Case Series: Temporal Lobe Encephalocele (TE) in Adult-Onset Drug Resistant Mesial Temporal Lobe Epilepsy (MTLE)

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Objective: Case series to evaluate for under-diagnosed temporal lobe encephalocele as a possible etiology of adult-onset drug-resistant mesial temporal lobe epilepsy

Background: Mesial temporal lobe epilepsy (MTLE) is the most common form of drug resistant focal epilepsy. Mesial temporal lobe epilepsy often has a relatively reproducible clinical history with seizures early in life and then seizure recurrence in adolescence after a latent period. Temporal lobe encephalocele (TE) may be a common, yet under-recognized, etiology of drug resistant MTLE in adult-onset epilepsy. This case series reviews 6 cases of adult-onset drug resistant MTLE related to TE.

Design/Methods: This is a case series of 6 patients undergoing epilepsy presurgical evaluations at Henry Ford Hospital and Beaumont Royal Oak Hospital. Each patient was presented at the patient management conference and chart review was completed for patient demographic and historical data. MRI was re-reviewed by neuro-radiologists. Neurophysiologic data, including sEEG, was reviewed by fellowship trained epileptologists involved in the cases.

Results: Of 6 included patients with drug-resistant mesial temporal lobe epilepsy, the median age of epilepsy onset was 39 (27–48) years old, with four of the six being female. Three of the six patients had a right temporal encephalocele, while three patients had a left temporal encephalocele. Three of the six patients had comorbid migraines/headaches. Additionally, three of the six patients had a BMI > 30. In those patients who have undergone sEEG implantation, a seizure-onset zone was identified within the mesial temporal structures.

Conclusions: This case series illustrates the importance of MRI re-review (with T2-SPACE sequence) to evaluate for temporal lobe encephalocele in patients with adult-onset drug resistant MTLE, especially if comorbid migraine/headache or high BMI are present. Although the epileptic lesion involves the temporal pole, ictal onsets may be present within the hippocampus and amygdala. This may suggest TE initiates epileptogenesis within the adjacent mesial temporal structures.





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