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Review
. 2022 Mar 15:13:804128.
doi: 10.3389/fneur.2022.804128. eCollection 2022.

The Temporal Lobe as a Symptomatogenic Zone in Medial Parietal Lobe Epilepsy

Affiliations
Review

The Temporal Lobe as a Symptomatogenic Zone in Medial Parietal Lobe Epilepsy

Nadim Jaafar et al. Front Neurol. .

Abstract

Some surgical failures after temporal lobe epilepsy surgery may be due to the presence of an extratemporal epileptogenic zone. Of particular interest is the medial parietal lobe due to its robust connectivity with mesial temporal structures. Seizures in that area may be clinically silent before propagating to the symptomatogenic temporal lobe. In this paper, we present an overview of the anatomical connectivity, semiology, radiology, electroencephalography, neuropsychology, and outcomes in medial parietal lobe epilepsy. We also present two illustrative cases of seizures originating from the precuneus and the posterior cingulate cortex. We conclude that the medial parietal lobe should be strongly considered for sampling by intracranial electrodes in individuals with nonlesional temporal lobe epilepsy, especially if scrutinizing the presurgical data produces discordant findings.

Keywords: cingulate gyrus; epilepsy surgery; intractable epilepsy; parietal lobe epilepsy; precuneus cortex; temporal lobe epilepsy.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Brain imaging of the patient with right precuneus neurocysticercosis and left temporal lobe seizure involvement. (A) Head CT showing calcified lesion in the right precuneus. (B) Double inversion recovery MRI showing the lesion with surrounding gliosis. (C) T2-weighted image showing the lesion. (D) Postoperative MRI T1 sequence showing the cavity. (E) Coregistration of FDG-PET with MRI showing hypometabolism in the left temporal lobe. (F–H) Diffusion tensor imaging through the level of the lesion showing asymmetrical findings with respect to the parietal white matter [adapted from (8)].
Figure 2
Figure 2
(A) X-rays showing the locations of the intracranial electrodes. (B) Scalp (top) and intracranial (bottom) electrodes in the amygdala, hippocampus, insula, and posterior cingulate gyrus in addition to the strips sampling right parietal lesion. The EEG shows onset around the right parietal lesion with secondary propagation to the contralateral temporal lobe [adapted from (8)].
Figure 3
Figure 3
Depth electrode recordings of two consecutive EEG pages showing the ictal onset in the posterior cingulate area before later propagation to the ipsilateral mesial temporal structures. The seizure was semiologically silent before it involved the hippocampus and amygdala (9).

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