Temporal lobe epilepsy with a contralateral parietal seizure‐onset zone

Abstract

Achieving sustained seizure freedom following epilepsy surgery remains a challenge in some patients. Lesional temporal lobe epilepsy (TLE), for example, in patients with mesial temporal sclerosis or other MRI abnormalities, carries a good prognosis for seizure freedom compared to significantly lower chances of seizure freedom in patients with non-lesional epilepsy. However, even in some lesional TLE cases, persistent post-operative seizures suggest seizure onset from a brain region that is clinically and electrographically silent but manifests only after propagation to the temporal lobe. A notable example of such a brain region is the parietal lobe, which has extensive connectivity to various brain regions. While certain seizure semiologies, for example, sensory seizures, suggest parietal lobe onset, some medial parietal seizures may be semiologically indistinguishable from temporal lobe seizures. Here, we report a patient with focal impaired awareness seizures that manifested semiologically and electrographically as left TLE but proved to originate from the contralateral medial parietal lobe. We discuss putative seizure propagation pathways.

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

“…(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 )].…”

“…(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 )].…”

“…Here, we review medial parietal lobe epilepsy (PLE) as a seizure onset zone with preferential propagation to the temporal lobe, potentially masquerading as TLE. We present two lesional cases of seizures originating in the precuneus ( 8 ) and the posterior cingulate cortex (PCC) ( 9 ), manifesting as TLE. Finally, we highlight the importance of having a multimodal integrated evaluation of the implicated anatomical connectivity, semiology, neuroimaging, neuropsychological testing, and electroencephalography to optimize surgical outcomes.…”