EEG Prediction of Post‐Traumatic Epilepsy

Jennett, Bryan; Sande, Jesse van de

doi:10.1111/j.1528-1157.1975.tb06055.x

Cited by 62 publications

(39 citation statements)

References 4 publications

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“…Similar results were obtained in vitro in the organotypic hippocampal slice culture model of epileptogenesis (Dyhrfjeld-Johnsen et al 2010). These studies undertook a simple but important step beyond prior EEG biomarker studies by greatly increasing the duration of the EEG sample from the standard clinical EEG of tens of minutes up to 24-h recording epochs (Jennett and Van De Sande 1975). Although the results in these experimental studies are promising and support the possibility that EEG biomarkers may be useful for the prediction of acquired epilepsy, the predictive power of electrographic biomarkers has not been systematically compared with the predictive power of traditional physical descriptors of injury, such as lesion size and location.…”

Section: Electrographic Biomarkerssupporting

confidence: 55%

Epileptogenesis

Pitkänen

Łukasiuk²,

Dudek

et al. 2015

Cold Spring Harb Perspect Med

279

173

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Epileptogenesis is a chronic process that can be triggered by genetic or acquired factors, and that can continue long after epilepsy diagnosis. In 2015, epileptogenesis is not a treatment indication, and there are no therapies available in clinic to treat individuals at risk of epileptogenesis. However, thanks to active research, a large number of animal models have become available for search of molecular mechanisms of epileptogenesis. The first glimpses of treatment targets and biomarkers that could be developed to become useful in clinic are in sight. However, the heterogeneity of the epilepsy condition, and the dynamics of molecular changes over the course of epileptogenesis remain as challenges to overcome.

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Section: Electrographic Biomarkerssupporting

confidence: 55%

Epileptogenesis

Pitkänen

Łukasiuk²,

Dudek

et al. 2015

Cold Spring Harb Perspect Med

279

173

View full text Add to dashboard Cite

show abstract

“…This is an issue on which previous investigations have been inconclusive. Jennett and Van De Sande (35) maintained that EEG does not improve the accuracy of the prediction based on clinical data and thus does not contribute usefully to the prediction of traumatic epilepsy. By contrast, Pampiglione (36) found relations between trauma evolution, EEG, and PTE when the analysis was performed 4-6 weeks after trauma.…”

Section: Discussionmentioning

confidence: 99%

Posttraumatic Epilepsy Risk Factors: One‐Year Prospective Study After Head Injury

et al. 1999

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Summary:Purpose: Prospective evaluation of risk factors for posttraumatic epilepsy (PTE) by using clinical, EEG, and brain computed tomography (CT) data in four assessments from the head injury (HI) acute phase to 1 year later; and evaluation of the possible epileptogenic role of hemosiderin as shown by brain magnetic resonance imaging (MRI).Methods: Risk factors for PTE were evaluated by using Kaplan-Meier curves, log-rank test, and the Cox model in 137 consecutively enrolled adult inpatients. Percentage differences of patients with brain hyperintense and/or hemosiderin areas shown by MRI 1 year after HI were statistically evaluated by univariate tests considering two subgroups [e.g., patients with (FTE) and without (WLS) late seizures].Results: The PTE subgroup included 18 patients with at least two seizures between the second and twelfth months. KaplanMeier curves demonstrated that Glasgow Coma Scale low score, early seizures, and single brain CT lesions are PTE risk factors, as is the development of an EEG focus 1 month after HI. No significant percentage difference was found between PTE and WLS patients with hemosiderin spots shown by MRI 1 year after HI.Conclusions: the Cox model indicates that, for HI patients with early seizures and brain CT single temporal or frontal lesions in the acute phase, the PTE risk is 8.58 and 3.43 times higher, respectively, than for those without. An EEG focus 1 month after HI is a risk factor 3.49 times higher than for patients without such EEG changes. One year after HI, a higher percentage of PTE than WLS patients had cortical MRI hyperintense areas including hemosiderin. Key Words: Posttraumatic epilepsy-Clinical-Brain CT-MRI-EEG follow-upHemosiderin.Posttraumatic epilepsy (PTE), known since the time of Hippocrates, is still a puzzle because of the variety of methods used in the different studies and the wide range of their results. Dalmady-Israel and Zasler ( I ) provided a critical analysis of the literature on PTE emphasizing the lack of standardized definitions of both epilepsy and head injury (HI). Differences in inclusion/exclusion criteria and inadequacy in the follow-up of patients generate inconclusive or controversial results on incidence and risk factors.Many of the retrospective studies evaluated outcome when there was no standardized way of managing the

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“…Patients with focal spikes do not necessarily develop epilepsy (20). Several authors considered an epileptic EEG pattern for the decision about AED treatment (15,21).…”

Section: Discussionmentioning

confidence: 99%