Convulsions are diagnostic for eclampsia. These are caused by excessive release of excitatory neurotransmitters-especially glutamate; massive depolarization of network neurons; and bursts of action potentials (Meldrum, 2002). Clinical and experimental evidence suggests that extended seizures can cause signiicant brain injury and later brain dysfunction.
Blindness is rare with preeclampsia alone, but it complicates eclamptic convulsions in up to 15 percent of women (Cunningham, 1995). Blindness may develop up to a week or more following delivery (Chambers, 2004). There are at least two ypes of blindness, as discussed subsequently.
Generalized cerebral edema may develop and is usually manifest by mental status changes that vary from confusion to coma. This situation is particularly dangerous because fatal transtentorial herniation can result.
Last, women with eclampsia have been shown to have some cognitive decline when studied 5 to 10 years following an eclamptic pregnancy. This is discussed further in the inal section (p. 745).
With CT imaging, localized hypodense lesions at the gray-and white-matter junction, primarily in the parietooccipital lobes, are typically found in eclampsia. Such lesions may also be seen in the frontal and inferior temporal lobes, the basal ganglia, and thalamus (Brown, 1988). These hypodense areas correspond to petechial hemorrhages and local edema. Edema of the occipital lobes or difuse cerebral edema may cause symptoms such as blindness, lethargy, and confusion (Cunningham, 2000). Widespread edema can appear as marked compression or even obliteration of the cerebral ventricles. Such women may develop signs of impending life-threatening trans tentorial herniation.
Several MR imaging acquisitions are used to study eclamptic women. Common findings are hyperintense T2lesions-namely, posterior reversible encephalopathy syndrome (PRES)-in the subcortical and cortical regions of the parietal and occipital lobes (see Fig. 40-12). Also, the basal ganglia, brainstem, and cerebellum are relatively commonly involved (Brewer, 2013; Zeeman, 2004a). Again, these lesions represent focal cerebral edema. Although these PRES lesions are almost universal in women with eclampsia, their incidence in women with preeclampsia approximates 20 percent (Mayama, 2016). Lesions are more likely in women who have severe disease and who have neurological symptoms. And although usully reversible, a fourth of these hyperintense lesions represent cerebral infarctions that have persistent indings (Loureiro, 2003; Zeeman, 2004a).
Scotomata, blurred vision, or diplopia are common with severe preeclampsia and eclampsia. hese usually improve with magnesium sulfate therapy and/or lowered blood pressure. Blindness is less common, is usually reversible, and may arise from three potential areas. These are the visual cortex of the occipital lobe, the lateral geniculate nuclei, and the retina. In the retina, pathological lesions may be ischemia, infarction, or detachment (Handor, 2014; Roos, 2012).
Occipital blindness is also called amaurosis-from the Greek dimming. With imaging, afected women usually have evidence of extensive occipital lobe vasogenic edema. Of 15 women cared for at Parkland Hospital, occipital blindness lasted from 4 hours to 8 days, but it resolved completely in all cases (Cunningham, 1995). Rarely, extensive cerebral infarctions may result in total or partial visual defects.