Abstracts

SUBCORTICAL SHAPE ANALYSIS IN TEMPORAL LOBE EPILEPSY

Abstract number : 3.186
Submission category : 5. Neuro Imaging
Year : 2013
Submission ID : 1750063
Source : www.aesnet.org
Presentation date : 12/7/2013 12:00:00 AM
Published date : Dec 5, 2013, 06:00 AM

Authors :
S. Keller, J. O Muircheartaigh, C. Traynor, K. Towgood, G. Barker, M. P. Richardson

Rationale: Prior imaging studies of temporal lobe epilepsy (TLE) emphasise mesial temporal lobe abnormalities. Extrahippocampal subcortical volume atrophy has been reported in TLE, but this is typically demonstrated as global volume loss (1, 2). In the present study, we mapped regional atrophy of the hippocampus and three extrahippocampal subcortical structures that are variably reported (3) to be abnormal in TLE: thalamus, putamen and caudate.Methods: We recruited 23 patients with well-characterised unilateral TLE (11 left-onset; mean age 40.9 years) attending King s College Hospital London and 23 healthy controls (mean age 35.3 years; no significant difference between patients and controls: p=0.27). Diagnosis and localisation of TLE was determined by comprehensive evaluation including detailed history and seizure semiology, EEG, and clinical MRI. 3D T1-weighted (IR-SPGR) images acquired on a 3 Tesla GE Signa HDx MR system were analysed using FSL FIRST tools, which (i) automatically segmented the subcortical structures, (ii) parameterised volumetric labels (meshes) from the deformable surfaces of structures, and (iii) permitted vertex-wise shape analysis along the surface of the segmented structures. Comparisons were made between left TLE and controls and right TLE and controls separately. All results are reported corrected for multiple vertex comparisons (p<0.05, FDR).Results: Fig 1 shows the patterns of regional subcortical deflation - a proxy for atrophy - in patients relative to controls. Patients with left TLE had significant regional deflation of the ipsilateral hippocampus, and more dramatically within the thalamus and putamen bilaterally. There was additional regional deflation of the caudate, which while bilateral was more pronounced ipsilaterally. Patients with right TLE had significant regional deflation of the ipsilateral hippocampus, and a more restricted pattern of subcortical deflation, including the ipsilateral thalamus and bilateral putamen. Conclusions: These results indicate that, in our patients with well-characterised TLE: (i) hippocampal atrophy is modest compared to extrahippocampal subcortical atrophy; (ii) thalamic and putamenal atrophy is severe in both hemispheres, and encompasses regions that are directly anatomically connected with the mesial temporal lobe (e.g. pulvinar, dorsomedial and anterior thalamic regions (4) and ventral putamen regions (5)); and (iii) patients with left TLE have a wider and more bilateral distribution of subcortical abnormalities relative to patients with right TLE, which is consistent with previous work (6). It will be important to establish the influence of mesial temporal-subcortical connectivity on regional subcortical pathology in TLE. References 1.Dreifuss S. Neurology. 2001;57:1636. 2.Pulsipher DT. Epilepsy Behav. 2007;11:442. 3.Keller SS. Epilepsia. 2008;49:741. 4.Aggleton JP. J Comp Neurol. 1986;243:409. 5.Kelley AE. Neuroscience. 1982;7:615. 6.Keller SS. PLoS One. 2012;7:e46791.
Neuroimaging