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| NI FEATURE: THE EDITORIAL DEBATE-- PROS AND CONS |
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| Year : 2016 | Volume
: 64
| Issue : 5 | Page : 860-861 |
Hydrocephalus and vasculitis delay therapeutic responses in tuberculous meninigitis: The neurologist's perspective
Sunil Pradhan
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
| Date of Web Publication | 12-Sep-2016 |
Correspondence Address:
Sunil Pradhan
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.190293
How to cite this article:
Pradhan S. Hydrocephalus and vasculitis delay therapeutic responses in tuberculous meninigitis: The neurologist's perspective. Neurol India 2016;64:860-1 |
The dilemma of response to antimicrobial agents in any given situation is as old as the discovery of these agents themselves and tuberculous meningitis is no exception. Though the virulence of an organism also plays a role in the final outcome, we can presume its effect to be negligible in a chronic infection such as tuberculosis, particularly when both arms of the study are from the same community. However, the other very important factor that determines the outcome is the duration of infection before starting anti-microbial therapy.[1] This is very difficult to assess in patients with tuberculous meningitis because several patients remain asymptomatic in early stages of the infection, and some others may fail to appreciate the associated mild fever or headache as being symptoms of any grave consequence.[1] Further, one must understand that the detrimental complications in granulomatous infections are as much the consequence of chronicity of infection as of immuno-allergic response of the body to the causative organism. In this context, the author's observation that the two most important poor prognosticators of tuberculous meningitis are hydrocephalus and intracranial vasculitis, appear quite pertinent and pathophysiologically understandable. Both complications occur as a result of late start or poor response to anti-tuberculous treatment and both have significant immuno-allergic response to brain structures such as the basal leptomeninges in the case of hydrocephalus, and the medium and small sized cranial blood vessels in the case of vasculitis.[2],[3] It is also important to note that in both these conditions, blood supply and perfusion of the brain suffers because of increased extra-luminal pressure in hydrocephalus and decreased intra-luminal pressure in vasculitis. This decreased blood supply, apart from causing ischemia of the brain, carries another risk of decreased availability of anti-tuberculous drugs at the site of bacillary infection, thus adding to the delayed therapeutic response. Irrespective of the complexities of the pathophysiology of the disease, the findings of this paper provide a simplistic clinical view of the status of the patients at the time of starting anti-tuberculous therapy and the expected clinical response. These findings, however, need to be understood in the proper perspective.
The authors are correct in saying that hydrocephalus and vasculitis delay the resolution of symptoms of tuberculous meningitis (TBM) but their view that “in the absence of hydrocephalus or vasculitis, one-week of anti-tuberculous treatment is adequate for the resolution of TBM symptoms” could be statistically correct but very difficult to extrapolate on TBM patients from developing countries where several other factors affect the therapeutic response. For example, disease related, drug induced or hepatitis related vomiting prohibits the initial use of four or five anti-tuberculous drugs in several patients, and very often, one or two of these drugs are withdrawn and re-introduced later on. Another factor that delays or slows down the therapeutic response is the partial or complete resistance to one or two drugs, which remains unnoticed so far as labeling a patient as having drug-resistance is concerned, because of efficacy of the remaining two or three drugs.
Hence, we may infer that the delayed clinical response in TBM patients with hydrocephalus and CNS vasculitis can have two different connotations. Firstly, it may suggest the delayed initiation of anti-tuberculous treatment that has allowed these complications to set in; and secondly, decreased perfusion pressure (decreased intra-luminal flow and pressure in vasculitis and increased extra-vascular pressure in hydrocephalus) would cause decreased availability of anti-tuberculous drugs at the target sites from the very beginning. Also, a combination of hydrocephalus and vasculitis is not uncommon. Often vasculitis related multiple small deep white matter infarcts are masked by peri-ventricular cerebrospinal fluid ooze of hydrocephalus that surprises a neurosurgeon who finds no improvement in symptoms after shunt surgery; or, he/she sometimes comes across worsening of symptoms due to an increase in cerebral ischemia, if the anesthetist is not aware of the fact that even transient hypotension during shunt surgery results in a compromised cerebral circulation and may lead to worsening of cerebral ischemia.
| » References | |  |
| 1. | Murthy J. Tuberculous meningitis: The challenges. Neurol India 2010;58:716-22.  [ PUBMED]  |
| 2. | Javaud N, Certal Rda S, Stirnemann J, Morin AS, Chamouard JM, Augier A, Tuberculous cerebral vasculitis: Retrospective study of 10 cases. Eur J Intern Med. 2011;22:e99-104. |
| 3. | Rajshekhar V. Management of hydrocephalus in patients with tuberculous meningitis. Neurol India 2009;57:368-74. [ PUBMED] |
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