Cervical Spondylotic Myelopathy

  1. Disease/Disorder:

    A condition in which the spinal cord is damaged, either directly by traumatic compression and abnormal movement, or indirectly by ischemia due to arterial compression, venous stasis, or other consequences of cervical spondylosis.

    1. Cervical spondylotic myelopathy (CSM) results from degenerative changes in the cervical spine, including uncovertebral and facet joints, intervertebral discs, ligaments and connective tissue.
    2. A congenitally narrow canal lowers the threshold by which trivial trauma or degenerative changes may cause myelopathy.
    Epidemiology including risk factors and primary prevention
    1. CSM is the most common cause of spinal cord dysfunction in persons over age 55 in North America.
    2. Men are affected more than women.
    3. The more mobile mid-cervical segments, C5 to C7, are most frequently involved.
    4. Patients over age 60 often have multi-segmental disease.
    5. The average anterior-posterior (AP) diameter of the canal measures about 17 mm from C3-C7. The space required by the spinal cord averages 10 mm. Absolute spinal canal stenosis exists with a sagittal diameter below 10 mm. Stenosis is relative if the diameter is 10-13 mm.
    1. Both static and dynamic factors contribute to myelopathy.
    2. Static factors:
      1. Decreased height of desiccated intervertebral discs leads to increased sagittal diameter and disc bulging.
      2. Reactive hypertrophy occurs and osteophytes form at the vertebral end plates.
      3. Osteophytes can project from the uncovertebral and facet joints.
      4. Hypertrophy of facet capsules and ligamentum flavum can contribute.
    3. Dynamic factors:
      1. With hyperextension, the ligamentum flavum buckles into the canal, and the degenerative disc bulges posteriorly.
      2. With a kyphotic sagittal alignment, the cord can become tethered over spondylotic anterior elements during flexion even though canal diameter is increased.
      3. As spinal segments are stiffened by spondylotic change, adjacent segments may develop relative hypermobility and subluxation, causing cord impingement.
    4. Pathological cord findings include gray and white matter destruction, ascending and descending demyelination, with relative anterior column sparing.
    5. Interrupted blood flow through terminal branches of the anterior spinal artery may cause neuroischemia.
    6. Secondary neural injury likely involves glutamate toxicity, free radical mediated cell injury and apoptosis.
    Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
    1. Natural history of CSM is variable and inadequately defined.
    2. Onset is insidious but may be acute(e.g., after a fall with hyperextension injury).
    3. Some patients experience a benign clinical course with neurological improvement; complete resolution is infrequent.
    4. Many do not improve spontaneously and experience neurological deterioration over time. Stepwise neurological worsening with interspersed periods of quiescent stability is common; less commonly, slow, steady progression may occur.
    5. Motor symptoms are more progressive and less likely to improve than are sensory abnormalities.
    6. Balance loss is usually the first symptom patients notice, can become quite profound before addressed, and recovers stubbornly, slowly, after surgical treatment.
    Specific secondary or associated conditions and complications
    1. Cervical radiculopathy often occurs concomitantly with CSM.
    2. Co-existing lumbar stenosis has been reported in a subset of patients.
    3. Acute cord compression with central cord syndrome may occur with relatively minor hyperextension trauma.
    4. Differential diagnosis:
      1. Amyotrophic lateral sclerosis (ALS)
      2. Multiple sclerosis and other demyelinating conditions
      3. Other causes of spinal cord dysfunction
        1. Tumors
        2. Syringomyelia
        3. Infectious myelopathy
        4. Toxic, inflammatory and nutritional myelopathies
      4. Peripheral and entrapment neuropathies
      5. Intracranial pathology
      6. Systemic causes of hyperreflexia.
  2. Essentials of Assessment
    1. Symptoms depend on the magnitude and chronicity of the spinal cord dysfunction.
    2. Early symptoms include diminished hand dexterity and subtle changes in balance and gait with leg stiffness, incoordination, and/or weakness.
    3. Patients may present with frequent falls.
    4. Initial sensory complaints often predominate in the upper extremities.
    5. Compromised bladder or bowel function is less common, and occurs with greater disease severity.
    6. Occipital headache, neck and/or upper extremity pain from associated radiculopathy is common.
    Physical examination
    1. Spastic paraparesis is typical, reflecting early involvement of the corticospinal tracts.
    2. Pathological reflexes such as Hoffman sign, Babinski sign, lower extremity hyperreflexia, and clonus indicate cord compression. A normal jaw reflex distinguishes from intracranial pathology. Concomitant lumbar stenosis may mask lower extremity hyperreflexia.
    3. Upper motor neuron signs may be accompanied by lower motor neuron signs at the level of cord or root compression (e.g., intrinsic atrophy of hand muscle or muscle wasting and fasciculations of shoulder girdle).
    4. Altered vibratory and proprioceptive changes are common. Posterior column dysfunction may cause sensory ataxia.
    5. Patients with CSM who develop a central cord syndrome after hyperextension injury typically have disproportionately greater upper extremity than lower extremity weakness and relative sacral sensory sparing.
    6. Limited neck range of motion reflects the underlying spondylosis.
    7. L'hermitte’s phenomenon can occur.
    Functional assessment
    1. Gait, balance, and fall risk should be assessed.
    2. Activities of daily living should be evaluated with upper extremity involvement.
    3. The Functional Independence Measure (FIM) is commonly used during rehabilitation and follow-up.
    4. The myelopathy disability index (MDI) assesses activities of daily living.
    Laboratory studies

    Laboratory studies are done to rule out other conditions.

    1. Anterior-posterior (AP), lateral, and oblique radiographs should be performed. Spondylotic changes (disc space narrowing, osteophyte formation and listheses) should be interpreted cautiously because such changes are common with increasing age even in the absence of CSM.
    2. The absolute sagittal diameter of the spinal canal is measured from the posterior aspect of the mid-vertebral body to the spinolaminar line.  A reduction to 13 mm or less at C3-C7, or a ratio of canal diameter to mid-vertebral body diameter of 0.8 or less is stenotic.
    3. Lateral flexion and extension radiographs assess range of motion and instability.
    4. Magnetic resonance imaging (MRI) assesses soft tissues and neural elements. Good correlation has been reported between clinical severity of CSM and the presence of high signal intensity in T2-weighted MR images.
    5. Computerized tomography (CT) myelography may provide additional information about bony architecture and osseous structures.
    Supplemental assessment tools
    1. Electrodiagnostic testing evaluates root involvement and excludes conditions such as ALS or neuropathies.
    2. Lumbar spinal imaging assesses concomitant lumbar spinal stenosis.
    Early predictions of outcomes
    1. Favorable prognostic indicators:  symptoms of less than 1-year’s duration, mild myelopathic symptoms, and younger age at initial presentation.
    2. Motor symptoms tend to be more progressive and less likely to improve than sensory abnormalities.

    Given a high risk of falls, environmental interventions such as eliminating loose rugs to prevent tripping, optimizing ambient lighting, and installing grab bars in the bathroom are important. 

    Social role and social support system

    Old age and associated co-morbidities contribute to a high risk of loss of independence especially without an adequate social support system.

    Professional Issues

    Symptoms of CSM are often subtle and varied, thus the diagnosis may be missed or misattributed to other conditions.

  3. Rehabilitation Management and Treatments
    Available or current treatment guidelines

    Lack of high quality, randomized studies and varied natural history of the disease contribute to paucity of definitive treatment guidelines.

    At different disease stages
    1. Patients without major neurological deficits but with radiological evidence of cord compression may be treated conservatively and monitored. The role of surgical decompression in this setting remains controversial. A soft cervical collar may prevent additional injury by providing sensory feedback to restrain extremes of movement; proof of effectiveness is limited. Rigid collars are often discarded if prescribed for long-term use. Nonsteroidal anti-inflammatory drugs are used for symptomatic pain management. In the absence of surgery, instruction to avoid high-impact activities that are associated with hyperextension injuries is prudent in those with radiological signs of pronounced cord compression.
    2. In the setting of progressive neurological deterioration, surgical decompression should be considered. The long-term effectiveness of surgery remains inconclusive:
      1. Both anterior and posterior surgical approaches have been used. Choice of technique depends upon factors including location of the primary compressive lesion, presence of spinal instability, spinal alignment, number of levels involved, and surgeon preference.
      2. Anterior approaches include anterior cervical discectomy and fusion, or cervical corporectomy. The presence of cervical kyphosis usually requires an anterior approach.
      3. Patients with widespread stenosis and multisegmental cord compression, ligamentum flavum buckling, or with technical/mechanical factors that interfere with an anterior approach, may be candidates for posterior decompression.
      4. Laminectomy alone carries the risk of developing postoperative kyphotic deformity, which is decreased with laminoplasty or laminectomy with fusion.
    3. Rehabilitation interventions depend on the extent and type of deficits. Mobility assessment, gait training, and fall risk management are essential. Patients with upper extremity weakness and impaired hand dexterity need ADL assessment and training and prescription of appropriate adaptive equipment.
    4. Complications of myelopathy such as urinary infections, incontinence, and pressure ulcers should be prevented and promptly managed.
    Coordination of care

    CSM typically occurs in older individuals with co-morbidities that cumulatively impact function, thus a coordinated, interdisciplinary approach to care is important.

    Patient & family education

    Patients should be informed of the risks, benefits, and limitations of various surgical and nonsurgical treatment options.

    Emerging/unique Interventions

    Gait analysis, particularly walking speed.

    Impairment-based measurement:

    1. Grip strength evaluation with a dynamometer
    2. 10-second step test
    3. 10-second open-and-close-hand test
    4. Modified Japanese Orthopedic Association (mJOA) scale
    Translation into practice: practice "pearls"/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
    1. CSM should be considered if unexplained subtle gait abnormalities or hyperreflexia are present in elderly patients.
    2. Do not assume without evaluating for other conditions that CSM is the primary cause of neurological impairment, just because there is radiological evidence of cervical spondylosis.
  4. Cutting edge/emerging and unique concepts and practice
    Cutting edge concepts and practice

    Initial results of disc arthroplasty in conjunction with decompression procedures have been promising; longer follow-up is needed.

    1. Advances in neuroimaging techniques including spinal diffusion tensor imaging (DTI) and magnetic resonance spectroscopy (MRS) may play a key future role in assessment and management.
    2. Minimally invasive techniques can make surgery less invasive in the future.
  5. Gaps in the evidence-based knowledge
    Gaps in the evidence-based knowledge
    1. Controversies persist about the natural history of CSM, the role of conservative versus surgical treatment in patients with mild symptoms, and the comparative merits of various surgical approaches. Randomized clinical studies are needed.
    2. Research is needed to evaluate specific interventions to optimize rehabilitation outcomes.


    Klineberg E. Cervical spondylotic myelopathy: a review of the evidence. Orthop Clin North Am. 2010;41(2):193-202.

    Matz PG, Anderson PA, Holly LT, et al. The natural history of cervical spondylotic myelopathy. J Neurosurg Spine. 2009;11(2):104-11.

    McKinley WO, Tellis AA, Cifu DX, et al. Rehabilitation outcome of individuals with nontraumatic myelopathy resulting from spinal stenosis. J Spinal Cord Med. 1998;21(2):131-136.

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