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February 2008

Stroke Secondary to Meningococcal Meningitidis: A Potential Link Between Endothelial Dysfunction and Cytokines

Arch Neurol. 2008;65(2):282-284. doi:10.1001/archneurol.2007.36

The recent article by van de Beek et al1 described presentation of brainstem infarction secondary to Neisseria meningitidis. Unfortunately, the authors failed to explore a potential connection between brainstem infarction and cytokine network pathway. Meningococcal pathogenesis involves multiple links that interconnect in a highly intricate web of phenomena from neisserial attachment to meningitis or meningococcal sepsis.2 In fact, there are various pathways within the vascular compartment and in the subarachnoid space that are involved in the human-meningococcal interaction, such as the hemostatic system and cytokine network pathway.3 Cytokines are key mediators involved in mediating the systemic inflammatory response, and they have critical biological effects on coagulation cascade and many cell types such as endothelium. Meningococci can trigger an explosive inflammatory response in the central nervous system, characterized by elevated levels of cytokines, which can lead to a loss of endothelial homeostasis.4 We recently reported a case of neisserial infection, complicated by cerebral infarction.4 Concentrations of IL-6 were particularly elevated in the cerebrospinal fluid of the patient.

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