Cervical Spondylotic Myelopathy

Authors:
Eliel Arrey, MD, and Laura Rosas, BBA, MS-III
McGovern Medical School, Houston, Texas

Lynnette Mazur, MD, MPH
University of Texas Health Science Center at Houston

Citation:
Arrey E, Rosas L, Mazur L. Cervical spondylotic myelopathy. Consultant. 2017;57(9):566-567.

A routine checkup for a 62-year-old woman revealed some unexpected reflexes. Her relevant past history included a ruptured right anterior cruciate ligament with a bucket-handle tear of the medial meniscus at age 20. Due to increasing episodes of a “locked” knee, she had undergone right meniscectomy at age 30. At age 57, she had reinjured the knee and had developed a limp.

Physical examination. At presentation, the patient denied pain, stiffness, numbness, and weakness in her neck, arms, and legs. There were no bladder or bowel changes. Physical examination revealed hyperreflexia of all right-sided deep-tendon reflexes and sustained clonus of the right ankle. She had mute Babinski signs, negative Romberg and Lhermitte signs (an electrical shock-like sensation with neck flexion), and normal vibratory and position senses. Positive bilateral Hoffmann signs (flexion of the thumb after flicking the nail of the middle finger) and an abnormal gait (scraping the tip of the shoe when walking) suggested spinal cord compression.

Diagnostic tests. Magnetic resonance imaging of the cervical spine (Figure 1) showed multilevel intervertebral disk degeneration with stenosis of the spinal canal; the smallest measurement between the anterior and posterior ligaments was 6.4 mm.

Based on the imaging results and her clinical presentation, the patient received a diagnosis of cervical spondylotic myelopathy (CSM) and was referred for neurosurgery consultation.

Discussion. Desiccation of the intervertebral disks with age starts a cascade of events that compromise the spinal canal, nerve roots, and arteries. As the disks begin to collapse and lose height, the ligaments enfold into the canal, causing further narrowing and compression. To strengthen the disk, osteoblasts start a reparative process and form new bone. These bony spurs also narrow the canal and compress the spinal cord. The cervical spine is particularly vulnerable to CSM due to its mobility and its location above the less-mobile thoracic spine. A congenitally small spinal canal also plays a role.

Patients with CSM can experience a wide variety of symptoms that usually progress over time. Tingling or numbness in the arms, fingers, or hands; weakness in the muscles of the arms, shoulders, or hands; difficulty in grasping or holding onto items or dropping them; imbalance or frequent falling; loss of fine motor skills; trouble with handwriting, buttoning clothes, picking up small objects, and feeding oneself; and pain or stiffness in the neck are all possible as a result of the interruption of nerve impulses from the neck to other areas of the body.

A study reviewing varying cervical spinal canal diameters on plain radiographs of patients with CSM showed that diameters of less than 10 mm were associated with myelopathy, diameters of 10 to 13 mm were associated with premyelopathic changes, and diameters of 13 to 17 mm were associated less with myelopathy but more with symptomatic spondylosis; patients with diameters greater than 17 mm (the average diameter) were not prone to spondylosis.¹ A more recent study showed that patients with a congenitally narrow canal were at an increased risk of developing stenosis.²

Because compression may be silent and the development of symptoms unpredictable, evaluation of therapy is difficult.^3-6 One study showed no difference in outcomes between conservative and surgical treatments.⁷ However, when symptoms occur or worsen, or when patients desire to halt the progression, surgical decompression may be indicated.

Surgical treatment and the choice of optimal approach remain controversial. The anterior approach is muscle-sparing and is associated with faster recovery, but a posterior laminectomy with fusion or a laminoplasty are preferred in patients with 3 or more levels of CSM.⁸ In general, a laminectomy with fusion improves neck pain, prevents postlaminectomy instability and kyphosis, and preserves sagittal alignment better than laminoplasty. However, laminoplasty is motion-preserving and results in better range of neck motion.^9,10 While one study found similar outcomes between the procedures,¹¹ another showed that only laminoplasty consistently halted myelopathic progression, had higher patient satisfaction, and had lower complication rates.¹² Other factors to be considered when choosing a surgical approach include the patient’s age, the geometry of the spinal canal (canal size and intrinsic curvature of the cervical spine), and the intrinsic stability of the spine.¹²

Outcome of the case. Because of the risk of ongoing degeneration and the possibility of quadriplegia with an extension-flexion injury of the neck, the patient elected to have a posterior laminoplasty (Figure 2). Postoperatively, she developed numbness and weakness in her right upper extremity, which may take up to 18 months to stabilize.

This patient’s case illustrates that orthopedic injuries may mask the detection of CSM, and that a thorough neurologic examination is important for all patients. 

References:

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