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Journal Article

Brain iron redistribution in mesial temporal lobe epilepsy: A susceptibility-weighted magnetic resonance imaging study

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Bernhardt,  Boris C.
Department Social Neuroscience, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Citation

Zhang, Z., Liao, W., Bernhardt, B. C., Wang, Z., Sun, K., Yang, F., et al. (2014). Brain iron redistribution in mesial temporal lobe epilepsy: A susceptibility-weighted magnetic resonance imaging study. BMC Neuroscience, 15: 117. doi:10.1186/s12868-014-0117-3.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0025-1BA6-8
Abstract
Background The roles of iron in epilepsy and its pathophysiological significance are poorly understood, especially whether iron levels are abnormal in subcortcal structures. This study aims to demonstrate whole-brain iron alterations and its clinical relevancies in mesial temporal lobe epilepsy (mTLE) in vivo, using susceptibility-weighted magnetic resonance imaging (SWI). Methods We studied 62 patients with mTLE and 62 healthy controls. Brain iron concentration was quantified using SWI phase values. Voxel-wise analysis was carried out to compare iron levels between mTLE and controls, and to assess the relationship between altered iron concentration and clinical parameters in mTLE. Results Patients with mTLE showed decreases of iron levels in the subcortical structures such as substantia nigra, red nucleus, and basal ganglia. Conversely, iron levels were decreased in the cortex. Subcortical iron levels were negatively correlated to those in the cortex. Moreover, cortical and basal ganglia iron levels were related to clinical variables including epilepsy duration, age at seizures onset, and histories of precipitating factors. Conclusions Our SWI findings suggest a redistribution of iron between subcortical and cortical structures in mTLE. The degree of redistribution is affected by both progression of epilepsy and precipitating factors. Investigation on brain iron redistribution offers new insights into the pathogenesis of mTLE, and may be a potential biomarker for monitoring the clinical progression of epilepsy.