High-resolution imaging of cortical and subcortical structures in patients with intractable epilepsy

This summer, I have been using imaging modalities to study the neuroanatomical changes that occur in patients with intractable epilepsy or epilepsy that is unresponsive to pharmacotherapy. Previous work has shown that in patients with epilepsy, cortical and subcortical structures ipsilateral to the seizure focus are smaller or undergo greater atrophic changes in comparison to the structures contralateral to the focus. These changes have been observed in structures such as the hippocampus, caudate, thalamus and lenticular nuclei. Seizure duration, history of febrile seizures and head trauma may also contribute to the loss of tissue volume in these structures. While the thalamus has been studied for evidence of tissue volume loss, the individual thalamic nuclei, such as the anterior thalamic nucleus, have not been as well-studied. Recent work has demonstrated with some success the anticonvulsant effects of deep brain stimulation of the anterior thalamic nucleus in patients with generalized seizures. As part of the loop of Papez, the anterior thalamic nucleus shares connections with the mammillary bodies and cingulate gyrus. High-frequency stimulation of the anterior thalamic nucleus and the structures which project to the nucleus led to a reduction of seizure activity. In this project, I am examining the tissue volume loss of temporal and extratemporal structures in patients with intractable epilepsy, with a focus on changes in the anterior thalamic nucleus. I am interested in whether the anterior thalamic nucleus undergoes the same atrophic changes as demonstrated in other structures, specifically on the side ipsilateral to the seizure focus. In addition to studying the changes in the anterior thalamic nucleus with clinical variables such as epilepsy duration and history of febrile seizures, I am also looking at the relationship between tissue volume loss and a history of major depressive disorder, one of the most common comorbidities associated with epilepsy. The goal of my work is to determine whether there are changes in the anterior thalamic nucleus in patients with intractable epilepsy. If there are changes, are they observable with high-resolution imaging modalities? Are the changes consistent with other clinical variables associated with cortical and subcortical atrophy evident in epilepsy patients?