073  Magnetic resonance spectroscopy to detect markers of brain injury in tuberculous meningitis (TBM). Issue 6 (27th May 2022)

• Record Type: Journal Article
• Authors: Davis, Angharad; Robertson, Frances; Maxebengula, Mpumi; Meintjes, Ernesta; Wilkinson, Robert
• Is Part Of: Journal of neurology, neurosurgery and psychiatry. Volume 93:Issue 6(2022)
• Page Start: A123
• Page End: A123
• Publication Date: 2022-05-27
• Subjects: Neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; Psychiatry -- Periodicals; 616.8
• DOI: 10.1136/jnnp-2022-ABN.398
• Languages: English
• ISSNs: 0022-3050

Abstract

Abstract : Centre for Infectious Diseases Research in Africa; 4 UCT Medical Imaging Research Unit, Division of Bio- medical Engineering, UCT, RSA; 5 Cape Universities Body Imaging Centre, UCT and Neuroscience Institute, University of Cape Town, RSA; 6 Department of Medicine, Imperial College London 1H-Magnetic Resonance Spectroscopy (MRS) allows non-invasive quantification of the biochemical com- position of imaged tissue in a single voxel within the brain; including concentrations of the neuroinhibitory and neuroexcitatory metabolites, GABA and glutamate. Excessive glutamate and neuro-excitotoxicity contribute to pathogenesis in tuberculous meningitis (TBM)[1], and like in other neurological conditions[2] may lead to cell death and brain injury. We hypothesised that glutamate would be raised and GABA decreased, in TBM vs healthy controls (HC). 11 patients with TBM, and 8 HC underwent 3-T MRI imaging at the University of Cape Town, South Africa, at two timepoints (baseline, day-56). We used MEGA-PRESS spectroscopy and GANNET software[3] to estimate metabolite concentrations in a voxel placed within the 'tubercular zone'. Glutamate at baseline was significantly higher in TBM vs HC (15.9 vs 12.2 IU, p=0.042). This decreased by day-56, although did not return to levels seen in HC, suggesting ongoing neuro-excitation in the post-acute phase. By contrast, at baseline GABA was non-significantly decreased in TBM vs HC (3.79 vs4.02 IU, p=0.5). These findings provide further rationale for the investigation of glutamate/GABA as brain injury pathways and potential drug targets in TBM. 1. Rohlwink, U.K., et al., Nat Commun, 2019. 10(1): p. 3767 2. Meldrum, B.S., J Nutr, 2000. 130(4S Suppl): p. 1007S-15S. 3. Edden, R.A., et al., J Magn Reson Imaging, 2014. 40(6): p. 1445–52. [e-mail]