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COMPARATIVE STUDY
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Hippocampal sclerosis: MR prediction of seizure intractability.
Epilepsia 2007 Februrary
PURPOSE: Patients with refractory temporal lobe epilepsy (refractory TLE) often have hippocampal sclerosis (HS). However, some HS patients have less-severe, drug-responsive epilepsy (mild TLE). We investigated the pattern of MR changes in these two HS groups.
METHODS: We acquired a 3D volumetric sequence, T(2) relaxation times (T2) and proton MR spectroscopy (MRS) in 41 HS patients (24 refractory TLE, 17 mild TLE) and 60 controls. Hippocampal volumes were measured bilaterally. T2 was measured in the hippocampus, amygdala, thalamus, in the white matter of the anterior temporal lobe (ATL), and in the frontal lobe. The temporal lobe MRS established concentrations of N-acetylaspartate (NAA), choline, creatine, myoinositol and glutamine/glutamate.
RESULTS: The degree of hippocampal volume loss and hippocampal T2 increase was not different between the two HS groups. However, in refractory TLE, the T2 signal in the ipsilateral ATL was increased, and the ipsilateral NAA concentration was reduced (p < or = 0.05).
CONCLUSIONS: In this group of HS patients, the degree of HS was not related to the clinical course, possibly reflecting the common cause of epilepsy. In contrast, refractory TLE patients had pronounced white matter changes and metabolite disturbance in the ipsilateral temporal lobe. These abnormalities may indicate the refractory nature of the epilepsy.
METHODS: We acquired a 3D volumetric sequence, T(2) relaxation times (T2) and proton MR spectroscopy (MRS) in 41 HS patients (24 refractory TLE, 17 mild TLE) and 60 controls. Hippocampal volumes were measured bilaterally. T2 was measured in the hippocampus, amygdala, thalamus, in the white matter of the anterior temporal lobe (ATL), and in the frontal lobe. The temporal lobe MRS established concentrations of N-acetylaspartate (NAA), choline, creatine, myoinositol and glutamine/glutamate.
RESULTS: The degree of hippocampal volume loss and hippocampal T2 increase was not different between the two HS groups. However, in refractory TLE, the T2 signal in the ipsilateral ATL was increased, and the ipsilateral NAA concentration was reduced (p < or = 0.05).
CONCLUSIONS: In this group of HS patients, the degree of HS was not related to the clinical course, possibly reflecting the common cause of epilepsy. In contrast, refractory TLE patients had pronounced white matter changes and metabolite disturbance in the ipsilateral temporal lobe. These abnormalities may indicate the refractory nature of the epilepsy.
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