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Epilepsy
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Donald C. Barr, Andres M. Kanner
Genetic factors are being recognized as very important pathogenic mechanisms in various types of epilepsy syndromes. Genetic disturbances may be associated with generalized epilepsies (e.g. idiopathic generalized epilepsies) or epilepsies of focal origin (e.g. adult nocturnal frontal lobe epilepsy or familial TLE). Genetic disturbances associated with a progressive encephalopathic process may lead to treatment-resistant epilepsies (e.g. progressive myoclonic epilepsies), while those that occur in the absence of an encephalopathic process are often identified in epilepsies of benign prognosis (e.g. idiopathic generalized epilepsy presenting as childhood absence epilepsy or juvenile myoclonic epilepsy [JME]).
Subthalamic nucleus and substantia nigra pars reticulata stimulation: the Grenoble experience
Published in Hans O Lüders, Deep Brain Stimulation and Epilepsy, 2020
Alim-Louis Benabid, Adnan Koudsie, Stephan Chabardes, Laurent Vercueil, Abdelhamid Benazzouz, Lorella Minotti, Jean-François Le Bas, Philippe Kahane, Anne de Saint Martin, Edouard Hirsch
This was a 17-year-old male with autosomal dominant nocturnal frontal lobe epilepsy, suffering from left insulo-opercular seizures. In a month follow-up no significant improvement was observed after HFS of the STN. His father and an uncle as well as his grandfather also had frontal lobe epilepsy, with a favorable evolution. Seizures started at age 5. He has a feeling of fear and asphyxiation followed by hyperapnea, agitation, bilateral motor movements and yelling, without loss of contact and without postictal deficit. Initially, he had up to two seizures per night. The seizures then stopped until age 10. Seizures then recurred but a much higher rate of up to 20 per night. There is no postictal deficit. He was diagnosed as having familial frontal lobe epilepsy. Despite several trials of antiepileptic drugs, seizures persisted, occurring several times a day, predominantly at night. Occasionally, seizures happened in clusters, sometimes requiring dilantin intravenously and hospitalization in an intensive care unit. A pre-surgical depth electrode EEG recording showed that the seizures originate from the insular or insulo-opercular region spreading into the whole left frontal area. Ablative surgery was not possible. There was no sensorimotor deficit.
Epilepsy
Published in Anne Lee, Sally Inch, David Finnigan, Therapeutics in Pregnancy and Lactation, 2019
The known inherited/genetic conditions associated with epilepsy can be divided broadly into two groups. The first, the inherited/genetic epilepsies, include benign familial neonatal or infantile convulsions and familial frontal lobe epilepsy. Many of this group are autosomal dominant, which implies a risk of up to 50% of transmitting the gene to offspring.6
Thalamic neuromodulation in epilepsy: A primer for emerging circuit-based therapies
Published in Expert Review of Neurotherapeutics, 2023
Bryan Zheng, David D. Liu, Brian B Theyel, Hael Abdulrazeq, Anna R. Kimata, Peter M Lauro, Wael F. Asaad
Frontal lobe epilepsy, the second most common focal epilepsy, accounts for about one-quarter of medically refractory cases[205] and is often included in clinical trials such as SANTE. Yet evidence of abnormal frontothalamic correlates in epilepsy remain vague and inconclusive[206,207]. In the SANTE trial, ANT stimulation did not significantly reduce seizures from the frontal (as well as parietal and occipital) lobes[164]. Likewise, in a trial of CMT stimulation that included five patients with frontal lobe epilepsy, only one had clinically-reduced seizures[202]. A recent case report of a patient with bilateral frontotemporal epilepsy demonstrated a meaningful decrease in seizure frequency and intensity after RNS of the CMT complex combined with VNS, though improved awareness during seizures was perhaps the more notable result[208]. Interestingly, the degree of thalamic involvement has been linked to poorer postsurgical outcomes in a stereo-electroencephalography (SEEG) study involving a diverse series of patients comprising multiple epilepsy categories (TLE, ‘temporal plus,’ bitemporal, opercular, motor-premotor)[209]. These preliminary observations suggest there may be a role for thalamic neuromodulation in non-temporal focal epilepsies, but much work remains to be done.
Advantages of magnetoencephalography, neuronavigation and intraoperative MRI in epilepsy surgery re-operations
Published in Neurological Research, 2021
Julia Shawarba, Burkhard Kaspar, Stefan Rampp, Fabian Winter, Roland Coras, Ingmar Blumcke, Hajo Hamer, Michael Buchfelder, Karl Roessler
Due to the high number of MRI negative failed cases (81%) included in this study, we not only relied on semiology, MRI and video-EEG monitoring during reinvestigation of the failed cases. Additionally, we employed MEG for the investigation of localizing intracranial spikes. This approach is not new, but also described by El Tahry et al., who found positive MEG foci in up to 58% of failed epilepsy surgery cases [22]. Fortunately, 12 out of 35 (34%) of our MEG investigations, corresponding to 12/27 (44%) patients, accomplished true localizing spikes mainly around the previous resection cavity preoperatively. Moreover, this resulted in 83% (10/12) of patients with localizing MEG spots used for targeting the resection, who had a better seizure outcome after the second surgery, Table 1. Equally to that study, we already had successfully used MEG for detection of the epileptogenic zone in negative frontal lobe epilepsy cases in the past.[23]
Contemporary surgical management of drug-resistant focal epilepsy
Published in Expert Review of Neurotherapeutics, 2020
Jasmina R. Milovanović, Slobodan M. Janković, Dragan Milovanović, Dejana Ružić Zečević, Marko Folić, Marina Kostić, Goran Ranković, Srđan Stefanović
Genetic factors are involved in almost 70% of epilepsy cases [10], and usually variants of several genes are responsible in the same time, revealing polygenic nature of the disorder. However, relatively small number of well-defined epilepsy syndromes nowadays could be precisely diagnosed by commercially available gene panels: Dravet’s syndrome (the most important are variants of SCN1A gene, while many others are also involved, like SCN2A, SCN8A, SCN9A, etc.), autosomal dominant nocturnal frontal lobe epilepsy (KCNT1 mutation of the gene for nicotinic receptor), familial focal epilepsy with variable foci (certain variants of NPRL2, NPRL3 and DEPDC5 genes) and autosomal dominant temporal lobe epilepsy (mutations of LGI1 and RELN genes). Knowing precise genetic basis of an epilepsy syndrome in a patient is helpful to the clinicians not only to have better estimate of prognosis, but also to choose optimal treatment modality [11].