Tract‐specific atrophy in focal epilepsy: Disease, genetics, or seizures?

Vaughan, David N.; Raffelt, David; Curwood, Evan K.; Tsai, Meng Han; Tournier, Jacques‐Donald; Connelly, Alan; Jackson, Graeme D.

doi:10.1002/ana.24848

Cited by 39 publications

(48 citation statements)

References 49 publications

(138 reference statements)

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“…Therefore FC, which is thought to reflect accumulated axonal loss (Raffelt et al, ), may decrease progressively as this degeneration continues, however FC was not related to time post‐injury in the current study. In addition, thin WM structures (e.g., fornix, anterior commissure) may not be accurately assessed using FBA; although micro‐structural changes (FD) can be detected in small structures, FC can be insensitive and any macro‐structural changes may instead present as micro‐structural changes (FD) (Raffelt et al, ; Vaughan et al, ). This problem may be exacerbated by the large voxel size used to acquire the images (2.5 mm 3 ), in addition to partial volume effects, which occur when there are two or more different types of tissue present within a single voxel (e.g., WM, grey matter, cerebrospinal fluid) (Raffelt et al, ; Vos, Jones, Viergever, & Leemans, ).…”

Section: Limitationsmentioning

confidence: 99%

“…FBA has been used to examine a number of different neurological conditions, including multiple sclerosis (Gajamange et al, ), temporal lobe epilepsy (Vaughan et al, ), and Alzheimer's disease (Mito et al, 2018), but has yet to be used with a TBI sample. Overall, FBA appears to provide a promising technique for detecting micro‐ and macro‐structural changes that addresses one of the main limitations of DTI (multiple tracts and crossing fibres) and yields more readily interpreted data.…”

Section: Introductionmentioning

confidence: 99%

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A fixel‐based analysis of micro‐ and macro‐structural changes to white matter following adult traumatic brain injury

Wallace

Mathias

Ward

et al. 2020

Human Brain Mapping

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Diffusion tensor imaging is often used to assess white matter (WM) changes following traumatic brain injury (TBI), but is limited in voxels that contain multiple fibre tracts.Fixel-based analysis (FBA) addresses this limitation by using a novel method of analysing high angular resolution diffusion-weighted imaging (HARDI) data. FBA examines three aspects of each fibre tract within a voxel: tissue micro-structure (fibre density [FD]), tissue macro-structure (fibre-bundle cross section [FC]) and a combined measure of both (FD and fibre-bundle cross section [FDC]). This study used FBA to identify the location and extent of micro-and macro-structural changes in WM following TBI. A large TBI sample (N mild = 133, N moderate-severe = 29) and control group (healthy and orthopaedic; N = 107) underwent magnetic resonance imaging with HARDI and completed reaction time tasks approximately 7 months after their injury (range:98-338 days). The TBI group showed micro-structural differences (lower FD) in the corpus callosum and forceps minor, compared to controls. Subgroup analyses revealed that the mild TBI group did not differ from controls on any fixel metric, but the moderate to severe TBI group had significantly lower FD, FC and FDC in multiple WM tracts, including the corpus callosum, cerebral peduncle, internal and external capsule. The moderate to severe TBI group also had significantly slower reaction times than controls, but the mild TBI group did not. Reaction time was not related to fixel findings.Thus, the WM damage caused by moderate to severe TBI manifested as fewer axons and a reduction in the cross-sectional area of key WM tracts. K E Y W O R D Sadults, diffusion-weighted imaging, fixel-based analysis, neuroimaging, traumatic brain injury

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Section: Limitationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A fixel‐based analysis of micro‐ and macro‐structural changes to white matter following adult traumatic brain injury

Wallace

Mathias

Ward

et al. 2020

Human Brain Mapping

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“…The fact that diffusion anomalies may be present soon after diagnosis (Hutchinson et al, 2010) is suggestive of possible contributing role of neurodevelopmental processes; further evidence stems for animal models of epilepsy, suggesting their presence as a requisite for development of spontaneous seizures (Parekh et al, 2010). A recent study provided a multifactorial model of WM damage in TLE, in which genetic factors play a minimal role compared to the underlying pathology and effects of seizures (Vaughan et al, 2017).…”

Section: Applications In Temporal Lobe Epilepsymentioning

confidence: 99%

Histological and MRI markers of white matter damage in focal epilepsy

et al. 2018

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Growing evidence highlights the importance of white matter in the pathogenesis of focal epilepsy. Ex vivo and post-mortem studies show pathological changes in epileptic patients in white matter myelination, axonal integrity, and cellular composition. Diffusion-weighted MRI and its analytical extensions, particularly diffusion tensor imaging (DTI), have been the most widely used technique to image the white matter in vivo for the last two decades, and have shown microstructural alterations in multiple tracts both in the vicinity and at distance from the epileptogenic focus. These techniques have also shown promising ability to predict cognitive status and response to pharmacological or surgical treatments. More recently, the hypothesis that focal epilepsy may be more adequately described as a system-level disorder has motivated a shift towards the study of macroscale brain connectivity. This review will cover emerging findings contributing to our understanding of white matter alterations in focal epilepsy, studied by means of histological and ultrastructural analyses, diffusion MRI, and large-scale network analysis. Focus is put on temporal lobe epilepsy and focal cortical dysplasia. This topic was addressed in a special interest group on neuroimaging at the 70th annual meeting of the American Epilepsy Society, held in Houston December 2-6, 2016.

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“…It has been argued 2 that non-mnestic deficits in TLE might reflect extra-temporal structural pathology, [5][6][7] giving rise to the notion of TLE as a structural "network disease". 8 While structural "network disease" is unlikely to explain cognitive impairment in all cases, 9 the underlying concept can be expanded to incorporate functional network disease as well.…”

Section: Introductionmentioning

confidence: 99%

Cognitive impairment in epilepsy: the role of reduced network flexibility

Tailby

Kowalczyk

Jackson

2017

Ann Clin Transl Neurol

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ObjectiveThe dominant model of cognitive impairment in focal epilepsy has emphasised structural bases for cognitive deficits. Current theories of cognition in the healthy brain emphasise the importance of the reweighting of brain network interactions in support of task performance. Here, we explore the hypothesis that cognitive deficits in epilepsy arise through abnormalities of dynamic functional network interactions.MethodWe studied 19 healthy controls and 37 temporal lobe epilepsy (TLE) patients, using a behavioural measure of verbal fluency (the Controlled Oral Word Association Test) and an fMRI verbal fluency paradigm (Orthographic Lexical Retrieval).ResultsBehaviourally, verbal fluency was significantly impaired in TLE. Psychophysiological interaction analyses of the fMRI data, which capture state‐dependent changes in network connectivity, revealed reduced task‐dependent modulations of connectivity from left superior medial frontal cortex to left middle frontal gyrus in TLE patients. Individual differences in verbal fluency among TLE cases was correlated with task‐dependent changes in connectivity from left posterior cingulate to left superior medial frontal cortex, and from left superior medial frontal cortex to a range of right predominant brain areas.InterpretationThese data reveal that the typical pattern of task‐driven shifts in network connectivity is not observed in TLE. Our observations go beyond simple structure‐function associations and suggest that failure of network flexibility can be an important contributor to cognitive impairment in epilepsy.

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Tract‐specific atrophy in focal epilepsy: Disease, genetics, or seizures?

Abstract: 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 multifactorial model of white matter atrophy in focal epilepsy is proposed. Ann Neurol 2017;81:240-250.

Cited by 39 publications

References 49 publications

A fixel‐based analysis of micro‐ and macro‐structural changes to white matter following adult traumatic brain injury

A fixel‐based analysis of micro‐ and macro‐structural changes to white matter following adult traumatic brain injury

Histological and MRI markers of white matter damage in focal epilepsy

Cognitive impairment in epilepsy: the role of reduced network flexibility

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