Cognitive-metabolic Correlations in Temporal Lobe Epilepsy: A Systematic Review
Mathias Maisenbacher1, Ola Alshaqi1, Xiahoan Peng1, Cynthia M Schmidt2, Olha Taraschenko1
1Department of Neurological Sciences, 2Leon S. McGoogan Health Sciences Library, University of Nebraska Medical Center
Objective:
Evaluate the link between neurometabolic dysfunction and cognitive impairment in Temporal lobe epilepsy (TLE)
Background:
TLE is the most common focal epilepsy, affecting over 40 million individuals worldwide. While drug-resistant seizures drive much of the morbidity, cognitive decline contributes to disability and is poorly understood. Increasing evidence suggests that neurometabolic dysfunction contributes to this impairment. Characterizing metabolic changes in patients with TLE and cognitive impairment may identify biomarkers and inform new treatment strategies.
Design/Methods:
We conducted a systematic review of EMBASE, MEDLINE, CINAHL, PsycINFO, and Scopus through December 2024, in line with PRISMA guidelines. We included all observational studies correlating metabolic imaging in temporal lobe epilepsy with cognitive impairment. Data on metabolic alterations and their relationship to cognitive performance was extracted.
Results:
Of 1449 reports, 38 met inclusion criteria, encompassing 1441 patients aged 5–66 years. Most had drug-resistant epilepsy with seizure frequencies ranging from seizure-free to 18 per month. Twenty-four studies used positron emission tomography, most frequently fluorodeoxyglucose (FDG)-positron emission tomography (22 studies, 885 subjects), to measure glucose metabolism. Other tracers assessed synaptic density and β-amyloid deposition. Fourteen studies used proton magnetic resonance spectroscopic imaging to measure metabolites including N-acetylaspartate (NAA), creatine (Cr), choline (Cho), and gamma-aminobutyric acid (GABA). Common markers included Cr/NAA and NAA/(Cho+Cr). Reported alterations correlated with global cognition, verbal and visual memory, working memory, attention, executive function, and language. Some markers were also linked to depression, an important confounder. Most studies focused on the temporal lobe and its subregions; fewer reported changes in frontal lobes, insula, fusiform gyrus, or precuneus.
Conclusions:
Across imaging modalities, altered glucose metabolism, metabolite ratios, and synaptic density were linked to various cognitive changes in TLE. Verbal memory specifically was commonly affected. These neurometabolic signatures hold promise as biomarkers for identifying patients at risk of cognitive decline and could represent potential targets for future therapeutic intervention.
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