Occipital Lobe Epilepsy With Ictal Fear: Evidence From a Stereo-Electroencephalography (sEEG) Case

Ictal fear—a relatively rare phenomenon—is a semiological characteristic of epilepsy. Most patients with epilepsy with ictal fear have an epileptic zone in the mesial temporal lobe, which is the classical brain area involved in emotion processing. Herein, we report a case of epilepsy with ictal fear as the first manifestation in a 10-year-old boy. All noninvasive evaluation including scalp video electroencephalography (EEG), magnetic resonance imaging (MRI), and positron emission tomography/computed tomography (PET-CT) suggested a possible lesion in the left posterior brain region. Stereo-electroencephalography (sEEG) results showed high frequency direct current shift in the left occipital lobe 1 s before the fear manifestation which preceded in 12 s the discharge in the amygdala. This case highlights the epileptic network hypothesis which suggested occipital cortex may play an important role in the early emotional network independently of amygdala activation

The distribution and heterogeneity of excitability in focal epileptic network potentially contribute to the seizure propagation

IntroductionExisting dynamical models can explain the transmigration mechanisms involved in seizures but are limited to a single modality. Combining models with networks can reproduce scaled epileptic dynamics. And the structure and coupling interactions of the network, as well as the heterogeneity of both the node and network activities, may influence the final state of the network model.MethodsWe built a fully connected network with focal nodes prominently interacting and established a timescale separated epileptic network model. The factors affecting epileptic network seizure were explored by varying the connectivity patterns of focal network nodes and modulating the distribution of network excitability.ResultsThe whole brain network topology as the brain activity foundation affects the consistent delayed clustering seizure propagation. In addition, the network size and distribution heterogeneity of the focal excitatory nodes can influence seizure frequency. With the increasing of the network size and averaged excitability level of focal network, the seizure period decreases. In contrast, the larger heterogeneity of excitability for focal network nodes can lower the functional activity level (average degree) of focal network. There are also subtle effects of focal network topologies (connection patterns of excitatory nodes) that cannot be ignored along with non-focal nodes.DiscussionUnraveling the role of excitatory factors in seizure onset and propagation can be used to understand the dynamic mechanisms and neuromodulation of epilepsy, with profound implications for the treatment of epilepsy and even for the understanding of the brain

The potential scale-free network mechanism underlying the formation of focal epilepsy

Abnormal brain networks are likely to be the trigger of seizure generation of epilepsy. Clarifying the effects of abnormal structures on brain function is of great significance for brain diseases. Due to the complexity of brain networks, the relationship between structural and functional brain networks is not yet well-defined. In this letter, we apply a generative model depicting the interrelationship between structural and functional connectivity, to reproduce similar resting whole brain networks and focal epileptic networks through networks with different topologies. It is found that only the underlying network connected with scale-free structure can reproduce the properties of focal epilepsy network, while the resting network has a small probability of reproduction under both the small-world network and the scale-free network. In particular, this reproduction capacity is immune to the nodal distance modes of the underlying network. This suggests that there exists severe heterogeneity in the focal epilepsy network similar to the scale-free network, which may facilitate to the clinical structural inference of seizure location

The Sluggishness of Early-Stage Face Processing (N170) is Correlated with Negative and General Psychiatric Symptoms in Schizophrenia

Patients with schizophrenia exhibit consistent abnormalities in face-evoked N170. However, the relation between face-specific N170 abnormalities in schizophrenic patients and schizophrenia clinical characters, which probably based on common neural mechanisms, is still rarely discovered. Using event-related potentials (ERPs) recording in both schizophrenic patients and healthy controls, the amplitude and latency of N170 were recorded when participants were passively watching face and non-face (table) pictures. The results showed a face-specific N170 latency sluggishness in schizophrenic patients, i.e., the N170 latencies of schizophrenic patients were significantly longer than those of healthy controls under both upright face and inverted face conditions. Importantly, the face-related N170 latencies of the left temporo-occipital electrodes (P7 and PO7) were positively correlated with negative symptoms and general psychiatric symptoms. Besides the analysis of latencies, the N170 amplitudes became weaker in schizophrenic patients under both inverted face and inverted table conditions, with a left hemisphere dominant. More interestingly, the FIEs (the difference of N170 amplitudes between upright and inverted faces) were absent in schizophrenic patients, which suggested the abnormality of holistic face processing. These results above revealed a marked symptom-relevant neural sluggishness of face-specific processing in schizophrenic patients, supporting the demyelinating hypothesis of schizophrenia

Dynamic Correlations between Intrinsic Connectivity and Extrinsic Connectivity of the Auditory Cortex in Humans

The arrival of sound signals in the auditory cortex (AC) triggers both local and inter-regional signal propagations over time up to hundreds of milliseconds and builds up both intrinsic functional connectivity (iFC) and extrinsic functional connectivity (eFC) of the AC. However, interactions between iFC and eFC are largely unknown. Using intracranial stereo-electroencephalographic recordings in people with drug-refractory epilepsy, this study mainly investigated the temporal dynamic of the relationships between iFC and eFC of the AC. The results showed that a Gaussian wideband-noise burst markedly elicited potentials in both the AC and numerous higher-order cortical regions outside the AC (non-auditory cortices). Granger causality analyses revealed that in the earlier time window, iFC of the AC was positively correlated with both eFC from the AC to the inferior temporal gyrus and that to the inferior parietal lobule. While in later periods, the iFC of the AC was positively correlated with eFC from the precentral gyrus to the AC and that from the insula to the AC. In conclusion, dual-directional interactions occur between iFC and eFC of the AC at different time windows following the sound stimulation and may form the foundation underlying various central auditory processes, including auditory sensory memory, object formation, integrations between sensory, perceptional, attentional, motor, emotional, and executive processes