Pediatric Moyamoya Syndrome Secondary to Tuberculous Meningitis: A Case Report

Abstract

Objectives: Tuberculosis is uncommon in the United States and a rare cause of meningitis in children with severe neurologic consequences. Tuberculous meningitis (TBM) is an even rarer cause of moyamoya syndrome with only a handful of cases previously reported.

Methods: We report the case of a female patient who initially presented at 6 years of age with TBM and developed moyamoya syndrome requiring revascularization surgery.

Results: She was found to have basilar meningeal enhancement and right basal ganglia infarcts. She was treated with 12 months of antituberculosis therapy and 12 months of enoxaparin and maintained on daily aspirin indefinitely. However, she developed recurrent headaches and transient ischemic attacks and was found to have progressive bilateral moyamoya arteriopathy. At age 11 years, she underwent bilateral pial synangiosis for the treatment of her moyamoya syndrome.

Discussion: Moyamoya syndrome is a rare but serious sequalae of TBM and may be more common in pediatric patients. The risk of stroke may be mitigated by pial synangiosis or other revascularization surgeries in carefully selected patients.

Figure 1. Serial MRI and MRA of the Brain Show Tuberculous Meningitis With Progressive Moyamoya Arteriopathy

Arrows in upper MRI studies denote change in tuberculous lesion over time. Arrowheads in lower MRA studies denote changes in artery caliber over time. MRA = magnetic resonance angiography.

Figure 2. Progressive Moyamoya Arteriopathy With Transdural Collaterals

(A–D) Digital subtraction angiography of the internal carotid arteries 16 months (A, B) and 58 months (C, D) after initial presentation of TBM demonstrated progressive stenosis of the right A1 and bilateral M1 segments (C, D, arrowheads). There was evidence of increased arterial phase lag in the right MCA territory and diminished opacification of the ACA/MCA watershed territories bilaterally on the 58-month DSA compared with that on the 16-month DSA. Note the interval appearance of the distal left ACA despite worsened stenosis of the left A1 segment, suggesting decreased competing flow from the contralateral ACA consistent with progressive right A1 segment arteriopathy. Overall, the constellation of findings is consistent with interval progressive moyamoya arteriopathy with the ACA/MCA watershed territories most at risk. (E) Frontal and lateral views of selective injections of the right ECA at 58 months demonstrated intrinsic EC-IC transdural collaterals in the right frontal and parietal lobes (arrows). (F) Frontal and lateral views of selective injections of the left ECA at 58 months demonstrated intrinsic EC-IC transdural collaterals in the left frontal lobe. There were no transdural collaterals seen on the 16-month DSA (not shown). (G) Intraoperative photograph demonstrates intrinsic EC-IC transdural collaterals from the dura entering the arachnoid. ACA = anterior cerebral artery; DSA = digital subtraction angiography; ECA = external carotid artery; EC-IC = external carotid to internal carotid; MCA = middle cerebral artery; TBM = tuberculous meningitis.