ArticleAJNR. American journal of neuroradiology
Distributed, limbic gray matter atrophy in patients after bacterial meningitis.
Article in AJNR. American journal of neuroradiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Invasive meningococcal disease over five decades in the Faroe Islands: high incidence, low mortality, and implications for vaccination policy.IJID regions · 2026Article
- Rapidly progressive brain atrophy in ventilated patients: a retrospective descriptive study.Scientific reports · 2024Article
- Biomechanical instability of the brain-CSF interface in hydrocephalus.Brain : a journal of neurology · 2024Review
- The Clock Is Ticking - Brain Atrophy in Case of Acute Trauma?Korean journal of neurotrauma · 2019Article
- Structural deficits and cognitive impairment in tuberculous meningitis.BMC infectious diseases · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeThe 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. MATERIALS AND
methodsWe 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.
resultsWe 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.
conclusionsEven 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.
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