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Functional Connectivity in Mesial Temporal Lobe Epilepsy: A Dynamic Concept

Commentary Mesial temporal lobe epilepsy (m-TLE) is a network disease. Its manifestations extend beyond seizures that arise from a well-restricted and limited focus within the hippocampus to include a wide array of cognitive and psychiatric challenges. In patients with unilateral m-TLE, the most obvious explanation for such extensive disease implications relates to widespread structural cortical and subcortical abnormalities described within both temporal lobes and strategic extratemporal brain regions. Cortical atrophy is seen in the frontocentral, lateral temporal (mainly superior and middle temporal gyri), dorsal parietal, and mesiotemporal cortices bilaterally. Similarly, volume loss occurs in the ipsilateral mesial orbitofrontal cortex, cingulate, and thalamus in patients with drug-resistant unilateral TLE (1, 2). Many of these atrophied structures represent key components of the default mode network (DMN) (3) and the limbic network, together responsible for maintaining baseline brain activities related to cognition, self-awareness, episodic memory, and emotions. As such, it is not surprising that structural damage affecting critical components of these networks may disturb mood and cognitive function. “Space” is then a critical concept: With high-resolution structural brain imaging demonstrating, as detailed above, the extension of atrophy beyond the space of the hippocampus, we have expanded our appreciation of the space of the epilepsy to a network rather than an individual structure. Recent highresolution functional neuroimaging studies using functional magnetic resonance imaging (f-MRI) or EEG-triggered f-MRI— including work by Pittau et al. chosen for this commentary— Patterns of Altered Functional Connectivity in Mesial Temporal Lobe Epilepsy.