Abstracts

Rationale: Sleep and epilepsy share a bidirectional relationship involving many facets. These include activation of interictal and seizure activity in addition to fragmentation of sleep architecture by abnormal spikes. In 1965 Niedermeyer first decscribed "dyshormia" as an aberrant spiky arousal wave seen in sleep in association with normal K complexes in patients with generalized epilepsy. As an EEG biomarker it most likely reflects abnormal activation of deep centrencephalic structures and the cortex in a complex interrelationship. The relevance of this pattern for clinical epilepsy diagnosis and management may relate to abnormal clinical arousals, parasomnias, presence of nocturnal seizures and specific EEG patterns that are activated by sleep (ESES, generalized spikes). Methods: We retrospectively analyzed the clinical and EEG data of 95 patients aged 1-18 years diagnosed with generalized, multifocal or focal epilepsy. We classified the sleep related epileptiform activity in temporal relationship to K complexes and spindles. We analyzed at least 30 minutes of the EEG sleep recordings for every patient. Results: 54 patients had a diagnosis of generalized epilepsy, 29 patients focal epilepsy and 9 patients with multifocal epilepsy.Dyshormia (abnormal epileptiform arousal) was seen in 68.5 % of patients with generalized epilepsy, 46.6 % of patients with focal epilepsy and 44.4% of patients with multifocal epilepsy. Most frequently spikes were superimposed on the vertex K complex (79%). Spikes seen before and after spindle activity correlated to a high spike load during sleep. Dyshormia was more frequent in patients with poorly controlled epilepsy (70% cf to 48%). In the prirmary generalized genetic epilepsy syndromes dyshormia was seen in 100% of patients. In benign focal epilepsies the rate was 44%. Conclusions: Abnormal epileptiform arousals were frequent in generalized and focal epilepsies in childhood including the benign epilepsies. However dyshormia was seen most frequently in generalized epilepsy that was medically refractory.. This suggests an active coactivation of cortical and thalamic structures during sleep. This may carry a high significance for seizure and comorbidities outcome.