Continuing Education Activity

Cervical myelopathy describes a spinal cord compression at the cervical level of the spinal column resulting in spasticity (sustained muscle contractions), hyperreflexia, pathologic reflexes, digit/hand clumsiness, or gait disturbance. Classically, it has an insidious onset, progressing in a stepwise manner with functional decline. Management often involves surgery involving either anterior or posterior decompression of the tight area and likely fusion. A poor prognosis is associated with more than 18 months of symptomatic duration. Without treatment, patients may progress toward significant paralysis and loss of function. This activity reviews the etiology, presentation, evaluation, and management of cervical myelopathy and examines the role of the interprofessional team in evaluating, diagnosing, and managing the condition.

Objectives:

• Evaluate the pathophysiology of cervical myelopathy and cite the at-risk patient populations who are susceptible to this condition.

• Outline the orthopedic, neurological, laboratory, and imaging tests needed to adequately diagnose cervical myelopathy.

• Differentiate treatment options for cervical myelopathy, depending on precise etiology.

• Summarize interprofessional team strategies for improving care coordination and communication to improve outcomes in managing and treating cervical myelopathy.

Introduction

Cervical myelopathy describes a spinal cord compression at the cervical level of the spinal column resulting in spasticity (sustained muscle contractions), hyperreflexia, pathologic reflexes, digit/hand clumsiness, or gait disturbance.[1][2][3] Classically, it has an insidious onset, progressing in a stepwise manner with functional decline. Without treatment, patients may progress toward significant paralysis and loss of function. Surgery involves either anterior or posterior decompression of the tight area and likely fusion. A poor prognosis is associated with more than 18 months of symptomatic duration, decreased cervical spine range of motion, and female gender.[4][5]

Etiology

While myelopathy is a term relating to the results of the compression of the spinal cord, stenosis is a term describing a narrowing of a normally patent canal. In the cervical spine, certain patients are more predisposed to myelopathy due to a congenitally narrowed spine cervical canal. Subsequent progression of stenosis or a cervical disc herniation is more likely to result in myelopathy at this level. Degenerative changes are usually at C5 and C6 or C6 and C7 levels due to the increased motion permitted at these levels. Additional contributors to canal narrowing are the infolding of the ligamentum flavum, spondylolisthesis, osteophytes, and facet hypertrophy. Myelopathy develops in approximately 100% of patients with greater than 60% canal stenosis (less than 6 mm disc cord space). Age is the strongest predictor of perioperative morbidity and unfavorable neurologic recovery.

Epidemiology

Interestingly, patients with neck pain who have radicular symptoms following a dermatome are more likely to improve from operative correction than those without radicular pain. If the pain follows a particular myotome, it is more likely to have a predictable source and origin. About 65% of patients with neck pain and radicular symptoms benefit from surgical decompression. Asians are at increased risk of cervical myelopathy (1.9% to 4.3% of individuals older than 30 years) due to their increased prevalence of ossification of the posterior longitudinal ligament, which is a source of compression.

Pathophysiology

Cervical spondylotic myelopathy frequently involves compression of the lateral corticospinal tracts, resulting in (voluntary skeletal muscle control) and the spinocerebellar tracts (proprioception). Together, these deficits are responsible for the wide-based spastic gait with clumsy upper extremity function that is classic to cervical myelopathy. Additional commonly involved spinal cord regions are the spinothalamic tracts, which are responsible for contralateral pain and temperature sensation, the posterior columns, which are responsible for the ipsilateral position and vibration sense, and the dorsal nerve root, which is responsible for dermatomal sensation.[6][7][8]

History and Physical

Patients presenting with cervical myelopathy predominately experience upper extremity symptoms. These may include hand clumsiness and a limited ability to perform fine motor tasks such as buttoning a shirt, combing hair, holding small objects, and differentiating coin sizes. In cases of lower extremity signs, patients typically ambulate with a wide-based gait and weakness. Neck pain and radicular symptoms are also common. Additionally, physicians should examine for a Lhermitte sign (provocative positions that create an electric shock-like sensation either down the back or into an extremity). Indicators of poor prognosis include bowel or bladder dysfunction and general weakness. Obtaining a history from the patient should focus on the timeline of pain, radiation of pain, and inciting events. A presentation of radiating pain correlates with canal stenosis. Radiating pain as the main issue has a much more predictable surgical outcome than a presentation of non-specific neck pain that is likely related to muscle fatigue and strain. All physical examinations should evaluate the neurologic function of the arms, legs, bladder, and bowels. The key to a thorough exam is organization and patience. The clinician should evaluate not only strength but also sensation and reflexes. It is also important to examine the skin along the back and document the tenderness to compression or any prior surgical scars.

Evaluation

The following should specifically be examined in cervical myelopathy patients:

• Gait: Examine balance issues or spasticity issues
• Reflex examinations for hyperreflexia: Biceps, brachioradialis, patellar, Achilles
• Lhermitte sign: Neck flexion causes an electric shock-like (positive exam)
• Hoffman sign: The examiner extends the distal phalanx of the long finger (or flicks the end of the digit) and rapidly releases this digit. The patient responds with a reflex flexion of the thumb or index finger.
• Crossed radial reflex: Extension of both the biceps and wrist following a biceps reflex test
• Inverted radial reflex: Extension of both wrist extension and finger flexion following tapping the brachioradialis
• Finger escape sign: The patient is unable to hold the ulnar digits in extension and adduction.
• Grip test: Failure to repetitively make a tight fist  

Imaging

• X-ray: Radiographs of the AP and lateral spine are paramount to all spine evaluations. If possible, flexion and extension views help determine ligamentous stability.
• Torg ratio: Compares the cervical canal's diameter to the cervical body's width on the lateral view. Mid-posterior vertebral body to the nearest point on the lamina, divided by the width of the corresponding vertebral body. A ratio lower than 0.8 may indicate congenital stenosis (baseline narrowing).
• Magnetic resonance imaging (MRI): A canal space of less than 10 mm indicates stenosis. It is best to evaluate cord and disk space. Of note, up to 19% of asymptomatic patients have significant cervical abnormalities, which can be misleading. An MRI is imperative to evaluate spine pathologies. Compression and signal changes on T1 and T2 are indicative of myelopathy pathologies.

Treatment / Management

Non-surgical management should include anti-inflammatories, physical therapy, ultrasound modalities, and, at times, corticosteroid injections, but these all supply temporary pain relief.[9][10] These short-term alternatives are not definitive treatments for patients with progressive symptoms.[11][12] In the setting of progressive symptoms, surgical management should merit strong consideration. The goal of surgery is to increase the canal space, which lessens/eliminates cord compression. It is now a general recommendation to intervene earlier instead of a careful waiting period surgically. Surgical intervention can involve either an anterior or posterior approach. A posterior approach is preferable in lordosis deformities and when the pathology occurs at the posterior aspect of the canal. One option is a laminectomy (ideally with preoperative lordosis greater than 10 degrees and absence of instability). Posterior approaches possibly have higher infection rates compared to anterior. Anterior cervical discectomy and fusion is performed via an anterior approach. This can involve up to 3 disc levels. It is reported that 9% to 27% of patients have a transient sore throat and dysphagia, usually resolving within 12 weeks. The most common neurologic complication is recurrent laryngeal nerve palsy in 3% of patients.

Differential Diagnosis

The differential diagnosis for cervical myelopathy includes the following:

• Central cord syndrome
• Chiari malformation
• Guillain-Barre syndrome
• Multiple sclerosis
• Syrinx

Prognosis

An MRI can guide clinicians and patients about the potential for improvement. Based on a systematic review of MRI findings by Tetreault et al in 2013:

• High-intensity changes on T2 and low intensity on T1: poorer recovery rate, worse motor symptom improvements
• A high ratio of T2 signal intensity between non-compressed and compressed (C7 through T1) was associated with a poorer JOA recovery rate.
• More frequent high signal intensity on T2 predicts worse recovery.

Pearls and Other Issues

• The clinician should consider surgery if symptoms progress, there have been issues for more than 6 months, the compression ratio (cord sagittal /transverse) is less than 0.4, or, on MRI, the transverse area of the cord is less than 40 mm.
• There should be a consensus statement recommending surgical intervention once a diagnosis of cervical myelopathy has been made.
• The timeliness of intervention is critical. Patients with milder myelopathy and less than 6 months of symptoms have improved outcomes after surgery.

Enhancing Healthcare Team Outcomes

The diagnosis and management of cervical myelopathy are handled by an interprofessional team that includes a nurse practitioner, neurologist, neurosurgeon, orthopedic surgeon, physiotherapist, and physiatrist. Treatment depends on symptoms and the degree of spinal stenosis. Non-surgical management should include anti-inflammatories, physical therapy, ultrasound modalities, and, at times, corticosteroid injections, but these all supply temporary pain relief. It is clear that once the symptomatology has started its progression, these short-term alternatives cannot be a definitive treatment. In the setting of progression, surgical management merits strong consideration. Surgery aims to increase the canal space to lessen/eliminate cord compression. It is now a general recommendation to intervene earlier instead of a careful waiting period surgically. The surgical intervention can be done via an anterior or posterior approach. The outcomes of these patients depend on the cause. Even though surgery is effective, it also has serious complications that can be life-threatening. The prognosis is good for patients who obtain symptom relief with non-surgical treatment.[6]