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Primary Intramedullary Anaplastic Oligodendroglioma Of   Spinal Cord: A Case Report

 Ish Dhammi*,Jena S K**

* Specialist
**Senior Resident
Department Of Orthopaedics,University College Of Medical Sciences And Guru Tegh Bahadur Hospital, Shahdara, Delhi-110095

Address for Correspondence:

Dr. Santosh Kumar Jena 
F-17/125, Sector-8, Rohini  
Telephone No. 011-27945626



Primary intramedullary anaplastic oligodendroglioma is a rare tumor. We described a 27-year old male with primary intramedullary anaplastic oligodendroglioma. He underwent partial removal of tumor and spinal radiation therapy. The objectives were to present a case of intramedullary anaplastic oligodendroglioma and review the existing literature. A comparison of the clinical, radiologic and pathologic characteristics, as they relate to those already described in similar cases, was also attempted.

Key Words: anaplastic oligodendroglioma, intramedullary spinal cord tumor, radiation therapy

J.Orthopaedics 2007;4(4)e18


Primary intramedullary oligodendroglioma is a rare tumor and primary intramedullary anaplastic oligodendroglioma is even more uncommon (1). Forty five cases of primary intramedullary oligodendroglioma have been reported in the literature till date and only five of these tumors were anaplastic (1).

Case Report :

A twenty seven year old male presented to the orthopaedics emergency with a history of lower back pain radiating to the right lower limb associated with hypoesthesia in the distribution of L5 and S1 dermatomes in the right lower limb for the past 2 weeks. There was no preceding history of trauma, constitutional symptoms such as low grade fever, anorexia and weight loss. History of contact with a patient of pulmonary tuberculosis was present. .His father had suffered from pulmonary tuberculosis. On clinical examination, there was tenderness at lumbosacral junction with paraspinal muscle spasm. The straight leg raising test on the right side was 60 degrees as compared to 90 degrees on the left side. Extensor hallucis longus and extensor digitorum were weak (grade 4) on the right side with sensory hypoesthesia in the L5 and S1 dermatomes. Plain radiographs of the lumbosacral spine were normal. Based on the history and clinical examination, a diagnosis of intervertebral disc prolapse L4 - L5 was made and the patient was advised bed rest and non-steroidal anti-inflammatory drugs. He was even being considered for an epidural steroid injection.

Within a period of four days, the patient deteriorated neurologically with involvement of left lower limb and bladder as well. The muscle power in both the lower limbs progressively deteriorated to grade three and eventually ended in complete paraplegia with loss of control over bladder and bowel. An ascending lumbar myelogram was performed and it revealed complete block of the dye column at L1 level (fig.1).Magnetic resonance imaging scan revealed an intradural space occupying lesion opposite the bodies of D12 and L1 vertebrae. (Fig.-2).

Figure 1: Myelogram shows complete block of dye column at L1 level







Figure 2: MRI shows intradural space occupying lesion opposite the bodies of D12 and L1 vertebrae

Laminectomy from D11 to L1 was performed. The cord was found enlarged in a fusiform shaped swelling extending from D12 to L1.On incising the dura; dirty black tissue intermingled with the neural tissue bulged out. It was not possible to remove the whole tumor tissue, a debulking surgery was performed. The tissue was sent for histopathological examination.

Histopathology sections showed a highly cellular tumor with characteristic features of oligodendroglioma with the tumor cells arranged in a lobular pattern. The cells showed a perinuclear halo giving a honeycombed appearance to the clusters of cells. Micro calcification was seen in areas. There were foci suggestive of anaplasia with marked cytologic atypia and considerable nuclear hyperchromasia. Another notable feature was the presence of vascular hypertrophy and proliferation. Areas of necrosis with pseudopalisading were seen in an occasional field. (fig.3a, b). It was reported as an anaplastic oligodendroglioma.

Figure 3 a: Shows an area of classical oligodendroglioma with marked vascularity and endothelial proliferation (200X)

Figure 3 b: Another field from the same tumor showing necrosis, vascular proliferation and nuclear atypia (200X)

Postoperative period was uneventful but the patient did not show any neural recovery.   He was referred to the radiotherapy department for megavoltage radiotherapy. He did not report back to us. But records of radiotherapy department say he is still following in radiotherapy department at 16 months postoperatively. 


Primary spinal cord oligodendroglioma represents 0.8-4.7% of the tumors of the spinal cord and filum and 1.59% of oligodendrogliomas (1). In literature 5 cases of anaplastic oligodendroglioma of spinal cord have been reported till date to the best of our knowledge (1).

The peak age incidence of oligodendrogliomas of the cord is around 30-40 years with no sex preference (2). In Fortuna et al series, three of the reported cases were adults in the fifth decade and the other was an 18 year old woman (3). Nam et al reported anaplastic oligodendroglioma in a 38 month old boy (1). Our case is a 27 year old male.

In the spinal cord, approximately 30% of the tumors occur in the cervical spine, 60% in the thoracic spine and 10% in the lumbar spine (2). Out of the forty five reported cases of intramedullary oligodendrogliomas only three were holocord i.e., extending over nineteen to twenty cord segments (4). In our case, the tumor was located at the dorsolumbar junction extending over two cord segments i.e., D12-L1.

Most of the patients present with pain, weakness and paraesthesiae (3).Sphincter disturbances are never among the presenting symptoms (3). Scoliosis may be the only sign of the tumor even for several years without any other clinical sign.  In addition to these neural symptoms, primary intramedullary oligodendroglioma has peculiar clinical characteristic of preference for meningeal spread with intracranial hypertension and fluctuation of symptoms owing to spontaneous bleeding (1).

The plain radiographs may reveal indirect evidence of the lesion (scalloping of the posterior vertebral bodies, erosion of the pedicles, widening of the canal) (3). No such finding was seen in our patient. Myelography usually reveals the diagnosis of an intramedullary tumor (3). In our case, myelogram revealed complete block of the dye column at L1 level. Magnetic resonance imaging is the procedure of choice in the investigation of spinal cord tumors. It can delineate tumor extension, though edema may not be readily distinguished from neoplastic tissue; gadolinium DTPA enhancement might help (4).

Surgical removal and radiotherapy are the two described modalities of treatment (3). Surgical removal may be complete or only debulking of tumor if it is not possible to separate the tumor tissue completely from the neural tissue. In each of the patients reported by Fortuna et al and Nam et al, it was not possible to remove the tumor mass in toto and a debulking procedure was done. In our case too, a debulking surgery was done (3).

Macroscopically oligodendrogliomas has been described in majority of cases as a soft, gelatinous, infiltrating tumor, white or grayish pink in color indicating greater clinical malignancy (3, 5). In a few cases, the consistency of the tumor may be firm which is related with a better prognosis (3). In the present case, the tumor tissue resembled grayish, friable caseous material preoperatively. Microscopically, the tumor presents a honeycombed appearance (2). The cells are of uniform size and shape and a clear halo around the nucleus is displayed in each cell. Areas of calcification are frequently seen in oligodendrogliomas. Increased mitotic activity and presence of necroses are characteristically associated with an anaplastic change (2, 5). All these features were noticeable in the histopathology sections of the present case.

Radiotherapy is an effective modality in primary malignant anaplastic oligodendroglioma where considerable residual mass is left after surgical debulking (1, 3, 6).We referred our case to radiotherapy center for radiation therapy.

The prognosis of primary intramedullary anaplastic oligodendroglioma in 4 reported cases was so poor that none survived for three years (1). Radiation therapy may lead to a better prognosis (1, 3, 6). In a child of 38 months the debulking was followed by megavoltage radiation therapy and post radiation therapy MRI revealed marked decrease in size and at 50 months after surgery there was no evidence of progression (1). Thus once anaplastic oligodendroglioma is diagnosed more radical therapy such as craniospinal radiation with or without chemotherapy should be given for a better prognosis.

Reference :

  1. Nam Do-Hyun, Cho Byung-Kyu, Kim Yeon- Mee et al: Intramedullary anaplastic oligodendroglioma in a child. Child’s Nervous System, 14:127-130, 1998

  2. Nathoo A.R., Halliday N.P.: Spinal cord oligodendroglioma. Postgrad Med J., 43(506), 789-791, 1967.

  3. Fortuna A, Celli P, Palma L.: Oligodendrogliomas of the Spinal Cord. Acta Neurochirurgica, 52:305-329, 1980.

  4. Pagni C.A., Canavero S. Gaidolfi F.: Intramedullary “Holocord” Oligodendroglioma: Case Report. Acta Neurochirurgica, 113: 96-99, 1991.

  5. Russel D.S., Rubinstein L.J. : Pathology of tumors of the Nervous system. Ed. 5,172-187, Baltimore, Williams and Wilkins, 1989.

  6. Fountas KN, Karampelas I, Nikolakakos LG, Troup EC, Robinson JS.: Primary spinal cord oligodendroglioma: case report and review of Literature. Childs nervous system, 21(2):171-5, Feb 2005


This is a peer reviewed paper 

Please cite as : Ish Dhammi : Primary Intramedullary Anaplastic Oligodendroglioma Of   Spinal Cord: A Case Report

J.Orthopaedics 2007;4(4)e18





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