Identifying Ketamine Responses in Treatment-Resistant Depression Using a Wearable Forehead EEG
Zehong Cao, Chin-Teng Lin, Weiping Ding, Mu-Hong Chen, Cheng-Ta Li, Tung-Ping Su
arXiv Preprint Archive May 29, 2018 via arXiv
Summary
AI-generated from the abstractIn a randomized, double-blind, placebo-controlled trial, 55 outpatients with treatment-resistant depression received either 0.5 mg/kg ketamine, 0.2 mg/kg ketamine, or saline. Using a wearable forehead EEG device, responders to ketamine showed weaker theta power at baseline and increased alpha power with lower alpha asymmetry and theta cordance after treatment compared to non-responders. A baseline EEG predictor classified responders and non-responders with 81.3% accuracy, 82.1% sensitivity, and 91.9% specificity. The rapid antidepressant effects of mixed ketamine doses are linked to prefrontal EEG patterns, which may help identify likely responders before treatment.
Study at a glance
| Characteristics | Randomized controlled trial Placebo-controlled Double-blind Peer reviewed |
|---|---|
| Sample size | 55 |
| Population | Outpatients with treatment-resistant depression |
| Intervention | Ketamine |
| Dose | 0.5 mg/kg, 0.2 mg/kg |
| Keywords | Eess.sp Neuroscience Biomedical-sensors Depression-treatment Brain-wave-analysis |
| Key finding | Baseline prefrontal EEG patterns, particularly weaker theta power, can predict ketamine response in treatment-resistant depression with over 80% accuracy. |
Abstract
This study explores the responses to ketamine in patients with treatment-resistant depression (TRD) using a wearable forehead electroencephalography (EEG) device. We recruited fifty-five outpatients with TRD who were randomised into three approximately equal-sized groups (A: 0.5 mg/kg ketamine; B: 0.2 mg/kg ketamine; and C: normal saline) under double-blind conditions. The ketamine responses were measured by EEG signals and Hamilton Depression Rating Scale (HDRS) scores. At baseline, responders showed a significantly weaker EEG theta power than did non- responders (p < 0.05). Responders exhibited a higher EEG alpha power but lower EEG alpha asymmetry and theta cordance at post-treatment than at baseline (p < 0.05). Furthermore, our baseline EEG predictor classified responders and non-responders with 81.3 +- 9.5% accuracy, 82.1 +- 8.6% sensitivity and 91.9 +- 7.4% specificity. In conclusion, the rapid antidepressant effects of mixed doses of ketamine are associated with prefrontal EEG power, asymmetry and cordance at baseline and early post-treatment changes. The prefrontal EEG patterns at baseline may account for recognising ketamine effects in advance. Our randomised, double- blind, placebo-controlled study provides information regarding clinical impacts on the potential targets underlying baseline identification and early changes from the effects of ketamine in patients with TRD.