Impaired cerebral glucose metabolism in eclampsia: a new finding in two cases.

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.