Indian Spine Journal

: 2019  |  Volume : 2  |  Issue : 1  |  Page : 20--32

Imaging in cervical myelopathy

Rajavelu Rajesh, Shanmuganathan Rajasekaran, Sri Vijayanand 
 Ganga Medical Centre and Hospitals Pvt. Ltd., Coimbatore, Tamil Nadu, India

Correspondence Address:
Prof. Shanmuganathan Rajasekaran
Ganga Medical Centre and Hospitals Pvt. Ltd., Coimbatore, Tamil Nadu


This is a narrative review. The objective of this study is to provide an overview on the imaging modalities and their utilization in cervical myelopathy (CM). Using PubMed, studies published on the “imaging modalities in CM,” “cervical spondylotic myelopathy (CSM) imaging,” “computed tomography (CT) and magnetic resonance imaging (MRI) in CM,” “imaging in ossified posterior longitudinal ligament (OPLL),” “dural ossification in OPLL,” “diffusion tensor imaging (DTI) in CSM,” and “dynamic MRI, functional MRI, and magnetic resonance spectroscopy (MRS) in CSM” were evaluated. The review addresses the evaluation of CM with various imaging modalities ranging from radiographs, CT, and MRI to advanced imaging techniques such as DTI and MRS. Each investigation contributes specific detail to the disease process in a different dimension. Specific parameters for CSM and OPLL, and their influence on outcome are discussed. Imaging in CM plays an important role in analyzing the cause of myelopathy, defining the level of the lesion, parameters to assess the time of intervention and to predict the outcome.

How to cite this article:
Rajesh R, Rajasekaran S, Vijayanand S. Imaging in cervical myelopathy.Indian Spine J 2019;2:20-32

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Rajesh R, Rajasekaran S, Vijayanand S. Imaging in cervical myelopathy. Indian Spine J [serial online] 2019 [cited 2020 Jun 1 ];2:20-32
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Degenerative cervical myelopathy (DCM) is defined as symptomatic cervical myelopathy (CM) associated with a broad variety of degenerative changes of the extradural spinal tissues in the cervical spine. The spectrum includes cervical spondylotic myelopathy (CSM), ossified posterior longitudinal ligament (OPLL), and ossification of the ligamentum flavum.[1] Radiological assessment in CM helps in establishing the diagnosis and preoperative planning by localizing the site, assessing the contributing factors and severity of the disease.[2],[3],[4] Various modalities of imaging with their unique benefit are available ranging from roentgenogram to the more advanced diffusion tensor imaging (DTI). Magnetic resonance imaging (MRI) provides accurate and greatest range of information including the disc, ligaments, and neural elements, as compared to all the other available imaging.

 Plain Radiographs in Cervical Myelopathy

Even in the presence of advanced diagnostic imaging, plain radiographs are valuable initial radiological evaluation tool of the cervical spine in CSM. Anteroposterior (AP), lateral, and oblique radiographs show changes in the facet and uncovertebral joints, vertebral body morphology, osteophytes, abnormal ossifications (diffuse idiopathic skeletal hyperostosis), cervical alignment, and disc space. Normal vertebral bodies are symmetric and rectangular. A loss of disc space height with nonbridging and nonmarginal osteophytes or syndesmophytes is a classic finding in patients with degenerative spinal disease.[5] A lateral radiograph must include from the base of the skull to cervicothoracic junction, and an AP view should include C3 to T1. Weight-bearing plain lateral films in CM are used to assess (a) sagittal canal diameter, (b) alignment, and (c) evaluation of OPLL.

Assessment of sagittal canal diameter

Congenitally narrow spinal canal is proposed as a risk factor for myelopathy in cervical spondylosis[6] and is assessed in radiographs using Torg–Pavlov ratio (TPR). TPR [Figure 1] is calculated from the lateral cervical radiographs by the ratio between the distance between the midpoint of posterior surface of the vertebral body to the closest point on the spinolaminar line and the vertebral body diameter of the same level.[7] According to Pavlov et al.,[8] cervical stenosis is present if the ratio is ≤0.82.{Figure 1}

Studies have shown that TPR is lower in patients with CM than in normal people.[9],[10],[11] In contrast, some studies[12],[13] reported that the TPR was not necessarily associated with spinal stenosis in view of vertebral body size variability. However, the AP diameter assessment in radiographs has been largely replaced by computed tomography (CT) and MRI.[14]

Assessment of cervical alignment parameters

CSM has been associated with and potentially exacerbated by cervical sagittal mal-alignment. In CSM, loss of lordosis leads to forced draping of the spinal cord against the vertebral bodies and disc-osteophyte complexes and may predispose to myelopathy. With increase in kyphosis, tethering of the spinal cord may increase intramedullary pressure and result in neuronal loss and demyelination. Simultaneously, the smaller arterial feeders to the cord will be compressed and flattened, resulting in further cord injury.[4],[15] Surgical decompression alone may not reduce the cord tension due to kyphosis, if sagittal alignment is not taken into consideration. Poor spinal cord posterior migration and expansion, leading to poor neurological improvement after laminoplasty, have been reported in patients with kyphotic alignment.[16] Cervical curvature has been classified into lordosis and nonlordosis; the latter includes straight, sigmoid, reversed sigmoid, and kyphosis curvature[17] based on the relationship with the line drawn between the posteroinferior corner of the C2 body and posterosuperior corner of the C7 body (or the C6 body, if the C7 body was invisible behind the shadow of the shoulders) [Figure 2].{Figure 2}

Cervical alignment parameters are assessed in lateral cervical radiographs, and it includes (1) cervical lordosis, (2) sagittal plane translation, and (3) dynamic cervical parameters.

Cervical lordosis

The normal curvature of the cervical spine is lordosis, and this is the result of cervical vertebra shape and to compensate for the thoracic kyphosis. In normal volunteers, the mean total lordosis is approximately 40°. The largest percentage of cervical standing lordosis (75%–80%) is localized to C1–C2, and relatively, little lordosis exists in the lower cervical levels; only 15% of lordosis occurs at the lowest 3 cervical levels (C4–C7).[18]

There are three methods to assess cervical lordosis including Cobb angles [Figure 3]a, Jackson physiological stress lines [Figure 3]b, and the Harrison posterior tangent method [Figure 3]c.[19] The most commonly used method is Cobb angle, typically measured from C1 to C7 or C2 to C7. This is described in [Table 1].{Figure 3}{Table 1}

Lee et al.[20] analyzed the influence of cervicothoracic junction anatomy on cervical spine sagittal alignment in cervical sagittal radiographs. The authors introduced the concepts of neck tilt (NT), thoracic inlet angle (TIA), and T1 slope (T1S). NT was defined as an angle between 2 lines both originating from the upper end of the sternum with one being a vertical line and the other connecting to the center of the T1 endplate [Figure 4]a. The TIA has been defined as the angle between a line originating from the center of the T1 endplate and perpendicular to the T1 endplate and a line from the center of the T1 endplate and the upper end of the sternum. T1S is the angle between horizontal plane and T1 endplate. The authors found that large TIA increases T1 slope and finally increases cervical lordosis to obtain a horizontal gaze and vice versa [Figure 4]b. The normal calculated values in the study were as follows: TIA – 69.5 ± 8.6°, T1S – 25.7 ± 6.4°, and neck tilt – 43.7 ± 6.1°.{Figure 4}

C2 sagittal vertical axis

Sagittal plane translation is assessed using C2 sagittal vertical axis (CSVA) [Figure 5]. It is measured as the horizontal distance between a plumb line dropped from the center of the C2 vertebral body and the posterior-superior corner of C7. The CSVA ranges from 15 to 17 ± 11.2 mm. Tang et al.[21] reported that positive CSVA of >40 mm is correlated with poor health-related quality of life and neck disability index scores following multilevel cervical fusion.{Figure 5}

Dynamic cervical spine parameters

Lateral fl exion-extension views are used to assess the dynamic parameters such as (i) assessment of cervical instability, (ii) center of rotation, and (iii) cone of kinesis. Cervical instability is when translation of >3.5 mm and sagittal plane angulation of >11° are present [Figure 6].[22]{Figure 6}

Role of plain radiographs in ossified posterior longitudinal ligament

In OPLL, radiographs help in assessing the alignment and measurement of K-line and thus planning surgical procedures. Fujiyoshi et al.[23] described the K-line [Figure 7], which connects the midpoints of the spinal canal at C2 and C7 on neutral lateral radiographs, as a guide for making decisions regarding the surgical approach for cervical OPLL patients. Based on the position with that of OPLL, it may be K-line (+) or K-line (−). K-line (+) group has OPLL that does not exceed this line while K-line (−) group does. In K-line (−) after posterior decompression, lack of sufficient posterior shift of cord and neurological improvement was noted due to anterior compression. Hence, if OPLL mass falls behind the K-line, then anterior approach is preferred.[24]{Figure 7}

Lee et al.[25] described kappa line [Figure 8] to assess the postoperative neurological recovery and residual cord compression in ≤4-level laminoplasty. Kappa line is a straight line connecting the midpoints of the spinal canal at 1 level above and 1 level below the decompressed segments on the plain lateral radiograph in neutral position. Kappa (+) meant that the OPLL mass did not pass the kappa line, while kappa (−) meant that OPLL had grown posteriorly beyond the kappa line. The authors reported that the kappa line predicted neurologic recovery and remaining cord compression following ≤4-level laminoplasty more correctly than the K-line.{Figure 8}

K-line was originally measured in cervical lateral standing radiographs taken in neutral position. However, measurement of the K-line in CT images with sagittal reconstruction is being used, stating that it can clearly reveal the precise size and morphology of the ossification.[26] Ijima et al.[27] compared the K-line measured in standing lateral radiographs versus CT in lying position. About 11% showed a change from K-line (+) to (−) when CT was used to assess K-line, and the authors stated that CT-based measurement is an over-indication for anterior or posterior decompression and fusion instead of laminoplasty which is optimal for K-line (+) patients and hence concluded that K-line should be measured with plain radiographs of standing patients.

 Computed Tomography in Cervical Myelopathy

(a) Cervical spondylotic myelopathy

CT provides excellent information about the dimensions of the spinal canal and helps in differentiating the various causes for narrowing of the canal such as posterior osteophytes or hypertrophied facet joints and ossified ligaments. It plays a vital role in assessing the vertebral artery variations and cervical pedicle morphology and its diameter and thus helps to choose the surgical fixation modality. Anterior cervical compression secondary to disc osteophyte complexes and their extent, whether confined to the disc interspace or extension behind the vertebral body as depicted by CT, is important to choose the surgical procedure to address the pathology by either discectomy and fusion or corpectomy and reconstruction, respectively.[28]

(b) Ossified posterior longitudinal ligament (OPLL)

CT is essential in identifying the OPLL in lower cervical levels, less densely calcified OPLL mass, associated dural ossification (DO), and other ligamentous ossifications such as ossified ligamentum flavum and to differentiate between osteophytes and segmental OPLL.[29],[30],[31] Sagittal image in CT helps in measurement of K-line and occupancy ratio, and to classify the type of OPLL. The axial sequences help to assess the thickness, shape, and extension and to localize the OPLL (central or paracentral).

Based on longitudinal extent, OPLL is classified into four types [Figure 9]:{Figure 9}

Continuous OPLL [Figure 9]a: a long lesion extending over several vertebral bodies; Segmental OPLL [Figure 9]b: one or several separate lesions behind the vertebral bodies; Mixed OPLL [Figure 9]c: a combination of the continuous and segmental types; and Circumscribed OPLL [Figure 9]d: mainly located posterior to a disc space.

Continuous or mixed types constrict the spinal cord more severely.[32] In order of frequency, OPLL is found at levels C4, C5, and C6.[32],[33]

Space available for cord

The space available for cord (SAC) is measured by subtracting the anterior to posterior distance of the OPLL from the spinal canal. The risk of CM is high in patients with a SAC of <6 mm, and the risk is low in patients with a SAC of >14 mm.[34] A reduction of spinal canal AP diameter from 40% to 60%[35],[36] has been claimed as a high-risk factor for the development of myelopathy.

Based on ossified foci in transverse plane, three types have been described [Figure 10]: (1) square, lines tangential to the bilateral margin of the ossified mass are parallel; (2) mushroom shaped, the two lines cross ventrally; and (3) hill shaped, the lines cross dorsally.[37]{Figure 10}

Dural ossification (DO) in ossified posterior longitudinal ligament

DO increases the chance of dural tear and CSF leak in anterior surgeries, and the DO can be detected using a bone window on CT scans. Based on the appearance of DO in OPLL, three signs have been described: (1) single-layer sign, (2) double-layer sign[38] [Figure 11], and (3) unilateral or bilateral C signs.[39]{Figure 11}

The single-layer sign: An irregular but continuous ventral OPLL massDouble-layer sign: Ventral hyperdense mass and dorsal hyperdense intradural mass along with an intervening hypodense areaUnilateral or bilateral “C signs” [Figure 12]: OPLL presenting laterally in the spinal canal with an angular C-shaped configuration; this sign indicated that the lateral dura had become imbricated in the OPLL mass.{Figure 12}

Chances of dural tear in DO with OPLL is in the following order of frequency double-layer, single-layer, and C signs[39] and if width >40% or thickness >50% [Figure 13].{Figure 13}

Occupancy ratio

Occupancy ratio [Figure 14] was defined as distance between largest width of OPLL and posterior spinal canal divided by spinal canal diameter and multiplying by 100. A ratio of 30%–60% is predictive of the development of myelopathy, and in those with an occupancy ratio >60%, all of them develop myelopathy,[40] and an anterior approach gives better neurological recovery as compared to posterior decompression.[24],[41]{Figure 14}

One other extended use of CT in the cervical spine is T1S and helps in the measurement of cervical sagittal alignment. T1S changes with various positions and age; hence, it cannot be used as an absolute parameter for cervical lordosis; however, TIA can be taken as a fixed reference value.[42]

 Role of Magnetic Resonance Imaging in Cervical Myelopathy

MRI in CM provides better anatomical details of disc, vertebral bone, ligamentous changes, alignment, and spinal cord pathologies. Detailed MRI assessment is usually done in conventional T1-weighted (T1W) and T2-weighted (T2W) sagittal and axial sequences.[43] A minimum of 1.5-Tesla imaging is essential for spine imaging, and screening of the whole spine in single mid-sagittal plane of T2W MRI is a routine to rule out the coexisting tandem lesions, the prevalence of which is about 11%.[43],[44],[45] Whole-spine screening also helps in identifying other pathologies, the incidence of which is reported to be about 15.8%.[46] MRI gives a comprehensive detail about the site, location and degree of compression, tandem stenosis, and cord changes, thereby predicting prognosis and planning appropriate intervention. However, controversies exist around the prediction of neurological recovery through signal intensity (SI) changes.[47],[48],[49],[50],[51],[52],[53],[54] The recent advancements in MRI such as DTI and magnetic resonance spectroscopy (MRS) attempt to address these issues by providing micro-architectural details and function of the spinal cord.[43] In OPLL, MRI is less sensitive and specific in diagnosis, but it is useful to assess the associated cord compression and intramedullary cord lesions, such as cord edema and myelomalacia.

Spinal cord compression and cervical spondylotic myelopathy

The severity of cord compression can be evaluated by various methods such as maximum spinal cord compression, compression ratio (CR)[55] (CR ratio between the AP and transverse diameter), or cross-sectional area[56] at the compression site [Figure 15]. These parameters are useful in assessing severity of compression as well as to assess the cord expansion postsurgically.{Figure 15}

Signal intensity (SI) change in spinal cord and cervical spondylotic myelopathy

In CM, SI change appears as hyperintense on T2 sequences and hypointense on T1 sequences. Hypointensity in T1 sequences indicates ischemic death of nervous tissue, while hyperintensity in T2 is due to edema of the spinal cord[47],[48],[57],[58] [Figure 16]. However, T1 hypointense signal change will not occur without T2 hyperintensity signals, unless there is a hemorrhage. In the early and intermediate stages of myelopathy, cord shows a high SI on T2-weighted image (T2WI), whereas in the late stages, hypointensity on T1-weighted images (T1WIs) and a hyperintensity on T2WIs occur.[59]{Figure 16}

The role of SI changes in recovery was analyzed in detail by many with varied results. Patients with altered SI on both T1WI and T2WI have a relatively poor outcome compared with the patients with signal changes only on T2WI.[49],[57] Most studies show poor prognosis related to the presence of T1 (low) signal change.[49],[50] High SI changes on T2WIs indicated both pathologically reversible and irreversible changes in the spinal cord, while low SI changes on T1WI were considered to reflect pathologically irreversible changes.[50] Better recovery rate was noted if the SI decreased after surgery as compared to those who had increased or persistence of signal change postoperatively.[47],[48],[49],[50],[60] In contrast, some studies[51],[52],[53],[54],[61] reported that the altered SI on T2WIs was not related to the poor outcome. The size (sagittal extent and area) of T2WI signal hyperintensity is significantly associated with surgical outcome, indicating that the larger the signal change, the lower the odds of achieving an Modified Japanese Orthopedic Association (mJOA) ≥16.[62]

In a retrospective study to analyze the SI changes and its role in prognostication of outcome in patients who underwent cervical laminectomy,[63] the authors observed that resolution of signal changes in T2WI was noted in most patients postsurgically and found that there is no significant difference in the recovery rate of patients with different grades of SI change in the T2WI or with focal or multisegmental SI changes when pre- and postoperative MRI images were compared; however, patients with low SI changes in T1WI had poor surgical outcome and concluded that out of all SI changes, low SI in T1WI is the best predictor of surgical outcome.

Role of dynamic magnetic resonance imaging in cervical spondylotic myelopathy

In CSM, the cord compression is due to both static and dynamic factors. Dynamic MRI (dMRI) taken in both flexion and extension separately allows to assess the complex interaction between disc, spinal canal, neural foramina, and segmental instability. dMRI is done typically using 1.5-T MRI with special functional positioning device. The ideal angles for flexion and extension are 40°–45°.[64] Studies have demonstrated more levels of compression in extension position as compared to flexion and neutral position.[64],[65],[66],[67] The hyperintense intramedullary lesions are visualized more often in flexion MRI.[68] CM patients with increased intramedullary signals during flexion had a greater degree of neurological recovery.[69]

Role of diffusion tensor imaging (DTI) in cervical spondylotic myelopathy

MRI is able to delineate the extent of anatomic lesion of the cervical cord, but it is difficult to infer the degree of cervical cord dysfunction from MRI findings. DTI is a recent advancement in MRI that solves this physiological lacuna.[70] DTI assesses the microstructural architecture by measuring the three-dimensional shape and direction of diffusion via the apparent diffusion coefficient (ADC) and fractional anisotropy (FA). It helps in identifying the compression earlier as it shows the abnormalities well before the development of SI changes in MRI.[70],[71]

DTI is based on the principle of anisotropic diffusion of molecules in biological tissues. Anisotropic diffusion refers to the diffusion of molecules in a medium where the molecular movement is restricted to one particular direction because of physical barriers. Most biological tissues such as the muscle fibers and neurons are anisotropic, because the molecular diffusion in them is restricted by physical barriers such as the myelin sheath. In these tissues, the direction of molecular diffusion is preferential along their longitudinal axis, and the DTI characteristics are often quantified by FA and ADC. FA is a diffusion index that indicates the directional preference of the diffusion where 0 represents isotropic diffusion (along all directions) and 1 represents completely anisotropic diffusion (along single longitudinal direction). ADC represents the mean diffusivity that is measured from 3 orthogonal directions within the imaged structure. In neuronal axons, where horizontal diffusion is restricted, diffusion of water molecules primarily occurs along the length (parallel) of the axon, and the FA values are closer to 1 [Figure 17].[70]{Figure 17}

Acute compression of spinal cord tissue may result in a focal decrease in ADC as well as a focal increase in FA. Progressive, chronic compression of the spinal cord results in a significant increase in ADC and decrease in FA.[70],[71],[72],[73],[74] Patients with a higher preoperative FA at the site of compression have better functional recovery, implicating mean FA at the site of compression as a biomarker for determining favorable surgical candidates.[73] DTI parameters and ratios help in the prediction of functional recovery after surgery.[75],[76],[77] However, in contrast, Rajasekaran et al. showed that the preoperative DTI datametrics are not predictive of postoperative recovery;[70] the difference might have been due to the magnitude (1.5 vs. 3 Tesla) of the MRI used.

Tractography gives a visual representation of fiber tracts, which is generated by placing initial seed at C1–C2 level covering the same region of interest that was used for obtaining DTI datametrics. The criteria for cessation of tracking are to be set at FA values >0.2. Four patterns are described as completely intact, waisted, partially interrupted, or completely interrupted [Figure 18]. Fiber indentation at the compression level without interruption was taken as waisted pattern. Fiber interruption across parts of the axial plane was taken as partially interrupted. Fiber interruption across the entire axial plane was taken as complete interruption.[70] Tractography helps in prognostic prediction in CSM,[70],[72],[77] and neurological improvement is more common in those with intact tractography.[72]{Figure 18}

Rajasekaran et al. analyzed DTI datametrics and tractography and observed an increasing trend of preoperative DTI values between control, ambulant, and nonambulant patients with CSM.[70] The authors analyzed that the efficacy of DTI anisotropy indices in predicting the postoperative recovery in CSM patients and postoperative changes in the DTI indices based on neurological recovery after surgery and found that there was a significant improvement in postoperative DTI indices in patients who showed neurological recovery; however, the preoperative DTI evaluation could not predict postoperative recovery for patients with CSM.[78] In tractography, none of the patients had a normal tractography whereas all the controls had normal pattern. However, the distribution of abnormal patterns was variable between the patients without any specific trend, and there was no significant association with myelopathy severity,[70] while in multilevel compressions, tractography helps in identifying the most severely compressed level.[70] On comparing eigenvalues (E1 is the longest vector along the long axis of the axonal cylinder and represents the longitudinal diffusion in the white matter, and E2 and E3 are minor eigenvectors representing the transverse diffusion within the spinal cord), the authors observed that minor eigenvectors had significantly higher values, denoting the increased transverse diffusion and loss of anisotropy, similar to the results shown by Kang et al.[79]

Magnetic resonance spectroscopy in cervical spondylotic myelopathy

MRS helps in understanding the progressive cellular alteration and provides metabolic information such as cellular biochemistry and function of the neural structures.[80] It assays a series of biochemical markers such as N-acetylaspartate (NAA), lactate, choline (Cho), myo-inositol (Myo-I), glutamine-glutamate complex (Glx), and creatinine (Cr), with particular sensitivity to NAA and lactate.[81] NAA is found only in axons and neurons and is considered as a marker for neuronal integrity.[82] Salamon et al.[83] reported that the early MRS changes in patients with cervical stenosis and without spinal cord signal changes had higher Myo-I and Glx compared to that of the control group and suggested Myo-I as a potential early marker for spinal cord inflammation and early-stage demyelination. Increased Cho levels appear later as cervical spondylosis progresses to a symptomatic state, and significantly, higher Cho/Cr ratio is found in patients with spinal cord signal changes than the control. Higher Cho/NAA ratio is significantly associated with poorer neurological function, and Cho/NAA had a significant correlation with the mJOA score, providing a useful radiographic biomarker in the assessment of cervical spondylosis.

Imaging in postoperative period

Cervical spine imaging after surgery plays a vital role in the evaluation of level of surgery, adequacy of decompression, position of implants, restoration of cervical alignment, cervical fusion assessment, diagnosis of pseudoarthrosis, spinal cord signal changes and to correlate with clinical improvement from myelopathy. Cervical fusion can be assessed by either radiographs or CT. Multiple radiological fusion criteria have been described. The four most commonly used are the presence of bridging trabecular bone between the endplates, absence of a radiolucent gap between the graft and endplate, absence of or minimal motion between adjacent vertebral bodies on flexion-extension radiographs, and absence of or minimal motion between the spinous processes on flexion-extension radiographs. However, <1 mm of motion between spinous process on lateral flexion and extension radiographs is considered as the most reliable indicator for fusion.[84] Although assessment through CT is accurate, it overestimates the fusion rate as it is taken in static position, while dynamic analysis is done in radiographs.[85],[86] Exact assessment of fusion requires dynamic information obtained from fl exion-extension x-ray in association with high-resolution static information from CT.


Cervical spine imaging in CM plays an important role in analyzing the cause of myelopathy and defining the level of the lesion and parameters to assess the time of intervention and to predict the outcome preoperatively.

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1Nouri A, Tetreault L, Singh A, Karadimas SK, Fehlings MG. Degenerative cervical myelopathy: Epidemiology, genetics, and pathogenesis. Spine (Phila Pa 1976) 2015;40:E675-93.
2Karpova A, Arun R, Davis AM, Kulkarni AV, Massicotte EM, Mikulis DJ, et al. Predictors of surgical outcome in cervical spondylotic myelopathy. Spine (Phila Pa 1976) 2013;38:392-400.
3Fehlings MG, Wilson JR, Kopjar B, Yoon ST, Arnold PM, Massicotte EM, et al. Efficacy and safety of surgical decompression in patients with cervical spondylotic myelopathy: Results of the AOSpine North America prospective multi-center study. J Bone Joint Surg Am 2013;95:1651-8.
4Scheer JK, Tang JA, Smith JS, Acosta FL Jr., Protopsaltis TS, Blondel B, et al. Cervical spine alignment, sagittal deformity, and clinical implications: A review. J Neurosurg Spine 2013;19:141-59.
5Gore DR, Sepic SB, Gardner GM. Roentgenographic findings of the cervical spine in asymptomatic people. Spine (Phila Pa 1976) 1986;11:521-4.
6Edwards WC, LaRocca H. The developmental segmental sagittal diameter of the cervical spinal canal in patients with cervical spondylosis. Spine (Phila Pa 1976) 1983;8:20-7.
7Yue WM, Tan SB, Tan MH, Koh DC, Tan CT. The torg – Pavlov ratio in cervical spondylotic myelopathy: A comparative study between patients with cervical spondylotic myelopathy and a nonspondylotic, nonmyelopathic population. Spine (Phila Pa 1976) 2001;26:1760-4.
8Pavlov H, Torg JS, Robie B, Jahre C. Cervical spinal stenosis: Determination with vertebral body ratio method. Radiology 1987;164:771-5.
9Herzog RJ, Wiens JJ, Dillingham MF, Sontag MJ. Normal cervical spine morphometry and cervical spinal stenosis in asymptomatic professional football players. Plain film radiography, multiplanar computed tomography, and magnetic resonance imaging. Spine (Phila Pa 1976) 1991;16:S178-86.
10Hukuda S, Xiang LF, Imai S, Katsuura A, Imanaka T. Large vertebral body, in addition to narrow spinal canal, are risk factors for cervical myelopathy. J Spinal Disord 1996;9:177-86.
11Chen IH, Liao KK, Shen WY. Measurement of cervical canal sagittal diameter in Chinese males with cervical spondylotic myelopathy. Zhonghua Yi Xue Za Zhi (Taipei) 1994;54:105-10.
12Blackley HR, Plank LD, Robertson PA. Determining the sagittal dimensions of the canal of the cervical spine. The reliability of ratios of anatomical measurements. J Bone Joint Surg Br 1999;81:110-2.
13Moskovich R, Shott S, Zhang ZH. Does the cervical canal to body ratio predict spinal stenosis? Bull Hosp Jt Dis 1996;55:61-71.
14Rao RD, Currier BL, Albert TJ, Bono CM, Marawar SV, Poelstra KA, et al. Degenerative cervical spondylosis: Clinical syndromes, pathogenesis, and management. J Bone Joint Surg Am 2007;89:1360-78.
15Shimizu K, Nakamura M, Nishikawa Y, Hijikata S, Chiba K, Toyama Y, et al. Spinal kyphosis causes demyelination and neuronal loss in the spinal cord: A new model of kyphotic deformity using juvenile Japanese small game fowls. Spine (Phila Pa 1976) 2005;30:2388-92.
16Baba H, Maezawa Y, Uchida K, Furusawa N, Wada M, Imura S, et al. Plasticity of the spinal cord contributes to neurological improvement after treatment by cervical decompression. A magnetic resonance imaging study. J Neurol 1997;244:455-60.
17Kamata M, Hirabayashi K, Satomi K, et al. Postoperative spinal deformity by posterior decompression for cervical spondylotic myelopathy. East Japan J Clin Orthop 1990;2:86-9.
18Hardacker JW, Shuford RF, Capicotto PN, Pryor PW. Radiographic standing cervical segmental alignment in adult volunteers without neck symptoms. Spine (Phila Pa 1976) 1997;22:1472-80.
19Harrison DE, Harrison DD, Cailliet R, Troyanovich SJ, Janik TJ, Holland B, et al. Cobb method or Harrison posterior tangent method: Which to choose for lateral cervical radiographic analysis. Spine (Phila Pa 1976) 2000;25:2072-8.
20Lee SH, Kim KT, Seo EM, Suk KS, Kwack YH, Son ES, et al. The influence of thoracic inlet alignment on the craniocervical sagittal balance in asymptomatic adults. J Spinal Disord Tech 2012;25:E41-7.
21Tang JA, Scheer JK, Smith JS, Deviren V, Bess S, Hart RA, et al. The impact of standing regional cervical sagittal alignment on outcomes in posterior cervical fusion surgery. Neurosurgery 2012;76 Suppl 1:S14-21.
22White AA 3rd, Panjabi MM. Update on the evaluation of instability of the lower cervical spine. Instr Course Lect 1987;36:513-20.
23Fujiyoshi T, Yamazaki M, Kawabe J, Endo T, Furuya T, Koda M, et al. Anew concept for making decisions regarding the surgical approach for cervical ossification of the posterior longitudinal ligament: The K-line. Spine (Phila Pa 1976) 2008;33:E990-3.
24Gwinn DE, Iannotti CA, Benzel EC, Steinmetz MP. Effective lordosis: Analysis of sagittal spinal canal alignment in cervical spondylotic myelopathy. J Neurosurg Spine 2009;11:667-72.
25Lee DH, Kim H, Lee HS, Noh H, Kim NH, et al. The Kappa Line – A Predictor of Neurologic Outcome after Cervical Laminoplasty. CSRS; 2012.
26Kawaguchi Y, Matsumoto M, Iwasaki M, Izumi T, Okawa A, Matsunaga S, et al. New classification system for ossification of the posterior longitudinal ligament using CT images. J Orthop Sci 2014;19:530-6.
27Ijima Y, Furuya T, Ota M, Maki S, Saito J, Kitamura M, et al. The K-line in the cervical ossification of the posterior longitudinal ligament is different on plain radiographs and CT images. J Spine Surg 2018;4:403-7.
28Hsu W, Dorsi MJ, Witham TF. Surgical management of cervical spondylotic myelopathy. Neurosurg Q 2009;19:302-7.
29Nagata K, Sato K. Diagnostic imaging of cervical ossification of the posterior longitudinal ligament. In: Yonenobu K, Nakamura K, Toyama Y, editors. OPLL: Ossification of the Posterior Longitudinal Ligament. 2nd ed. Tokyo: Springer; 2006. p. 127-43.
30Miyasaka K, Nakagawa H, Kaneda K, Irie G, Tsuru M. Computed tomography of ossification and calcification of the spinal ligaments. In: Post MJ, editor. Computed Tomography of the Spine. Baltimore: Williams and Wilkins; 1984. p. 616-27.
31Suzuki Y. An anatomical study on the anterior and posterior longitudinal ligament of the spinal column: Especially on its fine structure and ossifying disease process. J Jpn Orthop Assoc 1972;46:179-95.
32Matsunaga S, Sakou T. Epidemiology of Ossification of the Posterior Longitudinal Ligament. Tokyo: Springer; 1997. p. 11-35.
33Tsuyama N, Terayama K, Ohtani K, Yamauchi Y, Yamaura I, Kurokawa T, et al. The ossification of the posterior longitudinal ligament of the spine (OPLL). J Jpn Orthop Assoc 1981;55:425-40.
34Nakamura K, Sinomiya K, Yonenobu K, Komori H, Toyama Y, Taguchi T, et al. Clinical Guidelines for OPLL (in Japanese). Clinical Guidelines Committee, Japanese Orthopaedic Association and Investigation Committee on the Ossification of Spinal Ligaments, Japanese Ministry of Public Health and Welfare. Tokyo: Nankodo; 2005. p. 59-75.
35Ono K, Ota H, Tada K, Hamada H, Takaoka K. Ossified posterior longitudinal ligament: A clinicopathologic study. Spine 1977;2:126-38.
36Seki H, Tsuyama N, Hayashi K, Kurokawa T, Imai S, Yamabe N, et al. Clinical studies of 185 patients with OPLL (in Japanese). Orthop Surg (Tokyo) 1974;25:704-10.
37Hirabayashi K, Satomi K, Sasaki T. Ossification of the posterior longitudinal ligament of the cervical spine. Cervical Spine Research Society Editorial Committee. The Cervical Spine. Philadelphia: Lippincott; 1989. p. 678-92.
38Hida K, Iwasaki Y, Koyanagi I, Abe H. Bone window computed tomography for detection of dural defect associated with cervical ossified posterior longitudinal ligament. Neurol Med Chir (Tokyo) 1997;37:173-5.
39Epstein NE. Identification of ossification of the posterior longitudinal ligament extending through the dura on preoperative computed tomographic examinations of the cervical spine. Spine (Phila Pa 1976) 2001;26:182-6.
40Matsunaga S, Nakamura K, Seichi A, Yokoyama T, Toh S, Ichimura S, et al. Radiographic predictors for the development of myelopathy in patients with ossification of the posterior longitudinal ligament: A multicenter cohort study. Spine (Phila Pa 1976) 2008;33:2648-50.
41Iwasaki M, Okuda S, Miyauchi A, Sakaura H, Mukai Y, Yonenobu K, et al. Surgical strategy for cervical myelopathy due to ossification of the posterior longitudinal ligament: Part 1: Clinical results and limitations of laminoplasty. Spine (Phila Pa 1976) 2007;32:647-53.
42Park JH, Cho CB, Song JH, Kim SW, Ha Y, Oh JK, et al. T1 slope and cervical sagittal alignment on cervical CT radiographs of asymptomatic persons. J Korean Neurosurg Soc 2013;53:356-9.
43Nagata K, Yoshimura N, Hashizume H, Ishimoto Y, Muraki S, Yamada H, et al. The prevalence of tandem spinal stenosis and its characteristics in a population-based MRI study: The Wakayama spine study. Eur Spine J 2017;26:2529-35.
44Epstein NE, Epstein JA, Carras R, Murthy VS, Hyman RA. Coexisting cervical and lumbar spinal stenosis: Diagnosis and management. Neurosurgery 1984;15:489-96.
45Dagi TF, Tarkington MA, Leech JJ. Tandem lumbar and cervical spinal stenosis. Natural history, prognostic indices, and results after surgical decompression. J Neurosurg 1987;66:842-9.
46Kanna RM, Kamal Y, Mahesh A, Venugopal P, Shetty AP, Rajasekaran S, et al. The impact of routine whole spine MRI screening in the evaluation of spinal degenerative diseases. Eur Spine J 2017;26:1993-8.
47Takahashi M, Yamashita Y, Sakamoto Y, Kojima R. Chronic cervical cord compression: Clinical significance of increased signal intensity on MR images. Radiology 1989;173:219-24.
48Mehalic TF, Pezzuti RT, Applebaum BI. Magnetic resonance imaging and cervical spondylotic myelopathy. Neurosurgery 1990;26:217-26.
49Morio Y, Teshima R, Nagashima H, Nawata K, Yamasaki D, Nanjo Y, et al. Correlation between operative outcomes of cervical compression myelopathy and mri of the spinal cord. Spine (Phila Pa 1976) 2001;26:1238-45.
50Suri 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;3:33-45.
51Matsumoto M, Toyama Y, Ishikawa M, Chiba K, Suzuki N, Fujimura Y, et al. Increased signal intensity of the spinal cord on magnetic resonance images in cervical compressive myelopathy. Does it predict the outcome of conservative treatment? Spine (Phila Pa 1976) 2000;25:677-82.
52Lee TT, Manzano GR, Green BA. Modified open-door cervical expansive laminoplasty for spondylotic myelopathy: Operative technique, outcome, and predictors for gait improvement. J Neurosurg 1997;86:64-8.
53Morio Y, Yamamoto K, Kuranobu K, Murata M, Tuda K. Does increased signal intensity of the spinal cord on MR images due to cervical myelopathy predict prognosis? Arch Orthop Trauma Surg 1994;113:254-9.
54Naderi S, Ozgen S, Pamir MN, Ozek MM, Erzen C. Cervical spondylotic myelopathy: Surgical results and factors affecting prognosis. Neurosurgery 1998;43:43-9.
55Fujiwara K, Yonenobu K, Hiroshima K, Ebara S, Yamashita K, Ono K, et al. Morphometry of the cervical spinal cord and its relation to pathology in cases with compression myelopathy. Spine (Phila Pa 1976) 1988;13:1212-6.
56Okada Y, Ikata T, Yamada H, Sakamoto R, Katoh S. Magnetic resonance imaging study on the results of surgery for cervical compression myelopathy. Spine (Phila Pa 1976) 1993;18:2024-9.
57Uchida K, Nakajima H, Takeura N, Yayama T, Guerrero AR, Yoshida A, et al. Prognostic value of changes in spinal cord signal intensity on magnetic resonance imaging in patients with cervical compressive myelopathy. Spine J 2014;14:1601-10.
58Al-Mefty O, Harkey LH, Middleton TH, Smith RR, Fox JL. Myelopathic cervical spondylotic lesions demonstrated by magnetic resonance imaging. J Neurosurg 1988;68:217-22.
59Ramanauskas WL, Wilner HI, Metes JJ, Lazo A, Kelly JK. MR imaging of compressive myelomalacia. J Comput Assist Tomogr 1989;13:399-404.
60Matsuda Y, Miyazaki K, Tada K, Yasuda A, Nakayama T, Murakami H, et al. Increased MR signal intensity due to cervical myelopathy. Analysis of 29 surgical cases. J Neurosurg 1991;74:887-92.
61Ratliff J, Voorhies R. Increased MRI signal intensity in association with myelopathy and cervical instability: Case report and review of the literature. Surg Neurol 2000;53:8-13.
62Nouri A, Tetreault L, Zamorano JJ, Dalzell K, Davis AM, Mikulis D, et al. Role of magnetic resonance imaging in predicting surgical outcome in patients with cervical spondylotic myelopathy. Spine (Phila Pa 1976) 2015;40:171-8.
63Avadhani A, Rajasekaran S, Shetty AP. Comparison of prognostic value of different MRI classifications of signal intensity change in cervical spondylotic myelopathy. Spine J 2010;10:475-85.
64Kolcun JP, Chieng LO, Madhavan K, Wang MY. The role of dynamic magnetic resonance imaging in cervical spondylotic myelopathy. Asian Spine J 2017;11:1008-15.
65Harada T, Tsuji Y, Mikami Y, Hatta Y, Sakamoto A, Ikeda T, et al. The clinical usefulness of preoperative dynamic MRI to select decompression levels for cervical spondylotic myelopathy. Magn Reson Imaging 2010;28:820-5.
66Dalbayrak S, Yaman O, Firidin MN, Yilmaz T, Yilmaz M. The contribution of cervical dynamic magnetic resonance imaging to the surgical treatment of cervical spondylotic myelopathy. Turk Neurosurg 2015;25:36-42.
67Muhle C, Metzner J, Weinert D, Falliner A, Brinkmann G, Mehdorn MH, et al. Classification system based on kinematic MR imaging in cervical spondylitic myelopathy. AJNR Am J Neuroradiol 1998;19:1763-71.
68Zeitoun D, El Hajj F, Sariali E, Catonné Y, Pascal-Moussellard H. Evaluation of spinal cord compression and hyperintense intramedullary lesions on T2-weighted sequences in patients with cervical spondylotic myelopathy using flexion-extension MRI protocol. Spine J 2015;15:668-74.
69Seki S, Kawaguchi Y, Nakano M, Yasuda T, Hori T, Noguchi K, et al. Clinical significance of high intramedullary signal on T2-weighted cervical flexion-extension magnetic resonance imaging in cervical myelopathy. J Orthop Sci 2015;20:973-7.
70Rajasekaran S, Yerramshetty JS, Chittode VS, Kanna RM, Balamurali G, Shetty AP, et al. The assessment of neuronal status in normal and cervical spondylotic myelopathy using diffusion tensor imaging. Spine (Phila Pa 1976) 2014;39:1183-9.
71Kara B, Celik A, Karadereler S, Ulusoy L, Ganiyusufoglu K, Onat L, et al. The role of DTI in early detection of cervical spondylotic myelopathy: A preliminary study with 3-T MRI. Neuroradiology 2011;53:609-16.
72Lee JW, Kim JH, Park JB, Park KW, Yeom JS, Lee GY, et al. Diffusion tensor imaging and fiber tractography in cervical compressive myelopathy: Preliminary results. Skeletal Radiol 2011;40:1543-51.
73Jones JG, Cen SY, Lebel RM, Hsieh PC, Law M. Diffusion tensor imaging correlates with the clinical assessment of disease severity in cervical spondylotic myelopathy and predicts outcome following surgery. AJNR Am J Neuroradiol 2013;34:471-8.
74Facon D, Ozanne A, Fillard P, Lepeintre JF, Tournoux-Facon C, Ducreux D, et al. MR diffusion tensor imaging and fiber tracking in spinal cord compression. AJNR Am J Neuroradiol 2005;26:1587-94.
75Maki S, Koda M, Kitamura M, Inada T, Kamiya K, Ota M, et al. Diffusion tensor imaging can predict surgical outcomes of patients with cervical compression myelopathy. Eur Spine J 2017;26:2459-66.
76Shen C, Xu H, Xu B, Zhang X, Li X, Yang Q, et al. Value of conventional MRI and diffusion tensor imaging parameters in predicting surgical outcome in patients with degenerative cervical myelopathy. J Back Musculoskelet Rehabil 2018;31:525-32.
77Wang K, Chen Z, Zhang F, Song Q, Hou C, Tang Y, et al. Evaluation of DTI parameter ratios and diffusion tensor tractography grading in the diagnosis and prognosis prediction of cervical spondylotic myelopathy. Spine (Phila Pa 1976) 2017;42:E202-E210.
78Rajasekaran S, Kanna RM, Chittode VS, Maheswaran A, Aiyer SN, Shetty AP, et al. Efficacy of diffusion tensor imaging indices in assessing postoperative neural recovery in cervical spondylotic myelopathy. Spine (Phila Pa 1976) 2017;42:8-13.
79Kang M, Anderer E, Elliott R, Kalhorn S, Cooper P, Frempong-Boadu A, et al. Diffusion tensor imaging of the spondylotic cervical spinal cord: A preliminary study of quantifiable markers in the evaluation for surgical decompression. Int J Head Neck Surg 2011;5:1.
80Henning A, Schär M, Kollias SS, Boesiger P, Dydak U. Quantitative magnetic resonance spectroscopy in the entire human cervical spinal cord and beyond at 3T. Magn Reson Med 2008;59:1250-8.
81Holly LT, Freitas B, McArthur DL, Salamon N. Proton magnetic resonance spectroscopy to evaluate spinal cord axonal injury in cervical spondylotic myelopathy. J Neurosurg Spine 2009;10:194-200.
82Kendi AT, Tan FU, Kendi M, Yilmaz S, Huvaj S, Tellioğlu S, et al. MR spectroscopy of cervical spinal cord in patients with multiple sclerosis. Neuroradiology 2004;46:764-9.
83Salamon N, Ellingson BM, Nagarajan R, Gebara N, Thomas A, Holly LT, et al. Proton magnetic resonance spectroscopy of human cervical spondylosis at 3T. Spinal Cord 2013;51:558-63.
84Oshina M, Oshima Y, Tanaka S, Riew KD. Radiological fusion criteria of postoperative anterior cervical discectomy and fusion: A systematic review. Global Spine J 2018;8:739-50.
85Ghiselli G, Wharton N, Hipp JA, Wong DA, Jatana S. Prospective analysis of imaging prediction of pseudarthrosis after anterior cervical discectomy and fusion: Computed tomography versus flexion-extension motion analysis with intraoperative correlation. Spine (Phila Pa 1976) 2011;36:463-8.
86Park DK, Rhee JM, Kim SS, Enyo Y, Yoshiok K. Do CT scans overestimate the fusion rate after anterior cervical discectomy and fusion? J Spinal Disord Tech 2015;28:41-6.