Analysis of dynamics and propagation of parietal cingulate seizures with secondary mesial temporal involvement

Abstract

Cingulate-onset seizures, particularly those originating from parietal cingulate regions, are inadequately described and confounded by patterns of propagation. We analyzed scalp and depth electrode recordings in a patient whose seizures originated from a lesion in the right posterior cingulate region and produced secondary seizure activity in ipsilateral mesial temporal structures. Analyses included the matching pursuit (MP) method of time-frequency decomposition and the Gabor atom density (GAD) measure of signal complexity. Although scalp recordings suggested a right temporal onset, seizures recorded with depth electrodes clearly began in the parietal cingulate region before producing a secondary discharge in ipsilateral mesial structures. GAD revealed a significant increase in complexity during ictal cingulate activity and a consistent pattern of subsequent complexity changes in the hippocampus 30 seconds later. MP and GAD measures were valuable supplements to confirm the stereotyped pattern of both time-frequency changes and complexity. This provides additional evidence for pathways between the parietal cingulate region and mesial temporal structures and raises questions as to whether parietal cingulate seizures can produce clinical symptoms independent of regional or remote propagation.

Figure 1

Axial T2 weighted image (A) and sagittal T1 weighted (B) images show the lesion (arrows), centered in the posterior cingulate gyrus. There was only mild patchy enhancement (not shown) and no significant edema or mass effect. Panel C shows a coronal T2 image with a depth contact proximal to the lesion, and panel D shows a sagittal T1 image with the location of another depth electrode. Not all depth contacts are visible because the trajectory of the depth arrays was not in the plane of the MR sections.

Figure 2

Panel A illustrates one of ten seizures recorded with scalp arrays suggesting a right temporal lobe seizure onset. The ten seizures were similar clinically and electrographically. Scalp recordings were done prior to depth recordings. Panel B illustrates one of the three seizure recorded with intracranial depth electrode arrays; the two ICEEGs are continuous. A prominent spike is seen from the cingulate region followed by low voltage fast activity better illustrated in the exploded view. Later prominent activity is recorded from the right hippocampal and amygdalar electrodes. No clinical signs or symptoms were seen or reported until the temporal lobe involvement with the seizures. All three seizures recorded with intracranial arrays were similar clinically and electrographically.

Figure 3

Panels A and C are time-frequency decompositions using the matching pursuit method for the same time periods after seizure onset (time 0) as for the seizure shown in Fig. 2B recorded with intracranial depth arrays; all seizures had similar patterns. The energy of the signal is color-coded (blue is low energy, red is high energy). The GAD is plotted as a black line representing the composite complexity of the signal for the same time period. The cingulate recording (from contact 2-3, see Figure 2B) shows the clear onset in the cingulate region and the gamma frequency bands as well as the increase in complexity represented by increased GAD. No GAD increase or ictal activity is identified in the mesial temporal recordings (hippocampal 2-3 shown) until approximately 30 seconds after seizure onset. At this time prominent activity is present in the hippocampus (7-8 Hz with associated harmonics). Only the first 45 seconds of the seizures are shown on the time-frequency maps. On the right two panels (B and D) the GAD plots for all three seizures are shown for the entire seizure duration showing the similar patterns for all three seizures supporting the cingulate origin of all three seizures with similar latencies of spread to hippocampal regions. The black GAD plot in panels B and D is the same as in panels A and C.