Presentation
Subacute onset of bilateral lower limb weakness, urinary incontinence, low grade fever, and severe weight loss.
Patient Data
MRI whole spine showed revealed disseminated intramedullary enhancing nodules with swollen cord and nodular leptomeningeal enhancement.The enhancing nodules appear isointense signal at T1 and T2 WI. No evidence of spondylodiscitis.
The axial cuts of the spine revealed bilateral pulmonary diffuse air-space consolidations and right upper apical large cavity with an air-fluid level.
MRI exam of the brain revealed right cerebellar small faintly enhancing lesion of persistent high signal at T1 and T2 WI which on CT scan appeared calcific. No evidence of basal cisternal arachidonitis..
CT scan of the chest and abdomen were made and revealed bilateral pulmonary scattered patches of air-space consolidations with tree-in-bud densities. Right apical large cavity with an fluid level as also noted. Enlarged mediastinal lymph nodes. The examined abdominal cuts showed multiple bi-lobar hypodense focal lesions.
CT scan of the brain showed right cerebellar calcific focus.
First image: showed MRI whole spine showed revealed disseminated intramedullary enhancing nodules with swollen cord and nodular leptomeningeal enhancement.The enhancing nodules appear isointense signal at T1 and T2 WI.
Second image: MRI exam of the brain revealed right cerebellar small faintly enhancing lesion of persistent high signal at T1 and T2 WI which on CT scan appeared calcific. No evidence of basal cisternal arachidonitis, impressive of reactivation of calcified TB granuloma.
Third image: CT scan of the chest and abdomen were made and revealed bilateral pulmonary scattered patches of air-space consolidations with tree-in-bud densities. Right apical large cavity with an fluid level as also noted. Enlarged mediastinal lymph nodes. The examined abdominal cuts showed multiple bi-lobar hypodense focal lesions.
Case Discussion
Cerebrospinal fluid (CSF) analysis showed elevated intradural oligoclonal IgG production, decreased CSF glucose level, and increased CSF protein level. CSF polymerase chain reaction for TB was positive. Sputum cultures revealed acid-fast bacilli.
This patient had extensive extra-pulmonary dissemination of TB with involvement of the spinal cord and the liver. Also, reactivation of old cerebellar calcific focus is noted.
The patient was treated with a four-drug ATT regimen (Ethambutol 500mg, pyrazinamide 5oomg, Rifampin 300mg, Isoniazid 150mg) for a period of 2 months. The patient was discharged after 2 months treatment and improvement of the neurological symptoms related to the spinal lesion with extended (rifampin and isoniazid) for further 6 months.
Spinal intramedullary tuberculomas are extremely rare, seen in only 2 of 100,000 cases of tuberculosis and 2 of 1000 cases of tuberculous CNS disease.Intraspinal tuberculoma is almost always secondary to tuberculous involvement elsewhere in the body, most commonly pulmonary tuberculosis, as in this case.
The most common location of intramedullary tuberculoma is in the thoracic spinal cord. The higher incidence involving the thoracolumbar region is explained on the basis of the regional blood flow to the spinal cord.
Tuberculomas of the spinal medulla should be considered in the differential diagnosis of subacute spinal cord compression, particularly in patients with evidence of extraneural tuberculosis disease.
Intramedullary tuberculoma may be difficult to differentiate from space-occupying lesions such as primary and metastatic spinal tumors and other chronic granulomatous diseases such as sarcoidosis, brucellosis, histiocytosis.
Leptomeningeal TB involvement is usually secondary to the dissemination of basal arachidonitis or less common via hematogenous spread. In this case, there was no evidence of basal arachidonitis.
MRI appearance of spinal intramedullary TB differs according to the stage, in the early stage the tuberculomas seem to be isointense on both T1WI and T2WI and enhancing homogeneously on contrast. Later, the tuberculoma capsule becomes richer in collagen and the surrounding inflammatory reaction may decrease or disappear, resulting in an isointense lesion on T1WI and isointense to hyperintense on T2WI, and ring enhancement with hypointense center.
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