Single, Repeated, and Maintenance Ketamine Infusions for Treatment-Resistant Depression: A Randomized Controlled Trial

Phillips, Jennifer L.; Norris, Sandhaya; Talbot, Jeanne; Birmingham, Meagan; Hatchard, Taylor; Ortiz, Abigail; Owoeye, Olabisi; Batten, Lisa A.; Blier, Pierre

doi:10.1176/appi.ajp.2018.18070834

Cited by 298 publications

(167 citation statements)

References 25 publications

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“…Position of the VOIs of the second scanning session were determined based on VOI placement of the baseline measurement. VOI1 was centered to the medial part of the corpus callosum to cover the hippocampus and insula bilaterally, with a VOI = 80 (l-r) × 90 (a-p) × 80 (s-i) mm 3 and a field of view (FOV) = 160 × 160 × 160 mm 3 , see Figure 1. The acquired matrix size of 10 × 10 × 10 (i.e.,~4 cm 3 nominal voxel size) was interpolated to a 16 × 16 × 16 matrix (i.e.,~1 cm 3 nominal voxel size) during spectral processing steps.…”

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

“…The acquired matrix size of 10 × 10 × 10 (i.e.,~4 cm 3 nominal voxel size) was interpolated to a 16 × 16 × 16 matrix (i.e.,~1 cm 3 nominal voxel size) during spectral processing steps. VOI2 was centered to cover the cingulate cortex with VOI = 80 (l-r) × 120 (ap) × 50 (s-i) mm 3 and field of view (FOV) = 160 × 160 × 160 mm 3 , see Figure 1. Siemens advanced shimming procedure with manual adjustments was used.…”

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

“…As a rapid acting and robust glutamatergic agent, ketamine occupies a unique position in antidepressant therapy. Numerous randomized controlled trials substantiate its efficacy in uni-and bipolar depression (1)(2)(3). The recent approval of an intranasal formulation by the U.S. Food and Drug Administration (FDA) and the European Medicines Agency (EMA) is likely to promote the use of ketamine in clinical care.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Ketamine on Limbic GABA and Glutamate: A Human In Vivo Multivoxel Magnetic Resonance Spectroscopy Study

et al. 2020

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Furthermore, no statistically significant associations between changes in any of the neurotransmitter ratios and plasma levels of ketamine, norketamine, or dehydronorketamine were observed (p corr > 0.05). Conclusion: This study provides evidence for decreased hippocampal GABA+/tCr ratio 2 h following ketamine administration. As MRS methodology measures total levels of intraand extracellular GABA, results might indicate drug induced alterations in GABA turnover. Our study in healthy humans suggests that changes in GABA levels, particularly in the hippocampus, should be further assessed for their relevance to ketamine´s antidepressant effects.

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Section: Magnetic Resonance Imagingmentioning

confidence: 99%

Section: Magnetic Resonance Imagingmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of Ketamine on Limbic GABA and Glutamate: A Human In Vivo Multivoxel Magnetic Resonance Spectroscopy Study

et al. 2020

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“…62 However, owing to risk of psychosis, it is used only acutely, but recent trials suggest that repeated ketamine administration may be effective and safe for treatment-resistant depression. [63][64][65] It also remains unclear to what extent ketamine's antidepressant actions in humans depend on neuroplasticity. In rodents, inhibitors of the mammalian target of rapamycin that reduce dendritic protein synthesis prevent ketamineinduced neuroplasticity and behavioural improvement, 66 suggesting a role for neuroplasticity, although additional mechanisms are implicated in ketamine action.…”

Section: Ketamine and Adult Neuroplasticitymentioning

confidence: 99%

Adult neuroplasticity: A new “cure” for major depression?

Albert

2019

jpn

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Neuroplasticity involves synaptic reorganization (Box 1) in response to environmental stressors or rewards and is thought to underlie our ability to adjust, learn and remember. 7 However, in mental illness, it is thought that maladaptive plasticity occurs, resulting in persistence of the depressive symptoms, such as rumination, anhedonia and others. 8 By harnessing corrective neuroplasticity (Box 2), it may be possible to reprogram the maladaptive behaviour and produce long-lasting remission. This editorial presents evidence that both pharmacological and brain stimulation antidepressant approaches may act by inducing corrective neuroplasticity to mediate remission. Increasingly, antidepressant effects on neuroplasticity are shown to correlate with behavioural improvement, both in humans 18 and in animal models, 19 raising the possibility that neuroplasticity could provide a new avenue for depression research. However, learning how to harness this capacity to enhance recovery remains a challenge.

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“…Ketamine is an effective antidepressant agent, especially in patients with treatment-resistant depressive (TRD) symptoms [10][11][12][13]. A single administration of ketamine (0.5 mg/kg) can induce immediate psychotomimetic symptoms that recede within 2 h in healthy adults [14].…”

Section: Introductionmentioning

confidence: 99%

Adjunct ketamine treatment effects on treatment-resistant depressive symptoms in chronic treatment-resistant schizophrenia patients are short-term and disassociated from regional homogeneity changes in key brain regions – a pilot study

Ye¹,

Lin²,

Jiang³

et al. 2019

Psychiatry and Clinical Psychopharmacology

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2019) Adjunct ketamine treatment effects on treatment-resistant depressive symptoms in chronic treatment-resistant schizophrenia patients are short-term and disassociated from regional homogeneity changes in key brain regions -a pilot study, Psychiatry and Clinical Psychopharmacology, 29:4, 907-915, ABSTRACT BACKGROUND: To investigate the effects of adjunct ketamine treatment on depressive symptoms and brain activity in chronic treatment-resistant schizophrenia (CTRS) patients with treatment-resistant depressive (TRD) symptoms. METHODS: Calgary Depression Scale for Schizophrenia (CDSS), positive and negative syndrome scale (PANSS), and regional homogeneity (ReHo) results were compared before versus after ketamine treatment in 12 CTRS patients with TRD symptoms. RESULTS: From 7 days to 14 days after the first ketamine administration, CDSS and PANSS total scores were reduced by 63.8% and 12.9%, respectively. By day 21, ReHo values had increased in the main components of the default mode network (DMN) and bilateral orbitofrontal cortex (OFC) after family-wise error correction. ReHo alterations did not correlate with TRD symptom changes. TRD symptoms relapsed by the 21-day time point, while increased ReHo was sustained. No adverse secondary effects (ASEs) necessitating medical intervention occurred. CONCLUSIONS: Adjunct ketamine alleviation of TRD symptoms lasted only a week, whereas increased ReHo in DMN regions and the OFC in CTRS patients was maintained beyond 2 weeks, indicating that adjunct ketamine is not well-suited for CTRS patients with TRD symptoms and that effects on functional activity dissociate from effects on TRD symptoms. This small-sample pilot study provides clues for further research into therapy for TRD symptoms in CTRS patients. ARTICLE HISTORY

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Single, Repeated, and Maintenance Ketamine Infusions for Treatment-Resistant Depression: A Randomized Controlled Trial

Cited by 298 publications

References 25 publications

Effect of Ketamine on Limbic GABA and Glutamate: A Human In Vivo Multivoxel Magnetic Resonance Spectroscopy Study

Effect of Ketamine on Limbic GABA and Glutamate: A Human In Vivo Multivoxel Magnetic Resonance Spectroscopy Study

Adult neuroplasticity: A new “cure” for major depression?

Adjunct ketamine treatment effects on treatment-resistant depressive symptoms in chronic treatment-resistant schizophrenia patients are short-term and disassociated from regional homogeneity changes in key brain regions – a pilot study

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