Impaired Cerebral Glucose Metabolism in Eclampsia: A New Finding in Two Cases

This is the authors' abstract. We don't add key points for this paper.

The pathophysiology of the reversible neurological manifestation in eclamptic women remains unclear. We report on 2 women with eclampsia who were repetitively examined by (1) transcranial Doppler (TCD), (2) magnetic resonance imaging (MRI) including T1- and T2-weighted images, fluid attenuated inversion recovery sequence, dynamic susceptibility-weighted perfusion imaging and magnetic resonance angiography (MRA), and (3) (18)fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET). In both cases repetitive TCD revealed no signs of vasospasm; the same was true for MRA. MRI perfusion imaging showed completely homogenous cerebral blood flow in both cases. In the initial phase T2-weighted images revealed hyperintensities in both patients (predominantly bilateral frontal and parietal in 1 and in the temporo-occipital subcortex and the basal ganglia in the other). FDG-PET showed inhomogeneous glucose metabolism (GM) in both patients. Primary increased glucose utilization in the hyperintense T2-weighted areas as well as an attenuated GM parieto-occipital were observed in the 1st case; a high GM was found bilaterally in the basal ganglia and an attenuated one in the occipital cortex in the 2nd. In both cases MRI, and FDG-PET normalized within 3 weeks. These case reports document an altered cerebral GM in the presence of homogenous perfusion in eclamptic women. The high GM may be explained by a decoupling of cerebral perfusion and GM, possibly indicating an increased neuronal activity. The attenuation of the GM is most probably due to a deafferentation of cortical neurons.