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Radiology
Case of the Month
| Case No. : | 15 |
| Month : | March |
| Year : | 2000 |
| Contributor : | Dr. Hemant Parmar |
A 60 year old lady presented with history of progressive paraparesis over 15 days. She also complained of bladder bowel incontinence. Low-grade fever and anorexia over past month was also present. . On examination, both tone and power in both lower limbs were decreased and the deep tendon reflexes were exaggerated. Sensations of touch and temperature were also mildly affected. Posterior column sensations were however normal. Her hemogram showed an ESR of 60 mm at the end of the first hour. Her ELISA test for HIV was negative. The plain chest radiograph was normal.
Plain radiographs of the dorso-lumbar spine showed age related degenerative changes and a compression fracture at L1 level. An MRI study was then performed.
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| Fig 1 | Fig 2 | Fig 4 |
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| Fig 3 | ||
The sagittal TI weighed image (fig 1) showed a fusiform dilatation of the spinal cord at D11-12 level, with an ill-defined hyperintensity at that level. Sagittal T2WI (fig 2) images showed a hyperintensity of the cord from D10-L1 level. In addition, a hypointensity at D12 level with central hyperintensity was noted. Axial T2W images (Fig 3) at D12 level showed a rounded hypointense lesion within the spinal cord surrounded by edema, suggestive of an intramedullary lesion. After administration of Godolinium-D.T.P.A. the hypointense lesion showed ring enhancement at D12 level (fig 4).
Differential Diagnosis : This includes granulomas such as tuberculomas and cystecercal granulomas, neoplastic lesions such as astrocytoma, metastasis or lymphoma. However, in this case, the size of the lesion combined with the classical ring enhancement and surrounding edema was thought to be typical of a tuberculous granuloma.
The patient underwent surgical excision of the lesion. Histopathology of the lesion showed focal caseating necrosis with a rim of translucent granulation tissue consisting of epitheloid cells, lymphocytes, Langerhan's giant cells and fibroblasts. This confirmed the MRI diagnosis of an intramedullary tuberculoma. The patient was subsequently started on anti tuberculous chemotherapy for 18 months. By the end of 5-6 months, her symptoms started improving, and at the end of the course of treatment, only minimal residual symptoms were present.
Intramedullary tuberculomas were first described by Serra in 1840 (1). Lin reviewed the literature of intramedullary tuberculomas in 1960 and found reports of 104 cases, 88 of which were found on postmortem (4). In a more recent study, Ratliff found only 148 cases of intramedullary tuberculomas mentioned in the literature (6). Bucy and Oberhill reported evidence of CNS tuberculomas in 1 in every 53 cases with evidence of tuberculosis elsewhere in body (8). The proportion of intracranial to intraspinal tuberculosis ranges from 20:1 and 42:1, depending upon the series (1,2,3). Intraspinal tuberculomas are usually associated with intracranial involvement (1). But, in our case no intracranial tuberculomas were detected.
Clinically, patients with intramedullary tuberculomas present with signs and symptoms depending on the location of tuberculoma in the spinal cord. History of previous tuberculosis or tuberculous contact is usually present. Although tuberculomas occur at any age and in either sex, the greatest incidence is found in young nulliparous women, attributed to reactivation of previous tuberculosis by pregnancy (8,9). Some of the cases of intramedullary spinal tuberculous abscess have been reported with spinal dysraphism and as a complication of diagnostic spinal puncture (3). Most of the reported cases of intramedullary tuberculomas are associated with foci of tuberculosis elsewhere in the body (1, 4). They are caused by the blood borne infection of the tubercle bacilli, secondary to tubercular infection elsewhere, commonly from the lung (4). These lesions are distributed evenly in the cervical, dorsal and lumbar portions of the spinal cord (1). CNS tuberculosis affects 0.5-2% of the patients with systemic tuberculosis (3). Bucy and Oberhill reported six cases of tuberculoma of spinal cord and of these three were associated with lesions elsewhere in the CNS (8). Though multiple tuberculomas are seen in 10–33% of cases of intracranial tuberculomas, multiple lesions of spinal cord are very uncommon and sparsely reported in the literature (1). Gupta et al reported multiple intramedullary lesions with skip areas in seven of their patients (11). Lin has also reported a case of multiple areas of spinal involvement by tuberculomas in a patient on treatment for tuberculous meningitis (12).
Earlier, the role of imaging in intramedullary tuberculoma was restricted to plain films and myelography, which are usually not much contributory, being able to show only cord swelling. However this has undergone radical change with the advent of MRI. The role of MRI in the diseases of spine and cord is well documented, as it helps in delineation and better characterization of these lesions. Intracranial tuberculomas have been described as low intensity lesions with or without central hyperintensity (because of varying amount of caseous necrosis) on T2WI and as hypo to isointense lesions on T1WI (13). Other series of brain tuberculomas describe iso to hyperintensity on T1WI, at the site of the tuberculoma with peripheral hypointensity due to edema / myelomalacia (14). The peculiar hypointensity or isointensity seen on T2WI in the tuberculomas may reflect restricted mobile protons within high protein content in organized caseation, cellular and collagenous layers, the presence of heterogeneously distributed free radicals produced by macrophages during active phagocytosis and / or highly immobile saturated fatty acids (14). Loose liquefied caseation in the centre may produce central hyperintensity on T2WI (14,15). Intense peripheral enhancement may be explained by prominent vascularity seen on microscopy (14,15). The MR findings in our cases correspond to the above mentioned morphological description and are similar to the characteristic appearance of intracranial tuberculomas on MRI. Many of the tuberculomas were often associated with intense adjacent arachnoiditis (2,16). Tuberculomas are surrounded by nervous tissue, which prevents significant meningitic response (10). On follow up studies, tuberculomas are known to swell following start of the treatment, due to inflammatory properties of tuberculin and other products of the bacilli (10). Edema is first to disappear with the treatment. Small residual lesions remains in few cases even after completion of the therapy, explaining the minor residual neurological deficit in many of these cases (17,18).
The differential diagnosis of intramedullary tuberculomas include neoplastic (astrocytoma, ependymoma, hemangioblastoma, metastasis, lymphoma), inflammatory, demyelinating (multiple sclerosis), vascular (malformations, infarctions) and granulomatous lesions (syphillis, pyogenic, mycotic, parasitic). (7,8,17,19). Some of these lesions also show hypointensity on T2WI. In HIV positive patients, vascular myelopathy due to HIV virus, cytomegalovirus, herpes simplex virus and Toxoplasma gondi infections of spinal cord are more common than tuberculomas. Primary non-Hodgkin lymphoma and cord infarctions due to vasculitis may also be seen in HIV positive patients (7). Though differentiation between these lesions sometimes becomes difficult, correlation of clinical findings, history and the peculiar signal intensities on MRI can help in making diagnosis of intramedullary tuberculoma easier. Suzer advocates microsurgical resection of the spinal cord and antituberculous chemotherapy as the treatment of choice for all patients suspected to have intramedullary tuberculomas (20). Sanchez and Jena however felt that there was no need of surgical procedures and imaging findings were reliable enough to start antituberculous therapy (17,18).
MRI has thus brought a total change not only in the imaging, but also in the management of intramedullary tuberculomas. The suggestive appearance of the disease (iso to hypointensity on T2WI with or without central hyperintensity, disc or ring enhancement etc.) with positive history of tuberculosis can help us to make a confident diagnosis of intramedullary tuberculoma and start anti tuberculous therapy. Thus the need for surgery is obviated. Patients only require follow up scans during the therapy, to assess the response to treatment.
References :
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Arseni C., Samitra D.C.: Intraspinal tuberculous granuloma. Brain 83 (1960), 285-92.
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Hanci M., Sarioglu A.C., Uzan M., Islak C., Kaynar M.Y., Oz B.: Intramedullary tuberculous abscess: A case report. Spine 21 (1996), 766-9.
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Lin T.H.: Intramedullary tuberculoma of the spinal cord. J Neurosurg 17 (1960), 497-99.
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Mathai K.V., Chandy J.: Tuberculosis infection of the nervous system. Clin Neurosurg 14 (1967), 145-7.
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Ratliff J.K., Conolly E.S.: Intramedullary tuberculoma of the spinal cord: A case report and review of literature. J Neurosurg Suppl 1. 90 (1999), 125-8.
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Melhan E.R., Wang H.: Intramedullary spinal cords tuberculoma in a patient with AIDS. AJNR 13 (1992), 986-8.
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Bucy P.C., Oberhill H.R.: Intradural spinal granulomas. J Neurosurg 7 (1950), 1-12.
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Dastur H.M., Shah M.D.: Intramedullary tuberculoma of the spinal cord. Indian Paediatrics 5 (1968), 468-71.
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Choksey M.S., Powell M., Gibb W.B.G., Casey A.T.H., Geddes J.F.: A conus tuberculoma mimicking an intramedullary tumour: a case report and review of the literature. Brit J Neurosurg 3 (1989), 117-22.
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Gupta R.K., Gupta S., Kumar S., Kohli A., Mishra U.K., Gujral R.B.: MRI in intraspinal tuberculosis Neuroradiology 36 (1994), 39-43.
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Lin S.K., Wu T., Wai Y.Y.: Intramedullary spinal tuberculomas during treatment of tuberculous meningitis. Clin Neurol Neurosurg 96 (1994), 71-8.
- Kim T.K., Chang K.H., Kin C.J., Goo J.M., Kook M.C., Han M.H.: Intracranial tuberculomas: Comparison of MR with pathologic findings. AJNR 16 (1995), 1903-8.