cells. In contrast, a decrease in NT-3 mRNA expression in the hippocampus was seen after kindled seizures. Changes were transient reaching maximal levels 1-4 h following the seizure and returning to baseline within 24 h. No change in trkA mRNA was observed. After generalized seizures, in- creases in BDNF mRNA expression were seen also in amygdala, piriform cortex, and neocortex. These mRNA changes are followed by alterations in protein synthesis as evidenced by elevated levels of NGF and trkB protein fol- lowing kindled seizures.

We have demonstrated that mRNAs for BDNF and its re- ceptor trkB are coexpressed in hippocampal and cortical neurons. Kindled seizures lead to increased levels of both BDNF and trkB within the same cell. The parallel increase in neurotrophin and receptor expression suggest an autocrine and/or paracrine trophic stimulation. Such trophic support might protect neurons against seizure-induced damage. Alternatively, elevated neurotrophin levels might lead to plastic changes and synaptic reorganization underlying in- creases in seizure susceptibility in kindling and possibly also during development of human epilepsy.

CALCIUM ACCUMULATION AFTER STATUS EPILEP- TICUS--EFFECTS OF HIGH POTASSIUM-INDUCED NEURONAL DEPOLARIZATION. B. S6derfeldt (Depart- ment of Neurology, University Hospital, LinkOpin~.

Using electron microscope and the combined oxalate- puroantimonate technique, calcium can be located in hip- pocampal neurons of rats with different types of pharma- cologically induced status epilepticus. Calcium overload of mitochondria may be an important cytotoxic mechanism producing selective neuronal loss.

In the present study, amygdal perfusion of high-K + was compared to contralateral perfusion of Krebs' solution on the degree of Ca 2+ deposition in damaged neurons.

The results for pilot animals of different study groups are presented. The results show that the combined oxalate- puroantimonate technique is useful to detect evidence of irreversible neuronal damage at an early stage.

POSITRON EMISSION TOMOGRAPHY (PET) WITH UC-DEUTERIUM-DEPRENYL IN TEMPORAL LOBE EPI- LEPSY. 1E. Kumlien, 3M. Bergstr6m, 2A. Lilja, 3j. Andersson, 1C.-E. Westerberg, 3G. Westerberg, 3G. Antoni, and 3B. IAng- str6m (Departments of 1Neurology, 2Diagnos~c Radiology, and 3Uppsala PET Center, University Hospital, Uppsala).

It is conceivable that markers of gliosis could be useful as detectors of epileptogenic tissue, since the most common pathology in partial epilepsy is gliosis. Monoamine oxidase type B (MAO-B) is a mitochondrial enzyme located in astrocytes. Increased MAO-B activities have been found in hippocampi from patients operated on because of temporal lobe epilepsy. Deprenyl is an inhibitor of MAO-B. An autoradiographic study has shown an increased binding of 3H-deprenyl in epileptic hippocampi. These observations formed the background of our hypothesis that positron emission tomography (PET) with Deprenyl would show an enhanced uptake of the ligand in epileptogenic regions.

Nine patients with mesiotemporal seizure onset were

SWEDISH EPILEPSY SOCIETY ABSTRACTS

examined with PET with UC-deuterium-deprenyl. Two of the patients had bilateral seizure onset.

Using 11C-deuterium-deprenyl, the focus region was de- termined visually on PET images and compared with the EEG focus as defined by ictal epileptiform discharges, and with PET with fluoro-deoxyglucose. In addition, the rela- tive accumulation rate was measured in standardized re- gions. Mean interlobar ratios were formed in order to make the two PET methods comparable, thus allowing interindi- vidual comparisons.

With this PET tracer, the temporal lobe containing the epi- leptic focus was identified in the seven unilateral cases. The two bilateral cases were correctly identified as such.

EPILEPSY AND PREGNANCY: SEIZURE CONTROL, PHARMACOKINETICS, AND RED-CELL FOLATE LEV- ELS. T. Tomson, U. Lindbom, and A. Sundquist (Depart- ments of Neurology, Karolinska and SOder Hospital, Stockholm).

Seizure control, plasma concentrations of antiepileptic drugs, and red-cell folate levels were determined in a pros- pective population-based study of 93 pregnancies (cases) of 70 patients with epilepsy. Most cases were on monothera- py, predominantly carbamazepine (CBZ) or phenytoin (PHT). The dosages were altered only in the case of poor seizure control. Plasma concentrations were determined at monthly intervals throughout pregnancy and compared to levels at least 10 weeks' postpartum. The seizure frequen- cy during pregnancy was, for the group as a whole, not different during pregnancy as compared to during the nine pregestational months. Total CBZ concentrations were slightly lower during the third trimester compared to base- line, whereas free concentrations were unchanged. PHT levels decreased steadily as pregnancy progressed. Total plasma concentrations were 39% of baseline during the third trimester, but free concentrations decreased to a much lesser extent, being 82% of baseline levels at the third tri- mester. Changes in ethosuximide concentrations were less consistent; the enantiomeric ratio of this racemic drug was unchanged, however. No clear-cut relationship could be demonstrated between seizure control and plasma concen- trations. Red-ceil folate concentrations during the first tri- mester were comparable to those found in nonepileptic pregnant women and in age-matched nonpregnant healthy women.

THE OUTCOME IN CHILDREN OF EPILEPTIC MOTH- ERS ON WELL-CONTROLLED TREATMENT DURING PREGNANCY: A POPULATION-BASED CASE-CON- TROL STUDY. IIC Wide, lB. Winbladh, 2B. K/~llen, 3K. Str6mland, and 4L. Jacobson (Department of 1Pediatrics, Kar- olinska Hospital and Sach's Childrens Hospital, Stockholm; 2De- partment of Embryology, Univeristy of Lund, Lund; ZDepartment of Pediatric Ophthalmology, University of Gothenberg, East Hos- pital, Gothenburg; 4Department of Ophthalmology, Huddinge Hospital, Stockholm).

The aim of this ongoing prospective study is to investi- gate the outcome regarding minor abnormalities and psy- cho-motor development in children of epileptic mothers treated under well controlled conditions.

j EPILEPSY, VOL. 7, NO. 4, 1994 325