Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16194
Title: Interictal spikes and epileptic seizures: their relationship and underlying rhythmicity
Austin Authors: Karoly, Philippa J;Freestone, Dean R;Boston, Ray;Grayden, David B;Himes, David;Leyde, Kent;Seneviratne, Udaya;Berkovic, Samuel F ;O’Brien, Terence;Cook, Mark J
Affiliation: Austin Health, Heidelberg, Victoria, Australia
Department of Medicine, The University of Melbourne, St. Vincent's Hospital, Fitzroy, Victoria, Australia
NeuroEngineering Research Laboratory, Department of Electrical and Electronic Engineering, The University of Melbourne, Parkville, Victoria, Australia
Centre for Neural Engineering, The University of Melbourne, Parkville, Victoria, Australia
NeuroVista Corporation, Seattle, WA, USA
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Department of Medicine, The University of Melbourne, Royal Melbourne Hospital, Parkville, Victoria, Australia
Issue Date: Apr-2016
metadata.dc.date: 2016-02-17
Publication information: Brain 2016; 139(4): 1066-1078
Abstract: We report on a quantitative analysis of electrocorticography data from a study that acquired continuous ambulatory recordings in humans over extended periods of time. The objectives were to examine patterns of seizures and spontaneous interictal spikes, their relationship to each other, and the nature of periodic variation. The recorded data were originally acquired for the purpose of seizure prediction, and were subsequently analysed in further detail. A detection algorithm identified potential seizure activity and a template matched filter was used to locate spikes. Seizure events were confirmed manually and classified as either clinically correlated, electroencephalographically identical but not clinically correlated, or subclinical. We found that spike rate was significantly altered prior to seizure in 9 out of 15 subjects. Increased pre-ictal spike rate was linked to improved predictability; however, spike rate was also shown to decrease before seizure (in 6 out of the 9 subjects). The probability distribution of spikes and seizures were notably similar, i.e. at times of high seizure likelihood the probability of epileptic spiking also increased. Both spikes and seizures showed clear evidence of circadian regulation and, for some subjects, there were also longer term patterns visible over weeks to months. Patterns of spike and seizure occurrence were highly subject-specific. The pre-ictal decrease in spike rate is not consistent with spikes promoting seizures. However, the fact that spikes and seizures demonstrate similar probability distributions suggests they are not wholly independent processes. It is possible spikes actively inhibit seizures, or that a decreased spike rate is a secondary symptom of the brain approaching seizure. If spike rate is modulated by common regulatory factors as seizures then spikes may be useful biomarkers of cortical excitability.
URI: http://ahro.austin.org.au/austinjspui/handle/1/16194
DOI: 10.1093/brain/aww019
ORCID: 0000-0003-4580-841X
PubMed URL: https://pubmed.ncbi.nlm.nih.gov/26912639
Type: Journal Article
Subjects: Epilepsy
Seizures
Interictal spikes
Circadian rhythms
Appears in Collections:Journal articles

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