Age at onset and seizure frequency affect white matter diffusion coefficient in patients with mesial temporal lobe epilepsy

Abstract

SummaryIn mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS), structural abnormalities are present not only in the hippocampus, but also in the white matter with ipsilateral predominance. Although the timing of epilepsy onset is commonly associated with clinical and semiological dissimilarities, limited data exist regarding white matter diffusion changes with respect to age at epilepsy onset. The aim of this study was to investigate diffusion changes in the white matter of unilateral MTLE-HS patients with respect to clinical parameters and to compare them to an age-and sex matched healthy control group. Apparent diffusion coefficients (ADCs) were derived using mono-exponential approaches from 22 (11 early and 11 late age at onset) unilateral MTLE-HS patients and 22 age-and sex matched control subjects after acquiring diffusion-weighted images on a 3T MRI system. Data were analyzed using two-tailed t-tests and multiple linear regression models. In the early onset MTLE-HS group ADC was significantly elevated in the ipsilateral hemispheric (p=0.04) and temporal lobe white matter (p=0.01) compared to controls. These differences were not detectable in late onset MTLE-HS patients. ADC of the early onset MTLE-HS group was negatively related to age at epilepsy onset in the ipsilateral hemispheric white matter (p=0.03) and the uncinate fasciculus (p=0.03), while in late onset patients ADC was no longer dependent on age at epilepsy onset itself, but rather on the seizure frequency in the ipsilateral uncinate fasciculus (p=0.03). Such diffusivity pattern has been associated with chronic white matter degeneration, reflecting myelin loss and higher extracellular volume which are more pronounced in the fronto-temporal regions and also depends on clinical features. In the early onset group, the timing of epilepsy seems to be the major cause of white matter abnormalities while in late onset disease it has a secondary role in provoking diffusion changes.

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