Thoracic intervertebral disc sequestrum migrated into the posterior epidural space
Authors:
D. Vysloužil 1; V. Hobza 1; J. Jandura 2; A. Bryčková 3
Authors‘ workplace:
Neurochirurgická klinika FN Hradec, Králové
1; Radiologická klinika FN Hradec Králové
2; Neurologická klinika FN Hradec Králové
3
Published in:
Cesk Slov Neurol N 2025; 88(2): 118-120
Category:
Letter to Editor
doi:
https://doi.org/10.48095/cccsnn2025118
Dear Editor,
disc herniation occurs most frequently in the lumbar region, followed by the cervical spine. Disc herniations of the thoracic spine are less frequent (0.25-1% of all disc herniations), which is stabilized by the rib cage compared to the cervical spine, its discs are less bulky and bear less load than the lumbar discs [1].
Up to 75% of thoracic herniations are found below the level of Th8 and most often in the most mobile segment of Th11/12. Medial hard osteochondral mounds are typical for the thoracic spine and are encountered in up to 40% of cases. Here, soft prolapses tend to be localized mediolaterally to laterally [1].
Although prolapse of the thoracic intervertebral disc is a less common diagnosis, there are descriptions of large series, e.g. by Quin et al [2] and Quraishi et al [3].
If part of the herniated disc loses continuity with the disc, we speak of a sequestrum, which may travel through the spinal canal, most commonly through the anterior epidural space cranially or caudally or laterally [1]. Rarely, a laterally migrated sequestrum travels to the posterior epidural space [4-7].
Migration of sequesters into the spinal canal under normal anatomical conditions is prevented by the posterior longitudinal ligament and the lateral diaphragm, medially attached to the posterior longitudinal ligament and laterally to the spinal canal wall. If the sequestrum penetrates this barrier, it usually arrests in the neuroforamen against the spinal nerve root. The epidural fat and venous plexus also have a barrier function [4-6].
Previous discogenic asymptomatic difficulties predispose to migration into the dorsal epidural space, when adhesions between the anulus fibrosus and the dural sac occur. The adhesions obturate the anterior epidural space, and the sequestrum must therefore continue laterally. Furthermore, dorsal migration of the sequestrum is predisposed by lateral tears of the anulus fibrosus, from where the sequestrum passes along the medial surface of the pedicle. Anatomical variations are another predisposition. Abnormal position of the intervertebral disc, cranial or caudal position of the neuroforamen, which are associated with an abnormal position of the nerve root, allow the sequestrum to penetrate into the posterior epidural space [4-6].
Dorsal migration of the thoracic disc sequestrum is a very rare condition, but not known in the literature [4-7].
Dorsal migration of lumbar intervertebral disc sequesters is pathophysiologically similar [4-6]. This phenomenon was first described in the literature by Lombardi in 1973 [8]. We have more literature sources on this issue, due to its higher frequency. For example, large ensembles are described by Akhaddar et al [9] and Elsharkawy et al [10].
We encountered a dorsally migrated sequestrum of thoracic disc herniation in a 60-year-old patient, an active smoker, with no previous vertebrogenic complaints, who felt sudden pain in the lumbar spine when handling furniture and carrying its contents during a rotational sitting movement with a load in his hands. The pain pseudoradicularly propagated along the back of the thighs bilaterally. He was seen in a neurological outpatient clinic three days later because of worsening pain. He denied propagation of pain and paresthesias to the lower limbs, sphincter disturbances and perianogenital sensation. Objectively, he was free of pareses, walking with an antalgic component. After examination, he was discharged home with a diagnosis of vertebrogenic algic syndrome of the lumbar spine with bilateral pseudoradicular syndrome.
On the eighth day after the onset of the difficulties, the patient could not move his right lower limb normally on waking in the morning and could not stand up. In the neurological outpatient clinic, he was objectively found to have impaired sensation distal to the groin and buttocks bilaterally and paretic to plegic involvement of the right lower limb. The patient reported that after urinating he had to go again in ten minutes when he finished the rest. After insertion of the indwelling urinary catheter, 300 mL of residue was voided, which the patient did not feel. An analgesic infusion with corticosteroid (Dexamed 8 mg/2 ml, Medochemie Ltd., Lemesos, Cyprus) was administered.
Given the history of previous vertebrogenic complaints, a spinal lesion was suspected. Non-contrast MRI of the lumbar and thoracic spine was performed and severe secondary stenosis of the primary narrow spinal canal with mild compressive myelopathy was noted at the Th11/12 level. The stenosis was due to a protrusion of the disc, followed by a herniation on the right and an oval mass in the posterior epidural space, which in the differential diagnosis most likely corresponded to a sequestrum; the possibility of meningioma and hematoma was also considered (Figures 1 and 2). A small Th10/11 disc protrusion with slight impingement into the spinal cord on the right was also described. Examination with contrast medium was not performed because the patient did not tolerate further examination due to pain.
(B) hernia Th11/12, (C) sequester.
sequester, (C) spinal cord.
The patient was acutely admitted to the Neurosurgery Clinic. On admission, hypesthesia of the lower limbs bilaterally symmetrically distal to the level of the groin and buttocks and a sensation of cold feet were found. Objectively paretic involvement of the right lower limb. Mingazzini inhibited drop to the mat, actively lifting the thigh to about 15° at the hip and lifting the entire limb flexed at the knee about 10 cm above the mat. Additionally, extension in the right knee was laterally impaired. More markedly, mobility was impaired in the right ankle, where plantar flexion was weakened against resistance, and dorsal flexion from neutral position was only suggested by the patient. Patellar hyporeflexion on the right, Achilles tendon hyperreflexion on the left, and a positive Babinski sign bilaterally were present. We attributed the improvement in neurostatus to the administration of a corticosteroid infusion. The left lower limb was free of paresis. Defecation was unremarkable. Initial lab work was normal.
In the evening, we performed a total laminectomy of Th11 and a partial laminectomy of Th12. After the laminectomy, we sequentially removed a large number of small softened sequesters epidurally and to the right of the foramen, followed by a partial foraminectomy and release of the Th11 root, around which we still observed and removed several smaller sequesters, partially localized subligamentally. We did not penetrate the disc itself. The procedure was uneventful, with a blood loss of 350 ml. A Redon drain was introduced and removed on the second postoperative day. The drain still lost about 400 ml.
The following morning, the patient reported improved sensation in the lower extremities and objectively, the mobility of the right lower extremity was improved - he was actively elevated above the mat in the hip to about 30°, and the range of dorsiflexion in the right ankle was increased. This improvement occurred prior to the initiation of rehabilitation, anti-edema treatment and vitamin therapy, which were started on the first postoperative day. The indwelling urinary catheter was intermittently closed after 4 h, the patient felt the bladder filling well, and normal volume portions of urine were voided at his request. On the second postoperative day, the urinary catheter was removed and the patient continued to urinate spontaneously. The patient was verticalized during the first postoperative day and training of walking in a high walker was started, in which he was walking independently from the second postoperative day.
In the differential diagnosis of pathological formations of the posterior epidural space we consider a tumor mass, epidural hematoma, or abscess, or synovial cyst. The diagnosis of sequestrum is based on the structural connection of the mass with the intervertebral disc. Similarly, we differentiate a synovial cyst if its association with the facet joint is evident.
The gold standard for differential diagnosis in this area is MRI with contrast agent. The sequestrum appears as hypo-/isosignal on T1WI and hypersignal on T2WI, and is peripherally opacified (saturation of ingrowing granulation tissue and neocapillary epidural fat) after contrast agent administration [4]. Such a finding also resembles a tumor lesion, epidural hematoma or abscess. A history of trauma or surgery leads to the diagnosis of epidural hematoma. A fresh hematoma will not saturate with contrast medium in the periphery. Clinical and laboratory evidence of inflammation leads us to the diagnosis of an abscess. Metastases saturate well with contrast, also causing skeletal changes. Knowledge of the cancer history is a clue, although it may be the initial manifestation of a previously unrecognized cancer. Meningeomas are iso-/hypersignal in T2WI and also have good homogeneous contrast uptake [4,7].
However, definitive certainty can sometimes only be obtained peroperatively [5]. If diagnostic uncertainty persists, some authors complement histological examination with the finding of fibrocartilaginous tissue with foci of calcification and lymphocytic infiltration [4,6].
Conflict of interests
The authors declare that they have no conflict of interest in relation to the subject of the study.
This is an unauthorised machine translation into English made using the DeepL Translate Pro translator. The editors do not guarantee that the content of the article corresponds fully to the original language version.
Sources
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3. Quraishi NA, Khurana A, Tsegaye MM et al. Calcified giant thoracic disc herniations: considerations and treatment strategies. Eur Spine J 2014; 23 (Suppl 1): S76–S83. doi: 10.1007/s00586-014-3210-5.
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6. Morizane A, Hanakita J, Suwa H et al. Dorsally sequestrated thoracic disc herniation – case report. Neurol Med Chir (Tokyo) 1999; 39 (11): 769–772. doi: 10.2176/nmc.39.769.
7. Miyakoshi N, Hongo M, Kasukawa Y et al. Posteriorly migrated thoracic disc herniation: a case report. J Med Case Reports 2013; 7 : 41. doi: 10.1186/1752-1947-7-41.
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Paediatric neurology Neurosurgery NeurologyArticle was published in
Czech and Slovak Neurology and Neurosurgery
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