title: Correlation of quantitative MRI and neuropathology in epilepsy surgical resection specimens--T2 correlates with neuronal tissue in gray matter.
abstract: Newer MRI methods can detect cerebral abnormalities not identified on routine imaging in patients with focal epilepsy. Correlation of MRI with histopathology is necessary to understand the basis of MRI abnormalities and subsequently predict histopathology from in vivo MRI. The aim of this study was to determine if particular quantitative MR parameters were associated with particular histological features. Nine patients with temporal lobe epilepsy were imaged at 1.5 T using standard presurgical volumetric and quantifiable sequences: magnetization transfer and FFT2. The resected temporal lobe was registered with the volumetric MRI data according to our previously described method to permit correlation of the modalities. Stereologically measured neuronal densities and field fraction of GFAP, MAP2, synaptophysin and NeuN immunohistochemistry were obtained. Analyses were performed in the middle temporal gyrus and compared with quantitative MRI data from the equivalent regions. There was a significant Spearman Rho negative correlation between NeuN field fraction and the T2 value in gray matter (correlation coefficient -0.72, p=0.028). There were no significant correlations between any neuropathological and MR measures in white matter. These preliminary findings suggest that T2 in gray matter is sensitive to the proportion of neuronal tissue. Novel quantitative MRI measures acquired with higher field strength magnets, and so with superior signal to noise ratios, may generate data that correlate with histopathological measures. This will enable better identification and delineation of the structural causes of refractory focal epilepsy, and will be of particular benefit in patients in whom current optimal MRI does not identify a relevant abnormality.
authors.affiliation: Department of Clinical and Experimental Epilepsy, Institute of Neurology, University College London, Queen Square, Box 29, London WC1N 3BG, UK.
authors.forename: S H
authors.initials: SH
authors.lastname: Eriksson
authors.forename: S L
authors.initials: SL
authors.lastname: Free
authors.forename: M
authors.initials: M
authors.lastname: Thom
authors.forename: L
authors.initials: L
authors.lastname: Martinian
authors.forename: M R
authors.initials: MR
authors.lastname: Symms
authors.forename: T M
authors.initials: TM
authors.lastname: Salmenpera
authors.forename: A W
authors.initials: AW
authors.lastname: McEvoy
authors.forename: W
authors.initials: W
authors.lastname: Harkness
authors.forename: J S
authors.initials: JS
authors.lastname: Duncan
authors.forename: S M
authors.initials: SM
authors.lastname: Sisodiya
mesh_terms: D000328:Adult; D001369:Axons / Q000473:pathology; D001927:Brain Diseases / Q000175:diagnosis* / Q000473:pathology / Q000601:surgery; D003712:Dendrites / Q000473:pathology; D004292:Dominance, Cerebral / Q000502:physiology; D004833:Epilepsy, Temporal Lobe / Q000175:diagnosis* / Q000473:pathology / Q000601:surgery; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D006624:Hippocampus / Q000473:pathology / Q000601:surgery; D006801:Humans; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D008869:Microtubule-Associated Proteins / Q000032:analysis; D008875:Middle Aged; D009474:Neurons / Q000473:pathology; D011612:Psychosurgery; D012680:Sensitivity and Specificity; D012984:Software; D013223:Statistics as Topic; D016708:Synaptophysin / Q000032:analysis; D013702:Temporal Lobe / Q000473:pathology / Q000601:surgery*
chemical_list: D005904:Glial Fibrillary Acidic Protein; C489788:MAP2 protein, human; D008869:Microtubule-Associated Proteins; D016708:Synaptophysin