Key result
Children with functional neurological disorder show lower SMA and pDMN neurometabolite ratios versus healthy controls.
Why the study?
Neurometabolic homeostasis and excitatory/inhibitory neurotransmitter balance in children with functional neurological disorder across specific brain regions were investigated using in vivo magnetic resonance spectroscopy.
Do neurometabolic alterations exist in children and adolescents with functional neurological disorder compared to healthy controls?
Observational (n=73)
Do neurometabolic alterations exist in children and adolescents with functional neurological disorder compared to healthy controls?
Children with functional neurological disorder exhibit neurometabolic alterations in the supplementary motor area and posterior default mode network, suggesting dysfunction at the neuronal and glial levels.
Neurometabolic alterations may occur in pediatric FND; hypothesis-generating and requires prospective confirmation before clinical relevance.
OBJECTIVES: In vivo magnetic resonance spectroscopy (MRS) was used to investigate neurometabolic homeostasis in children with functional neurological disorder (FND) in three regions of interest: supplementary motor area (SMA), anterior default mode network (aDMN), and posterior default mode network (dDMN). Metabolites assessed included N-acetyl aspartate (NAA), a marker of neuron function; myo-inositol (mI), a glial-cell marker; choline (Cho), a membrane marker; glutamate plus glutamine (Glx), a marker of excitatory neurotransmission; γ-aminobutyric acid (GABA), a marker of inhibitor neurotransmission; and creatine (Cr), an energy marker. The relationship between excitatory (glutamate and glutamine) and inhibitory (GABA) neurotransmitter (E/I) balance was also examined. METHODS: MRS data were acquired for 32 children with mixed FND (25 girls, 7 boys, aged 10.00 to 16.08 years) and 41 healthy controls of similar age using both short echo point-resolved spectroscopy (PRESS) and Mescher-Garwood point-resolved spectroscopy (MEGAPRESS) sequences in the three regions of interest. RESULTS: In the SMA, children with FND had lower NAA/Cr, mI/Cr (trend level), and GABA/Cr ratios. In the aDMN, no group differences in metabolite ratios were found. In the pDMN, children with FND had lower NAA/Cr and mI/Cr (trend level) ratios. While no group differences in E/I balance were found (FND vs. controls), E/I balance in the aDMN was lower in children with functional seizures-a subgroup within the FND group. Pearson correlations found that increased arousal (indexed by higher heart rate) was associated with lower mI/Cr in the SMA and pDMN. CONCLUSIONS: Our findings of multiple differences in neurometabolites in children with FND suggest dysfunction on multiple levels of the biological system: the neuron (lower NAA), the glial cell (lower mI), and inhibitory neurotransmission (lower GABA), as well as dysfunction in energy regulation in the subgroup with functional seizures.
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Charney et al. (2023) conducted an observational in Functional neurological disorder (n=73). Functional neurological disorder vs. Healthy controls was evaluated on Neurometabolic homeostasis (metabolite ratios including NAA/Cr, mI/Cr, and GABA/Cr) in the SMA, aDMN, and pDMN. Children with functional neurological disorder had lower NAA/Cr, mI/Cr, and GABA/Cr ratios in the supplementary motor area and posterior default mode network compared to healthy controls.
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