Thalamostriatal disconnection underpins long-term seizure freedom in frontal lobe epilepsy surgery
Poster No:
2173
Submission Type:
Abstract Submission
Authors:
Davide Giampiccolo1, Lawrence Binding2, Lorenzo Caciagli3, Roman Rodionov2, Chris Foulon4, Jane de Tisi2, Alejandro Grandados5, Roisin Finn6, Debayan Dasgupta7, Fenglai Xiao7, Beate Diehl2, Emma Torzillo8, Jan van Dijk7, Matthias Koepp9, Andrew McEvoy8, Sallie Baxendale10, Fahmida Chowdhury8, John Duncan11, Anna Miserocchi8
Institutions:
1UCL Queen Square Institute of Neurology/National Hospital for Neurology and Neurosurgery, London, London, 2UCL Queen Square Institute of Neurology, London, London, 3University of Bern, Bern, Bern, 4UCL Brain Sciences, London, London, 5King's College London, London, London, 6University of Southhampton, Southhampton, Southhampton, 7UCL Institute of Neurology, London, London, 8National Hospital for Neurology and Neurosurgery, London, London, 9UCL, London, London, 10UCLH, London, London, 11UCL Queen Square Institute of Neurology, London, United Kingdom
First Author:
Davide Giampiccolo
UCL Queen Square Institute of Neurology/National Hospital for Neurology and Neurosurgery
London, London
UCL Queen Square Institute of Neurology/National Hospital for Neurology and Neurosurgery
London, London
Co-Author(s):
Introduction:
Around 50% of patients undergoing frontal lobe surgery for focal drug-resistant epilepsy become seizure free post-operatively, however, only about 30% of patients remain seizure free in the long- term. Early seizure recurrence is likely to be caused by partial resection of the epileptogenic lesion, whilst delayed seizure recurrence can occur even if the epileptogenic lesion has been completely excised. This suggests a coexistent epileptogenic network facilitating ictogenesis in close or distant dormant epileptic foci. As thalamic and striatal dysregulation can support epileptogenesis and disconnection of cortico-thalamostriatal pathways through hemispherotomy or neuromodulation can improve seizure outcome regardless of focality, we hypothesise that projections from the striatum and the thalamus to the cortex may contribute to this common epileptogenic network.
Methods:
To this end, we retrospectively reviewed a series of 47 consecutive individuals who underwent surgery for drug-resistant frontal lobe epilepsy. We performed voxel-based and tractography disconnectome analyses to investigate shared patterns of disconnection associated with long-term seizure freedom.
Results:
Seizure freedom after 3 and 5 years was independently associated with disconnection of the anterior thalamic radiation and anterior cortico-striatal projections. This was also confirmed in a subgroup of 29 patients with complete resections, suggesting these pathways may play a critical role in supporting the development of novel epileptic networks.
Conclusions:
Our study indicates that network dysfunction in frontal lobe epilepsy may extend beyond the resection and putative epileptogenic zone. This may be critical in the pathogenesis of delayed seizure recurrence as thalamic and striatal networks may promote epileptogenesis and disconnection may underpin long-term seizure freedom.
Modeling and Analysis Methods:
Connectivity (eg. functional, effective, structural) 2
Neuroanatomy, Physiology, Metabolism and Neurotransmission:
White Matter Anatomy, Fiber Pathways and Connectivity 1
Keywords:
Epilepsy
Sub-Cortical
Thalamus
White Matter
WHITE MATTER IMAGING - DTI, HARDI, DSI, ETC
1|2Indicates the priority used for review
·Figure 1. Tractwise voxel-based analysis of disconnectome maps.
·Figure 2. Atlas-based disconnectome analysis.
Provide references using author date format
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