Spinal MRIs were performed using the Siemens Magnetom Aera 48 Channel 1.5 Tesla Machine (Siemens Healthcare GmbH, Erlangen, Germany) according to the standard protocol at our institution. T1W and T2W sagittal and axial images and phase contrast images were obtained for analysis.

Scan parameters used were as follows: (1) sagittal T1-weighted spin-echo (repetition time/echo time, 500/7.7 msec; section thickness, 4 mm; field of view, 230×230 mm); (2) sagittal T2-weighted spin-echo (repetition time/echo time, 2,000/87 msec; section thickness, 4 mm; field of view, 180×180 mm); (3) axial T1-weighted spin-echo (repetition time/echo time, 400/8.8 msec; section thickness, 4 mm; field of view 230×230 mm); and (4) axial T2-weighted spin-echo (repetition time/echo time, 4,500/99 msec; section thickness, 4 mm; field of view, 230×230 mm).

All MRI images were analyzed by two experienced radiologists. They noted the presence of VDDSC in 28 patients who were subsequently included in the study. The imaging criteria used to group the various pathological entities are described in detail in Table 1 [1234].

An arachnoid web/membrane is a milder form of VDDSC. Here, the septum posticum is fenestrated during development. Superimposed chronic degenerative disintegration of the septum may induce membrane formation, thick floating remnants, and adhesions in a subset of the population. Thick membranous remnants of the septum may result in arachnoid membrane/web formation (Fig. 2A, B). Arachnoid webs are likely to represent focal bands of arachnoiditis, but may be difficult to visualize on routine MRI sequences [6].

MRI findings include a mass effect on the posterior aspect of the thoracic spinal cord, causing flattening of the posterior margin [7]. There is also a mild ventral displacement of the thoracic cord at the involved levels without evidence of any mass or ventral cord herniation [8]. Cerebrospinal fluid (CSF) flow is preserved, as is the presence of CSF flow artifacts in the posterior subarachnoid space at that level. VDDSC, due to posterior focal indentation of the cord by the arachnoid bands, produces a ‘scalpel sign’ (Fig. 2C) [4]. There is a widening of the posterior subarachnoid space, causing progressive alteration of CSF flow dynamics. Adhesive membranes and turbulent CSF flow lead to cord compression. Long-standing arachnoid webs may result in syringohydromyelia; however, most patients are asymptomatic and the displacement is incidentally detected.

Arachnoid cysts are intra-arachnoid fluid filled cystic lesions. The presence of an arachnoid cyst and VDDSC is correlated [9], the most common location being the posterior subarachnoid space of the dorsal spine [29]. Intramural spinal arachnoid cysts appear to result from arachnoid trabeculae alterations. They may also occur secondary to CSF inflow into the septum posticum or through the arachnoid diverticula [4]. Intradural arachnoid cysts can thus be attributed to septum posticum derangement. Cysts cause a highly severe VDDSC compared with arachnoid membranes/webs. Hence, cysts can be grouped under moderate severity VDDSC.

Posterior intradural arachnoid cysts are diagnosed on the basis of their unique MRI findings. They appear as uniform fluid intensities on all MRI sequences, with loss of normal CSF pulsation artifacts during phase contrast imaging, with smooth symmetric anterior spinal cord displacements (Fig. 3A–D) [2].

Ventral spinal cord adhesion is defined as focal VDDSC without spinal cord herniation or intradural mass [3]. Anterior spinal cord herniation is the herniation of the spinal cord caused by a defect in the anterior dura mater [1].

MRI findings associated with ventral cord adhesion include focal VDDSC involving one or two vertebral segments in the upper thoracic spine and focal widening of the posterior subarachnoid space (Fig. 4A–D). Normal CSF flow artifacts are noted throughout the affected spinal cord levels without cord herniation [2]. Similar findings were observed in seven patients from our study group. Of these, one demonstrated a focal T2 cord hyperintensity.

The MRI findings of ventral cord herniation are typical, with cord herniation through the anterolateral or anterior dural defects. On sagittal section, an anterior C-shaped kink of the cord can be seen with an irregular posterior margin and expansion of the dorsal subarachnoid space (Fig. 5A, C). On axial section, the herniated cord is visible as a protrusion through the ventral dura mater with no intervening CSF (Fig. 5B, D). The herniated cord may be thinned out and may show signal changes due to cord atrophy. The presence of normal CSF pulsation artifacts and free CSF flow in phase contrast pulse cine MRI differentiates it from an arachnoid cyst. In the present study, 10 patients demonstrated spinal cord herniation through dural defects between the D3 and D7 vertebral levels. A focal widening of the dorsal subarachnoid space in all patients and focal cord hyperintensity in six patients was also observed. Ventral cord herniation caused posterior vertebral body scalloping in one patient.

Ventral spinal cord herniation and cord adhesion are the two ends of the same pathology, with cord adhesion being a less-severe form [8]. Because cord adhesion and herniation cause significant anterior displacement of the dorsal cord with pathological changes in the ventral dura, these entities can be graded as severe forms of VDDSC.

Despite several studies being conducted, the pathogenesis of these conditions still remains unclear. One study reports that the traction force generated by the anteriorly-placed Hoffman ligaments along with normal physiological kyphosis with normal ventral motion secondary to cardiac pulsations and pulmonary actions at that level, and the biomechanical impact of flexion extension movements on the thoracic spinal cord tend to pull the cord, causing VDDSC and subsequently leading to cord adhesion and herniation (more commonly in the thoracic level) [2510]. This keeps the cord in contact with the ventral dura. If this persists over time, it leads to irritation and inflammation [11], which ultimately ends in cord adherence over the ventral dura. If the process persists, it may eventually cause a ventral dural tear, resulting in a dural defect. CSF freely flows through the dural defects, leading to defect enlargement and tissue reaction. Dural defect widening and tissue reaction lead to spinal cord protrusion at the vertebral body [3].

Isu et al. [12] postulated that dorsal arachnoid cysts exert pressure effects over the spinal cord, and along with physiological events, lead to spinal cord adhesion and subsequent herniation, as described above [13]. Another study proposes an inflammatory etiology of spinal cord herniation at the intervertebral disk level. Intervertebral disk inflammation leads to adhesion with the adjacent ventral dura because of inflammatory thickening of the dentate ligament and arachnoid membrane. Subsequent resorption of the disk results in pathological cord displacement and eventual cord herniation [9].

Parmar et al. [3] stated that when a lax denticulate ligament fails to stabilize spinal cord movement during cardiac and respiratory actions, the spinal cord may anteriorly displace. Congenital dural deficiencies and ventral dural duplications can also lead to cord adhesion and herniation [14].

According to previous studies and the present one, dural defects along with physiological events alone cannot cause spinal cord adhesion and herniation; rather, spinal cord adhesions and herniations at the vertebral body and intervertebral disk levels can be explained by the following mechanisms.

Dural inflammation at the spinal cord adhesion site produces an extrinsic pressure due to turbulent CSF flow. This, along with posterior traction exerted over the dura due to repeated extension movement of the dorsal spine, increases dural stress ultimately resulting in dural tearing (Fig. 7A, B).

Rarely, a persistent neuroenteric canal associated with anterior spina bifida, anterior meningomyeloceles, or dorsal neuroenteric cysts leads to varying severity of VDDSC; these are considered congenital causes of VDDSC [61015].

In our study group, patients with arachnoid webs presented without symptoms and were incidentally diagnosed. Consequently, we graded this as a milder form without significant cord compression or need for surgical intervention (grade 1). Patients with arachnoid cysts presented with milder symptoms like back pain and VDDSC, not involving the ventral dura. We considered this etiology as grade 2. In these cases, the spinal arachnoid cysts require no immediate intervention, since surgery itself carries potential complications. If symptoms worsen over time, then intervention might be required. As with cord adhesion, cord displacement also involved the ventral dura and cord herniation, in addition to dural involvement with a protruding cord. Moreover, patients with cord adhesion and herniation presented with neurological symptoms like lower limb paraparesis and bladder and bowel disturbances. We considered these entities as grades 3 and 4, respectively; these grade pathologies required immediate intervention.

Because this was a retrospective study, we were unable to correlate these pathologies with the changes in patient condition; patient follow-up was also not possible. Distribution of the VDDSC spectrum from our study group and our proposed grading system, are indicated in Table 3.