With a prevalence of 0.8 to 1.2%, epilepsy represents one of the most frequent chronic neurological disorders; 30 to 40% of patients suffer from drug-resistant epilepsy (that is, seizures cannot be controlled adequately with antiepileptic drugs). Epilepsy surgery represents a valuable treatment option for 10 to 50% of these patients. Epilepsy surgery aims to control seizures by resection of the epileptogenic tissue while avoiding neuropsychological and other neurological deficits by sparing essential brain areas. The most common histopathological findings in epilepsy surgery specimens are hippocampal sclerosis in adults and focal cortical dysplasia in children. Whereas presurgical evaluations and surgeries in patients with mesial temporal sclerosis and benign tumors recently decreased in most centers, non-lesional patients, patients requiring intracranial recordings, and neocortical resections increased. Recent developments in neurophysiological techniques (high-density electroencephalography [EEG], magnetoencephalography, electrical and magnetic source imaging, EEG-functional magnetic resonance imaging [EEG-fMRI], and recording of pathological high-frequency oscillations), structural magnetic resonance imaging (MRI) (ultra-high-field imaging at 7 Tesla, novel imaging acquisition protocols, and advanced image analysis [post-processing] techniques), functional imaging (positron emission tomography and single-photon emission computed tomography co-registered to MRI), and fMRI significantly improved non-invasive presurgical evaluation and have opened the option of epilepsy surgery to patients previously not considered surgical candidates. Technical improvements of resective surgery techniques facilitate successful and safe operations in highly delicate brain areas like the perisylvian area in operculoinsular epilepsy. Novel less-invasive surgical techniques include stereotactic radiosurgery, MR-guided laser interstitial thermal therapy, and stereotactic intracerebral EEG-guided radiofrequency thermocoagulation.

Goals of automated detection of epileptic seizures using wearable devices include objective documentation of seizures, prevention of sudden unexpected death in epilepsy (SUDEP) and seizure-related injuries, obviating both the unpredictability of seizures and potential social embarrassment, and finally to develop seizure-triggered on-demand therapies. Automated seizure detection devices are based on the analysis of EEG signals (scalp-EEG, subcutaneous EEG and intracranial EEG), of motor manifestations of seizures (surface EMG, accelerometry), and of physiologic autonomic changes caused by seizures (heart and respiration rate, oxygen saturation, sweat secretion, body temperature). While the detection of generalized tonic-clonic and of focal to bilateral tonic-clonic seizures can be achieved with high sensitivity and low false alarm rates, the detection of focal seizures is still suboptimal, especially in the everyday ambulatory setting. Multimodal seizure detection devices in general provide better performance than devices based on single measurement parameters. Long-term use of seizure detection devices in home environments helps to improve the accuracy of seizure diaries and to reduce seizure-related injuries, while evidence for prevention of SUDEP is still lacking. Automated seizure detection devices are generally well accepted by patients and caregivers.

BACKGROUND AND PURPOSE: Temporal lobe epilepsy, structural or nonlesional, may negatively affect language function. However, little is known about the lesion-specific influence on language networks. We hypothesized that different epileptogenic lesions are related to distinct alterations in the functional language connectome detected by fMRI. MATERIALS AND METHODS: One hundred one patients with epilepsy due to mesiotemporal sclerosis (21 left, 22 right), low-grade mesiotemporal tumors (12 left), or nonlesional temporal lobe epilepsy (22 left, 24 right) and 22 healthy subjects performed 3T task-based language fMRI. Task-based activation maps (laterality indices) and functional connectivity analysis (global and connectivity strengths between language areas) were correlated with language scores. RESULTS: Laterality indices based on fMRI activation maps failed to discriminate among patient groups. Functional connectivity analysis revealed the most extended language network alterations in left mesiotemporal sclerosis (involving the left temporal pole, left inferior frontal gyrus, and bilateral premotor areas). The other patient groups showed less extended but also predominantly ipsilesional network changes compared with healthy controls. Left-to-right hippocampal connectivity strength correlated positively with naming function (P = .01), and connectivity strength between the left Wernicke area and the left hippocampus was linked to verbal fluency scores (P = .01) across all groups. CONCLUSIONS: Different pathologies underlying temporal lobe epilepsy are related to distinct alterations of the functional language connectome visualized by fMRI functional connectivity analysis. Network analysis allows new insights into language organization and provides possible imaging biomarkers for language function. These imaging findings emphasize the importance of a personalized treatment strategy in patients with epilepsy.

BACKGROUND AND PURPOSE: Automated volumetry of the hippocampus is considered useful to assist the diagnosis of hippocampal sclerosis in temporal lobe epilepsy. However, voxel-based morphometry is rarely used for individual subjects because of high rates of false-positives. We investigated whether an approach with high dimensional warping to the template and nonparametric statistics would be useful to detect hippocampal atrophy in patients with hippocampal sclerosis. MATERIALS AND METHODS: We performed single-subject voxel-based morphometry with nonparametric statistics within the framework of Statistical Parametric Mapping to compare MRI from 26 well-characterized patients with temporal lobe epilepsy individually against a group of 110 healthy controls. The following statistical threshold was used: P < .05 corrected for multiple comparisons with family-wise error over the region of interest right and left hippocampus. RESULTS: The sensitivity for the detection of atrophy related to hippocampal sclerosis was 0.92 (95% CI, 0.67–0.99) for the right hippocampus and 0.60 (0.31–0.83) for the left, and the specificity for volume changes was 0.98 (0.93–0.99). All clusters of decreased hippocampal volumes were correctly lateralized to the seizure focus. Hippocampal volume decrease was in accordance with neuronal cell loss on histology reports. CONCLUSIONS: Nonparametric voxel-based morphometry is sensitive and specific for hippocampal atrophy in patients with mesial temporal lobe epilepsy and may be useful in clinical practice.

To assess the influence of collaterals on the long-term follow-up after successful percutaneous transluminal coronary arteriography (PTCA), 120 consecutive patients were studied. Of these, 104 (87%) had an adequate reangiogram and were included. At the time of PTCA the collaterals were estimated by a scoring system. In addtion, the coronary wedge pressure was measured in 49 patients six months after PTCA, a follow-up angiogram was performed, and the patients were split up into a group with restenoses (stenosis >50%), 34 patients (32.7%); and a group without restenoses (stenosis <50%), 70 patients (67.3%). A total of 35 patients (30.7%) had collaterals. A comparison between both groups showed no significant differences in clinical parameters (age, angina duration, vessel involvement, lipids, blood sugar, and blood pressure), and stenoses-related parameters (degree of stenoses, eccentricity, balloon size, inflation pressure, dissection, gradient after dilatation, and residual stenoses). Patients with collaterals had a significantly higher incidence of restenoses than those without collaterals (45.7% vs. 26.1%, p<0.05). Patients with wedge pressure of 45 mmHg (n= 19) (restenosis rate 52.6%). It is concluded that the presence of collaterals indicates a high restenosis rate after PTCA within 6 months.