Abstract
Context: Dorsal migration of the sequestered lumbar intervertebral disc is an unusual and underrecognized pattern of lumbar disc herniation associated with pain and neurological deficit.
Findings: Three patients presented with lower limb- and low back pain. MR imaging showed intracanalicular mass lesions with compression of the spinal cord and allowed precise localization of lesions in the extradural or intradural space. Diagnosis was straightforward for the patients with the posterior and anterior epidural disc fragments, whereas various differential diagnostic considerations were entertained for the patient with the intradural mass lesion. All patients underwent surgical removal of the sequestered disc fragments, and recovered full motosensory function. Surgical repair of the dura mater due to CSF leak was required for the patient with intradural disc herniation.
Conclusion/clinical relevance: Posterior and anterior epidural, and intradural disc migration may manifest with clinical symptoms indistinguishable from those associated with non-sequestered lumbar disc hernias. Missed, migrated disc fragments can be implicated as a cause of low back pain, radiculopathy or cauda equina syndrome, especially in the absence of visible disc herniation. A high index of suspicion needs to be maintained in those cases with unexplained and persistent symptoms and/or no obvious disc herniation on MR images.
Keywords: Intervertebral disc, Lumbar, Disc herniation, Epidural space, Intradural space, Low back pain
Introduction
The ruptured disc may be displaced, extruded, or sequestered and the detached disc fragments can migrate from the parent disc in rostral, caudal, and lateral directions within the spinal canal. Disc fragments usually migrate in the anterior epidural space, with posterior epidural and intradural migration being reportedly rare.1–4 Posterior epidural or intradural disc fragment herniation has been associated with variable neuromuscular symptoms, motosensory deficit, and cauda equina syndrome.2,4–6
Because of the rarity of this condition, in the lumbar spine, symptoms resulting from dorsal migration of the sequestered disc can easily be attributed to a trivial and uncomplicated lumbar disc herniation. Thus, in the presence of bearable symptoms, the condition is observed as chronic degenerative disc disease and the clinical course is protracted with both exacerbations and remissions. MR imaging is helpful in working up diagnostic dilemmas and surgical candidates. Three unusual, but characteristic patterns of dorsal sequestration of lumbar disc herniation in the form of posterior and anterior epidural, and intradural migration are presented to call attention to this challenging diagnosis.
Case reports
Case 1
A 72-year-old man presented at an outpatient clinic with progressive pain in the lower extremities for several days. Gradually worsening pain radiated in the anterolateral aspect of the thigh on both sides. He experienced no low back pain, or abnormal bowel or bladder function. Previous history was unremarkable for trauma, lumbar surgery, fever, weight loss, or other constitutional symptoms. On examination, the upper lumbar spine was tender to palpation. The straight leg raising test was negative and there was diminished patellar reflex, which was worse on the left leg than on the right. Motor strength was 3/5 proximally on the left leg and 4/5 on the right leg, and 4/5 distally in both legs. Ill-defined loss of sensation to light touch and pinprick was appreciated on the left thigh. Laboratory values were within normal limits. MR imaging of the lumbar spine revealed a posterior epidural mass lesion at the L2–L3 level, compressing the spinal cord. The lesion was of T1-weighted intermediate and T2-weighted increased signal intensity, relative to the intervertebral disc (Fig. 1A,B). Within the spinal canal at the L2–L3, axial T2-weighted MR images displayed a tract-like structure extending from the intervertebral disc to the posterior epidural mass (Fig. 1C). After administration of gadolinium-containing contrast material, peripheral enhancement of the epidural mass was seen (Fig. 1D). There was linear enhancement of the structure connecting the mass with the disc (Fig. 1E). An extruded disc herniation that enhanced in its periphery also was seen at this interspace.
Figure 1.
A 72-year-old man with progressive pain in the lower extremities (Case 1). A and B, Sagittal T1-weighted (A) and T2-weighted (B) MR images show large, epidural mass of intermediate and increased signal intensity (arrow), respectively, at L2-L3 spinal level. Note herniation of the disc at this interspace, and marked compression of the spinal cord by the mass lesion. C, Axial T2-weighted MR image shows disc fragment (f) in the posterior epidural space, displacing the spinal cord (arrow) to the right. A tract-like structure (arrowhead) of intermediate signal intensity is seen connecting the epidural mass with the posterior portion of the parent disc. D, Sagittal T1-weighted MR image with fat saturation after gadolinium administration reveals contrast enhancement at periphery of disc fragment (thin arrow). E, Axial T1-weighted MR image with fat saturation after gadolinium administration reveals rim enhancement of the epidural disc material (arrow) and linear, tract-like enhancement (arrowhead) originating from the disc to the posterior-left epidural space, indicating the route of disc fragment migration.
Decompressive laminectomy was performed on the day of presentation that allowed identification of bulky epidural disk material dorsally, which was removed along with the extruded L2–L3 disc. Following decompression of the spinal canal, the patient recovered uneventfully.
Case 2
A 33-year-old woman presented at the emergency department with a two-week history of persistent pain in the leg and dorsum of her left foot and mild low back pain, without any preceding trauma. She complained of subjective weakness of her left leg. She had no bladder or bowel symptoms and her medical history was unremarkable. On examination she had bilateral paravertebral muscle spasm. Straight leg-raising was positive at 30° on the left. The ankle reflex was decreased in her left lower extremity. Muscle testing showed weakness of the extensor hallucis longus and anterior tibial muscles. There was mild hypoesthesia involving the L4 dermatome on the left. Laboratory work-up was normal. MR imaging showed a degenerative and extruded intervertebral disc at L4–L5 and a small mass lesion in the dural sac exhibiting increased signal intensity on both the T1-weighted and T2-weighted images as compared to the disc (Fig. 2A). The lesion was better demonstrated on the axial MR images as an intradural mass occupying the posterior segment of the spinal cord on the right side (Fig. 2B). The lesion showed prominent enhancement after the administration of a gadolinium-containing contrast medium (Fig. 2C). The peripheral portion of the extruded disc displayed contrast enhancement and appeared to connect to the intradural mass lesion. On the axial MR images, there was peripheral, rim-like enhancement of the mass (Fig. 2D). Prompt surgery involving 2-level laminectomy to extend the exposure identified intradural migration of a herniated disc fragment, which was successfully removed with synchronous closure of the ventral dural defect. The patient recovered promptly.
Figure 2.
A 33-year-old woman with persistent pain in the left lower extremity (Case 2). A, Sagittal T1-weighted MR image reveals intradural mass (arrowhead) of increased signal intensity posterior to the herniated disc (arrow) at the L4–L5 interspace. B, Axial T2-weighted MR image shows intradural mass lesion (arrow) of heterogeneous increased signal intensity at the L4–L5 level. C, Sagittal T1-weighted MR image after gadolinium administration reveals contrast enhancement of intradural mass lesion (arrowhead) which maintains continuity with the herniated intervertebral disc (thin arrow). D, Axial T1-weighted MR image after gadolinium administration reveals peripheral enhancement (arrowhead) of the intradural disc fragment (f).
Case 3
A 26-year-old man presented at the emergency department with right anterior thigh pain and weakness, and mild lumbar pain for three weeks that worsened significantly after lifting a weighty box. On examination, the straight leg raising test was negative and there were diminished knee and ankle reflexes. Motor strength was 3/5 proximally and there was decreased pinprick sensation in the L4–L5 dermatomes of the lower right extremity. MR imaging disclosed an anterior epidural mass lesion at the L4–L5 level, compressing the thecal sac (Fig. 3). The lesion displayed MR imaging characteristics similar to those in case 1, but location within the epidural space was antipodal. At surgery within day of presentation involving decompressive laminectomy and discectomy the voluminous extradural disc fragment was removed and symptoms resolved completely.
Figure 3.
A 26-year-old man with progressive pain in the right lower extremity (Case 3). A, Sagittal T2-weighted MR image shows anterior epidural disc fragment of intermediate signal intensity (arrow) at the L4–L5 level. B, Corresponding coronal T1-weighted MR image with fat saturation after gadolinium administration displays disc fragment (arrow) with peripheral enhancement, compressing the spinal cord (SC). S, sacrum.
Discussion
Regardless of the anatomic location, the herniated (ruptured) intervertebral disc may become extruded or sequestered. The term “disc extrusion” indicates that despite rupture of the annulus fibrosus, the nucleus pulposus maintains its connection with the parent disc, whereas the term “disc sequestration” is used to designate complete separation of the disc fragment from the donor disc. In sequestered lumbar discs, the disc fragments typically migrate in the anterior epidural space and usually lodge into one of its lateral compartments.1 In a combined MR imaging- anatomic study, Schellinger and co-workers1 have attributed this pattern of disc migration to the anatomy of the constrained anterior epidural space, which is confined by the posterior longitudinal ligament and the peridural membranes attached to it.
In 1973, Lombardi7 was first to document migration of a disc fragment in the posterior epidural space and attracted attention to this rare complication of disc herniation. In 2011, the known reported cases – 47 in all – were summarized in the neurosurgical literature and clinical presentation of posterior epidural migration that is indistinguishable from the typical disc herniation was discussed.8 In that review analysis the association of derangements in the anatomy favoring disc fragment migration with rarity of the condition, was emphasized. More recently, Elsharkawy and co-workers reviewed the medical literature and found 111 cases of posterior epidural disc migration reported from first description of this entity up to now.9 Most patients with the condition were men, and the presenting symptoms were typically radiculopathy, cauda equina syndrome, and low back pain. Although virtually any spinal level may be affected, this complication of posterior epidural migration tends to have a predilection for the upper lumbar spine. Previous investigators have reported more frequent occurrence of posterior migration at L3–L4 (40% of cases), which may be due to the anatomical relationship between the nerve root and disc space in the horizontal plane, which appears to compromise the barrier role of the nerve root at this level.9–11
In accordance with previously reported experience8,10 in our patient diagnosis could not be instituted on the basis of clinical findings alone. Diagnosis of posteriorly migrated disc fragments can be notoriously difficult because sequestered disc fragments may appear as other, common epidural space-occupying lesions. Included among them are infections, tumors, trauma, degenerative disease changes, and iatrogenic conditions.2,9,12 Clinical findings of infection, homogeneous enhancement or no enhancement of the lesions, relationship with the facet joints and a cyst-like appearance in a synovial process would eliminate the above mentioned diagnostic considerations. In our patient MR imaging with and without the intravenous administration of contrast material readily depicted the migrated disc material into the epidural space, which was also surgically confirmed. The imaging findings of the lesion in our case were similar to those reported in the literature.2,13 We observed peripheral ring enhancement of the migrated disc fragment indicating the formation of granulation tissue.8 Interestingly, the tract-like structure connecting the sequestered disc with the posterior epidural lesion was suggestive of the route of migration of the disc fragment, as also indicated in previous studies.13
In our second case initial clinical diagnosis was that of disc herniation, presumably at the L4–L5 level. The MR imaging diagnosis entertained lumbar disc herniation (in L4–L5 and other levels) with concomitant intradural tumor at that level. Finally, the diagnosis was made intraoperatively with confirmation of the intradural migration of disc material. Intradural disc herniation is exceedingly rare, comprising 0.2–0.3% of all disc herniations.3,14 Clinical symptoms of intradural disc herniation are those of acute-on-chronic exacerbation of low back pain and cauda equina syndrome. Our patient presented with the new onset of pain she experienced other than the intermittent exacerbations of low back pain.
In the lumbar spine, intradural herniation usually occurs at the L4–L5 similar to our case.3 Although the exact mechanism of penetration of the dura mater by the sequestered disc is unknown, it has been postulated that congenital, post-traumatic, postoperative, or inflammatory adhesions, forming predominantly in the L4–L5 interspace between the posterior longitudinal ligament, the ventral aspect of the dura and the annulus fibrosus prevent lateral migration of the disc fragments.14–17 Penetration of a midline adhesion, in turn, allows for direct passage of the disc fragment from the anterior epidural space, through penetration of the ventral dura into the thecal sac.3,17,18 Mut and co-workers17 however, further classified intradural disc herniations into two distinct types according to migration of the disc fragment into the dural sac, or the dural sheath of a nerve root, that is, intraradicular disc herniation.
Although intradural disc herniation now appears to have a broader spectrum of features than initially recognized, in its classic form, this condition is observed as abrupt interruption of the posterior longitudinal ligament at the disc level with intrusion of a beak-like mass representing the disc fragment, in the dural sac.3,18,19 Typically, there is continuity of the herniated, migrating disc material with intradiscal nuclear material in the posterior portion of the ruptured annulus fibrosus.20 An association of intradural disc herniation with epidural gas has been reported as well.15,16 The imaging diagnosis of intradural disc herniation is difficult and the differential diagnosis is therefore broad. Consideration must be given to a number of intradural tumors, including schwanomma, meningioma, ependymoma, epidermoid and dermoid tumors. After the intravenous administration of gadolinium-containing contrast media, schwanommas and meningiomas demonstrate homogeneous enhancement, whereas in epidermoid and dermoid tumors enhancement is lacking. Finally ependymomas, which show high signal intensity on the T2-weighted images, unlike disc fragments, demonstrate abnormal marked enhancement after injection of contrast material. Furthermore, on the gadolinium-enhanced MR images the presence of rim-like, peripheral enhancement of the avascular, intradural disc fragment(s) is used to differentiate disc from tumor.3,12,18–22 This latter imaging characteristic corresponding to the formation of granulation tissue around the lesion and neovascularization indicates chronic herniation of the intervertebral disc.16,19,23 In our experience, the administration of gadolinium-containing contrast media in those cases with equivocal findings of disc herniation is considered sine qua non for diagnosis.
In a previous report Floeth and Herdmann24 addressed the pivotal role of high-resolution MR imaging in the investigation of spinal pathology. The authors were justified to comment on the frequent non-availability of preoperative, high-quality diagnostic MR imaging examinations, which may indeed jeopardize the management of patients with complicated disc herniations, requiring expertise and skill in (neuro)-surgical treatment. In another review study, authors realized MR imaging was the most frequently used imaging method to diagnose posterior epidural disc fragment migration.12 As also shown in our study, in expert hands, MR imaging not only suggests diagnosis but also allows pathologic processes to be precisely localized within the spinal canal. In accordance with previously reported experience recommending early decompressive surgery to prevent severe neurological deficits, our patients underwent surgical removal of the migrated disc fragment.9,12,25 Laminectomy with discectomy was performed to identify disc material at the thecal sac and the cord, with a favorable outcome documented as significant postoperative motor, sensory, and functional recovery. In the absence of cauda equina syndrome or complications related to surgery, the patients were discharged 3–5 days later.
Clinical evaluation at 1 month after surgery, clearly indicated complete resolution of the symptoms in all cases, thus suggesting no remaining migrated disc fragments.
Our three cases feature a classic presentation of sequestered lumbar disc herniation in the patterns of posterior, anterior epidural and intradural migration. We believe that disc fragment migration may be more common than it is documented or recognized. This perception however, is intriguing given the implications misdiagnosis of complicated disc herniation can have on failed back syndrome.17 By considering – at least, the migrated disc in the differential diagnosis of intracanalicular lesions, or in the presence of persistent or unexplained symptoms not amenable to treatment, diagnostic and surgical odysseys can be safely avoided.
Disclaimer statements
Contributors None.
Funding There was no funding for this work.
Conflicts of interest The authors report no conflicts of interest.
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