Conditions involving more obvious destruction of brain parenchyma, such as hydrocephalus (Tullberg et al., 1998; Beems et al., 2003; Petzold et al., 2004) or cavitating lesions (Rosengren et al., 1994), might also be expected to contribute to increased spillage of GFAP into the extracellular space, and subsequently into CSF and blood. This evidence concerns the gene GFAP and Hydrocephalus.