Electrical stimulation induced self-related auditory hallucinations correlate with oscillatory power change in the default mode network.

Self-related information is crucial in our daily lives, which has led to the proposal that there is a specific brain mechanism for processing it. Neuroimaging studies have consistently demonstrated that the default mode network (DMN) is strongly associated with the representation and processing of self-related information. However, the precise relationship between DMN activity and self-related information, particularly in terms of neural oscillations, remains largely unknown. We electrically stimulated the superior temporal and fusiform areas, using stereo-electroencephalography to investigate neural oscillations associated with elicited self-related auditory hallucinations. Twenty-two instances of auditory hallucinations were recorded and categorized into self-related and other-related conditions. Comparing oscillatory power changes within the DMN between self-related and other-related auditory hallucinations, we discovered that self-related hallucinations are associated with significantly stronger positive power changes in both alpha and gamma bands compared to other-related hallucinations. To ensure the validity of our findings, we conducted controlled analyses for factors of familiarity and clarity, which revealed that the observed effects within the DMN remain independent of these factors. These results underscore the significance of the functional role of the DMN during the processing of self-related auditory hallucinations and shed light on the relationship between self-related perception and neural oscillatory activity.

Auditory verbal hallucination can be evoked by prefrontal epileptic seizure.

Auditory verbal hallucinations (AVHs) have been reported in neocortical temporal epileptic seizures and have been considered highly associated with implication of auditory cortex by epileptic discharges or electrical stimulation. Herein, we report two rare frontal epilepsy cases in which AVHs featured the habitual seizures. The epileptogenic zones of these two patients were localized in the dorsal and orbitomedial prefrontal cortex, respectively by stereoelectroencephalography (SEEG) monitoring. Comparing with the AVHs in schizophrenia, we postulated that the phenomenological similarities between the two sets of AVHs imply homology in mechanisms. Ictal SEEG confirmed that the wide involvement of prefrontal-cingulate-auditory cortical network by low-voltage fast activity corresponded the occurrence with AVHs during frontal epileptic seizures. Electrical stimulation study of one of the two cases highlighted the causal role of prefrontal-cingulate cortex in the emergence of AVHs. Based on our clinical observation, SEEG findings, and electrical cortical stimulation, we supposed that wide implication of prefrontal-cingulate-auditory cortical network during epileptic seizure underlie the emergence of AVHs, and further hypothesized that AVHs could be yielded by transient deficit of self-monitoring for inner speech in focal epileptic seizures.

Electrical stimulation mapping in the medial prefrontal cortex induced auditory hallucinations of episodic memory: A case report.

It has been well documented that the auditory system in the superior temporal cortex is responsible for processing basic auditory sound features, such as sound frequency and intensity, while the prefrontal cortex is involved in higher-order auditory functions, such as language processing and auditory episodic memory. The temporal auditory cortex has vast forward anatomical projections to the prefrontal auditory cortex, connecting with the lateral, medial, and orbital parts of the prefrontal cortex. The connections between the auditory cortex and the prefrontal cortex thus help in localizing, recognizing, and comprehending external auditory inputs. In addition, the medial prefrontal cortex (MPFC) is believed to be a core region of episodic memory retrieval and is one of the most important regions in the default mode network (DMN). However, previous neural evidence with regard to the comparison between basic auditory processing and auditory episodic memory retrieval mainly comes from fMRI studies. The specific neural networks and the corresponding critical frequency bands of neuronal oscillations underlying the two auditory functions remain unclear. In the present study, we reported results of direct cortical stimulations during stereo-electro-encephalography (SEEG) recording in a patient with drug-resistant epilepsy. Electrodes covered the superior temporal gyrus, the operculum and the insula cortex of bilateral hemispheres, the prefrontal cortex, the parietal lobe, the anterior and middle cingulate cortex, and the amygdala of the left hemisphere. Two types of auditory hallucinations were evoked with direct cortical stimulations, which were consistent with the habitual seizures. The noise hallucinations, i.e., "I could hear buzzing noises in my head," were evoked with the stimulation of the superior temporal gyrus. The episodic memory hallucinations "I could hear a young woman who was dressed in a red skirt saying: What is the matter with you?," were evoked with the stimulation of MPFC. The patient described how she had met this young woman when she was young and that the woman said the same sentence to her. Furthermore, by analyzing the high gamma power (HGP) induced by direct electrical stimulation, two dissociable neural networks underlying the two types of auditory hallucinations were localized. Taken together, the present results confirm the hierarchical processing of auditory information by showing the different involvements of the primary auditory cortex vs. the prefrontal cortex in the two types of auditory hallucinations.

A semiological marker of emotional insulo-cingulate network activation in epileptic human brain.

There are limited reports on the "chapeau de gendarme" (CDG) sign, which is considered reliable evidence for the verification of frontal epilepsy. However, several recent reports of scattered cases of extra-frontal epilepsy suggest the complexity of the cortical networks underlying CDG generation. The present study aimed to investigate the anatomo-electro-clinical correlations and explore the cortical mechanisms of the generation of CDG via video-stereoelectroencephalography (SEEG). Patients with focal epilepsy who underwent SEEG and epilepsy surgery in our center from March 2017 to December 2019 were retrospectively reviewed. Ten patients with epilepsy with habitual seizures presenting with CDG were included. Most CDG signs were discerned visually into two chronological components referred to as the "prodromal component" and the "major component." The CDG signs occurred at 2.4-26.1 s after electrical onset and lasted for 2.2-16.6 s. The two sequential components were visually discerned in 64 included seizures of the six patients. The epileptogenic zones were diverse in distribution. Cluster analysis was performed based on the neurophysiological features of distinct cortical areas, and the agranulo-dysgranular insular and cingulate cortices were emphasized. Pearson correlation and linear regression showed a linear relationship between the latencies of CDG onset and the latencies of co-activation of agranulo-dysgranular cingulate and insular cortex in gamma bands. Our results suggest that (1) the CDG sign should be interpreted as a type of facial behavior with social-emotional features and considered a semiological marker of emotional insulo-cingulate cortex involvement in focal epilepsy, and (2) epileptic discharges arising directly from or propagating indirectly into this anterior limbic network have a high likelihood of evoking the CDG sign.