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|Title:||Hippocampal sclerosis: development in adult life.||Austin Authors:||Jackson, Graeme D ;Chambers, Brian R ;Berkovic, Samuel F||Affiliation:||Brain Imaging Research Institute, Boronia Centre, West Heidelberg, Howard Florey Institute, Department of Medicine, University of Melbourne, Victoria, Australia||Issue Date:||1-Nov-1999||Publication information:||Developmental Neuroscience; 21(3-5): 207-14||Abstract:||Hippocampal sclerosis (HS) is the most common pathological lesion underlying intractable temporal lobe epilepsy. It is not known whether HS exists before the onset of epilepsy or whether it is caused by seizures. Its has been proposed that childhood seizures cause HS. Optimized magnetic resonance imaging (MRI), hippocampal volumes and T(2) signal quantitation were performed 2 weeks and 8 months following at tonic-clonic seizure in a 23-year-old man. MRI 14 days after the seizure showed symmetrical hippocampal volumes (ratio R/L = 1.03) with intact internal architecture bilaterally but marked signal change in the right hippocampus (T(2) right = 121, T(2) left = 103, normal < or = 108 ms). Eight months later this hippocampus showed severe atrophy with a volume ratio of 0.65 and T(2) values of 117 (right) and 109 ms (left). High-resolution imaging showed that volume loss occurred mainly in the CA1 region which showed high signal in the initial study. Characteristic MRI features of HS can develop in adults and HS cannot always be assumed to have its origins in childhood. Hypoxia in the context of seizures may be an important component in hippocampal damage. HS may be a preventable lesion and MRI signal change seen in the neuronal layers of the hippocampus may be an indication for neuroprotection.||Gov't Doc #:||10575244||URI:||http://ahro.austin.org.au/austinjspui/handle/1/9193||DOI:||17400||URL:||https://pubmed.ncbi.nlm.nih.gov/10575244||Type:||Journal Article||Subjects:||Adult
Magnetic Resonance Imaging.methods
|Appears in Collections:||Journal articles|
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