W Van Paesschen1, J S Duncan, J M Stevens, A Connelly. 1. Epilepsy Research Group, University Department of Clinical Neurology, National Hospital for Neurology and Neurosurgery, London, UK.
Abstract
PURPOSE: We wished to establish whether hippocampal changes occur in 1 year in adults with newly diagnosed partial seizures and, if so, to identify possible causes and mechanisms. METHODS: Thirty-six adult patients with newly diagnosed partial seizures underwent a magnetic resonance imaging (MRI) scan of the brain including hippocampal volume and T2 relaxation time (HCT2) measurement and had a follow-up quantitative MRI scan approximately 1 year after the baseline MRI scan. RESULTS: At baseline, 4 patients (11%) had hippocampal sclerosis (HS), 4 (11%) had abnormalities other than HS, and 28 had a normal MRI scan (78%). Twenty-three patients (64%) had recurrent seizures in the period between the two MRI scans. One of the 4 patients with HS, who had daily seizures, had significantly increased HCT2 values on follow-up, possibly reflecting progressive hippocampal damage. None of the 32 patients with MRI findings other than HS at baseline progressed to HS on follow-up. However, 2 of the 32 patients had significant hippocampal changes, probably related to resolution of inflammatory swelling or edema after seizures were controlled. CONCLUSIONS: Subtle changes in hippocampi can occur in 1 year in adults with newly diagnosed partial seizures, which could be due to resolution of edema after seizure control or to hippocampal changes associated with frequent and daily seizures. Follow-up of the studied cohort for several years will be required to settle the question of whether progressive hippocampal damage occurs in temporal lobe epilepsy (TLE).
PURPOSE: We wished to establish whether hippocampal changes occur in 1 year in adults with newly diagnosed partial seizures and, if so, to identify possible causes and mechanisms. METHODS: Thirty-six adult patients with newly diagnosed partial seizures underwent a magnetic resonance imaging (MRI) scan of the brain including hippocampal volume and T2 relaxation time (HCT2) measurement and had a follow-up quantitative MRI scan approximately 1 year after the baseline MRI scan. RESULTS: At baseline, 4 patients (11%) had hippocampal sclerosis (HS), 4 (11%) had abnormalities other than HS, and 28 had a normal MRI scan (78%). Twenty-three patients (64%) had recurrent seizures in the period between the two MRI scans. One of the 4 patients with HS, who had daily seizures, had significantly increased HCT2 values on follow-up, possibly reflecting progressive hippocampal damage. None of the 32 patients with MRI findings other than HS at baseline progressed to HS on follow-up. However, 2 of the 32 patients had significant hippocampal changes, probably related to resolution of inflammatory swelling or edema after seizures were controlled. CONCLUSIONS: Subtle changes in hippocampi can occur in 1 year in adults with newly diagnosed partial seizures, which could be due to resolution of edema after seizure control or to hippocampal changes associated with frequent and daily seizures. Follow-up of the studied cohort for several years will be required to settle the question of whether progressive hippocampal damage occurs in temporal lobe epilepsy (TLE).
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