Cervical Spondylotic Myelopathy: An Imaging Vignette

Cervical Spondylotic Myelopathy: An Imaging Vignette

Author: Logan University/Tuesday, January 5, 2016/Categories: December 2015

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A 60-YEAR-OLD FEMALE WAS SEEN at an outside hospital for complaints of upper limb weakness and numbness. She had experienced recurrent falls over the previous six months. Neurological examination revealed that motor strength of the upper extremity was 4/5. Deep tendon reflexes were increased in both upper and lower extremities. Hoffman sign was positive, and the sensory exam was normal. She underwent MRI of the cervical spine, which revealed significant degenerative central canal stenosis with accompanying compression and multilevel hyperintensities within the spinal cord. Cervical spondylotic myelopathy (CSM) was diagnosed (see Figures 1 and 2). The patient underwent a multilevel cervical laminectomy with instrumented laminaplasty from C4 to C6 (see Figure 3). [Editor’s Note: This patient was unfortunately lost to follow-up.]


This disorder is one of the most common etiologies of cervical cord compression; its natural history is slow with progressive neurological deterioration. Degenerative changes of the cervical joints and ligaments give rise to CSM. The clinical expression of CSM may range from an asymptomatic state, incidentally detected on MRI, clinical exacerbation from a quiescent state, or quadriparesis arising from a fall secondary to CSM-induced ataxia.

The pathophysiology of CSM is complex and multifactorial. It is primarily caused by static and dynamic mechanical compression, accompanied by both shear and distraction forces directed into the cervical spinal cord. These stenotic and compressive forces arise from intervertebral disc, uncovertebral and apophyseal joint degenerative hypertrophy and spondylophytosis. Redundant posterior longitudinal and flavum ligaments, resulting from disc space reduction, also encroach upon the dura and spinal cord. These degenerative changes engender the term spondylotic myelopathy. However, the CSM pathophysiology is not limited to compression. Secondary pathophysiological mechanisms include biochemical, cellular and histological derangement. Ischemia of the cervical spinal cord is also a significant contributor to the pathophysiology of CSM resulting from degenerative compression of the large anterior spinal cord vessels and smaller branches (anterior spinal artery) affecting cord microcirculation. The primary mechanical and secondary biological insults incur spinal cord pathology inclusive of inflammation, edema, gliosis and myelomalacia.(1)

CSM is more commonly seen after 50 years of age. The clinical findings of CSM include symptoms of reduced digital dexterity, poor coordination and bilateral upper extremity paresthesia with signs, such as increased deep tendon reflexes, positive pathological reflexes (i.e., Hoffman response), a wide-base ataxic gait and spasticity of the lower extremities. Gait disturbances, common in the elderly, increase the probability of falls, elevating the suspicion for CSM. Cervical spinal cord compression may be an incidental finding in 5 to 7 percent of the elderly.(2)

Radiographic Exam

Radiographic examination of the cervical spine may suggest findings that correlate with CSM. Pavlov described a ratio measurement of the cervical canal; with this method, the sagittal diameter of the spinal canal is divided by the sagittal diameter of the corresponding vertebral body. Using lateral cervical radiography, measures were obtained from C3-C6 with a ratio of <.80 indicating cervical spine stenosis. This method is reliable for determining cervical spinal stenosis and eliminates the confound arising from magnification distortion.(3)

The radiographic findings of degenerative anterolisthesis or retrolisthesis are prevalent in patients with CSM. In 79 patients who underwent surgical treatment for CSM, radiographic examination revealed 30 percent had vertebral displacement of 3.5 mm of anterolisthesis or retrolisthesis at C3/C4 or C4/C5. Ninety-three percent of the degenerative spondylolisthesis at C3/4 or C4/5 had significantly greater intersegmental cervical mobility than those with less spondylolisthesis. Severe cervical spinal cord compression seen on T1-weighted and high-intensity spinal cord signals seen on T2-weighted MRI scans corresponded with the levels of degenerative spondylolisthesis.(4)

Recent radiographic studies have identified altered alignment of the cervical sagittal vertical axis (SVA) in elderly males and have drawn attention to aging posture and CSM. A plumb line drawn from a center point of the C2 vertebral body and a point on the anterosuperior corner of C7 on a weight-bearing cervical radiograph defines the SVA. Increased measures (anterior weight-bearing) of the C2-C7 sagittal vertical axis (SVA) have been correlated with the extent of CSM. Increased values of C2-C7 SVA are thought to elevate intramedullary pressure and contribute to the development of CSM in elderly males.(5)


MRI provides high-resolution imaging of the spinal cord in CSM by displaying the histopathological changes provoked by CSM, such as myelomalacia, edema, gliosis and ischemic white matter. Standard MRI pulse sequences include T1 and T2. Some authors consider these findings evidence for irreversible spinal cord injury, while others maintain that these changes represent some recuperative potential. Several grading systems have been proposed to classify the MRI spinal cord signal change, but the specific grading remains a topic of considerable debate.

Patients with no intramedullary MRI signal change and those with signal changes only on T2-weighted images had better outcomes than those with both T1- and T2-weighted signal changes. Those patients with regression of intramedullary signal changes had significantly better outcomes.(6) In 2009, “Guidelines for the Surgical Management of Cervical Degenerative Disease” were published. They established the relationship between spinal cord MRI signal changes and clinical outcomes in CSM. Multilevel T2-weighted hyperintensity, T1-weighted focal hypointensity when combined with T2-weighted focal hyperintensity and spinal cord atrophy, predicted a poor prognosis following surgery. Uchida et al. confirmed this finding, reporting that a low T1-weighted and high T2-weighted low signal in the spinal cord was a harbinger of poor neurological recovery. Regression of high signal changes on T2-weighted images postoperatively, however, was correlated with improved functional outcome.(7) New and evolving imaging technologies may contribute to improved assessment of the spinal cord in CSM. Functional magnetic resonance imaging (fMRI) has shown evidence for increased blood oxygen level dependent (BOLD) activity in the contralateral motor cortex that correlated with improved motor function after decompression for spondylotic myelopathy.(8)


The treatment of mild and moderate CSM remains uncertain. Surgical decompression of the spondylotic compression of the spinal cord seems almost intuitive, but this approach lacks consensus. Studies are inadequate in quality as their design lacks controls, randomization, standardized criteria for clinical evaluation and short periods of follow-up. Furthermore, criteria for the indication and timing of the operation have not been established. Spinal surgery is an expensive procedure with both operative and postoperative risks. In addition, the differential diagnosis of myelopathy is challenging. A large number of conditions, including multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), megaloblastic anemia, vascular malformation, cervical cord tumor, syringomyelia, or their combination, may mimic the MRI diagnosis of CSM. On the other end of the spectrum is the asymptomatic CSM patient, as 41 percent of the spinal cord compressions found by MRI were asymptomatic.(9)

Neurological deterioration of CSM patients is a clear-cut surgical indication. However, mild and slowly or non-progressive CSM may be managed nonsurgically. Fifty-six percent of patients with mild CSM and increased signal intensity in the spinal cord on T2-weighted MRI did not deteriorate or undergo surgery at the ten-year follow-up. The adverse prognostic factors identified included a significant increased range of segmental motion, segmental kyphosis and instability arising at the narrowest point of the cervical spinal canal.(10)

Kong et al. reported a satisfactory outcome for conservative treatment in mild CSM patients. Twenty-six percent experienced a deterioration of myelopathy during a three-year or greater follow-up, demonstrating that in the majority of the mild CSM patients, neurological function either improved or deterioration was non-progressive. It remains to be determined whether patients with CSM and adverse prognostic factors should be surgically treated as soon as possible to avoid potential deterioration, even if their symptoms and signs are moderate. Thus, although they have a tendency to undergo deterioration, mild CSM patients presenting with segmental instability or cervical spinal stenosis may initially be treated conservatively with a close follow-up. When neurological deterioration of myelopathy is clearly identified, surgery should be performed in a timely manner, since CSM may progress rapidly and a long period of moderate or severe CSM may result in poor prognosis.(11) In order to broaden the interventions for mild/moderate CSM, research employing CAM approaches, such as manual therapy and acupuncture, is warranted.

In addition to conservative and surgical care, there is increasing interest in the influence of dietary factors on specific molecular systems, such as neurotransmitters and pathogenic mechanisms within the CNS.(12) Studies have shown some benefit of dietary supplementation on cerebral function, such as memory and learning, and the enhancement of neural repair. Disorders have included Alzheimer’s disease, epilepsy and traumatic brain injury. Little information has been published, however, regarding the use of dietary supplementation to enhance neuroprotection and neural repair in disorders of the spinal cord such as myelopathy.

Holly et al. developed an animal model of CSM by placing a non-resorbable polymer in the thoracic epidural space inducing a delayed myelopathy. Animals were fed a diet rich in docosahexaenoic acid (DHA) and curcumin (Cur) or the standard Western diet.

After six weeks, gait analysis revealed significantly worsened function in the Western diet group compared with the DHA-Cur group. Biochemical data also collected in this study demonstrated that DHA-Cur promoted spinal cord neuroprotection and neutralized the clinical and biochemical effects of myelopathy, possibly by inducing repair mechanisms in the neuron’s plasma membrane.(13)


1 Liu S, Lafage R, Smith JS, Protopsaltis TS, Lafage VC, Challier V, Shaffrey CI, Radcliff K, Arnold PM, Chapman JR, Schwab FJ, Massicotte EM, Yoon ST, Fehlings MG, Ames CP. Impact of dynamic alignment, motion, and center of rotation on myelopathy grade and regional disability in cervical spondylotic myelopathy. J Neurosurg Spine. 2015 Aug 28:1-11.

2 Nishimura H, Endo K, Suzuki H, Tanaka H, Shishido T, Yamamoto K. Gait analysis in cervical spondylotic myelopathy. Asian Spine J. 2015 Jun; 9(3):321-6.

3 Pavlov H, Torg JS, Robie B, Jahre C. Cervical spinal stenosis: determination with vertebral body ratio method. Radiology. 1987; 164:771–775.

4 Kawasaki M, Tani T, Ushida T, Ishida K. Anterolisthesis and retrolisthesis of the cervical spine in cervical spondylotic myelopathy in the elderly. J Orthop Sci. 2007; 12:207–213.

5 Oe S, Togawa D, Nakai K, Yamada T, Arima H, Banno T, Yasuda T, Kobayasi S, Yamato Y, Hasegawa T, Yoshida G, Matsuyama Y. The influence of age and gender on cervical spinal alignment among volunteers aged over 50. Spine (Phila Pa 1976). 2015 Jul 22. [Epub ahead of print].

6 Suri A, Chabbra RP, Mehta VS, Gaikwad S, Pandey RM. Effect of intramedullary signal changes on the surgical outcome of patients with cervical spondylotic myelopathy. Spine J. 2003 Jan-Feb;3(1):33-45.

7 Zhang C, Das SK, Yang DJ, , Yang, HF. Application of magnetic resonance imaging in cervical spondylotic myelopathy. World J Radiolo. 2014 Oct 28; 6(10):826-32.

8 Tam S, Barry RL, Bartha R, Duggal N. Changes in functional magnetic resonance imaging cortical activation after decompression of cervical spondylosis: case report. Neurosurgery. 2010 Sep; 67(3).

9 Kada ka Z, Bednarík J, Novotn O, Urb.nek I, Dušek L. Cervical spondylotic myelopathy: conservative versus surgical treatment after 10 years. Eur Spine J. 2011; 20:1533–1538.

10 Oshima Y, Seichi A, Takeshita K, et al. Natural course and prognostic factors in patients with mild cervical spondylotic myelopathy with increased signal intensity on T2-weighted magnetic resonance imaging. Spine (Phila Pa 1976) 2012; 37:1909–1913.

11 Kong LD, Meng LC, Wang LF, Shen Y, Wang P, Shang ZK. Evaluation of conservative treatment and timing of surgical intervention for mild forms of cervical spondylotic myelopathy. Exp Ther Med. 2013 Sep; 6(3):852-856. Epub 2013 Jul 16.

12 Mi W, van Wijk N, Cansev M, Sijben JW, Kamphuis PJ. Nutritional approaches in the risk reduction and management of Alzheimer’s disease. Nutrition. 2013 Sep; 29(9):1080-9. 

13 Holly LT, Blaskiewicz D, Wu A, Feng C, Ying Z, Gomez-Pinilla F. Dietary therapy to promote neuroprotection in chronic spinal cord injury. J Neurosurg Spine. 2012 Aug; 17(2): 134–140. 

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