Each patient had a specific epileptogenic network, independent from the number, size, or location of nodules and from the cortical malformation associated with. SEEG-guided RF-TC appears as a new and very effective diagnostic and therapeutic approach for DRE related to PNHs.

Summary Purpose:  Electroencephalography–functional magnetic resonance imaging (EEG‐fMRI) coregistration has recently revealed that several brain structures are involved in generalized spike and wave discharges (GSWDs) in idiopathic generalized epilepsies (IGEs). In particular, deactivations and activations have been observed within the so‐called brain default mode network (DMN) and thalamus, respectively. In the present study we analyzed the dynamic time course of blood oxygen level–dependent (BOLD) changes preceding and following 3 Hz GSWDs in a group of adolescent and adult patients with IGE who presented with absence seizures (AS). Our aim was to evaluate cortical BOLD changes before, during, and after GSWD onset. Methods:  Twenty‐one patients with IGE underwent EEG‐fMRI coregistration. EEG‐related analyses were run both at the single‐subject and at group level (random effect). The time‐course analysis was conducted for 3 s time windows before, during, and after GSWDs, and they were included until no further BOLD signal changes were observed. Key Findings:  Fifteen patients (nine female, mean age 28 years) had GSWDs during EEG‐fMRI coregistration (262 total events, mean duration 4 s). Time‐course group analysis showed BOLD increments starting approximately 10 s before GSWD onset located in frontal and parietal cortical areas, and especially in the precuneus‐posterior cingulate region. At GSWD onset, BOLD increments were located in thalamus, cerebellum, and anterior cingulate gyrus, whereas BOLD decrements were observed in the DMN regions persisting until 9 s after onset. Significance:  Hemodynamic changes (BOLD increments) occurred in specific cortical areas, namely the precuneus/posterior cingulate, lateral parietal, and frontal cortices, several seconds before EEG onset of GSWD. A dysfunction of these brain regions, some of which belongs to the DMN, may be crucial in generating GSWDs in patients with IGE.

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In the past 2 decades we have observed an extensive use of different neuroimaging techniques to evaluate patients with status epilepticus. Magnetic resonance imaging (MRI) in particular may show a broad spectrum of abnormalities that are either the causes or the consequences of sustained epileptic activity. Neuroimaging techniques can offer a contribution both in the clinical management of individual patients, identifying hemodynamic patterns that support the diagnosis, and also in the recognition of periictal reversible or irreversible alterations. For the future it is necessary to develop larger and prospective studies in which imaging techniques and electroencephalography (EEG) recordings are acquired closely to understand which EEG patterns are related to imaging biomarkers of neuronal damage.