Serial multimodal monitoring of cerebral manifestations in eclampsia and comparison with normal pregnancy: a clinical study

Abstract

Eclampsia is characterized by seizures, coma, or focal neurological deficits in pregnant women with pre-eclampsia. It is not known if brain lesions are caused by vasospasm with hypoperfusion or by hypertension-induced breakdown of cerebrovascular autoregulation with hyperperfusion [1–3]. Ultrasound studies reported an increase of flow velocities and assumed vasospasm but did not prove it by a pathological middle cerebral artery (MCA)/internal carotid artery (ICA) (Lindegaard)-index in combination with angiography [4, 5]. However, also cerebral hyperperfusion and decreased resistance (vasodilatation) of intracerebral arteries have been reported in eclampsia [5, 6]. Low intracranial Doppler resistance and pulsatility indices predict a high risk of developing pre-eclampsia [6]. It is not clear if raised intracranial blood flow velocities are due to vasospasm or hyperperfusion [7]. Serial and multimodal investigations have been requested to improve the understanding of eclampsia [4]. A 34-year-old pregnant patient developed arterial hypertension (up to 200/140 mmHg) and proteinuria (2 ?). After two epileptic seizures (focal and generalized tonic– clonic), she was admitted to our hospital at her 37th week of pregnancy with the diagnosis of eclampsia. She suffered from pulsating headache of maximal intensity. Her neurological examination was regular. Ultrasound showed partial placental abruption. She gave birth to a healthy male infant weighing 2,955 g by emergency cesarean section. Seizures ceased with short-term clobazepam and long-term carbamazepine. CRP, AST, ALT, LDH, and leukocytes were transiently increased (Table 1). EEG showed bilateral intermittent slow theta waves and sharp transients. One day postpartum, MRI (T2 and fluid-attenuated inversion recovery FLAIR) showed multifocal, non-confluating, non-enhancing hyperintensities in both cerebral hemispheres without diffusion restriction, indicating vasogenic edema (Fig. 1a). MRA detected multifocal irregular lumen constrictions of bilateral anterior, middle, and posterior cerebral arteries (Fig. 1c). The follow-up brain MRI and MRA demonstrated complete normalization after 1 year (Fig. 1b, d). Global cerebral blood flow (GCBF) was measured as the sum of blood volume flow in both internal carotid and vertebral arteries [8]. Cerebral blood flow velocities (CBFV) and pulsatility were assessed by transcranial duplex ultrasound (DUS). Three days postpartum, CBFV of all intracranial arteries were raised, and both MCA/ICA indices and GCBF were increased; the pulsatility index of both ICAs was decreased (Table 1; Fig. 1e). Ten days postpartum, intracranial peak systolic flow velocities, MCA/ICA indices, and GCBF decreased (Table 1). Twenty days postpartum, blood flow velocities, MCA/ICA J. E. Roehl and S. J. Schreiber contributed equally to this article.