This rigorous randomised controlled trial (n=73) found that ketamine has rapid (24 hours) anti-depressant effects (MARDS) for those with treatment-resistant depression (TRD). Compared to the placebo group (midazolam), ketamine led to greater improvements in MADRS scores by 7.95 points and the response rate was greater in the ketamine group.
Papers cited by this study that are also in Blossom
Berman, R. M., Cappiello, A., Anand, A. et al. · Biological Psychiatry (2000)
Objective
Ketamine, a glutamate N-methyl-D-aspartate (NMDA) receptor antagonist, has shown rapid antidepressant effects, but small study groups and inadequate control conditions in prior studies have precluded a definitive conclusion. The authors evaluated the rapid antidepressant efficacy of ketamine in a large group of patients with treatment-resistant major depression.
Method
This was a two-site, parallel-arm, randomized controlled trial of a single infusion of ketamine compared to an active placebo control condition, the anaesthetic midazolam. Patients with treatment-resistant major depression experiencing a major depressive episode were randomly assigned under double-blind conditions to receive a single intravenous infusion of ketamine or midazolam in a 2:1 ratio (N=73). The primary outcome was a change in depression severity 24 hours after drug administration, as assessed by the Montgomery-Åsberg Depression Rating Scale (MADRS).
Results
The ketamine group had greater improvement in the MADRS score than the midazolam group 24 hours after treatment. After adjustment for baseline scores and site, the MADRS score was lower in the ketamine group than in the midazolam group by 7.95 points (95% confidence interval [CI], 3.20 to 12.71). The likelihood of response at 24 hours was greater with ketamine than with midazolam (odds ratio, 2.18; 95% CI, 1.21 to 4.14), with response rates of 64% and 28%, respectively.
Conclusions
Ketamine demonstrated rapid antidepressant effects in an optimized study design, further supporting NMDA receptor modulation as a novel mechanism for accelerated improvement in severe and chronic forms of depression. More information on response durability and safety is required before implementation in clinical practice.
Major depressive disorder is a leading cause of disability worldwide and a substantial subgroup of patients fail to achieve clinically meaningful improvement despite multiple antidepressant trials and augmentation strategies. Treatment-resistant major depression is typically defined as inadequate response to at least two adequate antidepressant treatments and is associated with poor outcomes and a slow therapeutic onset for conventional agents, which generally act on monoamine systems and require 4–12 weeks to produce benefit. Converging evidence implicates glutamatergic dysfunction in depression, and small case series and crossover studies had suggested that the NMDA receptor antagonist ketamine can produce rapid antidepressant effects within hours of a single subanesthetic intravenous infusion; however, prior work was limited by small samples, inert placebos, and potential unblinding due to ketamine's psychoactive effects. Murrough and colleagues designed a two-site, parallel-arm, double-blind randomized controlled trial to test whether a single low-dose ketamine infusion produces a rapid antidepressant effect in patients with treatment-resistant major depression. To strengthen blinding and control for nonspecific anaesthetic effects they used midazolam as an active placebo comparator, selected 24 hours postinfusion as the primary endpoint to capture rapid effects while minimising contamination by acute psychoactive symptoms, and powered the study to detect clinically meaningful differences in clinician-rated depression severity.
This was a two-site (Baylor College of Medicine and Icahn School of Medicine at Mount Sinai) parallel-arm randomized controlled trial conducted between November 2010 and August 2012. Adults aged 21–80 with a primary DSM-IV diagnosis of major depressive disorder and treatment resistance (inadequate response to at least three antidepressant trials per the Antidepressant Treatment History Form) were eligible. Additional inclusion criteria required either recurrent major depressive disorder or a chronic current episode of at least 2 years plus a screening Inventory of Depressive Symptomatology-Clinician Rated score of 32 or greater. Key exclusions were lifetime psychotic illness or bipolar disorder, substance or alcohol abuse in the past 2 years, unstable medical illness, imminent suicidal or homicidal risk, a Mini-Mental State Examination score under 27, or use of contraindicated medications. Standard safety screening including physical examination, laboratory testing, urine toxicology and ECG was performed, and institutional review boards approved the protocol. Participants were medication-free for the study duration (with limited allowance for stable non-benzodiazepine hypnotics) and underwent washout prior to infusion (at least 4 weeks for fluoxetine, 1 week for other agents). Randomisation at a 2:1 ratio assigned patients to a single intravenous infusion of ketamine hydrochloride 0.5 mg/kg or midazolam 0.045 mg/kg, each administered over 40 minutes. Midazolam was chosen as an active placebo to mimic ketamine's onset and short half-life and to enhance blinding. Study personnel, clinicians, anaesthesiologists, raters and patients were masked to allocation; a research pharmacist prepared sealed envelopes with drug identity. Physiological monitoring was performed during and after infusion and trained raters who were blind to infusion-day side effects conducted symptom assessments. The primary outcome was change in depression severity on the Montgomery-Åsberg Depression Rating Scale (MADRS) at 24 hours postinfusion. Secondary outcomes included MADRS response rate (≥50% reduction), the Quick Inventory of Depressive Symptomatology-Self-Report, Clinical Global Impression (CGI) severity and improvement measures, and durability of benefit up to 7 days. Safety assessments captured general adverse events, dissociative states (Clinician-Administered Dissociative States Scale), and psychotomimetic symptoms (Brief Psychiatric Rating Scale positive symptom subscale). The protocol defined nonresponders as <50% improvement on MADRS; nonresponders were followed for 7 days while responders were followed biweekly until relapse or for an additional 4 weeks. The statistical plan used conservative effect-size estimates to power the trial: a planned sample of 72 randomized in a 2:1 ratio provided 80% power for continuous MADRS differences and 96% power for dichotomous response differences at 24 hours, assuming Cohen's d=0.71 and response rates of 60% versus 15%. Modified intention-to-treat analyses included all randomized patients with baseline and at least one postbaseline assessment. General linear modelling (mixed models) evaluated MADRS scores at 24 hours controlling for baseline MADRS and site; exact logistic regression analysed response rates adjusted for site. Secondary endpoints used analogous general linear or ordinal logistic models. Time-course analyses among responders employed mixed modelling of MADRS over follow-up. A significance threshold of p≤0.05 was applied and safety analyses were descriptive.
The primary outcome was reduction in depression severity as assessed on the clinician-administered MADRS (23) 24 hours following infusion. Trained raters, who were not involved in the infusion-day procedures and who were unaware of treatmentgroup assignment and infusion-related side effects, performed clinical assessments for the primary outcome at 24 hours and subsequent evaluations. The raters were experienced research staff extensively trained in the use of the instruments, and the MADRS rating conventions were pilot tested in prior ketamine studies in treatment-resistant major depression. The two primary raters at each site achieved a high level of interrater reliability, 0.988. Prior studies suggest that the peak antidepressant effects of ketamine occur within 24 hours of administration. We selected the 24-hour change in depression severity as the primary endpoint for the current study because the interval after infusion was considered long enough that acute sedating and other side effects were not likely to be contributory. The interval was sufficiently short such that the individuals who showed substantial mood improvement were unlikely to have already relapsed. Secondary outcomes included the MADRS response rate (defined as a reduction in the baseline score by 50% or more), change in score on the Quick Inventory of Depressive Symptomatology-Self-Report, scores on the Clinical Global Impression (CGI) severity and improvement measures, and durability of benefit for up to 7 days following infusion. We recorded general adverse events, dissociative states, and psychotomimetic side effects at regular intervals throughout the study, using the Patient Rated Inventory of Side Effects, the Clinician-Administered Dissociative States Scale, and the Brief Psychiatric Rating Scale positive symptom subscale, respectively.
In this two-site trial in treatment-resistant patients with moderate-to-severe and persistent depressive symptoms, we found that a single low dose of ketamine, as compared with a psychoactive placebo control medication, was associated with a rapid-onset antidepressant effect. We found marked improvements in clinician-administered and patient self-report ratings of depression severity 24 hours after the ketamine infusion. The ketamine responders generally maintained the gains for several days beyond the 24-hour time point; we no longer observed statistically significant differences between treatment groups 7 days following the infusion. These data provide new support for the hypothesis that NMDA receptor modulation can accelerate clinical improvement in patients with severe and chronic forms of depression. We consistently demonstrated the magnitude and duration of ketamine's benefit across two sites in an ethnically and racially diverse patient group, enhancing confidence in the reliability of these findings. The large and rapid antidepressant effect of ketamine we observed in these patients with a history of three or more failed antidepressant trials is especially significant given the poor prognosis for improvement with currently available antidepressant treatments in treatment-resistant major depression. To maximize internal and external validity, we standardized infusion-monitoring procedures and shielded the primary outcome rater from knowledge of side effects on the day of infusion. Improvements in secondary outcomes of global illness severity also supported the efficacy of ketamine in this trial. Patients in the ketamine group experienced transient psychoactive and hemodynamic effects consistent with those in previous reports and clinical experience. Ketamine treatment did not increase the risk of emergent a Response was defined as a decrease from baseline of at least 50% in score on the Montgomery-Åsberg Depression Rating Scale (MADRS). Relapse was defined as a MADRS score of 20 or higher maintained for two consecutive visits and meeting criteria for a major depressive episode for 1 week. psychotic or manic symptoms over the follow-up period (see Figurein the data supplement accompanying the online version of this article). These findings suggest that ketamine is safe in the short term for nonpsychotic depressed patients when administered at a subanesthetic dose of 0.5 mg/kg over 40 minutes. It is important to note that the safety and efficacy of ketamine in depression beyond a single infusion are largely unknown and that abuse liability and other safety concerns associated with ketamine dictate a cautious approach to its application outside of research. The observed hemodynamic changes in a subgroup of patients in our study encourage cardiorespiratory monitoring as an essential component of risk management. The use of the anesthetic benzodiazepine midazolam as a control condition is a strength of the current study, although there is likely no perfect control condition for ketamine. Our objective was to select an agent that would function as a placebo (devoid of specific antidepressant effects) yet induce transient psychoactive effects designed to enhance study blinding and mitigate the nonspecific salutary impact of receiving an anesthetic agent. While the rates of general adverse events were similar across the two conditions, transient dissociative side effects immediately following study drug infusion were higher in the ketamine condition. Other agents that we considered for use as an active placebo included a sympathomimetic agent such as amphetamine. Amphetamine would have mimicked more closely the known sympathomimetic effects of ketamine; however, in contrast to midazolam, amphetamine is devoid of anesthetic properties. Finally, while we considered using a true active comparator with intrinsic antidepressant properties, we found that no pharmaceutical agents were readily available that had established antidepressant properties across a time scale similar to that for ketamine. Following the establishment of the antidepressant properties of ketamine in an optimized placebo-controlled design, future studies may compare schedules of ketamine to active comparators such as electroconvulsive therapy or antidepressant-antipsychotic medication combinations. The biological mechanisms underlying ketamine's antidepressant activity remain largely unknown. The rapid onset of antidepressant activity we observed is consistent with preclinical work indicating that ketamine rapidly (within hours) increases the number and functioning of synaptic connections involving cortical or hippocampal neurons. Ketamine appears to rapidly reverse both behavioral and neuronal changes associated with chronic stress, in part through activation of the mammalian target of the rapamycin signaling pathway and stimulation of brain-derived neurotrophic factor signaling. It is interesting that a recent study of patients with major depressive disorder found that carriers of the Val66Met (rs6265) single nucleotide polymorphism-representing an attenuation of BDNF functioning-had a smaller antidepressant response to ketamine, in line with findings in animal models. Limitations of our trial include stringent enrollment criteria due to concerns about ketamine's psychoactive effects and abuse liability. We believe that the exclusion of patients with histories of psychotic symptoms or substance or alcohol use disorders does not diminish the generalizability of our findings but, rather, offers a clinically relevant risk-mitigation strategy. A proportion of screened patients (17.2%) refused or were unable to tolerate psychotropic medication washout prior to randomization, thereby restricting participants to medication-free individuals or those able to tolerate medication washout. The efficacy of ketamine as an adjunct to ongoing therapies is a clinically relevant question not addressed in our study. Finally, we tested the efficacy of a single infusion over a brief followup period. The transient antidepressant response to ketamine highlights the need to identify strategies to maintain and prolong the initial response. Two studies of the glutamate-modulating drug riluzole failed to find benefit in prevention of relapse following ketamine administration. Additional infusions of ketamine have recently been explored to prolong the antidepressant response, although controlled data testing this strategy are not currently available. In conclusion, treatment-resistant patients in a major depressive episode showed a rapid antidepressant response to a single infusion of ketamine. To our knowledge, the current study represents the largest investigation to date of ketamine in treatment-resistant major depression. Utilizing an optimized active placebo design, the trial provides new evidence for the specific antidepressant effects of ketamine, apart from its nonspecific anesthetic properties. Future research is required to test the antidepressant effects of ketamine beyond a single administration and to characterize its longer-term safety profile.
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Murrough, J. W., Perez, A. M., Pillemer, S. et al. · Biological Psychiatry (2012)
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Of 116 patients who consented, 73 met eligibility and were randomized in a 2:1 ratio. The extracted text reports that all but one randomized patient (assigned to ketamine) received study medication and completed 24-hour assessments; 67 patients completed assessments through postinfusion day 7. The ketamine and midazolam groups were reported as well matched on demographic and clinical baseline characteristics and overall represented a chronically ill, moderate-to-severe treatment-resistant cohort. Primary outcome: At 24 hours postinfusion the ketamine group showed significantly greater reduction in MADRS scores than the midazolam group. After adjustment for baseline MADRS and site, the mean MADRS score was 7.95 points lower in the ketamine group (95% CI, 3.20 to 12.71), corresponding to Cohen's d=0.81. MADRS differences at 24 hours did not differ by site. Secondary outcomes at 24 hours: Response rates (≥50% reduction in MADRS) were higher with ketamine: 64% versus 28% with midazolam, yielding an odds ratio of 2.18 (95% CI, 1.21 to 4.14; p≤0.006) and a number needed to treat of 2.8. Self-reported depressive symptoms (Quick Inventory of Depressive Symptomatology-Self-Report) were lower in the ketamine group by 3.40 points (95% CI, 0.78 to 6.01; p≤0.02), Cohen's d=0.63. Ketamine also increased the odds of CGI-rated improvement at 24 hours. Durability: Treatment differences diminished over time. When modelling response probability across time, there were main effects of time (increasing nonresponse probability) and treatment (greater probability of response with ketamine), but no significant treatment-by-time interaction, indicating parallel trajectories. After adjustment for site and baseline scores, MADRS and self-report scores at day 7 no longer showed statistically significant differences between groups. At day 7, four midazolam patients and 21 ketamine patients still met response criteria and continued in the study; time-to-relapse over the subsequent 4 weeks is reported for this subgroup in the supplement. Safety and tolerability: The most common adverse events within 4 hours of infusion in the ketamine group were dizziness, blurred vision, headache, nausea/vomiting, dry mouth, poor coordination, poor concentration and restlessness; the midazolam group reported general malaise, dizziness, headache, restlessness, nausea/vomiting, dry mouth, decreased energy and poor coordination. Significant dissociative symptoms were observed in 8 of the 47 patients reported as receiving ketamine (17%); these resolved by 2 hours postinfusion. No severe psychotic symptoms occurred during follow-up. Mild transient increases in blood pressure were observed on average; two ketamine infusions were discontinued for hemodynamic changes. In one case infusion was stopped after 30 minutes for an elevated blood pressure (peak 187/91 mm Hg) that normalised within 10 minutes of cessation; in another case pronounced hypotension and bradycardia resolved without sequelae after overnight observation. The extracted text indicates serious adverse events are described in the online supplement but does not detail them in the main text.
Murrough and colleagues interpret the findings as evidence that a single low-dose ketamine infusion produces a rapid-onset antidepressant effect in patients with treatment-resistant major depression when compared with an active psychoactive placebo. The investigators emphasise robust clinician- and patient-rated improvements at 24 hours and note that responders commonly maintained benefit for several days, although statistically significant group differences were not present at day 7. They argue the two-site replication in an ethnically and racially diverse sample bolsters the reliability of the effect. The authors place their results in a biological context consistent with preclinical work showing rapid synaptic and functional changes after NMDA receptor antagonism, including activation of mTOR signalling and modulation of brain-derived neurotrophic factor pathways; they note emerging evidence that genetic variation in BDNF may moderate response to ketamine. They also stress that, while short-term administration at 0.5 mg/kg appeared safe in this trial for nonpsychotic patients with close monitoring, the longer-term safety, durability of effect and abuse liability of ketamine remain unknown and warrant caution regarding clinical implementation outside research settings. Cardiorespiratory monitoring is recommended given observed hemodynamic changes in a subgroup. Limitations acknowledged by the authors include stringent enrollment criteria (excluding psychotic disorders and recent substance use) and a medication washout requirement that limited participation to those able to tolerate discontinuation; these criteria were defended as clinically relevant risk-mitigation strategies but do constrain generalisability. The study tested only a single infusion with brief follow-up, leaving open the question of how to maintain and prolong the antidepressant response. The authors note that trials of riluzole after ketamine have not prevented relapse and that while repeated ketamine infusions have been explored an absence of controlled data limits conclusions. They suggest future work should evaluate repeated dosing schedules, compare ketamine to active standard treatments such as electroconvulsive therapy, and characterise longer-term efficacy and safety before routine clinical use.
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