Spontaneous intradural disc herniation with focal distension of the subarachnoid space in a dog

Abstract

Myelo-computed tomography of a paraparetic 14-year-old dog revealed subarachnoid distension with an intradural filling defect above the T13–L1 disc space. T12–L1 hemilaminectomy followed by durotomy allowed removal of a large piece of degenerated disc material that compressed the spinal parenchyma. Full return to function was achieved 10 days post-surgery. The distension was likely secondary to the intradural herniation, and is a rare and distinct finding.

Spontaneous intervertebral disc extrusions produce varying degrees of extradural compressive myelopathy. It is unusual for extruded material to penetrate the dura and enter the spinal cord (1). Dural penetrating disc herniations are rarely reported in the veterinary literature. Ten cases of possible intradural or intramedullary disc extrusions (2–9) have been reported, among which only 5 were confirmed at surgery (5–9) and only 1 had a secondary subarachnoid fistula associated with the disc extrusion (5). All but 1 (6) had a traumatic event following physical activity (running, jumping, racing) and all but 2 (6,7) had dural tear with extradural leakage of contrast medium. The formation of a secondary subarachnoid distention that can mimic a subarachnoid cyst is even less common and has been reported only once (5). Most subarachnoid cysts are thought to be congenital, but they have been reported in association with trauma, intervertebral disc disease (IVDD) and post spinal surgeries (10–12).

We present the first case of a spontaneous disc herniation that penetrated the dura to form a secondary subarachnoid cyst with a large component of the degenerated disc material lying against and compressing the spinal cord. No evidence of dural tear or leakage was observed on preoperative images. The diagnosis was made preoperatively based on myelo-computed tomography findings. The dog was treated surgically with hemilaminectomy followed by durotomy and recovered uneventfully.

Case description

A 14-year-old spayed female mixed-breed dog, weighing 9.3 kg was presented to the Koret School of Veterinary Medicine Teaching Hospital (KSVMTH) with an acute onset of non-ambulatory pelvic limb paresis. In the previous week the dog had experienced difficulty rising with normal ambulation. The left front leg had been amputated 6 years prior to the current presentation due to an old injury. The results of the rest of the physical examination were unremarkable. Neurological examination revealed mild voluntary motor movements in both hind limbs with the left being worse than the right. Conscious proprioception was decreased on the right and absent on the left hind limb. No back pain was elicited and spinal reflexes were normal bilaterally. An asymmetric T3–L3 myelopathy was suspected with differential diagnoses that included: IVDD, vascular event, neoplasia, trauma, fibrocartilaginous emboli, larval migration of Spirocerca lupi and acute myelitis. Complete blood cell count and serum biochemistry results were within reference ranges; an electrocardiogram was unremarkable.

Survey radiographs revealed spondylosis deformans throughout the vertebral column from T10 to S1 with narrowing of the T12–T13 and T13–L1 intervertebral disc spaces. A myelogram, performed through lumbar puncture using 3 mL of iohexol (Omnipaque, 300 mg/mL; Nycomed Imaging AS, Oslo, Norway), showed both ventral and dorsal attenuation of the dye column over the T12–T13 disc space with marked ventral contrast medium accumulation cranial to the compression site (Figure 1A). Mild attenuation of the ventral subarachnoid space over the T13–L1 intervertebral disc space was also noticed. A ventrodorsal view at the T12–T13 intervertebral disc space revealed 2 round radiolucent filling defects on the left side of the spinal cord within the area of the accumulated contrast medium (Figure 1B).

Figure 1.

Lateral and ventrodorsal views of the dog’s spine following injection of iohexol through a L5–L6 lumbar puncture. A — Note the severe ventral compression (black arrow) and contrast medium accumulation cranial to the point of compression at the level of T12–T13 disc space (arrowhead). There is mild attenuation of the ventral subarachnoid space over the T13–L1 disc space. B — Ventrodorsal view of the affected spinal cord segment showing widening of the left subarachnoid space at the level of T12 cranial to the intervertebral disc space with left spinal cord compression and 2 radiolucent circular filling defects centered in the middle of the fluid accumulation (arrows).

Transverse (Figure 2A), reconstructive sagittal (Figure 2B) and reconstructive coronal (Figure 2C) views of a computed tomography (CT) scan performed following the myelogram revealed widening of the left subarachnoid space at the level of T12 cranial to the intervertebral disc space. The spinal cord appeared compressed by the contrast medium accumulation and by the circular filling defect centered in its middle. Extradural ventrolateral compression was also noted over the T13–L1 intervertebral disc space, primarily on the right.

Figure 2.

Transverse and reconstructive sagittal and coronal views of T12–T13 spinal segments. CT scan was performed following a myelogram. A — transverse section cranial to intervertebral disc space T12–13; note the widening of the subarachnoid space with fluid accumulation and a filling defect in the middle (arrow). B — sagittal reconstructive image showing the intradural ventral compression at the T12–T13 disc space with contrast medium accumulation and filling defect (white arrow). Extradural compression at the T13–L1 disc space is also noted. C — coronal reconstructive image at the level of T12–T13; note the intradural compression on the spinal cord with the contrast accumulation and the circular filling defect located in the middle.

Based on the acute spontaneous onset, the accordance between the neurolocalization of the lesion and the imaging findings, our main differential diagnosis was intervertebral disc extrusion that had penetrated the dura mater at T12–T13 and was compressing the cord and causing the widening of the subarachnoid space. A right-sided T13–L1 extradural disc extrusion was also suspected. Neoplasia as well as other causes for the spinal fluid accumulation at the level of T12–T13 could not be ruled out but seemed less likely.

A left-sided large hemilaminectomy extending from the cranial borders of T12 to the end of T13 was performed. Removal of a small amount of disc material from the spinal canal at this location enabled the surgeon to detect an adhesion between the dura matter and the ruptured annulus. Cranial to this adhesion, a fluid-filled cystic cavity was detected beneath the dura matter. A 5-mm durotomy above the observed cyst revealed a large amount of degenerated disc material within the subarachnoid space embedded in the pia and compressing the cord. The disc material was carefully removed to allow reduction of the dura’s swelling and decompression of the spinal cord. The dura was left open and an absorbable gelatin sponge (Cutanplast; Mascia Brunelli, Millano, Italy) was placed over the hemilaminectomy site to attenuate the CSF leakage and protect the cord. A right-side hemilaminectomy performed at T13–L1 articulation revealed a moderate amount of hard bulging chronic disc that was also removed. Closure was routine at both sites and recovery was uneventful. The dog was able to walk on the second day after surgery, although she was still ataxic. No neurological abnormalities were detected at the follow-up examination 10 days after surgery, and the dog was still doing well 12 mo later.

Histological evaluation of the tissue removed from the subarachnoid space confirmed its origin to be degenerated fragments of cartilage. The largest piece was composed of hyaline cartilage and in most of the remaining pieces the chondroid matrix contained fibers consistent with fibrocartilage. The degenerate hyaline cartilage is typical of extruded disk material.

Discussion

Intradural extrusion of disc material is a rare form of IVDD in dogs (1) and the formation of a secondary subarachnoid widening is even less common. In humans, intradural disc herniations are considered rare and account for 0.26% to 0.30% of disc herniations (13). Ten dogs with presumptive or definitive intradural or intramedullary disc herniations were reported in the veterinary literature, most of which (9/10) occurred during excessive physical activity such as jumping, running, or racing and the event was considered traumatic. Post myelogram contrast leakage was reported in 8 of these 10 cases (2–9), suggesting a dural tear. Five dogs (5/10) had mild spinal cord compression and were treated conservatively (2,3). Three dogs were euthanized (3/10) and were found to have disc material within the spinal cord parenchyma at postmortem examination (7–9). One dog was operated on and intramedullary disc material was successfully removed from the spinal cord (1/10) (6), and 1 that was diagnosed with subarachnoid-pleural fistula and a dural tear was found to have intradural disc material at surgery (1/10) (5).

We report the first case of a spontaneous intradural disc herniation in which a pre-surgical diagnosis was made using routine lumbar myelogram followed by CT scanning of the disrupted spinal cord segments. Finding of an intradural extramedullary space-occupying lesion as was seen in our case is usually associated with neoplasia (14). In our dog the lesion was located above the disc space, a component of extradural compression was also present, and the acute onset of clinical signs led us to the presumptive diagnosis of intradural disc herniation. The spinal fluid accumulation cranial to the disc material was caused by widening of the subarachnoid space at this point and is better interpreted as an enlarged “golf tee” sign rather than a secondary arachnoid cyst. Contrast accumulation at the site of a current or previous disc herniation was reported previously in 2 dogs and 1 cat (10,11). In 2 of the reports (1 dog and 11 cats) the so-called cyst was only apparent a few years following surgery that was performed to remove a herniated disc at T13–L1 and L1–L2 intervertebral disc spaces, respectively (10). Another report described a dog with a subarachnoid cyst and extradural ventral compression due to a disc herniation at C6–C7 intervertebral disc space that was assumed to be the cause of the contrast accumulation at the same site (11). As in the case reported here, contrast accumulation with no leakage was observed in all previous reports but no intradural disc component was detected on imaging or at surgery in any of these 3 cases. In our dog, the subarachnoid distention was identified at the ventral aspect of the spinal cord unlike the previous publications in which the pseudo-cyst was detected at the dorsal part of the subarachnoid space, as in most cases of secondary and primary subarachnoid cysts reported in the veterinary literature (10,11). No contrast medium leakage was evident on imaging studies of our patient, nor was a dural tear or minor CSF leakage observed during surgery. Blockage of the tear by the disc fragment or adhesions formed between the disc material and the dura mater can explain the lack of CSF leakage in the present dog. Although we assume that the subarachnoid distention in our dog was secondary to the intradural disc extrusion, we do not have pre-herniation imaging hence the presence of the subarachnoid distention prior to the extrusion cannot be completely ruled out and may even have predisposed our dog to the intradural extrusion due to adhesions of the dura to the dorsal longitudinal ligament in the area.

Definitive pre-surgical diagnosis of intradural disc herniations is considered difficult in humans, and the diagnosis is often made during surgery (15,16). The presence of a small, post myelogram, filling defect located over a disc with no sign of enhancement on CT scanning following intravenous contrast administration and with the same density as that of the intervertebral disc, is highly suggestive of intradural disc herniation. In our dog, the small mass detected within the subarachnoid space appeared to have similar density as the intervertebral disc both on the myelogram (Figure 1B) and on the coronal CT view (Figure 2C). Magnetic resonance imaging (MRI) is considered the preferred diagnostic modality for intradural disc herniation in humans. In contrast to the acute onset reported in dogs, the disease in humans tends to be chronic and to provoke a reactive inflammatory response with formation of vascular granulation tissue around the herniated disc. This process accounts for the unique ring enhancement surrounding the disc fragment on post contrast T1-weighted images highly suggestive of intradural disc herniation. In more acute events in humans, resembling the ones reported in dogs, the herniated disc material is not yet sequestered by granulation tissue nor has it developed the vascularization that is the basis of the ring enhancement, thus making pre-surgical diagnosis more challenging. One presumptive diagnosis of intramedullary disc herniation based on MRI is reported in the veterinary literature. In that dog the degenerated tissue removed from within the spinal parenchyma at surgery was sent to histology and found to be disc material (6).

The present case is the first that describes a spontaneous intradural disc herniation in a dog with a suspected secondary cyst-like distention of the subarchnoid space with contrast medium accumulation, in which the pre-surgical diagnosis was achieved by myelogram followed by CT scanning of the involved spinal segments. It is thought that sudden trauma may tear the annulus causing an explosive extrusion of healthy nucleus pulposus that produces a strong contusion injury with less compression effect than when associated with mineralized material of degenerated disc (17). However, some of these disc extrusions may involve a large volume of nucleus pulposus as well (18). In our dog the degenerative changes were evident throughout the spine indicating a long-standing instability. The disc extrusion was acute and spontaneous and the material removed from the intradural space contained degenerated hyaline cartilage typical of extruded disc material.

In the present case we assume that degenerated intervertebral discs, spondilytic changes, and chronic inflammation resulted in the dural adhesions to the dorsal longitudinal ligament that were noted at surgery. These adhesions prevented the normally movable dura matter from shifting and accommodating the extruded disc in the extradural space. The weakened dura was then ruptured enabling the disc material to penetrate the subarachnoid space. The fluid-filled cavity was subsequently formed cranial to and around the fragments of disc material due to spinal fluid accumulation in the gap formed between the arachnoid and the pia matter. It was the accumulation of contrast medium in this cavity that enabled us to make the diagnosis of intradural disc extrusion.

We conclude that an intradural disc extrusion is a possible differential diagnosis in cases of both traumatic and spontaneous disc herniation and should be considered whenever a fluid-filled cavity is evident above or slightly cranial to the suspected herniated disc space. Furthermore, it is important to note that not seeing any contrast medium leakage does not preclude the possibility of a penetrating intradural or intramedullary disc extrusion. The use of myelogram followed by CT scanning is a well-accepted method for the diagnosis of IVDD and proved to be valuable in demonstrating the presence of fragmented disc material in the dilated subarachnoid space in our patient. CVJ