Summary: Purpose:  Previous neuroimaging studies provide growing evidence that patients with juvenile myoclonic epilepsy (JME) have both structural and functional abnormalities of the thalamus and frontal lobe gray matter. However, limited data are available regarding the issue of white matter (WM) involvement, making the microstructural WM changes in JME largely unknown. In the present study we investigated changes of WM integrity in patients with JME, and their relationships with cognitive functions and epilepsy‐specific clinical factors.Methods:  We performed diffusion tensor imaging (DTI) and neuropsychological assessment in 25 patients with JME and 30 control subjects matched for age, gender, and education level. Between‐group comparisons of fractional anisotropy (FA) and mean diffusivity (MD) were carried out in a whole‐brain voxel‐wise manner by using tract‐based spatial statistics (TBSS). In addition, both FA and MD were correlated with cognitive performance and epilepsy‐specific clinical variables to investigate the influence of these clinical and cognitive factors on WM integrity changes.Key Findings:  Neuropsychological evaluation revealed that patients with JME had poorer performance than control subjects on most of the frontal function tests. TBSS demonstrated that, compared to controls, patients with JME had significantly reduced FA and increased MD in bilateral anterior and superior corona radiata, genu and body of corpus callosum, and multiple frontal WM tracts. Disease severity, as assessed by the number of generalized tonic–clonic seizures in given years, was negatively correlated with FA and positively correlated with MD extracted from regions of significant differences between patients and controls in TBSS.Significance:  Our findings of widespread disturbance of microstructural WM integrity in the frontal lobe and corpus callosum that interconnects frontal cortices could further support the pathophysiologic hypothesis of thalamofrontal network abnormality in JME. These WM abnormalities may implicate frontal cognitive dysfunctions and disease progression in JME.

Objective: We aimed to explore cortical thickness abnormalities in a homogeneous group of patients with migraine without aura and to delineate possible relationships between cortical thickness changes and clinical variables. Methods: Fifty-six female migraine patients without aura and T2-visible white matter hyperintensities and 34 female controls were scanned on a 3T magnetic resonance imager. Cortical thickness was estimated and compared between patients and controls using a whole-brain vertex-by-vertex analysis. Correlation analysis was conducted between cortical thickness of significant clusters and clinical variables. Results: Compared to controls, migraine patients had cortical thickening in left rostral middle frontal gyrus and bilateral post-central gyri. Region-of-interest analysis revealed cortical thickening of bilateral post-central gyri in migraine patients relative to controls. The average thickness of bilateral post-central gyri positively correlated with disease duration as well as estimated lifetime headache frequency. Conclusions: We have provided evidence for interictal cortical abnormalities of thickened prefrontal cortex and somatosensory cortex in female migraine patients without aura. Our findings of greater thickening of the somatosensory cortex in relation to increasing disease duration and increasing headache frequency suggest that repeated migraine attacks over time may lead to structural changes of the somatosensory cortex through increased noxious afferent input within the trigemino-thalamo-cortical pathway in migraine.

Summary: Although it is well documented that long‐term therapy with older antiepileptic drugs (AEDs) leads to an increase in risk for atherosclerosis, there has been only limited information regarding the vascular risk in patients who are treated with new AEDs. We therefore conducted a prospective longitudinal study to assess the potential effects of new AEDs on the circulatory markers for vascular risk in patients with newly diagnosed epilepsy. We recruited adult patients with epilepsy who began to receive monotherapy with one of the new AEDs, including levetiracetam (LEV), oxcarbazepine (OXC), and topiramate (TPM). Circulatory markers of vascular risk were measured twice before and after 6 months of AED monotherapy. A total of 109 patients completed the study (LEV, n = 40; OXC, n = 40; TPM, n = 29). Six months of monotherapy resulted in significant increases in low‐density lipoprotein cholesterol (LEV, from 90.2 to 98.5 mg/dl, 9.2% increase, p = 0.025; OXC, from 96.5 to 103.2 mg/dl, 7.0% increase, p = 0.049), homocysteine (LEV, from 7.9 to 10.4 μm, 31.6% increase, p = 0.001; OXC, from 8.7 to 11.5 μm, 32.2% increase, p < 0.001; TPM, from 8.3 to 12.3 μm, 48.2% increase, p < 0.001), apolipoprotein B (LEV, from 63.6 to 77.4 mg/dl, 21.7% increase; OXC, from 67.0 to 83.2 mg/dl, 24.2% increase; TPM, from 66.7 to 84.4 mg/dl, 26.5% increase; all p < 0.001), and apolipoprotein B/apolipoprotein A1 ratio (LEV, from 0.51 to 0.61, 19.6% increase; OXC, from 0.52 to 0.67, 28.8% increase; TPM, from 0.50 to 0.67, 34.0% increase; all p < 0.001). Serum apolipoprotein A1 and folate were significantly decreased in TPM (from 139.1 to 132.1 mg/dl, 5.0% decrease, p = 0.014) and OXC (from 8.1 to 6.4 ng/ml, 21.0% decrease, p = 0.046) groups, respectively. There were no significant changes in total cholesterol, triglyceride, high‐density lipoprotein cholesterol, lipoprotein(a), and vitamin B12 in all three groups. Our findings suggest that treatment with some new AEDs might be associated with alterations in circulatory markers of vascular risk, which could contribute to the acceleration of atherosclerosis and increased risk of vascular diseases.