PMC

Magnetic resonance imaging (MRI) shows posterior temporal dysplasia leading to cyst not connected to ventricle. A depth electrode runs in the cleft between the two sides of the dysplasia. Electrode 1, is in the cyst and electrode 2 (arrow), is at the deepest point of the dysplasia. In the electroencephalography (EEG), seizure onset is electrode 2. Note that electrodes 3, 4, and 5, which are adjacent, but more superficial, are not involved. The next involved set of electrodes is a number of seconds later at the mesial temporal contacts (the electrodes labeled “EC”). Resection of the dysplasia resulted in seizure freedom. This case demonstrates how focal seizures can be in onset and how the spread is not always to adjacent structures. It also emphasizes that surface recordings (strips or grids) will not reveal seizure onset from underlying cortical abnormalities

Thalamic involvement in limbic seizures. (a) Spontaneous limbic seizure from a rat with limbic epilepsy. Onset is synchronized between the medial dorsal thalamic nucleus and the hippocampus (HC). Time bar is 2 sec. (b) Seizure induced in the HC with direct electrical stimulation. Top trace is baseline recording. Bottom trace follows infusion of inhibitory drug muscimol in medial dorsal nucleus of the thalamus, which results in a significant shortening of seizure duration and prevention of secondary generalization. Infusion adjacent to, but outside the medial dorsal nucleus has no effect on any seizure characteristic. These data demonstrate the involvement of a specific thalamic nucleus in limbic seizures and how precise the placement of the therapeutic intervention has to be. It also demonstrates the importance of the concept of circuit in epilepsy. Time bar is 5 sec