Abstracts

Rationale: Long-term invasive monitoring of patients with intractable epilepsy has demonstrated propensity of mesial temporal lobe seizures to propagate to the contralateral hippocampus, without clear involvement of the contralateral neocortex. Identifying the pathways of seizure propagation between the mesial temporal lobes is important, as it may explain false lateralization of some temporal lobe seizures when recorded by scalp EEG, and may even shed light on mechanisms of secondary epileptogenesis. In addition, such pathways may constitute an important target for deep brain stimulation for treatment of intractable bitemporal lobe epilepsy. Although some authors reported absence of direct connectivity between contralateral limbic structures, a postmortem study of human brains has identified the dorsal hippocampal commissure (DHC) as an easily recognizable and sizeable pathway. To date, no in vivo electrophysiological demonstration of this pathway has been reported. Methods: A 32 year-old right handed woman started to have seizures at the age of 10 months in the setting of bacterial meningitis. Her current seizures are of two types. One type consists of feeling a metallic taste with no clear alteration of awareness, and the other consists of an abdominal aura with oral automatisms and decreased responsiveness. Her Brain MRI was normal. Her seizures were refractory to maximal medical therapy. Scalp EEG monitoring revealed independent, bilateral temporal lobe seizure onsets. Thus, depth electrodes were implanted in bilateral hippocampi, parahippocampi, and amygdalae, among other regions. In addition, one depth electrode probe was implanted in the DHC from the right side and another from the left (Fig. 1). Single pulse stimulation (frequency 1 Hz, pulse width 0.5 msec, and current intensity 2-10 mA) was applied to the right and left DHC electrodes as well as to the hippocampi, and the EEG was averaged off line. Results: Cerebro-cerebral evoked potentials (CCEPs) were recorded bidirectionally between the hippocampi and the DHC (Fig. 2-4). Early and late components were seen. The early components of the CCEPs recorded in the hippocampi upon stimulation of the DHC, as well as those recorded in the opposite direction, had a latency of ~8 msec (Fig. 2). Conclusions: This is the first in vivo demonstration of connectivity between the DHC and bilateral mesial temporal structures. The results suggest that seizure propagation from one medial temporal lobe to the other, without involvement of neocortex, may be mediated by the DHC. In addition, the DHC may constitute a target for stimulation in patients with intractable bitemporal lobe epilepsy.