MISLEADING EEG LATERALIZATION ASSOCIATED WITH MIDLINE SHIFT
Abstract number :
2.157
Submission category :
3. Neurophysiology
Year :
2014
Submission ID :
1868239
Source :
www.aesnet.org
Presentation date :
12/6/2014 12:00:00 AM
Published date :
Sep 29, 2014, 05:33 AM
Authors :
Sergiu Abramovici and Gena Ghearing
Rationale: Focal ictal and interictal EEG discharges are often recorded ipsilateral to a brain lesion, and parasagittal midline epileptiform discharges and seizures have been described with focal lesions that result in midline shift (MLS). However, periodic or seizure discharges arising contralateral to a known lesion have not previously been described as a sign of MLS. Methods: We present two cases of 47 year old women with subdural fluid collections over the right hemisphere, resulting in significant right to left MLS and focal status epilepticus arising from the left hemisphere. The patients were followed using serial clinical evaluations, standard 5 mm slice CT brain imaging, and 22 channel digital continuous video EEG recordings. Results: Patient 1 underwent a right amygdalohippocampectomy and anterior temporal lobectomy for refractory epilepsy. On postoperative day (POD) 2 the patient had altered mental status, right leg shaking and perioral automatisms. CT demonstrated a MLS of 12 mm, and EEG was remarkable for left temporal intermittent rhythmic delta activity (TIRDA), which intermittently evolved into rhythmic 3 Hz spikes and sharp waves, consistent with left temporal non-convulsive status epilepticus. On POD 3 MLS measured 13 mm and EEG demonstrated 6 seizures of left temporal origin intermixed with left sided lateralized periodic discharges (LPDs). On POD 4 the MLS measured 8 mm and EEG demonstrated 2 seizures originating in the left temporal lobe. However, on the EEG recorded on POD 5 there were no longer seizures, and left temporal LPDs resolved on POD 6. Since then, the patient continued to have occasional left temporal and bi-frontal sharp waves without clinical manifestation. The patient continues to suffer occasionally from seizures clinically originating in the right hemisphere. Patient 2 suffered from a spontaneous subdural hematoma initially associated with 11 mm of MLS. She underwent right craniotomy and evacuation of the hematoma. On POD 3 the patient complained of left face and arm twitching. CT demonstrated a MLS of 7 mm and EEG was remarkable for occasional right temporal sharp waves and a continuous, evolving left temporal 5-7 Hz rhythmic sharp theta activity, consistent with non-convulsive status epilepticus. The patient had no further complaints or clinical manifestation. On POD 4 there was still sub-clinical left temporal seizure activity on EEG and MLS was 6 mm. On POD 5 the left temporal discharges resolved. EEG on POD 6 showed no discharges and CT showed no MLS a week after discharge. The patient continues to be seizure-free. Conclusions: In both cases, the discharges contralateral to the lesion gradually subsided as the MLS resolved without surgical intervention. LPDs and seizures arising contralateral to the site of a patient's known lesion may accompany lesions with mass effect and significant MLS. While the mechanism by which mass effect causes contralateral discharges is poorly understood and mostly speculative, it is important to be aware of this clinical association because the recording of periodic and seizure activity contralateral to the lesion may indicate significant MLS.
Neurophysiology