F121. Patterns of propagation in parietal lobe epilepsy

Abstract

Parietal lobe epilepsy accounts for about 5% of all the focal epilepsies. Seizures of the parietal lobe origin can be difficult to diagnose because of the diverse ictal manifestations. Moreover, the ictal semiology may be related to the propagation from the epileptogenic zone (EZ) to other areas of the brain, such as the motor cortex or temporolimbic area. The scalp EEG often doesn’t accurately localize the EZ requiring the use of Stereo-EEG (SEEG).The parietal lobe resection is the least commonly performed resective surgery for drug-resistant epilepsy (DRE) with limited publications. We present a case of parietal lobe epilepsy in a patient with previous history of hemorrhagic stroke affecting the left parietal lobe secondary to a cerebral venous thrombosis who was admitted to our epilepsy monitor unit for scalp and SEEG. Patient was a 66 years old right-handed woman who experienced hemorrhagic stroke over the left parietal-posterior frontal area, while she was receiving chemotherapy for her acute lymphoblastic leukemia. She was 62 years old when she acutely presented with clonic movements of the right arm consistent with epilepsia partialis continua (EPC) recurred for several hours at a time and was followed by aphasia. She was treated with levetiracetam with good control of her seizures for two years. After that she had recurrent episodes of clonic movements in the right arm with/without prolonged aphasia. She tried lacosamide, clobazam, clonazepam, on top of the levetiracetam, which did not result in control of the seizures. Video-EEG telemetry showed interictal epileptic spikes (IEDs) in the left temporal region and one typical EPC followed by aphasia with diffuse onset over the left hemisphere. SEEG was required with depth electrodes into the left temporal, frontal, parietal, insular, cingulate cortex and 4 lines surrounding the hemorrhagic lesion in the left parietal lobe. IEDs were abundant in the lines posterior and lateral to the lesion followed by the cingulate and temporal neocortex. Many electrographic seizures were captured manifesting with low voltage fast activity (LVFA) in the lines lateral and posterior without clinical symptoms. One typical EPC that lasted for 3 h was captured. SEEG showed onset as LVFA in the electrodes lateral and posterior to the lesion without clinical symptoms. Then it spread to the electrodes anterior to the lesion (behind the central sulcus) that caused clonic jerking of the right arm and then aphasia when spread to the neocortical temporal. Low voltage stimulation of the electrodes anterior to the lesion produced prolonged afterdischarges and typical clonic movements of the right arm. Seizures of the parietal lobe origin can be a silent at onset, not expressing symptoms until they propagate to the other lobes. In this case, SEEG confirmed parietal lobe epilepsy with spread to the Rolandic cortex to cause clonic movements/EPC and to the posterior temporal neocortex to cause receptive aphasia.