Neurology India
menu-bar5 Open access journal indexed with Index Medicus
  Users online: 6560  
 Home | Login 
About Editorial board Articlesmenu-bullet NSI Publicationsmenu-bullet Search Instructions Online Submission Subscribe Videos Etcetera Contact
  Navigate Here 
 Resource Links
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
    Article in PDF (1,331 KB)
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this Article
   Article Figures

 Article Access Statistics
    PDF Downloaded46    
    Comments [Add]    

Recommend this journal


Table of Contents    
Year : 2015  |  Volume : 63  |  Issue : 1  |  Page : 110-112

Cervical burst fracture caused by brown tumor

1 Department of Neurosurgery, Baskent University Faculty of Medicine, Adana Practice and Research Center, Adana, Turkey
2 Department of Pathology, Baskent University Faculty of Medicine, Adana Practice and Research Center, Adana, Turkey

Date of Web Publication4-Mar-2015

Correspondence Address:
Fatih Aydemir
Department of Neurosurgery, Baskent University Faculty of Medicine, Adana Practice and Research Center, Adana
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.152680

Rights and Permissions

How to cite this article:
Aydemir F, Kardes O, Cekinmez M, Tufan K, Kocer NE. Cervical burst fracture caused by brown tumor. Neurol India 2015;63:110-2

How to cite this URL:
Aydemir F, Kardes O, Cekinmez M, Tufan K, Kocer NE. Cervical burst fracture caused by brown tumor. Neurol India [serial online] 2015 [cited 2022 May 25];63:110-2. Available from: https://www.neurologyindia.com/text.asp?2015/63/1/110/152680


Brown tumors (BT) are benign focal bony lesions caused by increased osteoclastic activity and fibroblastic proliferation. They are encountered in primary or secondary hyperparathyroidism. [1] Patients with chronic renal failure (CRF) on long-term hemodialysis are at risk of developing secondary hyperparathyroidism due to phosphate retention and lowered calcitriol levels. [2] BTs can arise as a solitary or multiple lesions of any bone and are more common in the extremities, clavicles, ribs, and pelvis. [3] Spinal involvement is very rare. The diagnosis and treatment options of a C7 vertebral burst fracture caused by secondary hyperparathyroidism (SHP) are discussed in this presentation.

A 29-year-old male patient was admitted with neck pain, and left hand numbness and weakness. In his medical history, he had been undergoing hemodialysis for the past 10 years as he was suffering from chronic renal failure. About 7 years ago, he had been diagnosed to be having SHP and had undergone a total parathyroidectomy. His neurological examination revealed hypoactive left triceps reflex and loss of flexion of the distal phalanx of the left hand (4/5 power). Cervical computed tomography (CT) of the patient revealed a burst fracture (and a lytic lesion) of the C7 vertebral body as well as lytic lesions in the C6 spinous process and the T2 vertebral body. Cervical magnetic resonance imaging (MRI) revealed an expansile-lytic lesion in the C7 vertebral body that was hypointense on T1 and T2 imaging and contrast enhancing following gadolinium injection [Figure 1]. The laboratory findings were as follows; parathyroid hormone: 3377 pg/ml (normal range; 10-70 pg/ml), calcium: 8,77mg / dL (normal range: 8.4-10.2mg/dl), phosphate: 6.46 mg/dL (normal range: 2.7-4.5mg/dL), alkaline phosphatase: 1429 IU/L (normal range: 25-100 IU/L), respectively. Parathyroid scintigraphy and neck MRI revealed an 18 x 18 x 11 mm lesion behind the manubrium sterni consistent with parathyroid tissue. A C7 anterior corpectomy was performed. Fusion with polyether ether ketone (PEEK) cage and synthetic bone putty and C6-T1 anterior plate-screw fixation were performed. A repeat parathyroidectomy of the residual tissue was performed by the general surgeons in the same session. No postoperative neurological deficits were detected and laboratory values of parathyroid hormone and calcium on the first postoperative day were 18.68 pg/ml and 6.06 mg/dl, respectively. Histopathological examination of the resected tissue revealed a BT [Figure 2]. In the early postoperative period, the CT scan showed relief of cord compression and restoration of C7 body height. A cervical MRI and CT scan done after a year showed a proper PEEK cage placement [Figure 3].
Figure 1: Lytic lesion in C7 vertebral body causing burst fracture and spinal cord compression on T2-weighted sagittal (a) and axial MR images (b), sagittal CT images (c) and axial CT images (d)

Click here to view
Figure 2: Microphotograph reveals the lesion adjacent to cortical bone (a). Lesion is composed of numerous osteoclastic giant cells embedded in spindle cell stroma (b) (a: HE x40, b:HE x100)

Click here to view
Figure 3: Postoperative three-dimensional CT (a) shows the placement of PEEK cage, plates and screws. At one year follow up, T2-weighted sagittal MR images (b) and sagittal CT images (c), it is seen that the cord compression has ceased and the height of C7 vertebral body has been restored

Click here to view

A total of 47 cases BT (including the present case) have been reported in literature. Twenty eight of them were due to SHP and 19 were due to primary hyperparathyroidism [4],[5] SHP may occur in any condition that causes chronic low calcium levels in serum. A plasmocytoma, lymphoma, giant cell tumor, and metastasis are included in the differential diagnosis of BTs. [4],[5],[6],[7]

BTs are brown in color on gross examination due to a rich vascularity, hemorrhage, and hemosiderin deposition. The microscopic examination shows typically osteoclast-like multinucleated giant cells and hemosiderin scattered in a fibrovascular stroma. BTs are histologically similar to other giant cell lesions such as a giant cell tumor, aneurysmal bone cyst, and a reparative giant cell granuloma. [5] There are no obvious radiological features. Only the clinical manifestations and endocrinological status help in differentiating BTs from other giant cell lesions.

The mainstay in the treatment or prevention of occurrence of a BT is the elimination of the underlying metabolic disorder. Keeping calcium and phosphate levels within a normal range in patients with CRF is essential for the prevention of SHP. Total or subtotal parathyroidectomy may be indicated as it promotes bony remineralization, rapid bone healing, and resolution of the tumor tissue. [6] Patients without neurological deficit often show tumor regression following a parathyroidectomy and medical treatment for hyperparathyroidism. [7],[8],[9],[10] Even when surgery is required for a lesion compressing the thecal sac, to ensure complete tumor resolution and to prevent recurrence, a parathyroidectomy and bisphosphonate therapy before and after surgery may be necessary. [3] Serum phosphate levels should be controlled, dietary phosphorus intake restricted, and a high phosphate clearance dialyzer selected. Use of phosphate binders, vitamin D, oral calcium supplements, and calcimimetics are recommended as treatment. [4] The present case represents the second published report of a patient with a BT induced by residual parathyroid tissue. [6]

The aim of surgery in the present case was to eliminate pressure on the thecal sac and to promote spinal stability. Osteoporosis and impaired bone healing may often interfere with bony fusion. [11]

Thus, BTs should be considered in the differential diagnosis of spinal lesions of patients with CRF. Patients who have had a parathyroidectomy should be followed at regular interval for recurrence.

  References Top

Bullough PG. Neoplastic diseases of bone. In: Mills SE, editor, Sternberg's diagnostic surgical pathology, 4th ed. Vol 1. Philadelphia: Lippincott Williams & Wilkins; 2004. p. 245-64.  Back to cited text no. 1
Mak KC, Wong YW, Luk KD. Spinal cord compression secondary to brown tumour in a patient on long-term haemodialysis: A case report. J Orthop Surg (Hong Kong) 2009;17:90-5.  Back to cited text no. 2
Kaya RA, Cavuþoðlu H, Tanik C, Kahyaoðlu O, Dilbaz S, Tuncer C, et al . Spinal cord compression caused by a brown tumor at the cervicothoracic junction. Spine J 2007;7:728-32.  Back to cited text no. 3
Tayfun H, Metin O, Hakan S, Zafer B, Vardar AF. Brown tumor as an unusual but preventable cause of spinal cord compression: Case report and review of the literature. Asian J Neurosurg 2014;9:40-4.  Back to cited text no. 4
[PUBMED]  Medknow Journal  
Khalatbari MR, Moharamzad Y. Brown tumor of the spine in patients with primary hyperparathyroidism. Spine (Phila Pa 1976) 2014;39:E1073-9.  Back to cited text no. 5
Fargen KM, Lin CS, Jeung JA, Yachnis AT, Jacob RP, Velat GJ. Vertebral brown tumors causing neurologic compromise. World Neurosurg 2013;79:208.e1-6.  Back to cited text no. 6
Hoshi M, Takami M, Kajikawa M, Teramura K, Okamoto T, Yanagida I, et al. A case of multiple skeletal lesions of brown tumors, mimicking carcinoma metastases. Arch Orthop Trauma Surg 2008;128:149-54.  Back to cited text no. 7
Bohlman ME, Kim YC, Eagan J, Spees EK. Brown tumor in secondary hyperparathyroidism causing acute paraplegia. Am J Med 1986;81:545-7.  Back to cited text no. 8
Ganesh A, Kurian S, John L. Complete recovery of spinal cord compression following parathyroidectomy. Postgrad Med J 1981;57:652-3.  Back to cited text no. 9
Azria A, Beaudreuil J, Juquel JP, Quillard A, Bardin T. Brown tumor of the spine revealing secondary hyperparathyroidism. Report of a case. Joint Bone Spine 2000;67:230-3.  Back to cited text no. 10
Fineman I, Johnson JP, Di-Patre PL, Sandhu H. Chronic renal failure causing brown tumors and myelopathy. Case report and review of pathophysiology and treatment. J Neurosurg 1999;90:242-6.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3]


Print this article  Email this article
Online since 20th March '04
Published by Wolters Kluwer - Medknow