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J Neurol Neurosurg Psychiatry. 2016 Sep;87(9):930-6. doi: 10.1136/jnnp-2015-312980. Epub 2016 Apr 13.

Epilepsy-related cytoarchitectonic abnormalities along white matter pathways.

Author information

1
Center for Biomedical Imaging, Medical University of South Carolina, Charleston, South Carolina, USA Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, South Carolina, USA Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA.
2
Center for Biomedical Imaging, Medical University of South Carolina, Charleston, South Carolina, USA Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, South Carolina, USA.
3
Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, South Carolina, USA.
4
Department of Neurology, New York University, New York City, New York, USA.
5
Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK Department of Clinical Neuroscience, Institute of Psychiatry, King's College London, London, UK.
6
Department of Neurology, Medical University of South Carolina, Charleston, South Carolina, USA.

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.

PMID:
27076491
DOI:
10.1136/jnnp-2015-312980
[Indexed for MEDLINE]

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