Neocortical and medial temporal seizures have distinct impacts on brain responsiveness.

Focal epileptic seizures are characterized by abnormal neuronal discharges that can spread to other cortical areas and interfere with brain activity, thereby altering the patient's experience and behavior. The origin of these pathological neuronal discharges encompasses various mechanisms that converge toward similar clinical manifestations. Recent studies have suggested that medial temporal lobe (MTL) and neocortical (NC) seizures are often underpinned by two characteristic onset patterns, which, respectively, affect and spare synaptic transmission in cortical slices. However, these synaptic alterations and their effects have never been confirmed or studied in intact human brains. To fill this gap, we here evaluate whether responsiveness of MTL and NC are differentially affected by focal seizures, using a unique data set of cortico-cortical evoked potentials (CCEPs) collected during seizures triggered by single-pulse electrical stimulation (SPES). We find that responsiveness is abruptly reduced by the onset of MTL seizures, despite increased spontaneous activity, whereas it is preserved in the case of NC seizures. The present results provide an extreme example of dissociation between responsiveness and activity and show that brain networks are diversely affected by the onset of MTL and NC seizures, thus extending at the whole brain level the evidence of synaptic alteration found in vitro.

Cortical and subcortical intraoperative-monitoring of the visual pathway under general anesthesia in epilepsy surgery.

OBJECTIVE: The purpose of this study was to evaluate the applicability of visual evoked potentials (VEP) for intraoperative visual pathway monitoring in epilepsy surgery of the posterior hemispheric quadrant (PHQ) and to correlate it with post-operative visual field status. METHODS: VEP monitoring was performed in 16 patients (12 females, 7 children). Flash-induced VEP were recorded with strip electrodes from the banks of the calcarine cortex. Latency and amplitude of the first component of VEP (V1-lat, V1-amp) were monitored. Evaluation of the visual field was performed pre- and post-operatively in all patients. RESULTS: All procedures were successfully completed without adverse events. In 10 patients the strip covered both the inferior and superior calcarine banks, while only one bank was sampled in 6 cases (inferior in 4, superior in 2). Considering one of the two calcarine banks, at the end of the resection VEP had disappeared in 4 patients, whereas a decrease >33.3% in 4 and <20% of V1-amp was recorded in 5 and in 4 cases respectively. The percentage of V1-amp reduction was significantly higher for the patients who experienced a post-operative visual field reduction (p < 0.001). Post-operative visual field deficits were found in patients presenting a reduction >33.3% of V1-amp. CONCLUSIONS: VEP monitoring is possible and safe in epilepsy surgery under general anesthesia. SIGNIFICANCE: Intraoperative recording of VEP from the banks of the calcarine cortex allows monitoring the integrity of post-geniculate visual pathways during PHQ resections for epilepsy and it is pivotal to prevent disabling visual field defects, including hemianopia and inferior quadrantanopia.

Thalamic feedback shapes brain responses evoked by cortical stimulation in mice and humans.

Cortical stimulation with single pulses is a common technique in clinical practice and research. However, we still do not understand the extent to which it engages subcortical circuits which contribute to the associated evoked potentials (EPs). Here we find that cortical stimulation generates remarkably similar EPs in humans and mice, with a late component similarly modulated by the subject's behavioral state. We optogenetically dissect the underlying circuit in mice, demonstrating that the late component of these EPs is caused by a thalamic hyperpolarization and rebound. The magnitude of this late component correlates with the bursting frequency and synchronicity of thalamic neurons, modulated by the subject's behavioral state. A simulation of the thalamo-cortical circuit highlights that both intrinsic thalamic currents as well as cortical and thalamic GABAergic neurons contribute to this response profile. We conclude that the cortical stimulation engages cortico-thalamo-cortical circuits highly preserved across different species and stimulation modalities.