Distributed, limbic gray matter atrophy in patients after bacterial meningitis

The structural basis of cognitive sequelae after bacterial meningitis in humans is still poorly understood. In animal models and human autopsy cases, neuronal apoptosis of the hippocampal formation in particular seems to play an important role. Here, we aimed to analyze if BM entails MR imaging stru...

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Bibliographic Details
Published in:American journal of neuroradiology : AJNR 2013-06, Vol.34 (6), p.1164-1167
Main Authors: Focke, N K, Kallenberg, K, Mohr, A, Djukic, M, Nau, R, Schmidt, H
Format: Article
Language:English
Subjects:
Adult
Aged
Atrophy - complications
Atrophy - pathology
Bacteria
Brain
Epilepsy, Temporal Lobe - etiology
Epilepsy, Temporal Lobe - pathology
Female
Gyrus Cinguli - pathology
Hippocampus - pathology
Humans
Limbic System - pathology
Magnetic Resonance Imaging - methods
Male
Meningitis, Bacterial - complications
Meningitis, Bacterial - pathology
Middle Aged
Retrospective Studies
Temporal Lobe - pathology
Thalamus - pathology
Young Adult
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Summary:The structural basis of cognitive sequelae after bacterial meningitis in humans is still poorly understood. In animal models and human autopsy cases, neuronal apoptosis of the hippocampal formation in particular seems to play an important role. Here, we aimed to analyze if BM entails MR imaging structural consequences in humans in vivo. We applied voxel-based morphometry in a cohort of BM survivors with normal conventional MR imaging after resolution of the acute inflammation to assess morphologic differences. We found clear gray matter volume loss in the limbic system including the hippocampal formation, thalamus, and cingulate gyri bilaterally as well as in the temporal lobe. These results were corroborated by an alternative atlas-based method. Even in patients with normal routine MR imaging results, clear-cut gray matter atrophy with a mesial temporal/limbic pattern was evident. The anatomic distribution is compatible with the neuropsychological deficit commonly observed in patients after BM. The similarity of the observed atrophy may point to causal link between BM and mesial temporal epilepsy.
ISSN:0195-6108
1936-959X
DOI:10.3174/ajnr.a3351