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The phenomenon of déjà vu (DV) has intrigued scientists for decades, yet its neurophysiological underpinnings remain elusive. Brain regions have been identified in which morphometry differs between healthy individuals according to the frequency of their DV experiences. This study built upon these findings by assessing if and how neural activity in these and other brain regions also differ with respect to DV experience. Resting-state fMRI was performed on 68 healthy volunteers, 44 of whom reported DV experiences (DV group) and 24 who did not (NDV group). Using multivariate analyses, we then assessed the (fractional) amplitude of low-frequency fluctuations (fALFF/ALFF), a metric that is believed to index brain tissue excitability, for five discrete frequency bands within sets of brain regions implicated in DV and those comprising the default mode network (DMN). Analyses revealed significantly lower values of fALFF/ALFF for specific frequency bands in the DV relative to the NDV group, particularly within mesiotemporal structures, bilateral putamina, right caudatum, bilateral superior frontal cortices, left lateral parietal cortex, dorsal and ventral medial prefrontal cortex, and the posterior cingulate cortex. The pattern of differences in fALFF/ALFF measures between the brains of individuals who have experienced DV and those who have not provides new neurophysiological insights into this phenomenon, including the potential role of the DMN. We suggest that the erroneous feeling of familiarity arises from a temporary disruption of cortico-subcortical circuitry together with the upregulation of cortical excitability.

A clear concept of epileptic zones remains of high clinical relevance in presurgical evaluation of refractory epilepsy patients and in resection planning. Recent advances in understanding how each of the epileptic zones is functionally organized strengthened the importance of the network concept. It has been shown that neuronal networks underlying the individual epileptic zone may involve multiple brain structures with complex interactions between them. The network concept has impact not only for better understanding of pathophysiology of partial epilepsy but also for clinical practice, particularly for epilepsy surgery. This review examines recent reports on the use of advanced imaging techniques which enable to map the epileptic zones and their structural and functional organization. Magnetic resonance postprocessing substantially improved the accuracy in detection of the epileptogenic lesions. The seizure-onset zone is primarily determined by electrophysiology but can also be localized using single photon emission computed tomography. The functional deficit zone is commonly assessed by a number of tests including methods of functional neuroimaging (positron emission tomography) which can delineate hypometabolic cortical areas and subcortical structures. Hemodynamic fluctuations associated with interictal epileptiform discharges can be detected by novel functional magnetic resonance technique which is nowadays widely used for the irritative zone localization. These techniques open new prospect for epilepsy surgery in patients who were previously considered as not suitable candidates of surgical treatment.

The objective of the study was to find out whether, under the conditions of a double-blind, placebo coil controlled study, high-frequency repetitive transcranial magnetic stimulation (TMS) over the left prefrontal cortex will show positive effects on working memory with simultaneous assessment of respective changes in neuronal activation.Stimulation treatment led to a reduction of seriousness of negative schizophrenia symptoms in both comparative groups. However, mutual comparison of real (n=19) and sham (n=11) rTMS, respectively, has shown that the effect of real rTMS was statistically significantly higher compared with placebo stimulation. During stimulation treatment an improvement in working memory performance was also found. No statistically significant difference between the real and placebo sham rTMS, respectively, was established. The rate of neuronal activation did not change at all during rTMS treatment.From clinical point of view rTMS seems to be a well-tolerated neurostimulation method for treatment of negative schizophrenia symptoms with favourable of impact on cognitive functions.

to investigate potential neuronal dysfunction within the thalamus in patients suffering from mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE/HS).we examined twenty epileptic patients suffering from mesial temporal lobe epilepsy with hippocampal sclerosis (17 females, 3 males) and twenty sex- and age-matched healthy controls. H MR spectroscopic imaging (SI) was performed over the right and left thalamus in all patients and controls. In addition both hippocampi were investigated by the H MR spectroscopic single voxel (SV) technique in both groups.statistical analysis of compared data in both groups demonstrated that the total thalamic NAA level was significantly decreased in patients with MTLE/HS as compared to healthy controls. Detailed analysis revealed a statistically significant reduction of NAA, NAA/Cr and NAA/(Cr+Cho) ratios in the thalamus ipsilateral to hippocampus affected with hippocampal sclerosis in patients compared to controls, while no significant changes were observed in the thalamus contralateral to sclerotic hippocampus. A comparison of values in ipsilateral and contralateral thalami in patients showed statistically significant difference with lower values of NAA and both ratios in the ipsilateral thalamus. Previously reported reduced hippocampal concentration of NAA, NAA/Cr and NAA/(Cr+Cho) ratios on the side of hippocampal sclerosis compared with contralateral hippocampus in patients and both hippocampi in controls was confirmed.the present MRS data clearly indicate neuronal dysfunction within the thalamus ipsilateral to the sclerotic hippocampus of patients with mesial temporal lobe epilepsy. In agreement with other recent functional and structural neuroimagings our results confirm the role of the ipsilateral thalamus in the medial temporal/limbic epileptic network.