Microstructural and volumetric abnormalities of the putamen in juvenile myoclonic epilepsy

Abstract

and zDepartment of Radiology, University of Mü nster, Mü nster, Germany SUMMARY Purpose: Patients with juvenile myoclonic epilepsy (JME) show evidence of microstructural white matter (WM) damage of thalamocortical fiber tracts and changes of blood oxygen level dependent (BOLD) signal in a striatothalamocortical network. The objective of the present study was to investigate microstructural and volumetric alterations of the putamen in patients with JME using diffusion tensor imaging (DTI) and conventional magnetic resonance imaging (MRI). Methods: We performed DTI and MRI for 10 patients with JME and 59 age-matched neurologically healthy volunteers. Evaluation of microstructural damage was investigated using calculation of mean fractional anisotropy (FA) values in a priori regions of interest (ROIs) for the putamen, frontal lobe, and a thalamocortical region, after application of an improved eddy current correction method and a new statistical parametric mapping (SPM)-compatible toolbox incorporating intensive multicontrast FA image registration. Stereologic analysis on MRI was performed to estimate macroscopic volume of the putamen in both cerebral hemispheres for all subjects.Key Findings: Relative to controls, patients had significantly reduced FA in the frontal lobe (p = 0.01) and thalamocortical fiber WM (p < 0.001). In contrast, putamen FA was bilaterally increased (p = 0.01) and correlated with decreasing putamen volume (r 2 = )0.63, p = 0.004) in patients only. Putamen FA correlated negatively with onset of JME (total: r 2 = )0.50, p = 0.01), duration of JME (r 2 = 0.52, p = 0.01), and thalamocortical fiber FA (r 2 = )0.47, p = 0.01). Significance: This is the first evidence of combined microstructural and macrostructural putamen abnormalities in patients with JME, with early age of onset and a longer duration of epilepsy being significant predictors for greater architectural alterations. These findings are consistent with studies indicating neurophysiologic abnormalities of frontostriatal networks in patients with JME, and may contribute to explain the frequent presentation of executive dysfunction in these patients. Confirmation and further exploration of the increase in putamen FA in patients with JME is required in larger samples.

Diffusion tensor imaging abnormalities in photosensitive juvenile myoclonic epilepsy

“…This is consistent with findings of prior studies that focused on microstructural abnormalities in the internal capsule [6,16,17,22]; however, this is the first study showing a clear mean FA reduction in the Table 2 Eta values of clinical parameters ARAS LGN GIC ICP VMT L R L R L R L R FA MD FA MD FA MD FA MD FA MD FA MD FA MD FA MD GIC in pPPR JME patients in contrast to the nPPR group when compared to healthy controls. The GIC predominantly contains motor fibers between the thalamus and the premotor cortex including the supplementary motor area [26].…”

Evaluation of subcortical grey matter abnormalities in patients with MRI-negative cortical epilepsy determined through structural and tensor magnetic resonance imaging

“…In addition to changes in the hippocampus, they also observed the significantly reduced volumes of the left thalamus, left caudate nucleus and bilateral lenticular nuclei [27]. Consequently, the amygdala [15], putamen [10,12-14,16], caudate nucleus [11,14-16], globus pallidus [11] and hippocampus [11,13-15] were also found to show atrophy in patients with temporal lobe epilepsy with or without MRI-visible hippocampal lesions. Thereafter, patients with IGEs, including absence epilepsy, juvenile myoclonic epilepsy (JME) and primary generalised tonic-clonic seizures, were also found to have subcortical abnormalities [3-10].…”

“…It has been reported that patients with temporal lobe epilepsy (TLE) and idiopathic generalised epilepsy (IGE) have structural alterations in the subcortical nuclei and, more generally, in the thalamus [3-16]. Furthermore, the changes in subcortical GM correlate with the age at seizure onset and the duration of epilepsy [3,4,10,15,16]. A small number of longitudinal studies have shown that recurrent seizures may lead to progressive microstructural alterations [17,18].…”

Applications of Blood-Oxygen-Level-Dependent Functional Magnetic Resonance Imaging and Diffusion Tensor Imaging in Epilepsy

“…Widespread postictal diffusion changes around the seizure focus and remote areas (eg, thalamus and basal ganglia) have been shown in patients with focal and generalized epilepsy. 165,184,[198][199][200] Recurrent seizures, earlier age at seizure onset, and longer duration of epilepsy may also lead to microstructural changes along the seizure spread pathways. 167,172,199,201 Detecting Postoperative Changes Acute and chronic diffusion abnormalities, ipsilateral and contralateral to the epileptic focus, have also been seen after ATLR.…”

“…in more extensive diffusion abnormalities involving ipsilateral and contralateral temporal neocortex and medial temporal structures, ipsilateral frontal lobe white matter, corpus callosum, basal ganglia, thalamus, and cerebellum. [163][164][165][166][167][168][169][170][171][172][173][174][175][176] Similarly, significant widespread diffusion abnormalities are found in the white matter tracts adjacent to and distant from lesions (eg, focal cortical dysplasia 177-179 ; in frontal lobes in children with drug-resistant focal epilepsy 180 ; in corticothalamic network in IGE and its subtypes, JME and childhood absence epilepsy [181][182][183][184][185][186] ). These widespread changes are not detected by conventional structural imaging and may reflect microstructural damage in a network distribution.…”