Preeclampsia constitutes a heterogeneous multisystemic disorder defined by the new onset of
hypertension and proteinuria after 20 weeks of gestation.1 The incidence of preeclampsia in
Switzerland is estimated at 2.31 % of pregnancies (95% CI 1.62-3.28%), about 1'911 cases/year
can be expected to occur on the national level. Preeclampsia and eclampsia are considered a
continuum in the hypertensive disorders of pregnancy. When convulsions or coma occur in
addition to hypertension the condition is referred to as eclampsia. Up to 2-3% of severely
preeclamptic women will have eclampsia,4 with a consecutive mortality rated between 0-14%.5
The diagnosis of preeclampsia is challenging, because of clinical heterogenity, especially at
early stages. Until recently no routine laboratory test or biological marker other than
presenting clinical symptoms such as severe headache or arterial hypertension, decreased
plasmatic thrombocyte count and proteinuria were available for diagnostic purposes.
The only curative treatment of severe preeclampsia and eclampsia consists of delivery of
fetus and placenta. Since the 2002 Magpie trial, the mainstay of eclampsia prevention in
severely preeclamptic patients relies on the prophylactic use of intravenous magnesium,
either when prompt delivery can be performed, or if it has to be delayed for fetal reasons.
Obviously, eclampsia prevention is critical, considering that eclampsia onset can occur pre,
intra, or postpartum. Hereby the prophylactic magnesium treatment is mostly maintained
throughout a period of several days before and after delivery of the fetus and placenta, as
up today there is no reliable clinical or diagnostic approach to predict the risk of
eclamptic seizures.
The actual gold standard in high-risk maternities is to assess clinical symptoms as described
above and perform newer laboratory essays, in order to estimate the parturient's risk for
preeclamptic complications. Insofar changes in serum levels of fms-like tyrosine kinase-1
(sFlt-1) and placental growth factor (PGIF) were lately revealed and have been currently
approved as diagnostic aid in preeclampsia. Circulating maternal serum levels of sFlt-1 are
increased, and PGIF are decreased in preeclampsia. As an antagonist of PGIF and vascular
endothelial growth factor, sFlt-1 causes vasoconstriction and endothelial damage. Noteworthy
a sFlt-1:PIGF ratio lower than 38 can be used as to predict a short-term absence of
preeclampsia in women with suspect clinical symptoms.
Interestingly novel knowledge points to a strong link in between plasmatic steroid hormones
and epilepsy, with strong animal data pointing towards a higher epileptogenic potential in
high estrogenic states; whereas androgens, namely progesterone seem to induce a protective
state through agonism on extrajunctional GABAA receptors.
EEG slopes are good markers for epileptiform activity. EEG changes have been reported in
eclampsia and in severe preeclampsia, with differences also reported between severe
preeclampsia and eclampsia.Recently, slow waves most frequently localized in the occipital
lobe, as well as spike discharges in EEG, were reported as warning signs of deterioration of
brain function in preeclampsia or eclampsia. Neither have electroencephalic correlates of
sFlt-1, PGIF or hormonal states been investigated in preeclampsia. EEG is not in routine use
for convulsive risk assessment in maternity wards, when preeclampsia screening is performed.
One of the reasons might be that performing EEGs is time consuming and involves significant
human resources for urgent EEG analysis. These resources might be lacking even in tertiary
hospitals. Novel reliable, noninvasive and technically easy to perform simplified EEG methods
have become available, these are especially in use during anesthesia for detection of
clinically silent epileptic potentials.