The pathogenesis of cerebral vasospasm in bacterial meningitis

Abstract Introduction Cerebral inflammation in bacterial meningitis has been associated with vasospasms of cerebral arteries and arterioles. Vasospasm has been associated with permanent neurological deficits and death. The objective of the review was to summarise evidence for the involvement of inflammatory mediators in the pathogenesis of cerebral vasospasm. Materials and methods Databases Pubmed, EMBASE and the Cochrane Library were searched and reference list of retrieved articles was taken using keywords, including cerebral vasospasm, meningitis and inflammation. Results Increased levels of interleukin-1 may be involved in vasospasm through the release of vasoconstrictor endothelin-1. Another key factor in the pathogenesis of cerebral arterial vasospasm may be the reduced bioavailability of the vasodilator nitric oxide. Therapeutic trials in vasospasm related to inflammation showed a reduction of vasospasm through calcium antagonists. The importance of inflammation in causing vasospasm has been highlighted by the successful reduction of features of vasospasm and morbidity by anti-inflammatory agents, including steroids and acetylsalicylic acid, which merit further study in all conditions with cerebral inflammation in double blind placebo controlled randomised trials. Conclusion Key factors in the pathogenesis of cerebral vasospasm in bacterial meningitis are the depletion of nitric oxide and effects of endothelin and interleukin-1. Auxiliary treatment increasing nitric oxide levels and antagonising the other inflammatory mediators may be able to reduce ischaemic brain injury associated with neurological deficits and increased mortality in bacterial meningitis.