Brian Nils Lundstrom1, Christian Meisel2, Jamie Van Gompel3, Matt Stead4, Greg Worrell4. 1. Department of Neurology, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA. Electronic address: lundstrom.brian@mayo.edu. 2. Department of Neurology, University Clinic Carl Gustav Carus, Fetscherstrasse 74, 01307 Dresden, Germany. 3. Department of Neurosurgery, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA. 4. Department of Neurology, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA.
Abstract
OBJECTIVES: To develop quantitative measures for estimating seizure probability, we examine intracranial EEG data from patient groups with three qualitative seizure probabilities: patients with drug resistant focal epilepsy (high), these patients during cortical stimulation (intermediate), and patients who have no history of seizures (low). METHODS: Patients with focal epilepsy were implanted with subdural electrodes during presurgical evaluation. Patients without seizures were implanted during treatment with motor cortex stimulation for atypical facial pain. RESULTS: The rate and amplitude of spikes correlate with qualitative seizure probability across patient groups and with proximity to the seizure onset zone in focal epilepsy patients. Spikes occur earlier during the negative oscillation of underlying slow activity (0.5-2 Hz) when seizure probability is increased. Similarly, coupling between slow and fast activity is increased. CONCLUSIONS: There is likely a continuum of sharply contoured activity between non-epileptiform and epileptiform. Characteristics of spiking and how spikes relate to slow activity can be combined to predict seizure onset zones. SIGNIFICANCE: Intracranial EEG data from patients without seizures represent a unique comparison group and highlight changes seen in spiking and slow wave activity with increased seizure probability. Slow wave activity and related physiology are an important potential biomarker for estimating seizure probability.
OBJECTIVES: To develop quantitative measures for estimating seizure probability, we examine intracranial EEG data from patient groups with three qualitative seizure probabilities: patients with drug resistant focal epilepsy (high), these patients during cortical stimulation (intermediate), and patients who have no history of seizures (low). METHODS:Patients with focal epilepsy were implanted with subdural electrodes during presurgical evaluation. Patients without seizures were implanted during treatment with motor cortex stimulation for atypical facial pain. RESULTS: The rate and amplitude of spikes correlate with qualitative seizure probability across patient groups and with proximity to the seizure onset zone in focal epilepsypatients. Spikes occur earlier during the negative oscillation of underlying slow activity (0.5-2 Hz) when seizure probability is increased. Similarly, coupling between slow and fast activity is increased. CONCLUSIONS: There is likely a continuum of sharply contoured activity between non-epileptiform and epileptiform. Characteristics of spiking and how spikes relate to slow activity can be combined to predict seizure onset zones. SIGNIFICANCE: Intracranial EEG data from patients without seizures represent a unique comparison group and highlight changes seen in spiking and slow wave activity with increased seizure probability. Slow wave activity and related physiology are an important potential biomarker for estimating seizure probability.
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