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Research paper
Epilepsy-related cytoarchitectonic abnormalities along white matter pathways
  1. G Russell Glenn1,2,3,
  2. Jens H Jensen1,2,
  3. Joseph A Helpern1,2,3,
  4. Maria V Spampinato2,
  5. Ruben Kuzniecky4,
  6. Simon S Keller5,6,
  7. Leonardo Bonilha7
  1. 1Center for Biomedical Imaging, Medical University of South Carolina, Charleston, South Carolina, USA
  2. 2Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, South Carolina, USA
  3. 3Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA
  4. 4Department of Neurology, New York University, New York City, New York, USA
  5. 5Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK
  6. 6Department of Clinical Neuroscience, Institute of Psychiatry, King's College London, London, UK
  7. 7Department of Neurology, Medical University of South Carolina, Charleston, South Carolina, USA
  1. Correspondence to Dr Leonardo Bonilha, Comprehensive Epilepsy Center, Department of Neurology, Medical University of South Carolina, 96 Jonathan Lucas St, Suite 301, Charleston 29425, SC, USA; bonilha{at}musc.edu

Abstract

Objective Temporal lobe epilepsy (TLE) is one of the most common forms of epilepsy. Unfortunately, the clinical outcomes of TLE cannot be determined based only on current diagnostic modalities. A better understanding of white matter (WM) connectivity changes in TLE may aid the identification of network abnormalities associated with TLE and the phenotypic characterisation of the disease.

Methods We implemented a novel approach for characterising microstructural changes along WM pathways using diffusional kurtosis imaging (DKI). Along-the-tract measures were compared for 32 subjects with left TLE and 36 age-matched and gender-matched controls along the left and right fimbria-fornix (FF), parahippocampal WM bundle (PWMB), arcuate fasciculus (AF), inferior longitudinal fasciculus (ILF), uncinate fasciculus (UF) and cingulum bundle (CB). Limbic pathways were investigated in relation to seizure burden and control with antiepileptic drugs.

Results By evaluating measures along each tract, it was possible to identify abnormalities localised to specific tract subregions. Compared with healthy controls, subjects with TLE demonstrated pathological changes in circumscribed regions of the FF, PWMB, UF, AF and ILF. Several of these abnormalities were detected only by kurtosis-based and not by diffusivity-based measures. Structural WM changes correlated with seizure burden in the bilateral PWMB and cingulum.

Conclusions DKI improves the characterisation of network abnormalities associated with TLE by revealing connectivity abnormalities that are not disclosed by other modalities. Since TLE is a neuronal network disorder, DKI may be well suited to fully assess structural network abnormalities related to epilepsy and thus serve as a tool for phenotypic characterisation of epilepsy.

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