{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T11:58:59Z","timestamp":1785499139851,"version":"3.56.0"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T00:00:00Z","timestamp":1783296000000},"content-version":"vor","delay-in-days":5,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Health Research Council New Zealand project","award":["HRC 20-112"],"award-info":[{"award-number":["HRC 20-112"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Neurotic disorders\u2014major depressive disorder (MDD), panic disorder, social anxiety disorder, generalized anxiety disorder, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), and specific phobia\u2014have differing pharmaceutical profiles. But all, even when resistant to conventional treatment (TR), respond quickly to low-dose (0.5-1.0\u00a0mg\/kg I.M.) ketamine. We explore the variation in the neural effects of ketamine across its treatments of TR-MDD, TR-PTSD, and TR-OCD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>We recorded 10 min of resting frontal activity and diagnosis-related scale measures, before and 2\u00a0h after fentanyl (50\u00a0mcg) or ketamine (0.5 or 1.0\u00a0mg\/kg, I.M.) counterbalanced across 3 sessions at least a week apart. Average power spectra were calculated for delta, theta, alpha1, alpha2, beta, and gamma bands. Analysis of variance compared TR-PTSD (20\u00a0F, 2\u00a0M) with TR-MDD (12\u00a0F, 13\u00a0M). Preliminary TR-OCD (5\u00a0F, 2\u00a0M) data were also obtained.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>TR-PTSD patients showed dose- and band frequency-dependent electroencephalography (EEG) power changes (particularly alpha at 0.05\u00a0mg\/kg), while TR-MDD patients did not. TR-OCD differed qualitatively from both. The correlation of power change with score change was maximal for different bands and electrodes across the different scales (Impact of Events Scale-Revised, Montgomery-\u00c5sberg Depression Rating Scale, Hospital Anxiety and Depression Scales, Hamilton Anxiety Scale, Fear Questionnaire, and Yale-Brown Obsessive-Compulsive Scale).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Ketamine effects and their therapeutic links vary in band and site with conventional diagnosis\u2014including previous TR anxiety results. The EEG results appear to detect changes in the disorder-specific systems that conventional treatments target selectively and directly and these appear to require a ketamine-sensitive factor (as a \u201cdouble hit\u201d) to generate disorder.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ijnp\/pyag037","type":"journal-article","created":{"date-parts":[[2026,7,6]],"date-time":"2026-07-06T12:41:19Z","timestamp":1783341679000},"source":"Crossref","is-referenced-by-count":0,"title":["Ketamine effects on EEG and their links to therapy differ across treatment-resistant major depression, post-traumatic stress disorder, and obsessive-compulsive disorder"],"prefix":"10.1093","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3607-3469","authenticated-orcid":false,"given":"Shabah M","family":"Shadli","sequence":"first","affiliation":[{"name":"Department of Psychology, University of Otago , Dunedin ,","place":["New Zealand"]},{"name":"Department of Psychology, Charles 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