Saad Moussa Elmi1,2, Alngar Djimrabeye1,2, José Dimbi Makoso1,2, Rayhane Hamdaoui1,2
  1. Department of Neurosurgery, Ibn Sina University Hospital, Rabat,
  2. Faculty of Medicine and Pharmacy, University of Mohammed V, Rabat, Morocco.

Correspondence Address:
Saad Moussa Elmi, Department of Neurosurgery, IBN SINA University Hospital, Rabat, Mohammed V University of Rabat, Morocco.


Copyright: © 2023 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

How to cite this article: Saad Moussa Elmi1,2, Alngar Djimrabeye1,2, José Dimbi Makoso1,2, Rayhane Hamdaoui1,2. Spinal cord compression caused by a brown tumor secondary to primary hyperparathyroidism. 24-Mar-2023;14:108

How to cite this URL: Saad Moussa Elmi1,2, Alngar Djimrabeye1,2, José Dimbi Makoso1,2, Rayhane Hamdaoui1,2. Spinal cord compression caused by a brown tumor secondary to primary hyperparathyroidism. 24-Mar-2023;14:108. Available from:

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Background: Brown tumors (BTs) are rare non-neoplastic lesions that arise secondary to hyperparathyroidism largely involving mandible, ribs, pelvis, and large bones. Spinal involvement is extremely rare and may result in cord compression.

Case Description: A 72-year-old female with the primary hyperparathyroidism developed a thoracic spine BT causing T3–T5 spinal cord compression warranting operative decompression.

Conclusion: BTs should be included in the differential diagnosis in lytic-expansive lesions involving the spine. For those who develop neurological deficits, surgical decompression may be warranted followed by parathyroidectomy.

Keywords: Brown tumor, Primary hyperparathyroidism, Spinal cord compression


Brown tumors (BTs) are rare benign and non-neoplastic lesions that arise secondary to hyperparathyroidism (i.e., primary, or rarely secondary).[ 6 - 11 ] They most commonly involve the mandible, ribs, pelvis, and large bones, and only rarely the spine.[ 7 ] Here, a T3–T5 thoracic BT, arising secondary to hyperparathyroidism, contributed to cord compression and a paraparetic deficit that resolved following decompressive surgery.


Clinical presentation

A 72-year-old female presented with the upper back pain of 6 months’ with one month of acute worsening associated with the onset of paraparesis (i.e., 3/5 deficit). Laboratory studies showed; a serum calcium level of 144 mg/L (normal: 90–105 mg/L) and a slightly high parathyroid hormone level (pg/mL; normal is 10–53 pg/mL). A thyroid ultrasound proved negative, but the parathyroid scintigraphy with Tc-99 m showed focal activity in the inferior right thyroid lobe consistent with a parathyroid adenoma.

Spine computed tomography (CT) and magnetic resonance (MR) studies showing cord compression due to BT at T3–T5 levels

Both the CT and MR studies showed BTs compressing the cord from T3 to T5 secondary to hyperparathyroidism. The thoracic CT demonstrated multiple osteolytic lesions of the vertebral bodies and posterior elements from Th3 to Th5 level [ Figure 1 ]. The thoracic MR thoracic revealed a large expansile T3–T5 vertebral mass with extradural extension resulting in significant cord compression; it was isointense on T1, and hyperintense on T2-weighted images [ Figure 2 ].

Figure 1:

Computed tomography of the thoracic spine sagittal (a) and axial (b) images showing an osteolytic lesion regarding T3-T4-T5 with endocanalar extension.


Figure 2:

Sagittal T1-weighted (a), axial T2-weighted (b and c) images showing an expansile mass lesion with spinal cord compression at T3-4-5 level.


Surgery, pathology, and outcome

Following an emergent Th3-5 laminectomy, the extradural mass was totally excised, and the cord was adequately decompressed. The histopathological examination confirmed a BT secondary to hyperparathyroidism. Postoperatively, the patient’s symptoms resolved within 3 weeks. Subsequently, she was referred for a parathyroidectomy.


We identified 25 similar cases of BTs attributed primary hyperparathyroidism impacting the spine (since 1968 to present) [ Table 1 ].[ 1 - 25 ] Most patients were female (62.9 %) averaging 46.5 years of age who presented with predominant thoracic lesions (59%) contributing to varying degrees of myelopathy [ Table 1 ].[ 7 - 22 ] Surgical options included; biopsy, decompression/resection, or decompression/ instrumentation with fusion. Of the 25, 23 benefitted from parathyroidectomy. Typically, CT imaging documented BTs as well-defined soft-tissue masses with local bony erosion, expansion, while on magnetic resonance imaging studies, these lesions appear hypointense on T1, hypo- or hyperintense on T2-weighted images, with homogenous contrast enhancement.[ 7 - 22 ] The differential diagnoses these spinal lesions included; metastatic tumors, multiple myeloma, plasmacytoma, giant cell tumors, lymphoma, and aneurysmal bone cysts.[ 12 - 18 ]

Table 1:

Reported cases of spinal brown tumor secondary to primary hyperparathyroidism.


The gold standard for the treatment for BTs due to primary hyperparathyroidism remains gross total removal of the spine lesion (i.e., biopsy, decompression with/without fusion for those with neurological deficits) followed by parathyroidectomy.[ 7 - 18 ]


BTs should be included in the differential diagnosis of spinal lytic-expansive lesions with or without neurological deficits. The standard treatment is gross spinal total tumor excision followed by parathyroidectomy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent.

Financial support and sponsorship

Publication of this article was made possible by the James I. and Carolyn R. Ausman Educational Foundation.

Conflicts of interest

There are no conflicts of interest.


The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs.


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