Abstract
A case of multiple intracranial tuberculomas diagnosed by enhanced brain CT scan and MRI, which developed during the course of miliary tuberculosis under anti-tuberculous chemotherapy was experienced. Chemotherapy with an increased dose of each agent and corticosteroid was administered, and eventually intracranial tuberculomas nearly disappeared.
After 1970, there have been 29 reported cases of intracranial tuberculomas in Japan, which were diagnosed by brain CT and treated with anti-tuberculous agents.
Among them, 27 evaluable cases were classified into 3 groups. Group A: Intracranial tuberculomas were proved by CT before chemotherapy in 7 cases. Four of them enlarged during chemotherapy. Group B: During chemotherapy of tuberculous meningitis, neurological symptoms worsened or prolonged, and finally intracranial tuberculomas were found by CT in 9 cases. In 5 of them, after meningitis was improved by chemotherapy, neurological symptoms worsened and intracranial tuberculomas were found. Group C: During chemotherapy of pulmonary tuberculosis or miliary tuberculosis, neurological symptoms appeared and intracranial tuberculomas were found by CT in 11 cases (including our own case). Getting 3 groups together, intracranial tuberculomas seem to have worsened during chemotherapy in 24 out of 27 evaluable cases. In view of response to chemotherapy, these 24 cases can be divided into 2 categories: 1) non-responders to chemotherapy; 2) cases finally cured by chemotherapy (“transient worsening”).
Based on a review of the literature, the cause of non-responders can be attributed to the following: (1) anti-tuberculous agents do not penetrate well into tuberculomas because of their fibrous capsule, which is believed to be reflected on enhanced CT scans as ring-enhancement finding, (2) angitis is complicated and so local brain edema and tissue hypoxia is caused, and (3) intrathecal infiltration of anti-tuberculous agents is reduced once meningitis is improved.
Then, what is the cause of “transient worsening”? No previous reports have mentioned it. In our own case, during chemotherapy intracranial tuberculomas were supposed to have developed because headache worsened and right hemiplegia appeared. At the same time, pulmonary lesion of miliary tuberculosis also worsened. But eventually both of them were cured by continuation of chemotherapy. Similarly, in several reported cases, not only intracranial tuberculomas enlarged but pulmonary lesion worsened or hilar and cervical lymph nodes enlarged during chemotherapy, and eventually both of them were cured by chemotherapy.
Taking these clinical courses into consideration, it is suggested that the “transient worsening” of intracranial tuberculomas may be the same phenomenon as worsening of pulmonary lesions, appearance of pleural effusion, and enlargement of lymphnodes transiently seen in some cases of pulmonary tuberculosis during chemotherapy.
