Posterior cingulate epilepsy is a rare and diagnostically challenging form of epilepsy owing to the particular anatomical position of the posterior cingulate . In the present study, we analysed semiological characteristics and EEG/SEEG data to identify anatomic-electrical-clinical relationships in 12 patients with posterior cingulate epilepsy.
Previous studies have revealed that posterior cingulate epilepsy is associated with several types of premonitory auras.In one such study, dyscognitive aura(déjà vu, jamais vuor depersonalization),abdominal aura,gustatory aura,and sensations of falling or movement were reported in three patients. Two patients had multipleauras.The dyscognitive aura and abdominal aura were elicited by stimulation of the limbic structures of the temporal lobe.Our findings are mostly consistent with these previous studies, although visual and vestibular aura occurred more frequently in our patient group, which was elicited by electrical stimulation of the humanposterior cingulate cortex.
It was difficult to localize the ictal onset areas based on scalp EEG.Previous reports have shown that scalp interictal and ictal EEG lateralize or localize the seizures correctly in 50%-60% of posterior cingulate epilepsy cases. In the present study, we found that interictal or ictal epileptiform discharges were most observed in the temporo-parieto-occipital region but little in the temporal region, which was different from that observed in TLE. Interictal and ictal discharges in temporal areas were detected in the scalp EEG in only three patients (pts.2,4 and 10). However, two patients (pts.2 and 10), whose seizures resembled temporal lobeseizures[4, 9], underwent anterior temporal lobectomy but failed to achieve a seizure-free outcome.We used SEEG to reevaluate patients and found that the seizure onset zone (SOZ) was localized in the posterior cingulate gyrus.Two patients who had undergone posterior cingulate gyrus surgery were seizure-free at the end of the follow-up period.
Therefore, it is difficult to distinguish PCG from non-PCE via scalp EEG, particularly the mesial-temporal lobe epilepsy.SEEG represents a unique method for identifying and characterizing the underlying physiological mechanisms of PCE.
In SEEG methodology, the EZ is defined as the site of origin for epileptic seizures.Therefore, we focused our SEEG analyses mainly on the identification of the brain regions in which specific ictal patterns developed during seizures.The regions associated with the primary organization of ictal discharges and subsequent propagation were correlated with the anatomical positions of the electrodes that displayed the maximal abnormal activity and with the evolution of clinical seizure signs.
We analysed a case series of twelve patients in the present study, seven of whom exhibited temporal lobe seizures[1, 2, 4], and the remaining patients had complex motor behaviours. Our study revealed that the semiologyof PCE can involve dialeptic or automotor seizures, which depended upon the seizure spreading to mesialtemporal structures,the precuneusor the IPL.Structural connections via cingulate tracts were found between the IPL and PCC in all subjects with both streamline and probabilistic analyses[14, 15]. These findings are consistent with the previous hypothesisthat alterationsin consciousness and automatisms in PCE reflect the involvement of the temporal lobes[1, 4, 9].
Complex motor behaviours may also be observed in the latecourse of posterior cortex seizures, once the seizure propagates to more anterior regions.In the present study,the most common clinical characteristics of complex motor behaviours were exploratory gaze movements and bilateral hand fumbling movements. In these patients, complex motor behaviours were observed only when ictal activity assessed by SEEG had spread to the precuneus, MCC, medial temporal lobe and superior temporal gyrus[12, 16].The cingulum bundle was predominantly composed of cingulate fibres that head in either a rostral or caudal direction, with the majority bifurcating to go in both directions.The PCG interlinks medial parts of the frontal, parietal, and temporal lobes by the cingulum bundle.The highest number of active sites was found in the ventral and dorsal aMCC, whose stimulation triggered a variety of goal-oriented behavioursinvolvingreaching and grasping actions and exploratory gaze movements.Therefore, the clinical characteristics of posterior cingulate epilepsy vary among patients that are different from the mesial-temporal lobe epilepsy.
This preliminary impression could suggest a higher specificity of the SEEG method in mapping the EZ.Among this group, seven of twelve patients who underwent PCG resection were seizurefree at the end of the follow-up period. The three of five patients who underwent RF-TC achieved seizurefreedom, and the remaining patients had 30%-50% fewer seizures. SEEG methodology is both safe and effective in patients with difficult-to-localize, medically intractable, focal epilepsies.RF-TC selectively disrupts critical hubs in the epileptic network through contiguous contacts within the range of a single electrode and provides a more curative effectin regions such as the small and deeply epileptogenic foci,PCG.
Accurate description of the brain regions involved in seizure genesis is a crucial objective in the context of epilepsy surgery. However,the identification of the EZ is based on the abilities of experienced clinical neurophysiologists to identify the relevant anatomic-electrical-clinical correlations and SEEG patterns.In the present study, two patients (pts.3 and 4) had posterior cingulate lesions identified by MRI but had contralateral hippocampal onset identified by SEEG in our study.One patient(pt.4) who underwentposterior cingulate lesion resection was seizurefree.After treating the posterior cingulate lesion using SEEG-guided RT-FC, the discharge of the hippocampus was obviously reduced(pt.3).On the one hand,postoperative pathology was FCDIIIb(FCD Icand ganglion glioma), which is often associated with malformations during cortical development, in particular focal cortical dysplasia (FCD), which is most often the basis of epilepsy lesions.Invasive EEG investigations may provide useful information, although in GNT-associated focal epilepsy, the main goal of intracerebral recordings is usually to map the eloquent cortex in the proximity of the neoplasm.
On the other hand,the posterior cingulate cortex is known to project to the hippocampus via the entorhinal and parahippocampal cortex and to receive direct and indirect connections from the hippocampus.The inferior cingulum bundle is a white matter tract projecting from the PCC to the hippocampus or parahippocampus and the entorhinal cortex[21, 22]. Ictal propagation to the cingulate gyrus has frequently been observed among patients with temporallobe epilepsy.However,YCShih found in patients with left mesial temporal lobe epilepsy with hippocampal sclerosis, the left inferior cingulum bundle underwent degeneration in tandem with the left hippocampus volume, whereas intrinsic functional connectivity seems to react by compensating for the loss of connectivity. Their results suggested that increased intrinsic functional connectivity of the contralesional hippocampus was a compensatory response to decreased hippocampal connectivity on the lesion side.According to the hypothesis, we speculate that the PCG lesion and hippocampus functional connectivity decreased,but the contralesional PCG and hippocampus have extensive unctional connections. Fundamental to the original concept of the EZ was the idea of one or more regions of brain involved in the primary organization of the ictal discharge, rather than a ‘‘focus’’.Indeed, from the outset of SEEG development, the EZ was seen as a set of interconnected regional systems. The now widely accepted notion of epileptogenic networks stems from these early observations and is intrinsically related to the SEEG method of recording.The EZ in the PCG may be an epileptogenic network that is distributed across the limbic system and is complex.
This study has some limitations.First, this study was definitely limited by the location or number of implanted electrodes designed to treat these epilepsy patients.This spatial limitation in the recordings may have caused difficulties in identifying the wholeseizure pathway.Second, the sample size in this study was relatively small.Further studies employing a large number of participants would be helpful to confirm these preliminary results. We should apply CCEP or other methods to precisely track the pathway through which the seizures spread.