Research Review By Dr. Josh Plener©


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Date Posted:

September 2020

Study Title:

Cervical Spondylotic Myelopathy: A Guide to Diagnosis and Management


McCormick JR, Sama AJ, Schiller NC et al.

Author's Affiliations:

University of Miami Leonard M. Miller School of Medicine, Department of Education; University of Miami Hospital, Department of Orthopaedic Surgery; The Rothman Institute, Thomas Jefferson University Hospital, Philadelphia Pennsylvania, United States.

Publication Information:

The Journal of the American Board of Family Medicine 2020; 33(2): 303-313.

Background Information:

Cervical spondylotic myelopathy (CSM) is an insidious, progressive disease resulting from compression of the spinal cord and/or surrounding blood vessels (1). In North America, CSM accounts for 54% of non-traumatic spinal cord injury (1-3) – making it the most common cause. Unfortunately, diagnosis is still often delayed! Approximately 10% of patients aged 55 and older display clinical signs of CSM, but in the coming decades this number is expected to increase in prevalence as the population of people over the age of 60 increases (4). CSM has the potential to cause long-term disability and major neurological impairments. Therefore, identifying patients with CSM in a timely manner is critical for practicing chiropractors (and all primary care clinicians!). This clinical review paper summarized contemporary knowledge on CSM for practicing clinicians.


Pathophysiology of CSM

There are a variety of pathologies that can lead to cervical cord compression, such as cervical spondylosis and disc herniations. Cervical spondylosis is the progressive, degenerative disease that affects the vertebrae, intervertebral discs, facets and associated ligaments (most relevant here is the ligamentum flavum). However, the pathophysiology is still not fully understood. Multiple studies have demonstrated a diminished vascular supply through the anterior spinal artery and radicular arteries as they are stretched over a disc or vertebral body (5, 6). This can lead to ischemia of oligodendrocytes, leading to apoptosis and neural demyelination (7). Other factors that are believed to play a role in CSM include: impairment of intracellular energy metabolism, free radical-mediated injury, and cation-mediated cell injury (8). The end result of spinal cord damage in CSM is neuronal dysfunction, which leads to the long-tract signs that are observed clinically (9).

Spinal cord compression and subsequent neuronal damage are classified as either static or dynamic mechanical compression (5, 10). Static compression risk factors are constant and result in injury of the cervical canal through stenosis, whereas dynamic factors involve repetitive injury.

Examples of static risk factors include:
  • Congenital spinal stenosis: This is a narrowing of the spinal column which can lead to local ischemia, neural cell injury and apoptosis, ultimately leading to cervical myelopathy (11-13).
  • Disc herniation: Herniated discs can compress the spinal cord, or the lateral walls of the annulus fibrosis can tear (14). Disc herniations and/or annulus fibrosis tears can lead to increased stress on the vertebrae, leading to osteophyte development, which can further contribute to cord and surrounding vasculature compression.
  • Ossification of the ligamentum flavum or posterior longitudinal ligament: This can lead to narrowing of the spinal canal and progressive cervical myelopathy (11).
Dynamic risk factors for CSM involve repetitive injuries. Typically, the repetitive injury is caused by flexion or extension of the cervical spine, which can stretch the axons leading to greater susceptibility for secondary injury. Dynamic compression can result from movement beyond the typical range of motion. For example, neck hyperextension could lead to collapsing of the ligamentum flavum into the spinal canal, or neck flexion can lead to anterolisthesis that compresses the spinal cord if an underlying pathology is present (8, 11).

Natural History of CSM

Despite the fact that only a small percentage of spondylosis ultimately results in CSM, age related degeneration remains the primary cause of this condition. Risk factors for the development of CSM have been reported to be the male sex and having labor-intensive occupations (15). Some negative prognostic factors for CSM patients include the degree of disease progression upon diagnosis, age, and the duration of symptoms (1, 16). For patients undergoing surgery, prognostic factors that help indicate post-op outcomes include age, symptom duration, and preoperative neurological function (2). With regards to the progression of CSM in patients, further investigation is required as some patients report a benign form of the disease, where others report a progressive deterioration of motor and sensory function (17, 18).

Signs, Symptoms and Diagnosis

Clinically, CSM is difficult to diagnosis in a timely manner, as initial symptoms such as difficulties with fine hand dexterity and gait instability or falls tend to be subtle (19). Research has demonstrated that CSM has an average delay in diagnosis of 6.3 years, during which time patients decline an average of 2 Nurick grades (See below for an explanation of the Nurick grading system) (18).

Signs and symptoms include both upper and lower extremity findings. Upper extremity findings include:
  • Decreased hand dexterity: 75% of patients experience a decrease in intrinsic hand muscle dexterity and notice trouble with fine motor tasks such as shirt buttoning, handwriting and typing (19, 20).
  • Lower motor neuron signs: These can include muscle weakness, atrophy, fasciculation, hyporeflexia and hypotonia.
  • Sensory changes: These can include changes in pain, temperature, proprioception and general dermatomal sensation deficits. These are caused by compression of the spinothalamic tract, posterior column, and spinal roots (7). In addition, 50% of patients with CSM experience neck pain, 38% experience radicular pain, and 27% experience a positive L’hermitte sign (21).
  • Hoffman sign (an involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down): The prevalence of this sign in the general population is 2%, but it has a positive predictive value of 68% and a negative predictive value of 70% in CSM patients. Therefore, this test is useful in the diagnosis of CSM but should be used as an adjunct (22, 23).
  • Inverted radial reflex: If compression occurs at C6, this reflex may be present. This reflex is elicited by tapping the distal brachioradialis tendon, and a positive finding is hyperdynamic finger flexion on testing.
  • Hyperactive pectoralis reflex: For myelopathy at C2 to C4, this reflex has a sensitivity of 84.8% and specificity of 96.7%. This is elicited by taping the pectoralis tendon in the deltopectoral groove and a positive finding is adduction and internal rotation of the arm.
  • “Myelopathy hand”: This is characterized by a positive finger escape sign, grip and release test and intrinsic hand muscle wasting (24). The finger escape sign (also called Wartenberg’s sign) is visualized when the patient holds their fingers extended and adducted for 30 seconds. A positive finding is abduction and flexion of the ulnar two or three digits (often described as only the 5th digit). The grip and release test is visualized when the patient makes a fist and releases as many times as possible in 10 seconds. A positive finding is failure to do 20 open-close cycles. Intrinsic hand muscle wasting is assessed visually.
Lower extremity findings are related to upper motor neuron lesions that are below the affected vertebral level. The findings include:
  • Impairment of gait and/or falls: Gait dysfunction is seen in 80.3% of patients and is a key sign of CSM.
  • Upper motor neuron signs (weakness, hyperreflexia, hypertonia): Lower extremity weakness is most frequently seen in the iliopsoas muscle (38.8%), followed by the quadriceps (26.3%) (20). This can result in changes in patient’s gait as demonstrated by slower gait speed, decreased step length, longer stride time and increased step width compared to healthy controls (25).
  • Change in pain, temperature, proprioception, dermatomal sensation: Proprioception deficits are secondary to posterior spinal column involvement, which may be investigated by the Romberg test and heel-to-toe walking.
  • Motor deficits
  • Babinski reflex/sign: This has 100% specificity for CSM, but only 13% sensitivity (26).
  • Sustained foot clonus: This is defined as > 3 beats in succession. This has a high specificity (96%) but low sensitivity (11%) (22).
  • Bladder sphincter tone changes: This finding is seen in 44% of patients.
A retrospective analysis demonstrated CSM patients had the following symptoms: 91% had gait abnormality, 85% had any hyperreflexia with 81% having lower extremity hyperreflexia and 67% having upper extremity hyperreflexia, 83% had a positive Hoffman sign, and 44% had a Babinski reflex/sign (27).

Symptom Severity Scales for CSM

There are two scales that are used to evaluate CSM. Originally, the Nurick Scale for Clinical Myelopathy Evaluation was developed to assess symptom severity. The symptom score predominantly arises from the patient’s ability to walk and is graded from 0-5 with a higher score signifying greater impairment. On the scale, 0 represents signs and symptoms of root involvement without spinal cord disease, and 5 represents that the patient is chair bound or bedridden. The Japanese Orthopaedic Association Myelopathy Evaluation Questionnaire (JOA scale) has now largely replaced the Nurick scale. The JOA is a more comprehensive scale, which includes 6 sub-scores evaluating upper extremity motor, lower extremity motor, upper extremity sensory, lower extremity sensory, truncal sensory and bladder function (28). The JOA is scored from 0 to 17, with mild CSM defined as a score of 15 to 17, moderate CSM is defined as a score of 12 to 14, and severe CSM is defined as a score of 0 to 11.

Radiographic Evaluation

On initial presentation, plain film x-rays are usually carried out due to its ease of access and low cost. On films, spinal alignment and the Torg-Pavlov ratio can be determined. The Torg-Pavlov ratio is measured by dividing the canal diameter by the vertebral body diameter. Canal stenosis is suggested if the ratio is < 0.8. Furthermore, on the lateral view, the canal diameter can be determined as cord compression is correlated with a canal diameter < 12 mm. In addition, on the lateral view, one can assess the amount of neck flexion. A 2018 study demonstrated an association of milder myelopathy symptoms with increased C2-7 ROM and maximal flexion (29).

CT scans can also be used, which are the gold standard for diagnosing ossification of posterior longitudinal ligament (30-32). In addition, CT scans can be used when patients have contraindications for undergoing an MRI.

If suspicion of CSM is high, MRI is the gold standard for CSM diagnosis. MRI can visualize soft tissue, the severity of degeneration, and determine the severity of cord compression (33). Based on the MRI, there are some negative predictors for surgical outcomes which include a greater number of signal intensity segments on T2 weighted image, higher signal intensity ratio, and combined high signal intensity changes on T2 and low signal intensity changes on T1 (34). Furthermore, some factors that do not appear to be associated with post-surgical neurological outcome includes maximum cord compression ratio, number of discs causing cord compression and cord diameter.

Electrophysiological studies can be used to rule out other conditions that may simulate CSM such as carpal tunnel syndrome, multiple sclerosis and amyotrophic lateral sclerosis (ALS).


There is a lack of research comparing operative to nonoperative management. Typically, guidelines recommend a trial of non-operative management for mild CSM with close monitoring and the potential for surgery if any deterioration occurs. For moderate to severe CSM, surgical intervention is recommended (35). For patients with evidence of cord compression on imaging but a lack of myelopathy or root compression signs, education regarding signs and symptoms, the risk of progression and regular follow-up should occur (35).

Non-operative management:

There have been no studies to determine the optimal nonoperative treatment for CSM. Therefore, treatments should revolve around the patient’s symptoms with possible treatment modalities including bed rest, medications, steroids, injections, exercise, soft collar, rigid collar, cervical traction and thermal therapy (36). Some research has demonstrated rigid collars are unlikely to help and spinal manipulation has not resulted in long-term benefit (37). Further research is desperately needed as currently, a very low to low amount of evidence exists for the non-operative management of CSM.

Operative management:

The surgical approaches used for CSM patients consist of anterior, posterior or combined. Patients are frequently managed through an anterior approach if they have significant kyphosis, 1-2 vertebral level involvement or ossification of the posterior longitudinal ligament. Typically, the procedure includes anterior cervical discectomy (surgical removal of part or the entire intervertebral disc) and fusion, anterior cervical corpectomy (surgical removal of part or the entire vertebral body) and fusion, or cervical disk arthroplasty (38-40). Patients with > 3 levels involved, cervical stenosis, posterior compression, or congenital stenosis (41) are frequently managed through a posterior approach. Typically, the procedure consists of laminectomy with or without posterior spinal fusion and laminoplasty (42-45)

Asymptomatic patients who have no clinical signs of myelopathy are typically managed through a wait and see approach. Research has demonstrated that by the age of 50, up to 31.6% of the population has cord compression on MRI, which increases to 66.8% after 80 years of age (46). One review demonstrated that only 22.6% of patients with evidence of cord compression will develop myelopathy (47).

Clinical Application & Conclusions:

The diagnosis of CSM is often difficult to make initially, as signs and symptoms can be vague and emerge over a considerable period of time. As a result, it is important for primary care providers to be alert to the common symptomatology of CSM in order to provide patients with the best possible long-term outcome. Delaying diagnosis can result in deterioration of symptoms, leading to a decreased quality of life for patients.

Reviewer’s note: For chiropractors, physiotherapists and other clinicians who treat recurring neck pain patients, it is important to ensure that any new neck pain or arm symptoms are properly investigated, particularly as patients age. Treating new episodes of pain the same as previous episodes without a proper history and physical examination could (in some cases) be detrimental, as these signs may be the initial presentation of CSM, which would require further follow-up and likely specialist referral.

Editor’s note: Treating this condition can certainly be challenging. In my experience, these patients often respond well (albeit sometimes only temporarily) to an individualized application of manual cervical traction applied in a rhythmic, repetitive manner (in addition to mobilization and sometimes manipulation). This can involve general long-axis distraction, often with some degree of flexion or extension (depending on their comfort level and symptom response). Thoracic spine mobilization and manipulation can also be quite helpful (don’t forget to treat the whole person). Simple home range or motion and isometrics for the cervical spine are prudent additions for most patients. Ultimately, in the absence of high-quality evidence to guide us, our approach must be tailored to individual patients.

Study Methods:

This paper aimed to provide a clinical review of patients with CSM. Therefore, no statistical analysis was conducted nor was a specific description of their methodology provided.

Study Strengths / Weaknesses:

  • This article provides a comprehensive clinical review of CSM, discussing the clinical presentation, examination and management.
  • Further research on CSM is required, as currently research gaps exist. For example, the pathophysiology of CSM is not fully understood and there is very low to low quality research surrounding the effectiveness of non-operative treatment.

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