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- Elene Tsoures, Jan Lewerenz, Elmar Pinkhardt, Albert C Ludolph, and Susanne Fauser.
- Department of Neurology, University Hospital Ulm, Oberer Eselsberg 45, 89081 Ulm, Germany.
- Epilepsy Res. 2017 Sep 1; 135: 115-122.
IntroductionThalamo-cortical networks have mainly been studied in the generation of idiopathic (genetic) epilepsies. The purpose of this study was to analyze EEG patterns and the occurrence of focal (symptomatic) epileptic seizures in patients with acquired circumscribed thalamic lesions.Patients And MethodsAmong 596 patients with thalamic lesions, we identified 47 patients in whom circumscribed thalamic lesions were detected by MRI and who underwent an EEG examination at the same stay at hospital. EEG findings were divided into normal findings, unspecific pathological changes and epileptiform discharges. The EEG findings were correlated to the localisation of the lesion within the thalamus and to the patientś symptoms.ResultsIn 32 patients (68%) pathological EEG findings were observed. They were heterogeneous and comprised regional and generalized slowing, triphasic waves, generalized periodic and regional epileptiform discharges. However, some characteristic findings were seen: Regional slowing was associated with ipsilateral thalamic lesions independent of the thalamic subarea, epileptiform discharges were related to lesions in the ipsilateral medial thalamus and periodic generalized discharges/triphasic waves with lesions in the anterior-ventromedial thalamus. Epileptic seizures were also more common in patients with medial thalamic lesions. Patients with regional epileptiform discharges responded to antiepileptic treatment whereas patients with triphasic waves and generalized periodic patterns did not. In some cases, it remained difficult to decide whether the thalamic lesion was the cause or consequence of epileptic activity.ConclusionPathological EEG findings are common in patients with acute and chronic thalamic lesions. EEG patterns associated with circumscribed thalamic lesions were influenced by the affected thalamic subregion. As in idiopathic generalized epilepsy, also in symptomatic epilepsy, the medial thalamus revealed to play a role in the generation of epileptiform discharges. In the patients with generalized periodic discharges and acute lesions in the ventral-anterior-medial thalamus, however, EEG changes were more likely caused by a disinhibition of cortico-thalamic networks than by a status epilepticus and thus risks and benefits of an aggressive antiepileptic treatment must be thoroughly balanced.Copyright © 2017 Elsevier B.V. All rights reserved.
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