Antidepressant effects of ketamine in depressed patients
This double-blinded, randomised, placebo-controlled, within-subjects study (n=7) investigated the antidepressant efficacy of a single dose of ketamine (35mg/70kg) in patients with depression and found significant improvements in depressive symptoms within 72 hours after infusion.
Authors
- John Krystal
- Dennis Charney
Published
Abstract
Background
A growing body of preclinical research suggests that brain glutamate systems may be involved in the pathophysiology of major depression and the mechanism of action of antidepressants. This is the first placebo-controlled, double-blinded trial to assess the treatment effects of a single dose of an N-methyl-D-aspartate (NMDA) receptor antagonist in patients with depression.
Methods
Seven subjects with major depression completed 2 test days that involved intravenous treatment with ketamine hydrochloride (.5 mg/kg) or saline solutions under randomized, double-blind conditions.
Results
Subjects with depression evidenced significant improvement in depressive symptoms within 72 hours after ketamine but not placebo infusion (i.e., mean 25-item Hamilton Depression Rating Scale scores decreased by 14 6 SD 10 points vs. 0 6 12 points, respectively during active and sham treatment).
Conclusions
These results suggest a potential role for NMDA receptor-modulating drugs in the treatment of depression.
Research Summary of 'Antidepressant effects of ketamine in depressed patients'
Introduction
A growing body of preclinical research implicates NMDA-class glutamate receptors in the pathophysiology of major depression and in the mechanism of action of antidepressant treatments. Animal studies have shown that NMDA receptor antagonists can produce antidepressant-like effects in many, but not all, paradigms, while chronic administration of conventional antidepressants produces changes in NMDA receptor function and subunit mRNA expression. Early clinical work with agents that modulate NMDA-related sites (for example, amantadine and D-cycloserine) provided some support for this hypothesis but was limited by design and drug-specific issues; overall clinical data on selective NMDA antagonists remain sparse. Berman and colleagues conducted the present study to test whether ketamine hydrochloride, a potent NMDA receptor antagonist, produces antidepressant effects in patients with major depressive episodes. The study aimed to compare a single low-dose intravenous ketamine infusion with saline in a randomised, double-blind, crossover design and to assess mood, depressive symptoms, perceptual effects and safety over the subsequent 72 hours.
Methods
The investigators recruited nine patients (4 men, 5 women; mean age 37 ± 10 years, range 23–56; 2 Hispanic, 7 Caucasian) who met DSM-IV criteria for a major depressive episode (eight with recurrent unipolar major depression, one with bipolar disorder, depressed). Two participants had remote histories of alcohol abuse in remission; one had comorbid panic disorder. All patients were medically healthy, drug-free and unmedicated for at least two weeks before the first treatment, as confirmed by medical assessment and toxicology. Written informed consent was obtained and the study received institutional review board approval. Participants underwent two treatment days separated by at least one week in a randomised, double-blind, crossover fashion. On each test day they received an intravenous infusion over 40 minutes of either ketamine hydrochloride at a total dose of 0.5 mg/kg or saline. Four participants were randomly assigned to receive ketamine on the first test day. Two participants terminated before completing the second treatment day (one before placebo, one before ketamine), leaving seven subjects who completed both conditions; the extracted text also describes some analyses that refer to eight subjects, an inconsistency in the reported denominators. Mood and symptom assessments were made at multiple time points. The primary clinician-rated measure was the 25-item Hamilton Depression Rating Scale (HDRS) at baseline and at 80 minutes, 230 minutes, 24 hours, 48 hours and 72 hours after infusion start. Self-report using the Beck Depression Inventory (BDI) was obtained at the same time points plus 10, 40 and 110 minutes. Perceptual/intoxication effects were measured with a visual analogue scale for feeling "high" (VAS-high) at baseline and at 10, 40, 80 and 110 minutes. The Brief Psychiatric Rating Scale (BPRS) was administered at baseline and 10, 40, 80, 110 and 230 minutes. Data were analysed with repeated-measures analyses of variance, using a Huynh–Feldt correction, testing condition (ketamine versus saline), time and condition-by-time interaction effects on dependent variables.
Results
Analyses focused on the seven participants who completed both active and sham treatments; two patients withdrew prior to completing the second condition. Intravenous ketamine produced significantly greater reductions in HDRS scores than saline, with a significant condition-by-time interaction (F = 3.97, df 5,30, p = .02). Mean baseline HDRS scores reported in the extracted text were 33.0 ± 6.7 for the ketamine condition and 26.9 ± 5.8 for the placebo condition; this baseline difference was not statistically significant (paired t test, p = .10). The extracted text also notes one additional patient who completed only the active treatment and experienced marked improvement (baseline HDRS 33, final HDRS 16) but was excluded from the primary analyses. Self-reported depressive symptoms on the BDI showed robust decreases after ketamine (mean baseline 29.5 ± 8.2; final 16.8 ± 10.5) but not after saline (baseline 23.0 ± 8.2; final 25.2 ± 6.0). For the BDI there was a significant drug-by-time effect (F = 5.7, df 8,48, p = .0001). Reported response rates during the three-day follow-up period indicated that four of eight patients demonstrated ≥50% decreases in HDRS scores after active treatment versus one of eight after sham; however, the Fisher Exact test reported in the extracted text did not reach statistical significance (p > .05). Ketamine-associated mood improvement generally returned toward baseline by one to two weeks after infusion, although one subject who showed prolonged improvement began antidepressant medication before fully returning to baseline. Ketamine produced marked acute perceptual and euphoric effects. VAS-high scores were significantly greater after ketamine with significant condition-by-time, time and condition effects (condition-by-time F = 16.9, df 4,24, p = .0001). These subjective "high" ratings returned to baseline by 110 minutes post-infusion; all subjects showed maximum VAS-high scores >50 mm during ketamine testing and none did during sham. Ketamine also increased BPRS scores, particularly positive symptom items, but the extracted tests for BPRS-positive effects did not reach conventional significance (condition-by-time F = 4.14, df 5,30, p = .068; time F = 3.97, df 5,30, p = .06; condition F = 3.71, df 1,30, p = .10). Changes in BPRS or VAS-high did not correlate with percent decreases in HDRS (R2 < .05, p > .65), suggesting acute perceptual effects were temporally dissociated from antidepressant response. Item-level HDRS comparisons (uncorrected for multiple comparisons) indicated significant decreases during active treatment for depressed mood (p = .0025), suicidality (p = .02), helplessness (p = .008) and worthlessness (p = .015).
Discussion
Berman and colleagues interpret their findings as evidence that a single low-dose intravenous ketamine infusion is associated with rapid and robust reductions in depressive symptoms, with improvement emerging over the three days following administration. They note that while ketamine is a high-affinity NMDA receptor antagonist, it also has lesser affinities for opioid receptors and weak dopamine-transporter antagonist activity; consequently, antidepressant effects might arise from direct NMDA antagonism or secondary effects on monoamine and opioid systems. The investigators emphasise that ketamine also produced profound but transient cognitive disturbances and euphoria, consistent with prior observations in other populations. Importantly, the mood improvements persisted beyond the short-lived perceptual "high," returning to baseline after one to two weeks in most patients, which the authors take as evidence that the antidepressant effect is temporally dissociated from acute intoxication. They caution, however, that the perceptual effects made it easy for participants to distinguish active from placebo treatment, compromising blinding and potentially biasing self-reports and placebo responses. The authors situate their results within animal-model data supporting NMDA antagonists' antidepressant-like effects and note that rapid onset might in part reflect the intravenous route of administration. They acknowledge limitations to clinical applicability, including ketamine's psychotomimetic effects and abuse potential, and suggest that NMDA antagonists without prominent psychotomimetic properties (for example, memantine or eliprodil) merit further clinical testing for antidepressant activity.
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METHODS
Nine patients (4 men, 5 women; age 37 Ϯ 10 years, ranging 23 to 56 years; 2 Hispanic and 7 Caucasian) participated in the study, with two participants terminating prior to the last treatment condition (one each prior to placebo and ketamine treatment conditions). All participants fulfilled DSM-IV criteria for major depressive episodes (n ϭ 8, recurrent unipolar major depression; n ϭ 1, bipolar disorder, depressed), had no recent diagnosis of alcohol or substance abuse (two subjects had a history of alcohol abuse, in remission greater than 8 years), and had no lifetime diagnosis of any other Axis I disorder (except one patient with a comorbid diagnosis of panic disorder) as determined by the Structured Clinical Interview for Diagnosis, DSM-IV. All patients were drug-free, in good health, and unmedicated for at least 2 weeks prior to the first treatment condition, as determined by medical history, physical exam, routine blood labs, electrocardiogram, urinalysis, and urine toxicology. After receiving a complete description of the study (AC, RMB), written informed consent was obtained. The participants were informed that the study challenge might lead to significant mood changes, possibly causing a worsening of their depressive symptoms and potentially distressing cognitive disturbances. The study was approved by the IRB of the Veterans Administration Connecticut Healthcare Services, West Haven Campus. Patients underwent two treatment days separated by at least 1 week in a randomized, double-blinded manner, as described previously. A saline solution alone or containing ketamine hydrochloride (total dose of .5 mg/kg) was infused over 40 min. Ratings included the Hamilton Depression Rating Scale (HDRS; baseline as well as 80 min, 230 min, 24 hours, 48 hours, and 72 hours after starting infusion), Beck Depression Inventory (BDI; same time points plus 10, 40, and 110 min after infusion), Visual Analog Scales score for intoxication "high" (VAS-high; baseline as well as 10, 40, 80, and 110 min after infusion), and the Brief Psychiatric Rating Scale (BPRS; at baseline as well as 10, 40, 80, 110, and 230 minutes after infusion). Four participants were randomly assigned to receive ketamine (.5 mg/kg) prior to placebo infusion. Time points were chosen based on previous experience from our group. Data were evaluated with repeated measures analyses of variance with Huyn-Feldt correction, examining condition (saline vs. ketamine), time, and time-by-condition effects on dependent variables (HDRS, BDI, BPRS, and VAS).
RESULTS
Intravenous ketamine treatment produced significantly greater reductions on HDRS scores than saline treatment. Analyses included the seven participants who completed both active and sham treatment, with two patients electing to terminate the study (one each after active and sham infusions) for purposes of instituting antidepressant treatment. Analyses revealed significant condition-by-time (F ϭ 3.97, df 5,30, p ϭ .02) but not time (F ϭ 2.62, df 5,30, p ϭ .09) and condition (F ϭ 0.157, df 1,30, p ϭ .71) effects. Figuredepicts change in HDRS scores from baseline timepoint. Another patient, who was excluded from analyses because of completing only active treatment, experienced marked improvement in depressive symptoms (baseline HDRS 33, final HDRS 16). Mean baseline HDRS scores for ketamine (33.0 Ϯ 6.7) and placebo (26.9 Ϯ 5.8) infusions were not statistically different (paired t test, p ϭ 0.10). Among patients receiving active ketamine versus saline testing first, baseline scores were respectively 10.3 (Ϯ 9.0 SD) versus 3.0 (Ϯ 7.5) points lower for the second condition (p ϭ .29). Robust decreases in the BDI were observed during active (mean baseline score, 29.5 Ϯ 8.2; final score, 16.8 Ϯ 10.5) but not control (base, 23.0 Ϯ 8.2; final, 25.2 Ϯ 6.0) treatment. Drug-by-time (F ϭ 5.7, df 8,48, p ϭ .0001) but not drug (F ϭ .007, df 1,48, p ϭ .94) or time (F ϭ 1.63, df 8,48, p ϭ .21) effects were significant. Examined post hoc, order effects were not significant for HDRS and BDI measures (p Ͼ .3). Four of eight patients demonstrated 50% or greater decreases in HDRS scores during the 3-day follow-up period, whereas only one of eight subjects undergoing sham infusion demonstrated a similar response (i.e., 3, 6, 7, 8, and 74% decreases and three subjects remained 4, 22, and 33% above baseline during the follow-up period; Fisher Exact, p Ͼ .05). Ketamine-induced mood improvement returned to baseline levels (i.e., clinical impression and HDRS within 5 points of baseline) 1 to 2 weeks after infusion. An exception, one subject demonstrating marked mood improvement (i.e., baseline HDRS of 41 points; Day 3 HDRS of 7 points), was started on antidepressant medication without having returned to his baseline level of depression two weeks after the ketamine infusion (HDRS, 15 points). Ketamine infusion produced markedly greater scores on the VAS-high item, with significant condition-by-time (F ϭ 16.9, df 4,24, p ϭ .0001), time (F ϭ 16.9, df 4,24 p ϭ .0001), and condition (F ϭ 26.3, df 1,24, p ϭ .002) effects. VAS-high scores returned to baseline by 110 min after infusion. All patients demonstrated a maximum VAS-high score Ն 50 mm during ketamine testing, whereas no patients demonstrated any increases during sham testing. Ketamine infusion produced significantly greater scores on the BPRS, especially the positive symptoms. Condition-by-time (F ϭ 4.14, df 5,30, p ϭ .068), time (F ϭ 3.97, df 5,30, p ϭ .06), and condition (F ϭ 3.71, df 1,30, p ϭ .10) effects were not statistically significant for BPRS-positive scores. Changes in BPRS or VAS-high scores did not correlate with percent decreases observed in HDRS scores (R 2 Ͻ .05, p Ͼ .65). To determine how ketamine infusion affected specific symptoms of depression, baseline and final scores on individual HDRS items were compared. While undergoing active treatment, significant decreases were observed for items of depressed mood (paired t test, p ϭ .0025), suicidality (p ϭ .02), helplessness (p ϭ .008), and worthlessness (p ϭ .015), uncorrected for multiple comparisons. Control treatment was not associated with significant improvement in any of the HDRS items.
CONCLUSION
Results of this study suggest that low-dose ketamine infusion, as compared to placebo, is associated with robust decreases in depressive symptoms, emerging progressively within 3 days. Although ketamine is a high-affinity NMDA receptor antagonist, it has less, but potentially relevant, affinity for the opiate receptors and weak antagonist activity for the dopamine transporter. Additionally, NMDA receptor agents may potentially affect mood via known secondary effects on monoamineand opiatesystems. Profound and transient cognitive deficits and euphoria, as evidenced by increases in BPRS scores, were also induced by ketamine infusion, as also observed in other subject populations. The improvement associated with ketamine infusion reflects a lessening of core symptoms of depression and seems temporally disconnected from ketamine-induced euphoria or "high." In support, patients reported a diminution of depressive symptoms 3 days after infusion, whereas, feelings of "high" returned to baseline after hours. Nevertheless, patients were readily able to discern the active from placebo treatment based on ketamine's induced perceptual disturbances and "high." Hence, limitations in preserving study blind may have biased patient reporting by diminishing placebo effects, thereby potentially confounding results. These results are consistent with limited reports on the use of NMDA receptor antagonists in animal models of depression. Rapid response, however, may potentially reflect route of drug administration, as somebut not allstudies demonstrate rapid antidepressant response to intravenous administration of tricyclic antidepressants. Overall, the results of this study are consonant with hypotheses of NMDA receptor dysfunction in depression. Although our findings suggest the potential benefit of further exploration of NMDA antagonists as potential antidepressant agents, clinical applicability of this strategy may be limited by the psychotomimetic effects and the potential for abuse of many of these agents. Conversely, NMDA receptor antagonists without psychotomimetic properties in humans (e.g., memantine, eliprodil, and 1-aminocyclopropanecarboxylic acid) merit testing for antidepressant activity.
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Study Details
- Study Typeindividual
- Populationhumans
- Characteristicsdouble blindrandomizedplacebo controlledcrossover
- Journal
- Compound
- Topics
- Authors
- APA Citation
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