Introduction

Eclampsia is one of the most severe forms of central nervous system (CNS) involvement in the pre-eclampsia syndrome. Although pre-eclampsia has been known to be a multisystem disorder for over 100 years, much of the pathophysiology, including its molecular manifestations, has only come to light in the past 20 years. This is exemplified by the fact that the prominent causative role of endothelial activation has only been recently appreciated (Redman et al., 1999; Roberts and Redman, 1993; Roberts et al., 1989; Taylor and Roberts, 1999). Currently, the CNS findings in eclampsia can be grouped in two ways: (1) Cerebral blood flow changes associated with gestational hypertension resulting in either hyperperfusion or hypoperfusion, either of which can cause edema and ischemia. (2) Characteristic anatomical lesions documented with either computed-tomographic (CT) scanning or magnetic resonance imaging (MRI) with diffusion-weighted techniques (Brown et al., 1988; Cunningham and Twickler, 2000; Dahmus et al., 1992; Digre et al., 1993; Hauser et al., 1988; Morriss et al., 1997; Port et al., 1998; Schwartz et al., 1992, 2000; Zeeman et al., 2004). These groupings are obviously artificial and there is a large amount of overlap. Specifically, endothelial injury and subsequent leakage of plasma from the intravascular compartment may be associated with manifestations of both functional flow abnormalities and discreet anatomical lesions. In our current understanding of the vascular involvement of the brain in eclampsia, we assume that the cerebral blood vessels are directly involved – in a similar fashion to the peripheral circulation in pre-eclampsia (Hankins et al., 1984).