he second theory is that sudden elevations in systemic blood pressure exceed the normal cerebrovascular autoregulatory capacity (Hauser, 1988; Schwartz, 2000). Regions of forced vasodilation and vasoconstriction develop, especially in arterial boundary zones. At the capillary level, disruption of end-capillary pressure causes increased hydrostatic pressure, hyperperfusion, and extravasation of plasma and red cells through endothelial tight-junction openings. his leads to vasogenic edema. he recent description of a central nervous system lymphatic vasculature lends credibility to this theory (Louveau, 2015).
he most likely mechanism is a combination of the two.
hus, a preeclampsia-associated interendothelial cell leak develops at blood pressure (hydraulic) levels much lower than those that usually cause vasogenic edema and is coupled with a loss of upper-limit autoregulation (Fugate, 2015; Zeeman, 2009). With imaging studies, these manifest as theposterior reversible encephalopathy syndrome (Fig. 40-12) (Fugate, 2015; Hinchey, 1996). he lesions of this syndrome principally involve the posterior brain-the occipital and parietal cortices. But, in at least a third of cases, other areas are involved (Edlow, 2013; Zeeman, 2004a).
FIGURE 40-12 Cranial magnetic-resonance imaging in a nullipara with eclampsia. Multilobe T2-FLAIR high-signal lesions are apparent. FLAIR = fluid-attenuated inversion recovery. (Used with permission from Dr. Gerda Zeeman.)
Autoregulation is the mechanism by which cerebral blood flow sion pressure. Remember that cerebral perfusion pressure is the sure. In nonpregnant individuals, this autoregulation protects the brain from hyperperfusion when mean arterial pressures rise to as high as 160 mm Hg. hese are pressures far greater than those seen in all but a very few women with eclampsia. Thus, to explain eclamptic seizures, it was theorized that autoregu lation must be altered by pregnancy. Studies by Cipolla and colleagues (2007, 2009, 2015) have convincingly shown that autoregulation is unchanged across pregnancy in rodents. But, some investigators have provided evidence of impaired auto regulation in women with preeclampsia a anzarik, 2014; van
Veen, 2013).
Zeeman and associates (2003) showed that cerebral blood flow during the irst two trimesters of normal pregnancy is similar to nonpregnant values. But during the last trimester, low significantly drops by 20 percent. his group also found greater cerebral blood low in this trimester in women with severe preeclampsia compared with that in normotensive pregnant women (Zeeman, 2004b). Taken together, these findings suggest that eclampsia occurs when cerebral hyperperfusion forces capillary luid interstitially because of endothelial damage. This leak leads to perivascular edema characteristic of the preeclampsia syndrome.
Several neurological manifestations typiy the preeclampsia syndrome. Each signiies severe involvement and requires immediate attention.
First, headache and scotomata are thought to arise from cerebrovascular hyperperusion that has a predilection for the occipital lobes. Up to 75 percent of women have headaches, and 20 to 30 percent have visual changes preceding eclamptic convulsions (Sibai, 2005; Zwart, 2008). The headaches may be mild to severe and intermittent to constant. In our experiences, they are unique in that they do not usually respond to traditional analgesia, but they frequently improve ater magnesium sulfate infusion.