A 26-year-old male patient of Indian origin who had previously defaulted on his treatment for tuberculous peritonitis (Figure 1), without other known comorbidities, presented with ptosis and down and outward deviation of the left eye. Clinical examination was positive for meningeal signs and complete left oculomotor nerve palsy.
A lumbar puncture was performed, which yielded clear fluid with lymphocytic pleocytosis with very low cerebrospinal fluid (CSF) glucose level of 18 mg dl-1 (normal 45-80 mg dl-1). CSF adenosine deaminase level was 23.3 (normal 1-9 IU l-1). CSF polymerase chain reaction detected M. tuberculosis and M. tuberculosis complex consisting of M. bovis, M. microti and M. africanum. Serology was negative for human immunodeficiency virus infection. Cysticercosis immunoglobulin G level was found to be 0.9 ( >1.1 ng dl-1 is considered positive).
MRI of the brain with contrast performed at this time showed multiple parenchymal nodular enhancing lesions in all the lobes of the bilateral cerebral hemispheres with mild surrounding oedema. (Figure 2) A diagnosis of multiple parenchymal tuberculomas with TBM was made. The patient was restarted on antitubercular therapy (ATT) with the addition of steroids.
The left oculomotor nerve palsy clinically resolved with treatment. Repeat MRI performed 1 month later showed persisting basal meningeal enhancement with disappearance of most of the tuberculomas. However, the patient continued to have recurrent headaches. He completed the 9-month treatment course for the tuberculomas, but at follow-up 4 months after the conclusion of treatment, he presented with incontinence of urine for the past 2 months and one episode of generalized tonic-clonic seizures.
A repeat MRI showed evidence of multiple rounded lesions that were mildly T1 hyperintense compared with the cortex and isointense compared with the white matter, and T2 hypointense compared with the cortex. There was perilesional oedema and ring enhancement of the lesions in a racemose pattern in bilateral insular cortices and sylvian fissures, with ring-enhancing lesions in the cavernous sinus, the pituitary and suprasellar cisterns, floor of the third ventricle, perimesencephalic cistern abutting the cerebral peduncles on both sides and the quadrigeminal cistern. Meningeal enhancement was present in the parasellar regions (Figure 3). This led us to suspect the possibility of recurrence of the tuberculomas, and the patient was started on antitubercular chemotherapy. A differential diagnosis of paradoxical response was considered.
At this time, a chronic lacunar infarct in the left gangliocapsular region was noted (Figure 4). Despite extensive history taking and examination, no symptoms were attributable to this lacunar infarct.
A clinical decision to continue the antitubercular chemotherapy with corticosteroids was taken. Following this, the patient adhered strictly to the treatment regimen, which started with isoniazid, rifampicin, pyrazinamide, ethambutol and streptomycin for 6 months with corticosteroids, followed by maintenance therapy with isoniazid, rifamicin and ethambultol. Two further contrast-enhanced MRI studies of the brain were performed over the next year, 6 months apart (Figure 5). There was an increase in the size of one of the lesions, while the other lesions remained of similar size. There were no new lesions, no development of hydrocephalus or meningeal enhancement. MR spectroscopy (MRS) was performed owing to the lack of response to ATT. MRS showed evidence of reduced choline and N-acetyl-aspartate, with a lipid/lactate peak (Figure 6). The patient is currently asymptomatic on maintenance treatment with isoniazid, rifampicin and ethambutol with corticosteroids, with the ring-enhancing lesions showing minimal change over 12 months (three 6-monthly MRIs). A current lumbar puncture shows normal CSF cytology and biochemistry with normal adenosine deaminase levels (1.75 IU l-1).