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Acute Metabolic Changes Associated With Analgesic Drugs: An MR Spectroscopy Study
Author(s) -
Hansen Tine Maria,
Olesen Anne Estrup,
Simonsen Carsten Wiberg,
Fischer Iben Wendelboe,
Lelic Dina,
Drewes Asbjørn Mohr,
Frøkjær Jens Brøndum
Publication year - 2016
Publication title -
journal of neuroimaging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.822
H-Index - 64
eISSN - 1552-6569
pISSN - 1051-2284
DOI - 10.1111/jon.12345
Subject(s) - analgesic , creatine , medicine , venlafaxine , placebo , metabolite , glutamate receptor , pharmacology , anesthesia , in vivo magnetic resonance spectroscopy , anterior cingulate cortex , oxycodone , opioid , magnetic resonance imaging , antidepressant , psychiatry , receptor , pathology , hippocampus , alternative medicine , cognition , radiology
BACKGROUND AND PURPOSE Magnetic resonance spectroscopy (MRS) is used to measure brain metabolites. Limited data exist on the analgesic‐induced spectroscopy response. This was an explorative study with the aims to investigate the central effects of two analgesic drugs, an opioid and a selective serotonin and norepinephrine reuptake inhibitor, and to explore the association between metabolite changes and the analgesic effect and side effects. METHODS Single voxel proton spectroscopy measurements were performed in the anterior cingulate cortex, insula and prefrontal cortex in 20 healthy subjects before and after treatment for 5 days with oxycodone (eight doses of 10 mg extended release), venlafaxine (eight doses of 37.5 mg extended release) or placebo in a randomized double‐blind fashion. The metabolites of glutamate, N‐acetylaspartate, and myo‐inositol were analyzed in ratios to creatine. RESULTS Including all areas, the glutamate/creatine ratio was decreased ( P < .05) with 8.4% ± 0.3% after oxycodone treatment ( P = .02) and 6.6% ± 0.4% after venlafaxine treatment ( P = .07) as compared to placebo. No statistical significant differences in treatment effects across the areas were found ( P = .6). No treatment effect was seen for N‐acetylaspartate/creatine or myo‐inositol/creatine ratios (all P > .05). No associations between treatment induced glutamate/creatine changes and the analgesic effect and side effects were demonstrated (all P > .05). CONCLUSIONS MRS can be used to detect brain metabolites following acute analgesic treatments and glutamate is central in these mechanisms. Consequently, MRS might be a valuable tool to objectively evaluate analgesic effects and a potential biomarker to predict treatment outcomes and more research is needed.