Analysis of initial slow waves (ISWs) at the seizure onset in patients with drug resistant temporal lobe epilepsy.
BACKGROUND
The goal of this study is to analyze initial slow waves (ISWs) at seizure onset in patients with refractory temporal lobe epilepsy. ISWs are a specific type of ictal EEG pattern characterized by a slow wave at the seizure onset followed by low voltage fast activity.


METHODS
Investigations were carried out on 14 patients from the UCLA hospital (USA) and 10 from the Ghent University Hospital (Belgium) implanted with depth and grid electrodes for localization of the epileptogenic zone.


RESULTS
Sixty-one seizures in the UCLA group and 30 seizures in the Ghent group were analyzed. Fourteen UCLA and seven Ghent patients had ISWs at seizure onset. The duration of ISWs varied between 0.3 to 6.0 s and maximum amplitude varied from 0.2 to 1.4 mV. ISWs in three of 14 UCLA patients (30% of seizures) had a consistent positive polarity at the deepest contacts that were located in the amygdala, hippocampus, or entorhinal cortex and reversed polarity outside of these brain areas (ISWs1). ISWs in 11 of 14 UCLA patients (70% of seizures) had negative polarity at the deepest electrodes and their amplitude increased toward the recording contacts located in the white matter or neocortex (ISWs2). All ISWs from the seven Ghent patients were negative in the depth contacts (ISWs2) and positive on grid electrodes at the cortical surface. ISWs1 were associated with EEG spikes at the onset and on increase in amplitude of 10-20 Hz sinusoidal activity. In contrast, ISWs2 were associated with suppression of EEG amplitude, an increase in frequency in the range of 20-50 Hz, and did not have EEG spikes at the onset. Multiunit neuronal activity showed strong synchronization of neuronal discharges during interictal spikes, but multiunit synchronization was not obvious during ISWs2.


CONCLUSIONS
The existence of EEG spikes and phase reversal with ISWs1 indicates this type of seizure may be triggered by hypersynchronous neuronal discharges; however, seizures with ISWs2 at the onset may be triggered by different mechanisms, perhaps nonneuronal.
Bragin
Anatol
A
Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA. abragin@ucla.edu
Claeys
Pieter
P
Vonck
Kristl
K
Van Roost
Dirk
D
Wilson
Charles
C
Boon
Paul
P
Engel
Jerome
J
D000679:Amygdala / Q000503:physiopathology; D000927:Anticonvulsants / Q000627:therapeutic use; D001530:Belgium; D001921:Brain / Q000503:physiopathology*; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology; D003344:Cortical Synchronization / Q000706:statistics & numerical data; D004351:Drug Resistance; D004567:Electrodes, Implanted; D004569:Electroencephalography / Q000379:methods / Q000706:statistics & numerical data*; D018728:Entorhinal Cortex / Q000503:physiopathology; D004833:Epilepsy, Temporal Lobe / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D007839:Functional Laterality / Q000502:physiology; D006624:Hippocampus / Q000503:physiopathology; D006801:Humans; D008991:Monitoring, Physiologic; D013238:Stereotaxic Techniques; D014481:United States; D014743:Videotape Recording
D000927:Anticonvulsants