Our data show that:
Profound TCCS (AIS grade C and worse) typically results from hyperextension instability of the cervical spine.
Segmental instability and spinal cord signal may be located at different cervical segments.
Segmental instability may occur in more than one cervical segment.
Hyperextension instability is detected on high-quality MRI scans in 68% of patients by the radiologist on call and in 86% of patients by a specialized musculoskeletal MRI radiologist.
TCCS does not represent a recently defined clinical syndrome, but the first case report of TCCS rather dates back to 1887 . In 1954, Schneider et al.  reported on a case series of 15 patients (since then described as “Schneider’s syndrome” by some authors). It was stated that TCCS occurs in three situations: (a) fractures and dislocations of the cervical spine, (b) sudden protrusion of an intervertebral disc with consecutive compression of the spinal cord, and (c) hyperextension of the cervical spine without segmental instability in patients with preexisting degenerative conditions of the cervical spine (spondylotic TCCS). In the latter group of patients, radiographs were described as showing no signs of fractures or instability, whereas CT and MRI scans were not available in 1954. Accordingly, Schneider et al. stated that spondylotic TCCS occurs without apparent injuries of the cervical spine by forward bulging of the ligamenta flava into the spinal canal resulting in spinal cord compression (Taylor mechanism , Fig. 3).
CT and MRI scans allow for the diagnosis of more subtle injuries of the cervical spine nowadays. CT scans represent the gold standard imaging technique for the assessment of fractures and subluxations, while MRI is the method of choice for the evaluation of ligamentous and extraneural soft tissue injuries as well as for the assessment of the spinal cord [21, 23]. Despite continuous advances in imaging during the last decades, spondylotic TCCS is still considered to result from compression of the spinal cord without acute discoligamentous instability of the cervical spine by several authors [3, 7, 8, 11, 13, 14]. According to the results of our study, however, spondylotic TCSS mainly results from hyperextension instability of the cervical spine following disruption of the anterior tension band. Interestingly, re-assessing radiographs presented in the hallmark paper by Schneider et al.  in 1954 supports our hypothesis by showing subtle signs of hyperextension instability in two cases (Figs. 4, 5).
The aim of the present study was not to prove the Taylor mechanism of spondylotic TCCS without instability to be generally wrong or irrelevant. The goal of this study rather was to increase the awareness for hyperextension instability in patients with TCCS without apparent instability on CT scans. We interpret our findings as follows: Our results are based on intraoperative findings as a reference for the assessment of instability and indications for surgery followed institutional guidelines as described in the methods section. Patients with less severe neurological impairment or complete remission within the first days were therefore treated nonoperatively and were excluded from this study. It is reasonable to assume that spinal cord compression was minor in these patients, since recent studies have revealed a correlation between the severity of neurological impairment and stability of the cervical spine [3, 24]. Accordingly, mild TCCS and TCCS with rapid improvement may occur in patients with stable cervical spines and may be attributed to the Taylor mechanism of spondylotic TCCS. In patients with profound TCCS, however, we consider hyperextension instability of the spondylotic spine as a relevant factor leading to increased compression of the spinal cord resulting in more severe neurological deficits. We therefore propose subclassification of spondylotic TCCS into “spondylotic TCCS without segmental instability” and “spondylotic TCCS with hyperextension instability.”
Accordingly, it is mandatory to actively confirm or rule out hyperextension instability in patients with spondylotic TCCS. MRI is the gold standard for the assessment of the spinal ligaments and the spinal cord [21, 23]. The ALL is the key structure for the assessment of hyperextension instability. An intact ALL appears as a hypointense band in all sequences and is hardly discernible from adjacent hypointense structures such as cortical bone or the annulus. A disruption of the ALL appears as focal discontinuity of the hypointense band frequently combined with elevation of the ligament from adjacent structures by fluid . MRI findings were correlated with intraoperative findings as external reference following different types of cervical spine trauma in two studies [25, 26]. In 2006, Goradia et al.  used consensus reading of two radiologists of unknown experience and reported a sensitivity of MRI for ALL injuries of 0.71. A single senior trauma radiologist performed MRI reading in the study of Malham et al.  in 2009 with a sensitivity of 0.48 and a specificity of 1.00 for ALL injuries. The specificity of MRI was 1.00 in our study as well, while the sensitivity differed between the radiologist on call and the specialized MRI radiologist (0.61 and 0.88, respectively). Accordingly, hyperextension instability is detectable on MRI scans with an acceptable sensitivity in our opinion. It requires, however, high-resolution images with the entire bandwidth of available sequence and an experienced reader. Flexion–extension lateral radiographs may be an additional tool for the assessment of discoligamentous injuries of the cervical spine . In patients with spondylotic TCCS, however, we do not recommend to perform lateral radiographs in maximum extension in order to avoid further spinal cord compression. Regarding the spinal cord, diffusion tensor imaging (DTI) in addition to conventional MRI may allow for a more detailed radiological assessment of spinal cord damage in the future . DTI measures have been recently shown to correlate with the modified Japanese Orthopedic Association score in patients with cervical myelopathy  and may also provide useful information for treatment decision-making and predicting neurological outcome after TCCS.
Two further interesting findings of our study have to be discussed. First, the segmental level of spinal cord signal did not match the level of segmental instability in three patients. In these cases, the cord signal was found in the segment with the most pronounced spinal canal stenosis (Fig. 2). At first glance, this is a surprising finding which was not described in the literature yet. The spinal cord compression in spondylotic TCCS is the result of a pincer effect with the spinal cord being entrapped between the anterior spondylotic disc-osteophyte complex and the bulged posterior ligaments . Spinal cord compression increases with increased extension of the cervical spine. The restricted ROM of a spondylotic cervical spine therefore may “protect” the spinal cord from major compression in patients without acute discoligamentous instability. Hyperextension instability, however, increases the ROM of the cervical spine in extension to a pathological level and thus results in more severe compression of the spinal cord occurring at the most stenotic level. Second, in three of twenty-three patients, hyperextension instability was observed at two segments of the lower cervical spine (Fig. 2). After high-energy trauma, bi- or multilevel injuries of the spine are not an uncommon finding and typically occur in different regions of the spinal column [30, 31]. For example, combined injuries of the upper and lower cervical spine as well as combinations of injuries of the cervical and thoracic spine have been frequently described. The patients in this study, however, sustained low-energy hyperextension trauma of the cervical spine, which resulted in ALL rupture and disc avulsion in the most brittle segment of the lower cervical spine in 22 patients. Further hyperextension in this segment might have been stopped by both the PLL and the intact sclerotic facets according to our interpretation. Continuing hyperextension forces therefore might have resulted in disruption of the anterior tension band at an additional brittle segment in these three patients.
Indications and timing for surgical decompression after spondylotic TCCS are controversially discussed in the literature. While Schneider et al. advised against any surgical intervention (posterior laminectomy and transdural discectomy at that time), there is increasing evidence from several recent studies that anterior decompression and fusion results in favorable neurological outcome [1, 2, 8, 10, 11, 13, 32]. Although early (< 24 h after injury) surgical decompression has been reported to be associated with improved neurological outcome after traumatic spinal cord injury (tSCI) [33,34,35], a recent web-based survey among Dutch surgeons found that patients with TCCS (and particularly those without spinal column and/or discoligamentous injury) are preferably treated less urgently than those with other forms of incomplete tSCI . Our current institutional guidelines are based on an expert consensus , which recommends early surgical decompression in patients with AIS grade C and worse as well as initial observation of neurological recovery in less severe cases and optional surgery at a later date. In addition to these recommendations, we consider hyperextension instability as an indication for decompression and ACDF irrespective of the severity of neurological impairment. Nonoperative treatment may result in repetitive hyperextension at the injured segment and resulting compression of the spinal cord during the healing period even with the use of a cervical orthosis, which may impair neurological recovery.
Several limitations of this study need to be noted. First, this is a retrospective study with all limitations associated with this study design. Second, the number of patients included is relatively small due to the strict inclusion criteria. The latter, however, allowed for a homogeneous collective of patients with profound spondylotic TCCS and well-documented intraoperative findings, although TCCS in general represents a heterogeneous syndrome. Nevertheless, patients with mild TCSS or rapid neurological improvement within the first hours were treated nonoperatively and were therefore excluded from this study due to the unavailability of intraoperative findings. Third, the assessment of postoperative neurological recovery was not part of this study.