Jennifer A Williams1, Peter Bede2, Colin P Doherty2. 1. Department of Neurology,St. James's Hospital, James's Street, Dublin 8, Ireland; Academic Unit of Neurology, Trinity Biomedical Science Institute, Trinity College,152-160 Pearse Street, Dublin 2, Ireland. Electronic address: williaj7@tcd.ie. 2. Department of Neurology,St. James's Hospital, James's Street, Dublin 8, Ireland; Academic Unit of Neurology, Trinity Biomedical Science Institute, Trinity College,152-160 Pearse Street, Dublin 2, Ireland.
Abstract
PURPOSE: The aim of this review was to identify published studies in the literature relating to ictal induced MRI change and to identify certain common themes, practical points for clinicians and areas for future research. METHODS: We identified 96 articles that satisfied our inclusion criteria yielding 575 cases. All articles were analysed; number of subjects, spectrum of MRI and EEG change, aetiology, and follow-up (both clinical and imaging) were noted. RESULTS: The most frequent imaging changes were restricted diffusion, T2-hyperintensity and reduced ADC values. The mesial temporal structures and neocortex were most commonly affected locations though subcortical structures like the thalamus and pulvinar were also described. Practical clinical points included; the development of PLEDS concordant with ictal imaging change was associated with worse clinical prognosis, patients with seizures due to symptomatic aetiology may be more likely to develop ictal related imaging change and follow up is vitally important to ensure that ictal related oedema is not misidentified as a mass lesion or conversely that a mass lesion is not misidentified as ictal related change. CONCLUSION: Qualitative MRI studies have provided clinicians with useful in-vivo insights into the dynamic ictal neuronal environment. Changes are not only localised to the ictal focus but can be remote and irreversible. Small patient numbers varying study design and high numbers of symptomatic seizures makes comparison between studies problematic. Also there is possible microstructural quantitative MRI changes that are missed on qualitative MRI. There is a need for prospective quantitative MRI studies in patients with epilepsy peri-icatlly with a uniform period of follow up and comparison to control data.
PURPOSE: The aim of this review was to identify published studies in the literature relating to ictal induced MRI change and to identify certain common themes, practical points for clinicians and areas for future research. METHODS: We identified 96 articles that satisfied our inclusion criteria yielding 575 cases. All articles were analysed; number of subjects, spectrum of MRI and EEG change, aetiology, and follow-up (both clinical and imaging) were noted. RESULTS: The most frequent imaging changes were restricted diffusion, T2-hyperintensity and reduced ADC values. The mesial temporal structures and neocortex were most commonly affected locations though subcortical structures like the thalamus and pulvinar were also described. Practical clinical points included; the development of PLEDS concordant with ictal imaging change was associated with worse clinical prognosis, patients with seizures due to symptomatic aetiology may be more likely to develop ictal related imaging change and follow up is vitally important to ensure that ictal related oedema is not misidentified as a mass lesion or conversely that a mass lesion is not misidentified as ictal related change. CONCLUSION: Qualitative MRI studies have provided clinicians with useful in-vivo insights into the dynamic ictal neuronal environment. Changes are not only localised to the ictal focus but can be remote and irreversible. Small patient numbers varying study design and high numbers of symptomatic seizures makes comparison between studies problematic. Also there is possible microstructural quantitative MRI changes that are missed on qualitative MRI. There is a need for prospective quantitative MRI studies in patients with epilepsy peri-icatlly with a uniform period of follow up and comparison to control data.
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