Traumatic Cervical Myelopathy

h1 class=”calibre8″>19 Traumatic Cervical Myelopathy

Robert F. Heary and Raghav Gupta

Abstract

Traumatic cervical spinal cord injury (SCI) occurs in patients presenting with blunt trauma due to motor vehicle accidents (MVAs), sports-related injuries, falls, and injuries related to interpersonal violence. Cervical SCI can present with symptoms of myelopathy secondary to compression of the cervical spinal cord. A decrease in the sagittal diameter of the spinal canal has been found to correlate with an increased incidence of cervical myelopathy following trauma. Multiple conditions, such as spondylosis, ossification of the posterior longitudinal ligament (OPLL), and congenital spinal stenosis, can increase the risk for presentation with myelopathic symptoms after cervical trauma. These conditions are characterized in this chapter with respect to the mechanisms of injury, clinical presentations, and resulting patient outcomes that have been reported in the context of cervical trauma.

Keywords: cervical trauma, myelopathy, spondylosis, OPLL, SCI, spinal stenosis

19.1 Traumatic Cervical Spinal Cord Injury

The epidemiology of traumatic spinal cord injury (SCI) has been well characterized in the neurosurgical literature. It has an estimated annual incidence of 25 to 59 new cases per million individuals in the United States and occurs 3 to 4 times more commonly in men than in women. ¹ The underlying etiology for traumatic SCI varies and can include motor vehicle accidents (MVAs), acts of violence, sports-related injuries, falls, and other miscellaneous causes. MVAs are the leading cause of SCIs in the United States. Falls, meanwhile, account for most cases of SCI in elderly individuals (defined as adults over the age of 60 years). ² Traumatic cervical SCI is fairly common with 2.4% of patients who present with blunt trauma suffering from cervical spine injuries. ³

Acute traumatic cervical SCI can result in a clinical syndrome termed myelopathy resulting from compression of the spinal cord. While symptoms of cervical myelopathy can vary depending on the location and severity of cord compression, patients commonly present with disturbances in balance and/or gait, decreased hand dexterity, numbness in the hands and/or feet, bowel and bladder incontinence, and signs of upper and/or lower motor neuron dysfunction. Signs of myelopathy are detected on physical examination and include the presence of pathological reflexes including a positive Babinski sign, Hoffman sign, as well as ankle clonus and lower extremity hyperreflexia. ⁴ Increased lower extremity muscle tone, or spasticity, is another sign of myelopathy. While the most common etiology for cervical myelopathy is spondylosis, other etiologies can include, but are not limited to spinal neoplasms, ossification of the posterior longitudinal ligaments (OPLL), and congenitally narrowed spinal canals (▶ Fig. 19.1). A decrease in the sagittal diameter of the spinal canal has been found to correlate with an increased incidence of cervical myelopathy. ⁵ Given that each of the aforementioned etiologies of cervical myelopathy can result in a decrease in the sagittal diameter of the spinal canal, when superimposed upon trauma, these conditions can predispose one to presentation with myelopathy resulting from spinal cord compression.

Fig. 19.1 A 61-year-old woman with no known history of cervical spine disease was involved in a fall. She presented to the emergency department with symptoms consistent with a central cord syndrome including profound hand weakness and diminished sensation in the hands, trunk, and lower extremities. (a) Magnetic resonance imaging (MRI; T2-weighted sagittal) study obtained at the time of admission. Congenitally narrowed spinal canal with abnormal signal extending from C3 to C6 within the cord parenchyma. Also, abnormal signal is evident in the C4–C5 intervertebral disc with questionable fracture of the superior aspect of the C5 vertebra. (b) MRI (T2-weighted axial) images at the C4–C5 level demonstrate markedly narrowed spinal canal with increased signal within the cord parenchyma. (c, d) Plain film images (anteroposterior and lateral) obtained 6 months following the injury demonstrate solid fusions from C3 to C7 with anterior/posterior stabilization having been performed. The rationale for this single-setting, anteroposterior surgery was to increase the space available for the swollen spinal cord and improve the odds of neurological recovery. At 6 months out from surgery, she had improved hand function although weakness of the opponens and intrinsic muscles persisted to a moderate degree. Lower extremity power was within normal limits and some gait spasticity persisted. Sensory examination had gradually improved but was not yet normal in the hands or lower extremities.

19.2 Sagittal Diameter of the Spinal Canal and Torg–Pavlov Ratios

In the past, the anteroposterior diameter (or sagittal diameter) of the spinal canal on lateral radiographs has been used to diagnose critical cervical canal stenosis. A diameter < 13 mm had been proposed as the threshold under which pathological changes in the intervertebral discs have been observed. ⁶ However, given discrepancies in the canal diameter between patients of different ethnic backgrounds ⁷ and radiographic magnification variability, ⁴ the Torg–Pavlov ratio was developed for making the diagnosis of critical spinal canal stenosis. Here, the sagittal diameter of the spinal canal is divided by the sagittal diameter of the vertebral body at the same level. ⁸ In the original study where this ratio was proposed, a value of < 0.82 diagnosed cervical canal stenosis in 92% of cases. ⁸ When Torg–Pavlov ratios in patients with and without cervical spondylotic myelopathy were compared, the mean Torg–Pavlov ratio was found to be significantly smaller in patients with spondylotic myelopathy (0.72 vs. 0.95; p < 0.001). ⁹ In patients presenting with minor trauma to the cervical spine, a Torg–Pavlov ratio < 0.70 has been found to have the greatest positive likelihood ratio for predicting SCI. ¹⁰

19.3 Trauma in Patients with Cervical Spondylosis

Cervical spondylosis (or osteoarthritis) refers to a pair of entities including degenerative disc disease (DDD) and facet joint degeneration, which are both commonly observed in elderly patients. DDD results from compromised diffusion of oxygen and nutrients through the intervertebral discs over time leading to a radial redistribution of compressive forces within the vertebral column. This can present radiographically as a herniated disc, decreased intervertebral disc height, hypertrophy of the ligamentum flavum (▶ Fig. 19.2), and/or osteophyte formation. Osteophyte formation along the ventral aspect of the spinal canal is a physiological response to the increased stress on the vertebral endplates and stabilizes the neighboring vertebrae by increasing the surface area of the vertebral endplates. Myelopathy and radiculopathy can result from compression of the cervical spinal cord and cervical nerve roots, respectively, by these bony spurs. Clinical symptoms of cervical spondylosis can include neck pain, arm pain, upper extremity weakness, and/or neurological symptoms resulting from spinal cord or nerve root compression. The prevalence of radiographically determined cervical DDD in men and women above the age of 40 years has been estimated to be 21.7%. ¹¹^,¹² Meanwhile, the incidence of myelopathy resulting from cervical spondylosis has been estimated to be 4 per 100,000 person-years. Elderly male patients, however, are disproportionately affected more frequently in relation to other patient demographics.

Fig. 19.2 A 63-year-old male with no known history of pathology in the cervical spine was involved in a motor vehicle accident as the driver and he developed signs and symptoms of myelopathy. Upon presentation to the emergency department, his neurological examination was consistent with an ASIA D spinal cord injury. (a, b) Magnetic resonance imaging (MRI; T2-weighted sagittal) study (two images) demonstrates a minimal degree of subluxation at the C4–C5 level with a herniated disc compressing the spinal cord. Evidence of ligamentum flavum hypertrophy causing canal narrowing was present at the C4–C6 levels. (c) MRI (T2-weighted axial) demonstrates marked canal narrowing at the C4–C5 level with bright signal in the cord proper. (d, e) Plain film imaging (anteroposterior and lateral) obtained 6 months following posterior decompression and fusion surgery with lateral mass fixation at C4–C6 and bilateral pedicle screw fixation at the C7 level confirms successful fusion and satisfactory alignment. The rationale for this surgery was to decompress the neural elements and provide stabilization to prevent further cord impairment. At 6 months out from surgery, the patient made a complete recovery with no deficits evident on a detailed neurological examination.

Trauma in a patient with underlying cervical spondylosis can present paradoxically with a neurological deficit but little or no radiographic abnormalities. ¹³ In this subpopulation of patients, the traumatic event preceding the presentation with myelopathy is often minor. This underscores the disparity between the clinical presentation and the associated imaging findings. The mechanism by which SCI occurs is believed to be through bulging of the ligamentum flavum anteriorly into the spinal canal upon cervical spine extension. Posteriorly directed bone spurs and herniated discs, therefore, can compress the cord anteriorly while the ligamentum flavum enfolding does so posteriorly. In addition, hypertrophy of the laterally located uncovertebral facet joints can also contribute to narrowing of the overall spinal canal space. However, ligamentous and disc injury can occur if there is a rotational component to the extension. This can lead to intervertebral disc rupture and compression of the cord from the posteroinferior segment of the vertebral body above the ruptured disc (which has been displaced posteriorly), as well as the lamina of the vertebra at the level of the ruptured disc. ¹³^,¹⁴ Patients may be essentially asymptomatic, with previously unidentified spondylosis, and they may present with cervical myelopathy following a relatively minor traumatic episode. This leads to issues regarding insurance payments for spinal care as the patients clearly have abnormalities prior to the traumatic event but they are not symptomatic, and usually not even aware of any cervical pathology being present. In this scenario, the coverage by insurers for spine care is usually the responsibility of the motor vehicle insurance coverage.

In a series reported by Koyanagi et al on 42 patients who presented with acute traumatic cervical SCI over a 9-year period, and who had no evidence of fracture or dislocation, 38 patients (90.5%) were found to have degenerative changes of the cervical spine. ¹⁵

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