INTRODUCTION: We analyzed the imaging features of transient focal lesions in the splenium of the corpus callosum (SCC) in non-epileptic patients receiving antiepileptic drugs (AEDs). METHODS: We identified signal abnormalities in the SCC in three non-epileptic patients, all of them receiving AEDs. We examined two of these patients with multiplanar magnetic resonance (MR) imaging using 1.0-T equipment including fluid-attenuated inversion recovery (FLAIR), T2-weighted (TSE) and T1-weighted (SE) sequences before and after injection of contrast agent. The third patient was studied using 1.5-T equipment with the same sequences. Additionally, a T1 SE sequence with a magnetization transfer contrast pulse off resonance (T1 SE/MTC), diffusion-weighted imaging (EPI-DWI) and apparent diffusion coefficient (ADC) maps were obtained. RESULTS: We observed an identical pattern of imaging abnormalities in all patients characterized by round lesions, hyperintense on FLAIR and hypointense on T1 SE images, located in the central portion of the SCC. One lesion showed homogeneous gadolinium enhancement and perilesional vasogenic edema. This particular lesion showed restricted diffusion confirmed on the ADC map. This pattern was considered consistent with focal demyelination. Follow-up MR examinations showed complete disappearance or a clear reduction in lesion size. All patients had been treated with AEDs, but they did not show any clinical signs of toxicity, interhemispheric symptoms, or abnormal neurological findings (including seizures). CONCLUSION: We believe that our MR findings might be interpreted as transient lesions related to AED toxicity. They presumably resulted from focal demyelination in the central portion of the SCC.
INTRODUCTION: We analyzed the imaging features of transient focal lesions in the splenium of the corpus callosum (SCC) in non-epilepticpatients receiving antiepileptic drugs (AEDs). METHODS: We identified signal abnormalities in the SCC in three non-epilepticpatients, all of them receiving AEDs. We examined two of these patients with multiplanar magnetic resonance (MR) imaging using 1.0-T equipment including fluid-attenuated inversion recovery (FLAIR), T2-weighted (TSE) and T1-weighted (SE) sequences before and after injection of contrast agent. The third patient was studied using 1.5-T equipment with the same sequences. Additionally, a T1 SE sequence with a magnetization transfer contrast pulse off resonance (T1 SE/MTC), diffusion-weighted imaging (EPI-DWI) and apparent diffusion coefficient (ADC) maps were obtained. RESULTS: We observed an identical pattern of imaging abnormalities in all patients characterized by round lesions, hyperintense on FLAIR and hypointense on T1 SE images, located in the central portion of the SCC. One lesion showed homogeneous gadolinium enhancement and perilesional vasogenic edema. This particular lesion showed restricted diffusion confirmed on the ADC map. This pattern was considered consistent with focal demyelination. Follow-up MR examinations showed complete disappearance or a clear reduction in lesion size. All patients had been treated with AEDs, but they did not show any clinical signs of toxicity, interhemispheric symptoms, or abnormal neurological findings (including seizures). CONCLUSION: We believe that our MR findings might be interpreted as transient lesions related to AED toxicity. They presumably resulted from focal demyelination in the central portion of the SCC.
Authors: J Takanashi; A J Barkovich; T Shiihara; H Tada; M Kawatani; H Tsukahara; M Kikuchi; M Maeda Journal: AJNR Am J Neuroradiol Date: 2006-04 Impact factor: 3.825
Authors: S S Kim; K H Chang; S T Kim; D C Suh; J E Cheon; S W Jeong; M H Han; S K Lee Journal: AJNR Am J Neuroradiol Date: 1999-01 Impact factor: 3.825
Authors: H Ogura; M Takaoka; M Kishi; M Kimoto; T Shimazu; T Yoshioka; H Sugimoto Journal: AJNR Am J Neuroradiol Date: 1998 Jun-Jul Impact factor: 3.825