Abstracts

Rationale: Epilepsy is the most common neurologic complication presenting in over 50% of new neurologic diagnoses in pregnancy and postpartum periods. Eclamsia and acute stroke are less common, in this setting, and do not fully explain new cases of epilepsy. The cause of epilepsy associated with pregnancy has not otherwise been shown. Lipoprotein a (Lp(a)) has recently been shown to be a cause of cardiovascular disease, and has long been known to cause stroke. Atherosclerosis can cause ischemic lesions which are subclinical and might later lead to seizures. Pregnancy is well known to cause elevation of cholesterol and triglyceride levels, which when combined with high Lp(a) might predispose to cerebral ischemia. Lp(a)level may rise in pregnancy as well, although it is relatively stable throughout the lifespan. Methods: Eleven women who developed epilepsy during or after pregnancy (up to 5 years) without other risk factors for seizures were compared to 11 patients (4 were men) with epilepsy prior to or unrelated to pregnancy for Lp(a) levels. All patients were between the ages of 20 and 56 years. MRI of the brain and EEG were reviewed when available. The groups were matched for antiepileptic medications, although 3 of the women with postpartum epilepsy were not yet treated. None of the women with pregnancy related epilepsy had hypertension. Results: There was a strong statistical difference between the groups for higher Lp(a) levels in the postpartum epilepsy group. The Mann-Whitney U test for median differences was significant at p<0.01. The mean concentration of Lp(a) was 149 nmol/L in the postpartum epilepsy group and 14 nmol/L in controls. All of the patients with postpartum epilepsy had Lp(a) levels over 100 nmol/L (very high). MRI scans and reports were available for review in 9/11 postpartum epilepsy patients. These showed one or more discrete white matter lesions in all patients, which were hyperintense on flair with fewer lesions on T2 weighted studies. 5 of the scans available for visual inspection revealed at least one lesion that was juxtacortical. EEGs were normal, non-specific theta bursts, or positive for epileptiform activity (8 studies) which was frontal or parieto-occipital but not temporal in locationConclusions: These results indicate that postpartum epilepsy is strongly associated with high Lp(a) levels. This suggests higher Lp(a) levels may be the predisposing factor for epilepsy in this population. This is supported by the presence of small vessel ischemic white matter lesions in these patients. Monitoring and treatment of elevated Lp(a) may be indicated in this population to prevent early atherosclerosis and its complications.