Case Study

A 36 year old RHWM had drug-resistant localization-related epilepsy. He had a simple febrile seizure during childhood. Monthly focal seizures with and without impaired consciousness developed later. Auras of an indescribable feeling that would develop into a stare, impaired responsiveness, prominent lip smacking, and right upper limb dystonic posturing for 30-60 seconds following which he had trouble getting his words out for a few minutes. Convulsions did not occur. An MRI demonstrated left MTS. FDG-PET demonstrated left temporal lobe hypometabolism. Scalp-sphenoidal vEEG demonstrated left sphenoidal spikes and left temporal seizures. He underwent a left amygdalohippocampectomy and several years later developed seizure recurrence. He then underwent iEEG and subsequent lateral neocorticectomy with rare post-op seizures (Engel class 2) continuing with the identical temporal semiology…

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Figure: Transverse (A) and coronal (B) post-operative high-resolution brain MRI demonstrating extensive surgical resection of both the mesial and lateral temporal lobe.

What did the EEG Reveal?

The objective of temporal lobe surgery in patients with drug-resistant mesial temporal lobe epilepsy (mTLE) is to resect the epileptogenic zone responsible for generating seizures. Surgical approaches vary, though amygdalohippocampectomy with and without lateral predicts a favorable seizure free outcome when electro-clinical correlation is concordant with a structural lesion1. Additional electrodes and subtemporal electrodes (ie sphenoidals) may improve source localization of the interictal spikes in mTLE. Febrile seizures during childhood can evoke neuronal atrophy and sclerosis of the hippocampus. Despite the characteristic history and non-invasive evaluation strongly favoring mTLE, our patient was not rendered seizure free after surgery. Surrounding brain regions (ie insular cortex) may propagate to the temporal lobe or mimic TLE. Other pathologies such as end folium sclerosis and amygdalar sclerosis may represent the epiphenomenon of febrile seizures or seizures of extrahippocampal origin2. Our patient has had seizures persist though they have “run down” over the last decade since surgery.

References

  1. Spencer SS, Berg AT, Vickrey BG et al. Multicenter study of epilepsy surgery. Predicting long-term outcomes following epilepsy surgery. Neurology 2005;65:912-918.
  2. Diehl B, Najm I, Mohamed A, et al. Interictal EEG, hippocampal atrophy, and cell densities in hippocampal sclerosis and hippocamapal ssclerosis associated with mircscopic cortical dysplasia. J Clin Neurophysiol 2002;19:157-162.
Authored By: 
William O. Tatum DO
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Authored Date: 
10/2011