| ORIGINAL ARTICLE |
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| Year : 2015 | Volume
: 63
| Issue : 6 | Page : 926--932 |
Vascular complications of tuberculous meningitis: An autopsy study
Debajyoti Chatterjee1, Bishan Dass Radotra1, Rakesh Kumar Vasishta1, Kusum Sharma2
1 Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Medical Microbiology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Correspondence Address:
Bishan Dass Radotra
Department of Histopathology, Room No. 510, 5th floor, Research Block A, Sector-12, Postgraduate Institute of Medical Education and Research, Chandigarh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.170086
Aims: Vascular complications have the most serious consequences in patients with tuberculous meningitis (TBM). Although stroke is seen in approximately 20% of patients with TBM, the underlying vascular damage and infarction are much more extensive. This study has been undertaken to study the pathology at different levels of cerebral vessels and their resultant complications in TBM.
Materials and Methods: Fifty-one postmortem TBM brains were examined over a period of 16 years (1997–2012). The vascular pathology was studied in detail. Changes in middle cerebral artery (MCA) and basilar artery (BA) and their branches at different levels were analyzed in all cases.
Results: The age of the patients ranged from 3 months to 72 years. Infarcts were found in 37 cases, among which they were grossly visible in 27 cases. Macroscopic infarcts were more common in MCA territory whereas microscopic infarction was more in BA distribution—brainstem and cerebellum. Vascular involvement was almost universal, with smaller branches of both MCA (94%) and BA (100%) carrying the brunt of the disease, whereas the larger branches were variably involved. Infiltrative lesions were most common at all levels; necrotizing lesions were more common in smaller branches, whereas proliferative changes were seen more in larger branches.
Conclusion: This study showed extensive damage of cerebral vessels in TBM, which was responsible for the presence of widespread infarctions. Microscopic infarctions in the brainstem and cerebellum were much more common than reported by radiological studies. Thus, more aggressive management of TBM is required to combat its vascular complications.
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