Behavioral risk factors among Arizonans with epilepsy: Behavioral Risk Factor Surveillance System 2005/2006.

Modifiable risk factors to help improve health outcomes for people with epilepsy in Arizona were identified using the 2005-2006 Arizona Behavioral Risk Factor Surveillance System (BRFSS). Of 9524 adults who participated in this survey, 125 reported ever being diagnosed with epilepsy (lifetime prevalence=1.3%, 95% CI=1.1-1.6%). Individuals with active epilepsy (those who had seizures in the prior 3 months and/or were taking anticonvulsants) had an overall lower quality of life. This likely resulted from a large number of medical comorbidities and poor mental and physical health days. Regression models suggested that for individuals with active epilepsy, physical activity was associated with fewer activity-limited days, whereas for individuals with inactive epilepsy, medical comorbidity was positively associated with activity-limited days. Further research is needed to increase the reliability of the findings.

"Tectonic" hippocampal malformations in patients with temporal lobe epilepsy.

Histological analysis of hippocampi removed en bloc during surgical treatment of temporal lobe epilepsy revealed a subgroup of patients with bulbous expansions of the CA1 pyramidal cell/subicular layers that were consistently accompanied by "tectonic" invaginations of the adjacent dentate gyrus. Most hippocampi containing the CA1/subicular anomaly and the tectonically deformed dentate gyrus exhibited minor cell loss compared to hippocampi with typical hippocampal sclerosis, and retrospective analysis revealed that conventional imaging methods usually failed to detect subtle hippocampal atrophy or abnormal signal characteristics in patients with this anomaly. Cells within the anomaly exhibited the spherical appearance of undifferentiated pyramidal layer neurons, and were immunopositive for the neuronal marker NeuN. Immunostaining for the synaptic marker beta-synuclein suggested abnormal dentate gyrus lamination in segments containing the pyramidal cell layer anomaly, but not in unaffected areas of the same specimens. Despite differences in the extent of neuronal loss between patients with hippocampal sclerosis and those with the CA1/subicular anomaly, the incidence of antecedent febrile seizures was similar in both groups. In a comparison group of hippocampi obtained at autopsy, structural irregularities were evident, but were consistently less disruptive to hippocampal architecture than the anomalies observed in epilepsy patients. We hypothesize that developmental malformation of the CA1 pyramidal cell/subicular layers may adversely influence the subsequent development of the adjacent dentate gyrus, and may render temporal lobe structures hyperexcitable and more vulnerable to relatively innocuous seizures and injuries. Thus, these presumably developmental hippocampal anomalies may serve as substrates for early febrile seizures and subsequent epilepsy.