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From the Brain Imaging Research Institute (Drs. Mitchell, Jackson, and Fitt) and Departments of Radiology (Drs. Mitchell and Fitt), Neurology (Drs. Jackson and Berkovic), Anatomical Pathology (Dr. Kalnins), and Neurosurgery (Dr. Ashpole), Austin and Repatriation Medical Centre; and the Departments of Medicine (Drs. Jackson and Berkovic) and Neuropsychology (Dr. Saling), University of Melbourne, Australia.
Address correspondence and reprint requests to Dr. Anne Mitchell, Department of Radiology, Austin and Repatriation Medical Centre, Heidelberg (Melbourne), Victoria 3084, Australia.
OBJECTIVE: To examine the nature and frequency of anterior temporal lobe (AT) abnormalities that occur in intractable temporal lobe epilepsy (TLE).
METHODS: We reviewed the MR scans and clinical histories of 50 consecutive patients with intractable TLE. Histopathology was available in 42 surgically treated cases.
RESULTS: MRI demonstrated loss of the gray-white matter differentiation and decreased T1- and increased T2-weighted signal in the ipsilateral AT in 58% of the 50 patients. This appearance was observed in 64% of the 36 patients with hippocampal sclerosis (HS) but was also seen in patients without HS. These changes were associated with temporal lobe atrophy, a higher hippocampal T2 relaxation time, and a history of febrile convulsions. Pathologic examination showed that the MRI appearances were not caused by dysplasia, degenerative abnormalities, or inflammatory change. Histologic quantitation showed increased glial cell nuclei counts in the intractable TLE cases compared with controls. There was no difference in glial cell numbers between cases with AT abnormality and those without this appearance. Presence or absence of changes was not predictive of preoperative neuropsychology, postoperative change in neuropsychology, or seizure outcome after surgery.
CONCLUSIONS: These frequently seen ipsilateral changes are not caused by gliosis and may reflect a nonspecific increase in water content in the temporal lobe. This may be due to myelin abnormalities or some other as yet unidentified pathologic factor.
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