Abstracts

Rationale:
The piriform cortex is the major part of the primary olfactory cortex and has broad connections into fronto-temporal cortical and limbic networks. The piriform cortex has been demonstrated to be highly epileptogenic in rodents, sometimes the site of seizure onset in systemic chemoconvulsant models. However, its role remains to be confirmed in human epilepsy.
Method:
We identified 15 consecutive patients with medically intractable temporal lobe epilepsy (2 male, 12 female patients; age range 21 – 53 years) who underwent Stereoelectroencephalography (SEEG) and with at least one electrode contact in piriform cortex.  Demographic information, semiology, imaging data, intracranial monitoring results, subsequent surgical interventions, and seizure outcomes were analyzed. The SEEG trajectories accessing the piriform cortex were standardized and performed by single neurosurgeon. MRI brain, electrophysiology and semiology of seizures were reviewed by two epileptologists and the findings were compared to MRI and SEEG reports in the medical record. Engel outcome classification was used to divide patients into good (Engel I and II) and poor outcomes (Engel III-IV).
Results:
Seven and eight patients had at least one electrode contact in temporal or frontal piriform cortex, respectively. An average of 8.3 (range 4-16) seizures per patients were captured, and all were reviewed. Seizures invaded the piriform cortex within a mean of 19 seconds (range 2 – 48). Propagation within 10 seconds was noted in two patients at mean intervals of 3 and 6 seconds, respectively. In latter two patients, piriform involvement appeared to correlate with onset in ipsilateral amygdala. Electrographic patterns of piriform involvement were - rhythmic delta to beta frequencies or rhythmic spikes or low voltage fast activity.  In the two patients with earlier piriform involvement, the first patient with a contact in the frontal piriform area showed rhythmic theta, while the second patient with a temporal piriform contact displayed rhythmic delta. In each case, invasion of the piriform region was not correlated with the occurrence of a specific clinical sign or semiologic feature (but unreported aura were not completely excluded). Five patients had lesions by MRI and seven had ipsilateral hypometabolism on PET imaging.  All patients underwent ablative procedures by radiofrequency or laser ablation.  While ten out of 15 patients had Engel I and II outcomes (I = 8, II = 2. Four patients had Engel score of III and one patient did not undergo any procedure. There was no consistent finding in relation to piriform involvement and in only one case was there destruction of the sampled piriform region.
Conclusion:
Involvement of piriform cortex in this case series was typically late , was not found to be the ictal onset zone and there was no relationship with semiology or surgical outcomes in this highly selected series. Earlier involvement of the piriform cortex coincided with amygdala but not all patients with amygdala onset had involvement of the piriform cortex, perhaps highlighting the complex connectivity of the amygdala and the olfactory cortices. Further human studies are needed to understand the role of the piriform cortex in epilepsy. The role of the piriform cortex in human epilepsy is yet to be elucidated.          
Funding:
:None