Acute inflammation plays an important role in host tissue defense against injury and infection, and also subsequent tissue repair. In the central nervous system parenchyma, following many types of insults, the acute inflammatory response to rapid neuronal degeneration or challenge with inflammatory substances differs dramatically from that of other tissues. The rapid recruitment of neutrophils is virtually absent and monocytes are only recruited after a delay of several days. It appears that the microenvironment of the central nervous system has evolved mechanisms to protect it from the potentially damaging consequences of some aspects of the acute inflammatory response.