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Structural abnormalities remote from the seizure focus

A study using T2 relaxometry at 3 T

From the Brain Research Institute (Drs. Briellmann, Jackson, Pell, Mitchell, and Abbott) and Radiology Department (Drs. Jackson and Mitchell), Austin Health, Melbourne, and Department of Medicine (Drs. Briellmann and Jackson) and Radiology Department (Drs. Jackson and Mitchell), University of Melbourne, Victoria, Australia.

Address correspondence and reprint requests to Dr. G. Jackson, Brain Research Institute, Neurosciences Bldg., Austin Health, Heidelberg West, Victoria 3081, Australia; e-mail: BRI{at}brain.org.au

Objective: To determine the extent and severity of mesial temporal and subcortical signal abnormalities in patients with partial epilepsy.

Methods: T2 relaxation time maps were acquired in 50 consecutive patients and 55 control subjects on a 3 T MRI scanner. Twenty-two patients had hippocampal sclerosis (HS), 16 had malformations of cortical development (MCD), and 12 had no obvious MR abnormalities (normal MR). The following eight regions were measured bilaterally: hippocampus, anterior temporal lobe (ATL) white matter, amygdala, frontal lobe white matter, caudate, putamen, pallidum, and thalamus.

Results: In patients with HS, increased T2 relaxation times were found in the ipsilateral hippocampus and ATL but not in subcortical nuclei. In patients with MCD, increased T2 relaxation times were found in the temporal lobe (hippocampus, ATL) and in subcortical areas (caudate, putamen, and pallidum); in patients with normal MR, increased T2 relaxation times were found in the hippocampus and putamen. The degree of abnormality did not correlate with the duration of epilepsy or the estimated seizure load.

Conclusions: Mesial temporal structures show increased T2 relaxation times not only in patients with hippocampal sclerosis but also in patients with a seizure focus remote from the hippocampus. Patients with normal MR and focal malformations of cortical development have increased T2 relaxation times in subcortical structures. Therefore, abnormalities in T2 relaxation time can be found remote from the seizure focus. They cannot be simply attributed to secondary seizure effects.

Received March 22, 2004. Accepted in final form September 3, 2004.

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