Elevated GABA level in the precuneus and its association with pain intensity in patients with postherpetic neuralgia: An initial proton magnetic resonance spectroscopy study

Purpose: This study aimed to explore the changes in gamma-aminobutyric acid (GABA) and glutamate (Glu) levels, and their correlations with clinical indicators in patients with postherpetic neuralgia (PHN).Methods: A totally of 22 PHN patients and 21 sex-, age-, and education-matched healthy controls (HCs) under-went proton magnetic resonance spectroscopy scanning. The spectral data of GABA in the precuneus was ob-tained by Mescher-Garwood point-resolved spectroscopy, whereas the spectral data of Glu, total N-acetyl-L- aspartic acid (tNAA) and total choline (tCho) were obtained by point-resolved spectroscopy. The pain intensity of PHN was assessed by numeric rating scales (NRS). The edited GABA signal was displayed as GABA+ due to overlapping macromolecules and homocarnosine signals. Total creatine (tCr) level in individual was used as an endogenous reference. The neurometabolites levels of PHN patients were compared with those of healthy in-dividuals and the correlations with clinical variables (pain duration and intensity) were analyzed.Results: PHN patients had higher GABA+/tCr levels in the precuneus than HCs (P = 0.009), with no significant differences in the levels of Glu/ tCr, tNAA/ tCr and tCho/ tCr (all P > 0.05). The GABA+/ tCr levels were positively correlated with the NRS scores of the PHN patients (r = 0.473, P = 0.030).Conclusion: Increased GABA+/tCr levels in the precuneus and their association with pain intensity of PHN pa-tients suggested a key role of the abnormalities of regional GABAergic neurons in the pathophysiological mechanisms of pain in PHN.

Automated summary

This study found that PHN patients had higher GABA+/tCr levels in the precuneus compared to healthy controls, and these levels were positively correlated with pain intensity, suggesting a key role of abnormalities in regional GABAergic neurons in the pathophysiological mechanisms of pain in PHN.