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Preexisting severe cervical spinal cord compression is a significant risk factor for severe paralysis development in patients with traumatic cervical spinal cord injury without bone injury: a retrospective cohort study Takeshi Oichi, Yasushi Oshima, Rentaro Okazaki & Seiichi Azuma European Spine Journal ISSN 0940-6719 Eur Spine J DOI 10.1007/s00586-015-4142-4

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Author's personal copy Eur Spine J DOI 10.1007/s00586-015-4142-4

ORIGINAL ARTICLE

Preexisting severe cervical spinal cord compression is a significant risk factor for severe paralysis development in patients with traumatic cervical spinal cord injury without bone injury: a retrospective cohort study Takeshi Oichi1,2 • Yasushi Oshima2 • Rentaro Okazaki1 • Seiichi Azuma1

Received: 11 February 2015 / Revised: 14 July 2015 / Accepted: 14 July 2015 Ó Springer-Verlag Berlin Heidelberg 2015

Abstract Purpose The objective of this study is to investigate whether preexisting severe cervical spinal cord compression affects the severity of paralysis once patients develop traumatic cervical spinal cord injury (CSCI) without bone injury. Methods We retrospectively investigated 122 consecutive patients with traumatic CSCI without bone injury. The severity of paralysis on admission was assessed by the American Spinal Injury Association impairment scale (AIS). The degree of preexisting cervical spinal cord compression was evaluated by the maximum spinal cord compression (MSCC) and was divided into three categories: minor compression (MSCC B 20 %), moderate compression (20 % \ MSCC B 40 %), and severe compression (40 % \ MSCC). We investigated soft-tissue damage on magnetic resonance imaging to estimate the external force applied. Other potential risk factors, including age, sex, fused vertebra, and ossification of longitudinal ligament, were also reviewed. A multivariate logistic regression analysis was performed to investigate the risk factors for developing severe paralysis (AIS A–C) on admission. Results Our study included 103 males and 19 females with mean age of 65 years. Sixty-one patients showed

& Takeshi Oichi [email protected] 1

Department of Orthopedic Surgery, Saitama Red Cross Hospital, 8-3-33 Kamiochiai, Chuo-ku, Saitama 338-8553, Japan

2

Present Address: Department of Orthopedic Surgery, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

severe paralysis (AIS A–C) on admission. The average MSCC was 22 %. Moderate compression was observed in 41, and severe in 20. Soft-tissue damage was observed in 91. A multivariate analysis showed that severe cervical spinal cord compression significantly affected the severity of paralysis at the time of injury, whereas both mild and moderate compression did not affect it. Soft-tissue damage was also significantly associated with severe paralysis on admission. Conclusions Preexisting severe cervical cord compression is an independent risk factor for severe paralysis once patients develop traumatic CSCI without bone injury. Keywords Cervical spine  Spinal cord injury  Cervical spinal cord compression  Soft tissue damage  Fused vertebra

Introduction Increasing number of patients experiencing traumatic cervical spinal cord injury (CSCI) do not show any major fracture or dislocation on radiological examinations [1]. In Japan, the incidence of spinal cord injuries is reported to be 33.77 per million population, with 58.1 % of CSCI patients not showing bone injury. The incidence of spinal cord injuries might further increase in the current aging society [2]. Patients with CSCI without bone injury suffer from varying severity of paralysis, ranging from complete paralysis to mild numbness. The prognosis of patients with severe paralysis is generally poor; thus, disability, suffering, and socioeconomic burden to the individual and their caregivers are of particular importance [3]. Physicians engaged in the initial management of trauma patients

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should therefore be cognizant of the characteristics of CSCI without bony injury. CSCI occurs as a result of various factors. Among them, both dynamic factor (i.e., traumatic external force) and static factor (i.e., preexisting cervical spinal cord compression) are of particular importance [1, 4–6]. As for dynamic factor, high energy trauma is a well-known predictor of neurological outcomes in patients with CSCI [4, 7]. As for static factors, preexisting cervical spinal cord compression is a well-established risk factor for developing CSCI [1, 5, 8] but the degree of preexisting cervical spinal cord compression has been shown not to affect the severity of the paralysis [8–11]. Despite these reports, we often encounter patients with preexisting severe cervical spinal cord compression developing severe CSCI from a minor trauma, such as falling from standing. These experiences lead us to hypothesize that preexisting cervical spinal cord compression actually affects the severity of paralysis especially when the stenosis is severe. Studies focusing on this issue are limited, and thus the objective of this study was to investigate whether the presence of preexisting severe cervical spinal cord compression affects the severity of paralysis at the time of injury in patients with traumatic CSCI without bone injury. To investigate the independent effect of preexisting spinal cord compression, we adjusted for the influence of other important factors, including traumatic external force, using statistical measures.

Materials and methods We retrospectively investigated 122 consecutive patients with traumatic CSCI without bone injury, who were admitted to our facility within 2 days after trauma from April 2006 to April 2013. All patients or their families provided written informed consent. The study was approved by the internal review board of our institution. CSCI without bone injury was defined as (1) presence of neurological deficit referable to CSCI, (2) absence of major fracture or dislocation of the cervical spine on computer tomography (CT), and (3) presence of intramedullary high-intensity areas on T2-weighted magnetic resonance imaging (MRI). We excluded patients without intramedullary signal change on MRI to rule out patients with cervical concussion or hysteria. We also excluded CSCI patients who showed severe instability with dynamic radiographs that indicate a spontaneous reduction of dislocation. The neurological outcomes were assessed by the American Spinal Injury Association impairment scale (AIS) at admission (i.e., before receiving any treatments) and discharge [12]. We defined AIS grade A–C as severe paralysis, and AIS D or E as less-severe paralysis.

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Radiological evaluation All patients underwent plain radiography and CT at the time of admission, and an Aquilion Super 4 CT scanner (Toshiba Medical Systems, Tokyo, Japan) was used in this series. Horizontal slices were obtained at a slice thickness of 1 mm and a slice interval of 1 mm in all cases and 3 dimensional CT was generated. All patients underwent high-resolution MRI using a 1.5-Tesla imager (Signa; GE Medical Systems, WI), and transverse and sagittal images were obtained at 1-mm intervals. MRI was performed at an average of 0.8 days after admission (range, 0–10 days). T1-weighted images (T1WI) and T2WI of the cervical spinal cord were obtained using a fast spin echo sequence system. A phased-array surface coil was used. Slice width was 3 mm and the acquisition matrix was 320 9 256. Sequence parameters were repetition time (TR) 450 ms/ echo time (TE), 10 ms for T1WI, and TR 3000 ms/TE, 100 ms for T2WI. The presence of major fracture or dislocation and the presence of ossification of the posterior longitudinal ligament (OPLL) were assessed by 3-dimensional CT. Cases that were difficult to distinguish between OPLL and a bony spur were not defined as OPLL. The presence of fused vertebrae adjacent to the level of injury was also examined by 3-dimensional CT because it is a potential predictor of neurological outcomes [5]. The level of CSCI was determined on the basis of intramedullary signal change or apparent soft-tissue or ligamentous injury on MRI. The degree of preexisting cervical spinal cord compression was evaluated by calculating maximum spinal cord compression (MSCC) using mid-sagittal T2WI MRI (Fig. 1) [13]. MSCC is a reliable radiological measure for quantifying the degree of cord compression in patients with acute CSCI [14, 15]. Patients with higher MSCC mean that they have more severe cervical spinal cord compression. MSCC was calculated by the following equation: !! di MSCC ¼ 1   100 % ðda þ dbÞ= 2 di is the anteroposterior cord diameter at the injury level. da is the anteroposterior cord diameter at the nearest normal level above the level of injury, and db is the anteroposterior cord diameter at the nearest normal level below the level of injury. According to MSCC, the degree of preexisting spinal cord compression was divided into three categories: minor compression (MSCC \ 20 %), moderate compression (MSCC [ 20 and \ 40 %), and severe compression (MSCC [ 40 %).

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Fig. 1 Midsagittal T2-weighted magnetic resonance imaging from a representative case with acute traumatic CSCI without bone injury. The anteroposterior cord diameter at the injury level (di), the anteroposterior cord diameter at the nearest normal level above the level of injury (da), and the anteroposterior cord diameter at the nearest normal level below the level of injury (db) were used to estimate maximum canal compromise (see text, math equation)

CSCI patients with findings of soft-tissue damage on MRI are considered to have larger external force applied at the time of injury than those without soft-tissue damage [11, 16]. Because it is difficult to evaluate the degree of actual traumatic force from the situation at the time of injury, we examined the presence of soft-tissue damage using sagittal MRI to estimate the degree of external force applied instead. Findings of soft-tissue damage on MRI included prevertebral hyperintensity, injury of the interspinous ligament or posterior neck muscles, and intervertebral disk disruption (Fig. 2) as reported previously [11, 17–19]. Prevertebral hyperintensity was defined as increased signal intensity of the prevertebral tissues on T2WI MRI. Injury of the interspinous ligament or posterior neck muscles was considered positive if signal intensity on T2WI MRI was increased. Disk disruption was defined as increased signal intensity on T2WI MRI. The presence of soft tissue damage was defined as having one or more of the previously mentioned features.

Fig. 2 Midsagittal T2-weighted magnetic resonance imaging from a representative case with soft tissue damage in our series. Prevertebral hyperintensity (1), intervertebral disk disruption (2), and injury of the interspinous ligament or posterior neck muscles (3) were observed

The observer was blinded to the patients clinical and neurological data. MSCC was measured twice at different times and mean data were employed. Statistical analysis We divided the patients into 2 groups according to the AIS grade on admission: severe group (AIS A–C); and the lesssevere group (AIS D). Differences in each variable between the 2 groups were compared. For continuous variables, 2-group comparisons were performed using the nonparametric procedure of the Wilcoxon rank-sum test because all continuous variables (age and MSCC) did not approximate to normal distribution. Categorical variables were compared between the 2 groups using the Chi-square test. Then, a multiple logistic regression model yielding odds ratios (ORs) and 95 % confidence intervals (CI) was used to identify predictors of severe paralysis (AIS A–C) on admission. The model included age, sex, and variables showing a univariate association with neurological outcome (p \ 0.20). Data analyses were performed using the JMP software, version 9.0 (SAS Institute, Inc.); a p value of \0.05 was considered significant. All tests were 2-tailed.

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ligament (n = 4), Klippel–Feil syndrome (n = 3), and spondylosis (n = 4).

Results Clinical characteristics Of the 122 patients enrolled, 103 were males and the average age was 65 years (range, 16–93). The average follow-up period was 47 days (range, 2–320 days) after trauma. Overall causes of CSCI without bone injury were falls from standing or seated heights in 55 patients (45 %), falling from a height (including falling forwards down stairs) in 31 patients (25 %), traffic accidents in 29 patients (24 %), falling object from a height in 4 patients (3 %), and sports-related activities in 3 patients (2 %). Neurological outcomes Sixty-one patients (50 %) showed severe paralysis (AIS A– C) on admission. Forty-six patients (38 %) showed neurological recovery at discharge, as defined by Cgrade 1 improvement in AIS grade (Table 1). Preexisting cervical spinal cord compression The average MSCC was 22 % (range, -19 to 67 %). Minor compression was observed in 61 patients, moderate compression in 41 patients, and severe compression in 20 patients. Soft tissue damage Of the 122 patients, prevertebral high intensity was observed in 81 patients, intervertebral disk disruption in 49 patients, and injury of the interspinous ligament or posterior neck muscles in 27 patients. A total of 91 patients showed C1 of these 3 findings. Fused vertebrae adjacent to the level of injury Fused vertebrae adjacent to the level of injury were observed in 16 patients. Underlying pathologies included OPLL (n = 5), ossification of anterior longitudinal

Differences in each variable between the severe group and the less-severe group Table 2 shows the results of differences between the 2 groups on admission. Patients in the severe group were significantly older than those in the less-severe group. The average MSCC was 26 % (range, 219 to 67 %) in severe group and 19 % (range, 212 to 58 %) in less-severe group. No significant difference in MSCC between two groups was observed (p = 0.13, Wilcoxon rank-sum test). However, patients with severe compression develop severe paralysis significantly more frequently compared with those with minor or moderate compression (p \ 0.05, Chisquare test). The findings of soft-tissue damage were observed in the severe group more frequently than those in the less-severe group; however, this difference was not statistically significant (p = 0.09, Chi-square test). Sex, OPLL, and fused vertebra adjacent to the injury level did not affect the severity of paralysis significantly. Multivariate logistic regression analysis of severe paralysis (AIS grade A–C) on admission On the basis of the results of univariate analyses, age, sex, soft tissue damage, and the degree of preexisting spinal cord compression (mild, moderate, and severe) were considered as dependent variables. Preexisting severe compression was a significant predictor of severe paralysis (AIS A–C) on admission even after adjusting for other risk factors (OR, 4.50; 95 % CI, 1.50–15.5; p \ 0.05), whereas neither mild nor moderate compression was a significant predictor (Table 3). Older age and the presence of softtissue damage on MRI also significantly affected the severity of paralysis on admission (OR, 1.04; 95 % CI, 1.00–1.07; p \ 0.05 and OR, 2.81; 95 % CI, 1.08–8.06; p \ 0.05, respectively).

Discussion Table 1 AIS grade at admission and discharge AIS grade On admission

At discharge

Grades

A

B

C

D

E

A (n = 10)

7

2

1





B (n = 28)



8

9

11



C (n = 23) D (n = 61)

– –

– –

5 –

18 56

– 5

AIS American Spinal Injury Association impairment scale

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In this study, we made two important clinical observations. First, preexisting severe cervical spinal cord compression is a significant risk factor for developing severe paralysis in patients with CSCI without bone injury. Second, the findings of soft-tissue damage on MRI are associated with severe paralysis in patients with CSCI without bone injury. Preexisting severe cervical spinal cord compression is a significant risk factor for developing severe paralysis. Our results are congruent with those reported by Hayashi et al. [20]. He retrospectively investigated 31 CSCI patients

Author's personal copy Eur Spine J Table 2 Characteristics and radiographic findings on admission between severe group and less-severe group Severe group (AIS A–C) (n = 61)

Less-severe group (AIS D) (n = 61)

p value 0.01

Age (mean ± SD)

68 ± 13

61 ± 13

Sex (Male/Female)

53/8

50/11

0.62

MSCC (%)

26 ± 22

19 ± 14

0.13

Degree of spinal cord compression [no. of patients (%)] Minor compression

27 (44)

Moderate compression

18 (30)

34 (56) 23 (38)

Severe compression

16 (26)

4 (7)

Ossification of longitudinal ligament

16 (26)

12 (20)

0.52

Fused vertebrae adjacent to the injury level

8 (13)

8 (13)

1.00

Soft tissue damage

50 (82)

41 (67)

0.09

0.01

Continuous variables were compared using Wilcoxon rank-sum test; categorical data were analyzed using Chi-square test AIS American Spinal Injury Association impairment scale, MSCC maximum spinal cord compression, minor compression MSCC of less than 20 %, moderate compression MSCC exceeding 20 % and less than 40 %, severe compression MSCC exceeding 40 %

Table 3 Multivariate logistic regression analysis of severe paralysis (AIS A–C) on admission

Age

OR

95 % CI

p value

1.04

1.00–1.07

0.03

Sex Male

Reference

Female

0.54

0.18–1.58

0.26

2.81

1.08–8.06

0.03

Soft tissue damage

Degree of spinal cord compression Minor compression Moderate compression

Reference 1.06

Severe compression

5.3

0.44–2.55

0.90

1.5–24.1

0.01

AIS American Spinal Injury Association impairment scale, CI confidence interval, MSCC maximum spinal cord compression, OR odds ratio, minor compression MSCC of less than 20 %, moderate compression MSCC exceeding 20 % and less than 40 %, severe compression MSCC exceeding 40 %

without bone injury and reported that patients with preexisting severe spinal cord compression, which was defined as the narrowest spinal cord diameter being \2/3 of the diameter at C1 level, developed a more severe paralysis at the time of injury. In comparison, our study includes a relatively large sample size which enables us to adjust for other risk factors, such as age, sex, and traumatic external force, using statistical measures. Therefore, the results of our study are more reliable and further support that preexisting severe spinal cord compression is a significant predictor of severe paralysis in patients with CSCI without bone injury. Conversely, several studies have reported that the degree of preexisting cervical spinal cord compression does not affect the severity of the paralysis. Maeda et al. investigated 88 cases with acute traumatic CSCI without

bone injury and reported that the severity of paralysis at the time of injury does not correlate with the degree of cervical canal diameter [11]. Moreover, Chikuda et al. investigated 106 CSCI patients with OPLL and found no significant differences in maximal canal compromise between Frankel grade groups at admission [9]. Similarly, in our study, no significant differences in MSCC between severe and lesssevere groups were observed. However, when we stratified the patients according to the degree of spinal cord compression, our study revealed that patients develop severe paralysis more frequently only when the degree of compression is severe above some threshold level. Considering the results that minor or moderate compression did not affect the neurological outcomes at all, it is likely that the mere difference of MSCC does not affect the paralysis severity as long as the cord compression is mild or moderate. It seems reasonable to think that no liner correlation exists between the degree of preexisting compression and the severity of paralysis. We speculate that the spinal cord becomes more vulnerable to external forces, when the degree of cord compression exceeds a certain threshold. The results of the present study suggest that patients with preexisting severe cervical spinal cord compression are likely to suffer severe paralysis once they develop traumatic CSCI. Then the next issue to be resolved is whether prophylactic surgery should be considered in these patients to prevent developing severe CSCI. Fundamentally, we do not recommend the prophylactic surgery in asymptomatic patients because the actual incidence of CSCI in those with preexisting cervical spinal cord compression is low [6, 21]. Takao et al. reported only 0.0017 % of asymptomatic patients with preexisting cervical spinal canal stenosis can avoid traumatic CSCI if they undergo decompression surgery before trauma [6]. Furthermore, according to the nation-wide cohort study conducted by

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Wu et al., only 0.3 % of CSM patients can avoid CSCI if they undergo surgery before trauma [21]. However, especially in cases involving preexisting gait disturbance and a high risk of falling, prophylactic surgery can be considered to prevent developing severe CSCI. We believe that it is important to inform patients of the potential risks of severe cervical spinal cord compression. Soft-tissue damage The findings of soft-tissue damage on MRI are associated with severe paralysis in patients with CSCI without bone injury, possibly reflecting the amount of external force that was applied. Machino et al. investigated 100 consecutive patients with spinal cord injury without radiological abnormality and showed that the larger range of prevertebral high intensity is related to severe paralysis at admission [17]. Maeda et al. also reported that the presence of discoligamentous damage at the time of injury strongly affects the neurological status [11]. Similarly, in our study, the presence of soft tissue damage served as a significant predictor of severe paralysis even after adjusting for other risk factors. Our results clearly show that the severity of paralysis is significantly associated with the presence of soft tissue damage, which suggests a high level of external force applied. Limitations The present study is associated with several limitations. First, we excluded patients without intramedullary signal change on MRI; thus, it is possible that we might have underestimated the incidence of CSCI without bone injury. Second, the follow-up period was relatively short because our hospital is a tertiary referral center and most patients are usually transferred to other hospitals after acute medical care. Thus our results are applied to the neurological status only at the time of injury. Whether preexisting severe cervical canal stenosis affects long-term neurological recovery and whether surgical decompression after the injury should be considered in these patients remains unknown and thus warrants further examination. However, the severity of paralysis at the time of injury mainly determines the neurological prognosis of patients with CSCI [7], and we believe that our study provides valuable clinical information.

Conclusions Preexisting severe cervical cord compression is an independent risk factor for severe paralysis once patients develop traumatic CSCI without bone injury. Furthermore,

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the findings of soft-tissue damage on MRI are associated with severe paralysis in patients with CSCI without bone injury. The identification of these factors will help to provide appropriate information for patients and to aid in stratification of patients in future clinical trials or clinical therapeutic protocol. Compliance with ethical standards Conflict of interest The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

References 1. Koyanagi I, Iwasaki Y, Hida K, Akino M, Imamura H, Abe H (2000) Acute cervical cord injury without fracture or dislocation of the spinal column. J Neurosurg 93:15–20 2. Sakai H, Ueta T, Shiba K (2010) Current situation of medical care for spinal cord injury in Japan (in Japanese). J Spine Res 1:41–51 3. El Masri WS, Kumar N (2011) Traumatic spinal cord injuries. Lancet 377:972–974. doi:10.1016/s0140-6736(11)60248-1 4. Kawano O, Maeda T, Mori E, Yugue I, Takao T, Sakai H, Ueta T, Shiba K (2014) Influence of spinal cord compression and traumatic force on the severity of cervical spinal cord injury associated with ossification of the posterior longitudinal ligament. Spine (Phila Pa 1976). doi:10.1097/brs.0000000000000361 5. Kato H, Kimura A, Sasaki R, Kaneko N, Takeda M, Hagiwara A, Ogura S, Mizoguchi T, Matsuoka T, Ono H, Matsuura K, Matsushima K, Kushimoto S, Fuse A, Nakatani T, Iwase M, Fudoji J, Kasai T (2008) Cervical spinal cord injury without bony injury: a multicenter retrospective study of emergency and critical care centers in Japan. J Trauma 65:373–379. doi:10.1097/TA. 0b013e31817db11d 6. Takao T, Morishita Y, Okada S, Maeda T, Katoh F, Ueta T, Mori E, Yugue I, Kawano O, Shiba K (2013) Clinical relationship between cervical spinal canal stenosis and traumatic cervical spinal cord injury without major fracture or dislocation. Eur Spine J. doi:10.1007/s00586-013-2865-7 7. Wilson JR, Cadotte DW, Fehlings MG (2012) Clinical predictors of neurological outcome, functional status, and survival after traumatic spinal cord injury: a systematic review. J Neurosurg Spine 17:11–26. doi:10.3171/2012.4.aospine1245 8. Aebli N, Ruegg TB, Wicki AG, Petrou N, Krebs J (2013) Predicting the risk and severity of acute spinal cord injury after a minor trauma to the cervical spine. Spine J 13:597–604. doi:10. 1016/j.spinee.2013.02.006 9. Chikuda H, Seichi A, Takeshita K, Matsunaga S, Watanabe M, Nakagawa Y, Oshima K, Sasao Y, Tokuhashi Y, Nakahara S, Endo K, Uchida K, Takahata M, Yokoyama T, Yamada K, Nohara Y, Imagama S, Hosoe H, Ohtsu H, Kawaguchi H, Toyama Y, Nakamura K (2011) Acute cervical spinal cord injury complicated by preexisting ossification of the posterior longitudinal ligament: a multicenter study. Spine (Phila Pa 1976) 36:1453–1458. doi:10.1097/BRS.0b013e3181f49718 10. Okada S, Maeda T, Ohkawa Y, Harimaya K, Saiwai H, Kumamaru H, Matsumoto Y, Doi T, Ueta T, Shiba K, Iwamoto Y (2009) Does ossification of the posterior longitudinal ligament affect the neurological outcome after traumatic cervical cord injury? Spine (Phila Pa 1976) 34:1148–1152. doi:10.1097/BRS. 0b013e31819e3215

Author's personal copy Eur Spine J 11. Maeda T, Ueta T, Mori E, Yugue I, Kawano O, Takao T, Sakai H, Okada S, Shiba K (2012) Soft-tissue damage and segmental instability in adult patients with cervical spinal cord injury without major bone injury. Spine (Phila Pa 1976) 37:E1560– E1566. doi:10.1097/BRS.0b013e318272f345 12. Maynard FM Jr, Bracken MB, Creasey G, Ditunno JF Jr, Donovan WH, Ducker TB, Garber SL, Marino RJ, Stover SL, Tator CH, Waters RL, Wilberger JE, Young W (1997) International standards for neurological and functional classification of spinal cord injury. Am Spinal Inj Assoc Spinal Cord 35:266–274 13. Rao SC, Fehlings MG (1999) The optimal radiologic method for assessing spinal canal compromise and cord compression in patients with cervical spinal cord injury. Part I: An evidencebased analysis of the published literature. Spine (Phila Pa 1976) 24:598–604 14. Fehlings MG, Furlan JC, Massicotte EM, Arnold P, Aarabi B, Harrop J, Anderson DG, Bono CM, Dvorak M, Fisher C, France J, Hedlund R, Madrazo I, Nockels R, Rampersaud R, Rechtine G, Vaccaro AR (2006) Interobserver and intraobserver reliability of maximum canal compromise and spinal cord compression for evaluation of acute traumatic cervical spinal cord injury. Spine (Phila Pa 1976) 31:1719–1725. doi:10.1097/01.brs.0000224164. 43912.e6 15. Furlan JC, Fehlings MG, Massicotte EM, Aarabi B, Vaccaro AR, Bono CM, Madrazo I, Villanueva C, Grauer JN, Mikulis D (2007) A quantitative and reproducible method to assess cord compression and canal stenosis after cervical spine trauma: a study of interrater and intrarater reliability. Spine (Phila Pa 1976) 32:2083–2091. doi:10.1097/BRS.0b013e318145a91c

16. Kongsted A, Sorensen JS, Andersen H, Keseler B, Jensen TS, Bendix T (2008) Are early MRI findings correlated with longlasting symptoms following whiplash injury? A prospective trial with 1-year follow-up. Eur Spine J 17:996–1005. doi:10.1007/ s00586-008-0687-9 17. Machino M, Yukawa Y, Ito K, Nakashima H, Kanbara S, Morita D, Kato F (2011) Can magnetic resonance imaging reflect the prognosis in patients of cervical spinal cord injury without radiographic abnormality? Spine (Phila Pa 1976) 36:E1568– E1572. doi:10.1097/BRS.0b013e31821273c0 18. Miyanji F, Furlan JC, Aarabi B, Arnold PM, Fehlings MG (2007) Acute cervical traumatic spinal cord injury: MR imaging findings correlated with neurologic outcome–prospective study with 100 consecutive patients. Radiology 243:820–827. doi:10.1148/ radiol.2433060583 19. Song KJ, Kim GH, Lee KB (2008) The efficacy of the modified classification system of soft tissue injury in extension injury of the lower cervical spine. Spine (Phila Pa 1976) 33:E488–E493. doi:10.1097/BRS.0b013e31817b6191 20. Hayashi K, Yone K, Ito H, Yanase M, Sakou T (1995) MRI findings in patients with a cervical spinal cord injury who do not show radiographic evidence of a fracture or dislocation. Paraplegia 33:212–215. doi:10.1038/sc.1995.47 21. Wu JC, Ko CC, Yen YS, Huang WC, Chen YC, Liu L, Tu TH, Lo SS, Cheng H (2013) Epidemiology of cervical spondylotic myelopathy and its risk of causing spinal cord injury: a national cohort study. Neurosurg Focus 35:E10. doi:10.3171/2013.4. focus13122

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