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Letters to the Editor
4 (
3
); 374-375
doi:
10.4103/0976-3147.118775

Nitrite, vasodilation, and headache in bacterial meningitis: Theoretical approach

Address for correspondence: Prof. Viroj Wiwanitkit, Wiwanitkit House, Bangkhae, Bangkok, Thailand. E-mail: wviroj@yahoo.com
Licence

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Disclaimer:
This article was originally published by Medknow Publications & Media Pvt Ltd and was migrated to Scientific Scholar after the change of Publisher; therefore Scientific Scholar has no control over the quality or content of this article.

Sir,

Meningitis is an important neurological disorder. Bacterial meningitis is a common type of meningitis that is considered as a serious neurological infection. Severe headache with stiff neck is an important clinical manifestation of bacterial meningitis. Basically, it is proposed that the severe headache is due to a possible stimulation of nociceptive nerve-endings in the meningeal vessel wall.[1] However, the exact pathogenesis of the severe headache in bacterial meningitis has never been clarified. The author hereby discusses the theoretical approach to explain the ethiopathogenesis of headache in bacterial meningitis. On the basis of the basic biochemical theory, existence of bacteria in cerebrospinal fluid (CSF) results in several biochemical changes, including glucose utilization and production of nitrite.[2] Kornelisse et al. reported the elevation of nitrite in the CSF of the patients with bacterial meningitis, confirming this proposed mechanism.[3] The resulted nitrite, a potent vasodilator,[4] will be an important factor causing generalized vasodilatation in meninges and this can finally result in severe headache. In addition, triptans have recently found a role in headache management in meningitis patients.[5] Triptans, as a nitrite scavenger, acts at perivascular serotonin receptor, leading to vasoconstriction.[5] The author hereby proposes a theoretical discourse that the production of nitrite bacteria might have clinical relationship to severe headache in bacterial meningitis.

References

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  4. , , , . The nitrate-nitrite-nitric oxide pathway in physiology and therapeutics. Nat Rev Drug Discov. 2008;7:156-67.
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  5. , , , , , , . Triptans reduce the inflammatory response in bacterial meningitis. J Cereb Blood Flow Metab. 2002;22:988-96.
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