TY - JOUR
T1 - Right frontal theta
T2 - Is it a response biomarker for ketamine’s therapeutic action in anxiety disorders?
AU - Shadli, Shabah M.
AU - Delany, Robert G.
AU - Glue, Paul
AU - McNaughton, Neil
PY - 2022/7/4
Y1 - 2022/7/4
N2 - Anxiety disorders are the most prevalent mental disorders in the world, creating huge economic burdens on health systems and impairing the quality of life for those affected. Recently, ketamine has emerged as an effective anxiolytic even in cases resistant to conventional treatments (TR); but its therapeutic mechanism is unknown. Previous data suggest that ketamine anxiety therapy is mediated by reduced right frontal electroencephalogram (EEG) theta power measured during relaxation. Here we test for a similar theta reduction between population-sample, presumed treatment-sensitive, (TS) anxiety patients and healthy controls. Patients with TS DSM-5 anxiety disorder and healthy controls provided EEG during 10 min of relaxation and completed anxiety-related questionnaires. Frontal delta, theta, alpha1, alpha2, beta, and gamma power, Higuchi’s fractal dimension (HFD) and frontal alpha asymmetry (FAA) values were extracted to match ketamine testing; and we predicted that the controls would have less theta power at F4, relative to the TS anxious patients, and no differences in HFD or FAA. We provide graphical comparisons of our frontal band power patient-control differences with previously published post-pre ketamine TR differences. As predicted, theta power at F4 was significantly lower in controls than patients and FAA was not significantly different. However, HFD was unexpectedly reduced at lateral sites. Gamma power did not increase between controls and patients suggesting that the increased gamma produced by ketamine relates to dissociation rather than therapy. Although preliminary, and indirect, our results suggest that the anxiolytic action of ketamine is mediated through reduced right frontal theta power. Copyright © 2022 Shadli, Delany, Glue and McNaughton.
AB - Anxiety disorders are the most prevalent mental disorders in the world, creating huge economic burdens on health systems and impairing the quality of life for those affected. Recently, ketamine has emerged as an effective anxiolytic even in cases resistant to conventional treatments (TR); but its therapeutic mechanism is unknown. Previous data suggest that ketamine anxiety therapy is mediated by reduced right frontal electroencephalogram (EEG) theta power measured during relaxation. Here we test for a similar theta reduction between population-sample, presumed treatment-sensitive, (TS) anxiety patients and healthy controls. Patients with TS DSM-5 anxiety disorder and healthy controls provided EEG during 10 min of relaxation and completed anxiety-related questionnaires. Frontal delta, theta, alpha1, alpha2, beta, and gamma power, Higuchi’s fractal dimension (HFD) and frontal alpha asymmetry (FAA) values were extracted to match ketamine testing; and we predicted that the controls would have less theta power at F4, relative to the TS anxious patients, and no differences in HFD or FAA. We provide graphical comparisons of our frontal band power patient-control differences with previously published post-pre ketamine TR differences. As predicted, theta power at F4 was significantly lower in controls than patients and FAA was not significantly different. However, HFD was unexpectedly reduced at lateral sites. Gamma power did not increase between controls and patients suggesting that the increased gamma produced by ketamine relates to dissociation rather than therapy. Although preliminary, and indirect, our results suggest that the anxiolytic action of ketamine is mediated through reduced right frontal theta power. Copyright © 2022 Shadli, Delany, Glue and McNaughton.
KW - anxiety disorders
KW - ketamine
KW - electroencephalography (EEG)
KW - theta frequency
KW - response biomarker
U2 - 10.3389/fnins.2022.900105
DO - 10.3389/fnins.2022.900105
M3 - Article
C2 - 35860301
SN - 1662-453X
VL - 16
JO - Frontiers in Neuroscience
JF - Frontiers in Neuroscience
M1 - 900105
ER -