Rationale:
The anterior temporal lobectomy (ATL) is a long-used and standard treatment for drug-resistant (DRE) mesial temporal lobe epilepsy, which involves the removal of the amygdala, hippocampus, and temporal pole. Acute postoperative seizures (APOS) are defined as seizures occurring within 7-10 days after epilepsy surgery, and have variable significance for long-term prognostication. Some studies suggest that APOS are associated with future surgical failure, particularly when they are of the patient’s typical semiology [1,2]. Other studies suggest that there is no association with APOS and long-term outcomes, and that these seizures may be the result of acute surgical injury and will abate as the surgical cavity matures [3,4].
While there is electrocorticography literature of acute surgical injuries recorded during intraoperative procedures, to our knowledge, there is no current literature demonstrating the progression of electrophysiologic activity in the hippocampus after a partial acute surgical intervention.
We present a case where surgical limitations prevented total resection of the hippocampus, and responsive neurostimulator(RNS) electrocorticography(ECoG) data of the residual hippocampus were available from the immediate postoperative period.
Methods: NA
Results:
A 25-year-old right-handed man presented with a history of left temporal medulloblastoma s/p resection, radiation, and chemotherapy and subsequent DRE. He had daily seizures of chills or chest tightness followed by coughing/gagging and then expressive aphasia and loss of consciousness. He had bilateral hippocampal RNS placed 2 years prior, which was ineffective.
EEG showed intermittent L temporal delta range slowing interictally, and frequent L temporal seizures, both subclinical and clinical, matching with the above semiology. RNS data showed long episodes in the L hippocampus at a similar frequency to EEG.
He underwent L ATL, for removal of remaining hippocampus and gliotic tissue, with preservation of the RNS on the R hippocampus. The surgery was uncomplicated, however technical barriers prevented removal of the hippocampal tail, and the left hippocampal RNS lead was left in place and the most proximal contact at the resection border (figure 1). Postoperatively, ECoGs showed nearly continuous long episodes without clinical correlate, now confined to the resection border, lasting until postop day 3. Following this, there was a 5 day period with no long episodes recorded, after which (on postop day 8), long episodes recurred and remained, followed by recurrence of clinical seizures with typical semiology (figure 2).
Conclusions:
We present a case which used RNS data to show in-situ residual hippocampal activity in a postoperative period after a subtotal hippocampal resection. There was residual hippocampal status epilepticus in the immediate postoperative period for 3 days, followed by an abatement of epileptiform activity for 5 days, then a persistent recurrence of epileptiform activity. This data provides a window into the natural history of hippocampal APOS, and may have implications for causes of delayed surgical failure, and the lower success rates of subtotal ablative procedures (LITT).
Funding: None