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Table of Contents    
Year : 2016  |  Volume : 64  |  Issue : 5  |  Page : 862-863

Clinical indicators of an early therapeutic response in tuberculous meningitis

Department of Radiology and Imaging, Fortis Memorial Research Institute, Gurgaon, Haryana, India

Date of Web Publication12-Sep-2016

Correspondence Address:
Rakesh Kumar Gupta
Department of Radiology and Imaging, Fortis Memorial Research Institute, Gurgaon, Haryana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.190290

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How to cite this article:
Gupta RK. Clinical indicators of an early therapeutic response in tuberculous meningitis. Neurol India 2016;64:862-3

How to cite this URL:
Gupta RK. Clinical indicators of an early therapeutic response in tuberculous meningitis. Neurol India [serial online] 2016 [cited 2020 Sep 23];64:862-3. Available from:

It is well known that early diagnosis and treatment is the key to management of tuberculous meningitis (TBM). Cranial neuropathy, hydrocephalus and vasculitis are poor clinical predictors and have a bearing on the therapeutic response and prognosis.[1],[2] Cag et al., have examined the course of clinical parameters after start of anti-tuberculous treatment (ATT), with emphasis on the parameters delaying the therapeutic response. The study included eighty eight microbiologically-proven TBM cases with follow-up data for fever, headache and mental changes during the course of treatment.[3]

A range of demographic characteristics and pre-morbid conditions, stage of the disease, neurological symptoms, radiological findings, laboratory parameters, cerebrospinal fluid findings, and therapy-related data were compared for the duration of fever, mental changes, headache and clinical response time persisting beyond 7,9, 11 and 13 days, respectively. The duration of fever was increased beyond 7 days in the presence of vasculitis (n = 10, P = 0.015). The presence of hydrocephalus was associated with the duration of mental changes lasting beyond 9 days (n = 20, P = 0.003). Therefore, vasculitis (P < 0.001) and hydrocephalus (P = 0.01), were the main predictors of a delayed clinical response and consequently, were detected to be the risk factors for an unfavorable outcome.

The authors have demonstrated the low sensitivity of imaging studies, as evidenced by abnormal meningeal enhancement that was evident in only 35/88 patients.[3] Ten patients had imaging features of vasculitis and 20 had evidence of hydrocephalus.[3] There are studies which report a higher rate of abnormal meningeal enhancement in TBM, varying from 80-94% at the time of diagnosis.[4] It is also known that while the patients may clinically respond to symptoms and signs with imaging evidence of early meningitis, the full blown imaging features of meningeal enhancement are noted while the patient appears clinically better at follow up. In fact, a number of patients with TBM develop vascular narrowing within three months of treatment and develop infarction and are thought of as having a paradoxical response to treatment.[1],[4] It appears that inflammatory changes in the subarachnoid vasculature are the likely reason for vascular complications in tuberculous meningitis. Exudative basal meningitis, precipitating vaso-constriction and peri-arteritis results in the development of infarction. This is one of the reasons for the use of steroids in the early part of the treatment to prevent this complication from occurring, which may still be noted despite the use of steroids and aspirin.[1] Similarly, patients presenting with vasculitis and/or hydrocephalus, are to be treated more vigorously with multi-drug regimen, corticosteroids and cerebrospinal fluid diversion to improve the patient's consciousness, which may help in improving the therapeutic response and in reducing the morbidity and mortality.

The authors have tried to re-emphasise the role of early diagnosis and initiation of treatment for attainment of a better clinical response that may help to prevent the complications of TBM like vasculitis and hydrocephalus from developing, which are responsible for the precipitation of morbidity and mortality in these cases.[2],[3] However, an early amelioration of clinical symptoms may not always give the clinician the handle to a good therapeutic response as the patient may subsequently develop hydrocephalus and vasculitis, which are poor prognosticators of TBM and have often been described as a paradoxical response.[1]

It is known that diffusion weighted imaging (DWI) magnetic resonance imaging (MRI) is more sensitive in the detection of acute infarcts, which may not be picked up early on the conventional MRI. The authors have used the computed tomographic scans and MRI but have not defined the methodology to assess the true value of these techniques for the detection of vasculitis.[4],[5] We routinely perform a high resolution magnetic resonance angiography, perfusion MRI and DWI to detect the development of an early infarct and/or vasculitis in patients with TBM, as has been shown by a number of authors in the literature.[4],[5],[6]

I conclude that a high resolution imaging is the key to defining vasculitis, infarction, cranial nerve involvement and hydrocephalus. It may help in the appropriate management of these complications and in decreasing the incidence of morbidity and mortality associated with this devastating clinical condition.

  References Top

Tai ML, Nor HM, Kadir KA, Viswanathan S, Rahmat K, Zain NR, et al. Paradoxical manifestation is common in HIV-negative tuberculous meningitis. Medicine (Baltimore). 2016;95:e1997.  Back to cited text no. 1
Trivedi R, Saksena S, Gupta RK. Magnetic resonance imaging in central nervous system tuberculosis. Indian J Radiol Imaging 2009;19:256-65.  Back to cited text no. 2
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Cag Y, Ozturk-Engin D, Gencer S, Hasbun R, Sengoz G, Crisan A, et al. Hydrocephalus and vasculitis delay therapeutic responses in tuberculous meninigitis: Results of Haydarpasa-III study. Neurology India 2016;64:896-905.  Back to cited text no. 3
Anuradha HK, Garg RK, Agarwal A, Sinha MK, Verma R, Singh MK, et al. Predictors of stroke in patients with tuberculous meningitis and its effect on the outcome. Q J Med 2010; 103:671-8.  Back to cited text no. 4
Shukla R, Abbas A, Kumar P, Gupta RK, Jha S, Prasad KN. Evaluation of cerebral infarction in tuberculous meningitis by diffusion-weighted imaging. J Infect 2008;57:298-306.  Back to cited text no. 5
Garg RK, Malhotra HS, Jain A. Neuroimaging in tuberculous meningitis. Neurol India 2016;64:219-27.  Back to cited text no. 6
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