to be 17-18mm between C3 and C7
  • a narrow spinal canal is thought to lead to local spinal cord tissue damage and ischemia, further exacerbated by repetitive movement problems, and all conditions discussed above
  • dynamically, neck hyperextension narrows the canal by shingling the laminae and buckling the ligamentum flavum
  • normal flexion of the neck can also result in cord injury via axial strain to the cord – normal spinal cords are resilient to such forces but over time with associated anatomical problems, the tissue can surpass its threshold and become symptomatic
The Role of Ischemia
  • considerable evidence (animal and human) supports ischemia as a major underlying event in the etiology of myelopathy
  • the neural cell type thought to be most susceptible to ischemia is the oligodendrocyte (responsible for insulating myelin sheaths, and also known to undergo apoptosis after acute traumatic injury)
  • anterior cord compression compromises the anterior sulcal arteries, while posterior compression reduces perfusion of the intramedullary branches of the central gray matter
    reasonable differentials for cervical myelopathy include: Multiple Sclerosis, shoulder amyotrophy, syringomyelia, rheumatoid arthritis affecting the upper cervical spine, post-polio syndrome, spinal cord tumour, psychogenic disorders, and pernicious anemia

Conclusions & Practical Application:

Cervical myelopathy is a complex disorder with many contributing factors. It can be a difficult condition to assess and diagnose, but should remain in the astute clinician’s mind when patients present with vague neurological symptoms.

Additional information for this review was adapted from the following paper, also contained in the supplemental issue on the topic from The Spine Journal in December, 2006:

Salvi FJ, Jones JC & Weigert BJ. The assessment of cervical myelopathy. The Spine Journal 2006; 6: S182-S198.