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Abstract Details

Neuroimaging Evidence of Cortical-subcortical Network Involvement in Patients with Cortical Lateralized Periodic Discharges
Epilepsy/Clinical Neurophysiology (EEG)
P5 - Poster Session 5 (5:30 PM-6:30 PM)
1-004

To study if lateralized periodic discharges (LPDs) due to different brain pathologies can be associated with neuroimaging abnormalities in brain regions different from the site of the primary brain injury or the LPDs localization.

Structural brain injury typically underlies the development of LPDs, likely affecting the local cortical excitation and inhibition balance. LPDs increase the risk of focal metabolic failure and are associated with an increased risk of epilepsy. It is still under investigation if the mechanisms and effects of LPDs extend beyond the local site of injury, potentially involving cortico-subcortical networks.

We retrospectively selected a cohort of 19 patients with evidence of LPDs on EEG. Etiologies were heterogeneous (e.g., stroke, brain tumors, encephalitis, encephalopathy). All subjects had a brain MRI scan close to/or concomitant with the detection of LPDs on EEG. MRI images were independently reviewed by 2 board-certified neurologists to judge the presence of structural abnormalities in the thalami, and the hippocampi/amygdalae. In case of disagreement, the images were reviewed by a third neurologist.

We observed that 53% (10/19) of patients with LPDs showed neuroimaging abnormalities at the level of either the thalamus or hippocampus/amygdala on FLAIR and/or DWI/ADC sequences. In all cases, the abnormalities were in the hemisphere affected by the primary brain injury where also cortical LPDs were recorded. 30% of positive cases (3/10) displayed a concomitant injury of both the thalamus and hippocampus/amygdala. The majority of the thalamic abnormalities were at the level of the posterior thalamus/pulvinar with a common presence of cortical LPDs over temporal regions.

Cortical LPDs can be associated with neuroimaging abnormalities in subcortical regions such as the thalamus and the hippocampus. These signs could reflect the involvement of specific pathological cortical-subcortical networks in patients with LPDs.

Authors/Disclosures
Elena Monai, MD (University of Wisconsin-Madison)
PRESENTER
Dr. Monai has nothing to disclose.
Safoora Fatima, MD (Southern Illinois University) Safoora Fatima has nothing to disclose.
Justin A. Sattin, MD (University of Wisconsin) The institution of Dr. Sattin has received research support from NIH / NINDS.
Erick Tarula, MD Dr. Tarula has received personal compensation in the range of $500-$4,999 for serving as a Consultant for WellFleet RX.
Mariel Kalkach Aparicio, MD Mariel Kalkach Aparicio, MD has nothing to disclose.
Klevest Gjini (University of Wisconsin - Madison) Klevest Gjini has nothing to disclose.
Melanie Boly, MD (UW Medical Foundation Centennial Bldg) Dr. Boly has nothing to disclose.
Aaron F. Struck, MD (Washington University in St. Louis) The institution of Dr. Struck has received research support from Ceribell.