Ventral spinal cord herniation was first described in 1974 by Wortzman et al., when a herniated spinal cord was incidentally noticed during a thoracotomy operation for disc herniation (1). Since then, more than 246 cases have been reported in the literature (2). Due to this increased reporting of the disorder, a sufficient level of awareness has been created among clinicians (3).

The pathomechanism of this disorder is a ventral displacement of the spinal cord across a defect in the dura, leading to ventral adhesion to the vertebra. Because of the constriction of the spinal cord, blood flow to the herniated part decreases gradually, which leads to progressive ischemic myelopathy and neurological impairment. Symptoms may manifest before a herniation can be detected on magnetic resonance imaging (MRI). Idiopathic spinal cord herniation (ISCH) generally occurs in the upper thoracic spine, most often with the involvement of the T 4—T 8 level (4). Also most often, herniation occurs anteriorly to the spinal cord, with only two cases reported of a herniation that occurred posteriorly (5, 6).

A total of five patients (mean age: 66.2 ± 5.97 years) with spinal cord herniation underwent surgery at the Department of Neurosurgery of the University of Tuebingen between January 2015 and May 2023. Out of these five, we found one patient with spinal cord herniation associated with an intraspinal bone spur (also referred to as osteophyte). This finding of an intraspinal bone spur is in line with only a few previously reported cases (7–10).

A 56-year-old male patient suffered from a progressive myelopathy with features of the Brown-Sequard syndrome, which persisted for over a year. A neurological examination revealed an ataxic gait, limited walking distance, monoparesis (M4) of the right leg flexor, increased reflexes of the lower right extremity, and hypoesthesia for pain, touch, and temperature of the left leg and up to a level of T 7. Babinski sign was negative. The patient did not have any history of trauma, central nervous system inflammation, or spinal manipulation.

A magnetic resonance imaging of the spine revealed spinal cord displacement to the ventral location of the spinal canal at the level of T 6/7, a possible adhesion of the cord tissue to the upper part of the T 7 dorsal vertebral body, and a hyperintensity of the spinal cord in T2-weighted imaging at the same level (Figures 1A,B). In addition, disc protrusions at levels T4/5, T 7/8, and T 10/11 were present with a slight compression of the spinal cord at level T 7/8, which was below the spinal cord herniation. A supplementary thin-sliced computed tomography of the spine revealed a bone spur at the level of T 6/7 (Figure 2). Because of the progressive neurological deficits and correlated radiological findings, the option of surgical repair of the spinal cord herniation (laminectomy of T 6 and T 7, microsurgical release of the herniated spinal cord, and closure of the ventral dural defect) was discussed with the patient.

To date, many different pathophysiological factors have been postulated as a potential etiology for spinal cord herniation. However, no specific etiologic factor has been found.

One factor that has been suggested is congenital malformation (11, 12). What is critical to this suggestion is that there is delay in the occurrence of symptomatology; it occurs only during one’s middle age. However, the exact reason for the delayed occurrence of herniation is inadequately accounted for at present. One proposition (13) is that symptomatology might predate herniation, which accounts for the fact that a structural abnormality already exists at the herniation level; however, it does not explain why herniation per se should be delayed (14).

Previous studies have demonstrated that a congenital duplication of the ventral dura allows herniation of the spinal cord through the inner dura, which is possibly attributable to a neurenteric canal remnant. The spinal cord herniates within this defect and becomes strangulated, causing neurological deficits; this has been reported by Tyagi et al. (15).

According to Najjar et al. (16), it seems to be an acquired condition possibly caused by an inflammatory process, which results in adherence between the spinal cord and the dura, with erosion, formation of a dural defect, and then herniation occurring with cerebral spinal fluid (CSF) pulsations.

Reports about traumatic events associated with spinal cord herniation have also been published (17, 18). However, one must be careful not to attribute trauma as the scientific cause of the dural defect if no injury is reported at the relevant level (19). Often times, there is spontaneous cord herniation with a history of irrelevant or trivial trauma not differentiated from actual post-traumatic spinal cord herniation (18). In case of fractured vertebra, there is a sharp dural tear with herniation at the same level due to a fractured bone (20) or a penetrating (i.e., stab) injury (21) at the level of herniation, which may be legitimate post-traumatic cord herniation. This etiology may also be identified by its characteristics, which differ from those of non-traumatic spinal cord herniation. In traumatic spinal cord herniation, the level of herniation is not typically mid-thoracic ventral occurring mainly in middle age, but spinal cord herniation occurs at the level of trauma, which may be cervical or low-thoracic. Herniation may also occur at the dorsal level instead of at the ventral level, may be associated with nerve root avulsion, and occur at any age (22, 23).

Intraoperatively, an enlarged posterior arachnoid space can also be identified in a majority of patients which has to be differentiated from posterior arachnoid cyst (2, 3). Rather it is a co-occurrence due to the changed anatomy of the spinal cord with a reduced caliber and an increased amount of posterior intraspinal space.

ISCH almost always occurs at the thoracic level; this may be attributed to the anatomical characteristics of the thoracic spinal cord, with its typical kyphotic curve leading to the ventral position of the spinal cord in relation to the cervical and lumbar regions. During the performance of daily activities, the flexion and extension of the thoracic spine may lead to dural injury when there is an associated vertebral bony spur. It may lead to unrecognized trauma to the ventral dura mater and further dural laceration and spinal cord herniation. Dorsal thoracic dural defect with posterior spinal cord herniation has been reported only twice so far. Dorsal spinal cord herniation causing a perforation of the posterior elements has also been reported (5, 6).

The spinal cord develops adhesions to the dural defect and gradually becomes strangled, which, in turn, results in strangulation of the spinal tracts. The consequent tethering/distortion and ischemia of the neural elements lead to neurological deficits such as Brown-Sequard syndrome and paraparesis. A diagnosis of spinal cord herniation requires that the patient undergo an MRI of the spine. For symptomatic patients, operative retrieval of the herniated spinal cord and repair of the dural defect are recommended. Two different techniques are employed: one is direct closure of the defect by primary suturing and the second is placement of an artificial dural graft in some patients, which is accompanied by an enlargement of the dural defect to facilitate cord retraction. Widening of the dural defect is significantly associated with postoperative improved neurological functioning (2). Intraoperative ultrasound may be helpful in detecting the location of the herniation (24, 25).

In addition to the few previously reported cases (7–10), our case shows that intraspinal spur and disc herniation may be a cause of spinal cord herniation (similar to the pathophysiology of intracranial hypotension). Bone spur occurs exactly at the spinal cord herniation level, which is highly suggestive of the origin of the herniation. Mechanic stress caused by bone spur may lead to dural defect, followed by a herniation of the spinal cord through this defect. CSF leakage in the thoracic epidural space following dural laceration leads to CSF leakage with intracranial hypotension and position-dependent headache (9, 10). In 28.9% of ISCH patients, an extradural fluid can be detected (26). As a consequence, a decreased pressure in the thoracic epidural space facilitates the herniation process. In our patient, below the level of the herniation, at T 7/8, there was disc protrusion, which could lead to altered CSF flow and enhance herniation through a dural tear. Intraoperatively, at the spinal cord herniation level, a disc protrusion was identified, which was not very visible on preoperative MRI probably because of an anterior herniation of the spinal cord, subsequently, it was resected.

Tight dural closure is important for preventing dural leakage postoperatively. Otherwise, there is a risk for the development of intracranial hypotension and consequent subdural hematoma with neurological deterioration (27).

Brus-Ramer and Dillon (26) analyzed 70 published cases of patients with spinal cord herniation with associated disc protrusion and accompanying osteophytes. This study showed that in 67.1% of patients, herniation occurred at the disc level. In 30.2% of patients, there was herniated nucleus pulposus, and in 30.2%, osteophytes occurred. Because of this high percentage of associated nucleus pulposus herniation and osteophytes, it may be concluded that this factor plays a role in the pathogenesis of spinal cord herniation.

In this study, we reported a case of a patient with spinal cord herniation at the thoracic level, which was most probably attributed to a vertebral bone spur–induced dural tear and associated disc protrusion at the herniation level. Because of the kyphotic structure of the spine, sheering force exerted on the dura by movement, finally leading to dural rupture. Consecutive CSF leakage may result in intracranial hypotension. Because of altered CSF flow, the spinal cord may finally herniate through the defect in the dura. Strangulation of the cord leads to spinal cord impairment and clinical Brown-Sequard syndrome or spastic paralysis.

In addition to previously reported cases, our case supports the theory that intraspinal bone spur may cause spinal cord herniation and intracranial hypotension because of CSF leakage.