Abstracts

Rationale: Verbal memory is crucial for the development and adaptation of most communication, and likely involves complex neural circuitry spanning the temporal lobe. Correlates of this faculty (e.g. short-term memory, word-finding) can be severely affected in patients with epilepsy. How mesial memory networks (e.g. hippocampus and mesial temporal cortices) dynamically interact with lateral language-associated cortices (e.g. superior temporal gyrus; STG) to encode cues and recall verbal information is currently unknown.  Methods: Five patients with medically-refractory focal epilepsy underwent intracranial implantation with subdural grids and strips for pre-surgical monitoring. High-gamma band responses (50-200 Hz) were used as surrogates for subsequent principle component analysis assessing state-space dynamics of neural population activity. Patients performed a modified auditory naming paradigm, with auditory stimuli consisting of questions (noun-verb-noun syntax) followed by patients’ subsequent speech responses.  Results: The STG showed expected high-gamma increases during sentence stimuli (transient in posterior STG, while anterior STG showed sustained activations throughout stimuli), and smaller activations during speech responses. Subtle activations were also observed in mesial temporal cortices and the temporal pole shortly before speech responses. Principle component scores time-locked to AN task syntactic components showed some differentiation between grouped categorical stimuli, suggesting some spatiotemporal semantic separation in the temporal lobe. Conclusions: Beyond the expected robust activation of language-associated cortices during a verbal memory task, we observed parallel activation of mesial and anterior temporal structures before speech responses, suggesting concerted interplay of linguistic and memory networks. We also detected evidence of differential semantic categorical trends in parallel spatiotemporal processing among these distributed networks. Further work may inform strategies for mitigating memory and cognitive comorbidities in epilepsy and other brain diseases. Funding: Dr. Kleen was funded by NINDS (R25NS070680-07), Dr. Leonard was funded by the NIH (F32-DC013486) and Kavli Institute for Brain and Mind, and Dr. Chang was funded by the NIH (R01-DC012379, R00-NS065120, and DP2-OD00862) and the Esther A. and Joseph Klingenstein Fund.