Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16495
Title: Tract-specific atrophy in focal epilepsy: disease, genetics or seizures?
Austin Authors: Vaughan, David N;Raffelt, David;Curwood, Evan;Tsai, Meng-Han;Tournier, Jacques-Donald;Connelly, Alan;Jackson, Graeme D 
Affiliation: Austin Health, Heidelberg, Victoria, Australia
Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia
Department of Florey, University of Melbourne, Melbourne, Victoria, Australia
Department of Neurology, Austin Health, Heidelberg, Victoria, Australia
Department of Neurology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
Department of Nursing, Meiho University, Pingtung, Taiwan
Department of Biomedical Engineering, Division of Imaging Sciences and Biomedical Engineering, King's College London, UK
Centre for the Developing Brain, Division of Imaging Sciences and Biomedical Engineering, King's College London, King's College London, UK
Issue Date: 23-Dec-2016
metadata.dc.date: 2016-12-23
Publication information: Annals of Neurology 2016; online first: 23 December
Abstract: OBJECTIVE: To investigate whether genetics, underlying pathology or repeated seizures contribute to atrophy in specific white matter tracts. METHODS: Medically-refractory unilateral temporal lobe epilepsy with hippocampal sclerosis (HS-TLE, n=26) was studied as an archetype of focal epilepsy, using fixel-based analysis of diffusion-weighted imaging. A genetic effect was assessed in first-degree relatives of HS-TLE who did not have epilepsy themselves (HS-1°Rel; n=26). The role of disease process was uncovered by comparing HS-TLE to unilateral TLE with normal clinical MRI (MRI-neg TLE; n=26, matched for seizure severity). The effect of focal seizures was inferred from lateralized atrophy common to both HS-TLE and MRI-neg TLE, in comparison to healthy controls (n=76). RESULTS: HS-1°Rel had bilaterally small hippocampi, but no focal white matter atrophy was detected, indicating a limited effect of genetics. HS-TLE had lateralized atrophy of most temporal lobe tracts, and hippocampal volumes in HS-TLE correlated with parahippocampal cingulum and anterior commissure atrophy, indicating an effect of the underlying pathology. Ipsilateral atrophy of the tapetum, uncinate and inferior fronto-occipital fasciculus was found in both HS-TLE and MRI-neg TLE, suggesting a common lateralized effect of focal seizures. Both epilepsy groups had bilateral atrophy of the dorsal cingulum and corpus callosum fibers, which we interpret as a consequence of bilateral insults (potentially generalized seizures and/or medications). INTERPRETATION: Underlying pathology, repeated focal seizures and global insults each contribute to atrophy in specific tracts. Genetic factors make less of a contribution in this cohort. A multi-factorial model of white matter atrophy in focal epilepsy is proposed.
URI: http://ahro.austin.org.au/austinjspui/handle/1/16495
DOI: 10.1002/ana.24848
PubMed URL: https://pubmed.ncbi.nlm.nih.gov/28009132
Type: Journal Article
Appears in Collections:Journal articles

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