The relationship between white matter abnormalities and cognitive functions in new-onset juvenile myoclonic epilepsy |
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| Affiliation: | 1. Adiyaman University Training and Research Hospital, Neurology, Adiyaman, Turkey;2. Adiyaman University Training and Research Hospital, Radiology, Adiyaman, Turkey;3. Tekirdag Goverment Hospital, Child Psychiatry, Tekirdag, Turkey;4. Adiyaman University Training and Research Hospital, Physical Medicine and Rehabilitation, Adiyaman, Turkey;5. Adiyaman University Training and Research Hospital, Psychology, Adiyaman, Turkey;1. Department of Cardiology, University Hospital of Marburg and Gießen, Philipps-University Marburg, Marburg, Germany;2. Sleep Disorder Unit of the Department of Pneumology, University Hospital of Marburg and Gießen, Philipps-University Marburg, Marburg, Germany;1. Owensboro Medical Health System Neurology, USA;2. Department of Neurology, Vanderbilt University, Nashville, TN, USA;3. Hamad Medical Corporation, Doha, Qatar;1. Department of Neurology, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, United States;2. Department of Quantitative Health Sciences, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, United States;3. Department of Psychiatry and Psychology, Cleveland Clinic, 2070 East 90th Street, Cleveland, OH 44195, United States;4. Epilepsy Center, Cleveland Clinic, 9500 Euclid Avenue S51, Cleveland, OH 44195, United States;1. Epilepsy Unit, Pitié-Salpêtrière Hospital, APHP, Paris, France;2. Brain and Spine Institute, (Centre de Recherche de l''Institut du Cerveau et de la Moelle Epinière, ICM), Paris, France;3. Rothschild Foundation, Paris, France;4. Affiliated Teaching Hospital of Tsinghua University, Beijing, China;5. Psitec Laboratory (EA 4072), University of Lille, France |
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| Abstract: | Diffusion tensor imaging (DTI) has revealed evidence of subcortical white matter abnormalities in the frontal area in juvenile myoclonic epilepsy (JME). Decreased fractional anisotropy (FA) and increased mean diffusivity (MD) in the corticothalamic pathway have been detected in adult patients with JME. It has been demonstrated that, in adult patients with JME, frontal dysfunction is related to subcortical white matter damage and decreased volume in frontal cortical gray matter and the thalamus. Many studies have focused on adult patients.Twenty-four patients and 28 controls were evaluated. The group with JME had significantly worse results for the word fluency, trail-B, and Stroop tests that assessed executive functions. A significant decrease in FA values in the dorsolateral prefrontal cortex (DLPFC), the supplementary motor area (SMA), the right thalamus, the posterior cingulate, the corpus callosum anterior, the corona radiata, and the middle frontal white matter (MFWM) and an increase in ADC values in patients with JME were detected. The correlation between FA values in DLPFC and the letter fluency test results was positive, and the correlation with the Stroop and trail-B test results was negative. We found a negative correlation between SMA, anterior thalamus, and MFWM FA values and the trail-B test results and a positive correlation between the SMA, anterior thalamus, and MFWM FA values and the letter fluency test results.We detected white matter and gray matter abnormalities in patients with new-onset JME using DTI. In addition, we determined the relationship between cognitive deficit and microstructural abnormalities by evaluating the correlation between the neuropsychological test battery results and DTI parameters. We evaluated newly diagnosed patients with JME in our study. That leads us to believe that microstructural abnormalities exist from the very beginning of the disease and that they result from the genetic basis of the disease. |
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