Evaluation of cerebral white-matter micro-structural alterations in patients with medically refractory epilepsy using diffusion tensor tractography

Kori, Prakash; Garg, Ravindra Kumar; Malhotra, Hardeep Singh; Gupta, Rakesh K.; Verma, Rajesh; Singh, Maneesh; Rathore, Ram K.S.; Gupta, Pradeep Kumar

doi:10.1016/j.eplepsyres.2013.08.015

Cited by 11 publications

(7 citation statements)

References 31 publications

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“…Furthermore, mTOR complex 1 has been implicated in neurodegeneration leading to sustained seizure activity with increased mossy fiber spreading in the hippocampus [72]. This pre-clinical data is similar to persistent gliosis, cavitation, and hippocampal sclerosis in human TBI patients measured with diffusion tensor tractography [73]. Hippocampal sclerosis is associated with tauopathy in patients with PTE [68].…”

Section: Tau Pathologysupporting

confidence: 53%

Traumatic brain injury and epilepsy: Underlying mechanisms leading to seizure

Lucke‐Wold

Nguyen

Turner

et al. 2015

Seizure

128

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Post-traumatic epilepsy continues to be a major concern for those experiencing traumatic brain injury. Post-traumatic epilepsy accounts for 10-20% of epilepsy cases in the general population. While seizure prophylaxis can prevent early onset seizures, no available treatments effectively prevent late-onset seizure. Little is known about the progression of neural injury over time and how this injury progression contributes to late onset seizure development. In this comprehensive review, we discuss the epidemiology and risk factors for post-traumatic epilepsy and the current pharmacologic agents used for treatment. We highlight limitations with the current approach and offer suggestions for remedying the knowledge gap. Critical to this pursuit is the design of pre-clinical models to investigate important mechanistic factors responsible for post-traumatic epilepsy development. We discuss what the current models have provided in terms of understanding acute injury and what is needed to advance understanding regarding late onset seizure. New model designs will be used to investigate novel pathways linking acute injury to chronic changes within the brain. Important components of this transition are likely mediated by toll-like receptors, neuroinflammation, and tauopathy. In the final section, we highlight current experimental therapies that may prove promising in preventing and treating post-traumatic epilepsy. By increasing understanding about post-traumatic epilepsy and injury expansion over time, it will be possible to design better treatments with specific molecular targets to prevent late-onset seizure occurrence following traumatic brain injury.

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Section: Tau Pathologysupporting

confidence: 53%

Traumatic brain injury and epilepsy: Underlying mechanisms leading to seizure

Lucke‐Wold

Nguyen

Turner

et al. 2015

Seizure

128

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“…Full text was screened in 71 cases and reference lists were inspected to detect additional studies not identified with the initial search. Forty-two studies met the inclusion criteria for the meta-analysis (Ahmadi et al, 2009, Andrade et al, 2014, Arfanakis et al, 2002, Braakman et al, 2014, Campos et al, 2015, Concha et al, 2005, Concha et al, 2007, Concha et al, 2009, Deppe et al, 2008, Diao et al, 2015, Diehl et al, 2008, Duning et al, 2010, Gao et al, 2012, Govindan et al, 2008, Gross et al, 2006, Holt et al, 2011, Hutchinson et al, 2010, Keller et al, 2011, Keller et al, 2012, Kemmotsu et al, 2011, Kemmotsu et al, 2014, Kim et al, 2011, Knake et al, 2009, Kori et al, 2013, Labate et al, 2015, Lee et al, 2013, Lee et al, 2014, Li et al, 2010, Liacu et al, 2012, Lin et al, 2008, Liu et al, 2011, Mao et al, 2011, McDonald et al, 2008, Meng et al, 2010a, Nilsson et al, 2008, Powell et al, 2007, Pustina et al, 2015, Rodrigo et al, 2007, Scanlon et al, 2013, Vulliemoz et al, 2011, Wang et al, 2010, Xiao et al, 2014). The total number of people with epilepsy and controls was 1027 and 1122, respectively.…”

Section: Resultsmentioning

confidence: 99%

White matter abnormalities at a regional and voxel level in focal and generalized epilepsy: A systematic review and meta-analysis

Slinger

Sinke

Braun

et al. 2016

NeuroImage: Clinical

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ObjectiveSince the introduction of diffusion tensor imaging, white matter abnormalities in epilepsy have been studied extensively. However, the affected areas reported, the extent of abnormalities and the association with relevant clinical parameters are highly variable. We aimed to obtain a more consistent estimate of white matter abnormalities and their association with clinical parameters in different epilepsy types.MethodsWe systematically searched for differences in white matter fractional anisotropy and mean diffusivity, at regional and voxel level, between people with epilepsy and healthy controls. Meta-analyses were used to quantify the directionality and extent of these differences. Correlations between white matter differences and age of epilepsy onset, duration of epilepsy and sex were assessed with meta-regressions.ResultsForty-two studies, with 1027 people with epilepsy and 1122 controls, were included with regional data. Sixteen voxel-based studies were also included. People with temporal or frontal lobe epilepsy had significantly decreased fractional anisotropy (Δ –0.021, 95% confidence interval –0.026 to –0.016) and increased mean diffusivity (Δ0.026 × 10–3 mm2/s, 0.012 to 0.039) in the commissural, association and projection white matter fibers. White matter was much less affected in generalized epilepsy. White matter changes in people with focal epilepsy correlated with age at onset, epilepsy duration and sex.SignificanceThis study provides a better estimation of white matter changes in different epilepsies. Effects are particularly found in people with focal epilepsy. Correlations with the duration of focal epilepsy support the hypothesis that these changes are, at least partly, a consequence of seizures and may warrant early surgery. Future studies need to guarantee adequate group sizes, as white matter differences in epilepsy are small.

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“…Significant alterations occur in functional connectivity between brain structures in patients with GTCS ( Blumenfeld et al, 2009 ; Elshahabi et al, 2015 ; Ji et al, 2014 ; Song et al, 2011 ), presumably arising from loss of volume in neural structures ( Huang et al, 2011 ), or fiber injury ( Kori et al, 2013 ). The findings suggest a potential for involvement of insular and cingulate cortex regions, both of which mediate autonomic, and especially cardiovascular patterning ( Kimmerly et al, 2005 ; Oppenheimer, 2001 ; Oppenheimer et al, 1991 ).…”

Section: Introductionmentioning

confidence: 99%

Regional cortical thickness changes accompanying generalized tonic-clonic seizures

Ogren

Tripathi

Macey

et al. 2018

NeuroImage: Clinical

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ObjectiveGeneralized tonic-clonic seizures are accompanied by cardiovascular and respiratory sequelae that threaten survival. The frequency of these seizures is a major risk factor for sudden unexpected death in epilepsy (SUDEP), a leading cause of untimely death in epilepsy. The circumstances accompanying such fatal events suggest a cardiovascular or respiratory failure induced by unknown neural processes rather than an inherent cardiac or lung deficiency. Certain cortical regions, especially the insular, cingulate, and orbitofrontal cortices, are key structures that integrate sensory input and influence diencephalic and brainstem regions regulating blood pressure, cardiac rhythm, and respiration; output from those cortical regions compromised by epilepsy-associated injury may lead to cardiorespiratory dysregulation. The aim here was to assess changes in cortical integrity, reflected as cortical thickness, relative to healthy controls. Cortical alterations in areas that influence cardiorespiratory action could contribute to SUDEP mechanisms.MethodsHigh-resolution T1-weighted images were collected with a 3.0-Tesla MRI scanner from 53 patients with generalized tonic-clonic seizures (Mean age ± SD: 37.1 ± 12.6 years, 22 male) at Case Western Reserve University, University College London, and the University of California at Los Angeles. Control data included 530 healthy individuals (37.1 ± 12.6 years; 220 male) from UCLA and two open access databases (OASIS and IXI). Cortical thickness group differences were assessed at all non-cerebellar brain surface locations (P < 0.05 corrected).ResultsIncreased cortical thickness appeared in post-central gyri, insula, and subgenual, anterior, posterior, and isthmus cingulate cortices. Post-central gyri increases were greater in females, while males showed more extensive cingulate increases. Frontal and temporal cortex, lateral orbitofrontal, frontal pole, and lateral parietal and occipital cortices showed thinning. The extents of thickness changes were sex- and hemisphere-dependent, with only males exhibiting right–sided and posterior cingulate thickening, while females showed only left lateral orbitofrontal thinning. Regional cortical thickness showed modest correlations with seizure frequency, but not epilepsy duration.SignificanceCortical thickening and thinning occur in patients with generalized tonic-clonic seizures, in cardiovascular and somatosensory areas, with extent of changes sex- and hemisphere-dependent. The data show injury in key autonomic and respiratory cortical areas, which may contribute to dysfunctional cardiorespiratory patterns during seizures, as well as to longer-term SUDEP risk.

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Evaluation of cerebral white-matter micro-structural alterations in patients with medically refractory epilepsy using diffusion tensor tractography

Cited by 11 publications

References 31 publications

Traumatic brain injury and epilepsy: Underlying mechanisms leading to seizure

Traumatic brain injury and epilepsy: Underlying mechanisms leading to seizure

White matter abnormalities at a regional and voxel level in focal and generalized epilepsy: A systematic review and meta-analysis

Regional cortical thickness changes accompanying generalized tonic-clonic seizures

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