Illustrations
Figure 1
(A) SEEG traces; reduced montage. Electrodes are identified by letters and the recording leads are numbered from 1 to 18; low numbers correspond to the deepest structures. Im’ 11-12: left pre-frontal cortex; SA’ 1-2: left supplementary motor area; SA’ 6-7: left lateral pre-motor cortex; CP’ 4-5: left central sulcus; Lp’ 1-2: left posterior insula; CP’ 1-2 post-central lobule; PA’ 1-2: left precuneus; PA’ 7-8: left superior parietal lobule; PI’ 1-2: posterior cingular gyrus; PI’ 7-8 left polymicrogyric cortex in the supramarginal gyrus; B’ 1-2: left hippocampal gyrus; B’ 10-11: left medium temporal gyrus; H’ 8-9: left Heschl gyrus; FCA’ 2-3: left cuneus; OT’ 1-2: left lingular gyrus; OT’ 9-10: left anterior occipital sulcus; PI 1-2: right posterior cingular gyrus; PI 12-13: right polymicrogyric cortex in the inferior parietal lobule; OT 1-2: right lingular gyrus; OT 10-11: right medium temporal gyrus; Im 1-2: right anterior insula; Im 15-16 right post-central gyrus. Electrographically, the seizure started 2.5 s before the first clinical manifestations, with a rapid discharge in the beta-gamma band in the left parietal cortex, at the inferior part of intraparietal sulcus (electrode PI’, contacts 7-8) and within the posterior-superior insular cortex (electrode Lp’, contacts 1-2). Discharge is seen within the contralateral polymicrogyric cortex (inferior parietal lobule; electrode PI, contacts 12-13) and within the left temporo-occipital junction (electrode OT’, contacts 9-10). The seizure was brief, lasting less than 20 seconds. (B) MRI 3D mesh with electrode positions. Im: medium insula; SA: supplementary motor area; CP: paracentral; OP: parietal operculum; La: anterior lesion; PA: superior parietal lobule; PFG: posterior fusiform gyrus; Lp: posterior lesion; PI: inferior parietal lobule; FCA: anterior calcarine sulcus; OT: occipito-temporal; H: Heschl gyrus; B: hippocampal gyrus. The apostrophe denotes left electrodes.
Figure 1
Figure 2
(A) Normalized epileptogenicity index (EI) values. EI ranks brain structures according to the “tonicity” of the fast discharge (energy ratio of high frequency content over low frequency; red bars) and the delay of involvement at seizure onset. The normalized values range from 0 to 1 (blue bars), with 1 corresponding to the most epileptogenic region. To compute the EI, we used the plugin designed for the open-source AnyWave software (available at: http:// meg.univ-amu.fr). The max EI value was observed in the left supramarginal gyrus (PI’ 7-8) and high EI values (>0.3) in the left posterior inferior insula (Lp’ 1-2) and right supramarginal gyrus (PI 12-13). (B) 3D mesh and axial T1-weighted MRI with electrode positions and representation of EI. Max EI was observed in the left polymicrogyric cortex in the supramarginal gyrus (electrode PI’ contacts 7-8, red dot). High EI values were also found in the left posterior-superior insular cortex (electrode Lp’, contacts 1-2; yellow dot) and contralateral polymicrogyric cortex (electrode PI, contacts 12-13; yellow dot). The polymicrogyric cortex is indicated by arrows.
Figure 2
Auteurs
1 Department of Medical Sciences and Public Health, Neurology Section - University of Cagliari, Italy
2 Aix Marseille Univ, APHM, INSERM, INS, Inst Neurosci Syst, Timone Hospital, Epileptology Department, Marseille, France
3 APHM, Timone Hospital, Pediatric Neurology Department, Marseille, France
4 Aix Marseille Univ, APHM, INSERM, INS, Inst Neurosci Syst, Timone Hospital, Pediatric Neurosurgery Department, Marseille, France
* Correspondence: Fabrice Bartolomei
Service d’Epileptologie et Rythmologie Cérébrale,
CHU Timone - 264 Rue St Pierre
13005-Marseille, France
Autoscopic phenomena (AP) are characterized by seeing an image of oneself in extra-personal space. These phenomena are rare and the anatomy of brain regions producing these phenomena is not well defined. We report anatomical electroclinical correlations during a stereoelectroencephalography-recorded seizure with autoscopic hallucination (a form of AP in which the double of oneself is seen from an internal point of view). Seizure onset zone was quantified using the epileptogenicity index method (EI). Maximal EI values were obtained in the left lateral parietal cortex (supramarginal gyrus) and high values were also found in the left posterior-superior insular cortex, left temporo-occipital junction and contralateral inferior parietal lobule. Our case confirms the involvement of the inferior parietal lobule, temporo-parieto-occipital junction and posterior insula in the genesis of autoscopic hallucination.