Slow Wave Induction by Propofol to Eliminate Depression (SWIPED)
Study Details
Study Description
Brief Summary
Our overall hypothesis is that sleep slow-wave potentiation by propofol is a therapeutic pathway for enhancing slow wave sleep and alleviating treatment-resistant depression (TRD).
Condition or Disease | Intervention/Treatment | Phase |
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Phase 1/Phase 2 |
Detailed Description
Aim 1: Establish the safety and feasibility of multiple propofol infusions targeting of electroencephalographic (EEG) slow-wave activity (SWA) without burst suppression in geriatric patients with treatment-resistant depression (TRD) patients.
Aim 2: Compare sleep EEG SWA in geriatric patients with treatment-resistant depression (TRD) patients randomized to two arms: 1) multiple moderate-dose propofol infusions targeting of unconsciousness and electroencephalographic (EEG) slow-wave activity (SWA) without burst suppression vs 2) multiple low-dose propofol infusions targeting unconsciousness with minimal electroencephalographic (EEG) slow-wave activity (SWA) or burst suppression.
Study Design
Arms and Interventions
Arm | Intervention/Treatment |
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Experimental: Propofol infusion - moderate dose Serial propofol infusions to maximally and safely induce unconsciousness and EEG slow waves while minimizing burst suppression. |
Drug: Propofol
Targeted propofol infusion in TRD patients will induce sedation. Dosage of propofol is determined based upon EEG markers and treatment arm.
Other Names:
Diagnostic Test: Electroencephalography (EEG)
EEG will be recorded during propofol infusion and during overnight sleep. Sleep EEG data will be acquired for a minimum of one night prior to the first sedation session, providing a baseline measure. Additional overnight sleep recordings will be performed on day of sedation and subsequent nights.
Diagnostic Test: Slow-Wave Activity
Duration of slow waves during sedation will be evaluated using automated approaches. SWA during sedation will be calculated as the total power in the 0.5-4 Hz frequency band/total time in minutes. SWA during N2/N3 sleep will be calculated as the total power in the 0.5-4 Hz frequency band/total time in minutes in the N2 and N3 sleep stages. Delta sleep ratio will be computed from the SWA measured during the first and second N2/N3 cycles.
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Active Comparator: Propofol infusion - low dose Serial propofol infusions to safely induce unconsciousness while minimizing EEG slow waves and burst suppression. |
Drug: Propofol
Targeted propofol infusion in TRD patients will induce sedation. Dosage of propofol is determined based upon EEG markers and treatment arm.
Other Names:
Diagnostic Test: Electroencephalography (EEG)
EEG will be recorded during propofol infusion and during overnight sleep. Sleep EEG data will be acquired for a minimum of one night prior to the first sedation session, providing a baseline measure. Additional overnight sleep recordings will be performed on day of sedation and subsequent nights.
Diagnostic Test: Slow-Wave Activity
Duration of slow waves during sedation will be evaluated using automated approaches. SWA during sedation will be calculated as the total power in the 0.5-4 Hz frequency band/total time in minutes. SWA during N2/N3 sleep will be calculated as the total power in the 0.5-4 Hz frequency band/total time in minutes in the N2 and N3 sleep stages. Delta sleep ratio will be computed from the SWA measured during the first and second N2/N3 cycles.
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Outcome Measures
Primary Outcome Measures
- Duration of Slow Wave Activity [Up to 10 weeks following consent]
SWA during sedation will be calculated as the total power in the 0.5-4 Hz frequency band/total time in minutes. SWA during N2/N3 sleep will be calculated as the total power in the 0.5-4 Hz frequency band/total time in minutes in the N2 and N3 sleep stages. Delta sleep ratio will be computed from the SWA measured during the first and second N2/N3 cycles.
Eligibility Criteria
Criteria
Inclusion Criteria:
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Age of at least 60 years
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History of Treatment-Resistant Major Depressive Disorder (defined as non-responsiveness to at least two adequate trials of oral antidepressant medications)
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English Speaking
Exclusion Criteria:
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Symptomatic coronary artery disease
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Symptomatic congestive heart failure/cardiomyopathy (New York Heart Association > Class III or left ventricular ejection fraction < 40%)
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Allergy to Propofol
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Resting Bradycardia
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Current treatment with ECT/TMS
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Active vagal nerve implantation
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BMI > 35
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Columbia-Suicide Severity Rating Scale (C-SSRS) of 4 or greater
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Montreal Cognitive Assessment (MOCA) score < 23
Contacts and Locations
Locations
Site | City | State | Country | Postal Code | |
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1 | Washington University School of Medicine/Barnes-Jewish Hospital | Saint Louis | Missouri | United States | 63110 |
Sponsors and Collaborators
- Washington University School of Medicine
- National Institute of Mental Health (NIMH)
Investigators
- Principal Investigator: Ben Palanca, MD PhD, Washington University School of Medicine
Study Documents (Full-Text)
None provided.More Information
Publications
- Doghramji K, Jangro WC. Adverse Effects of Psychotropic Medications on Sleep. Psychiatr Clin North Am. 2016 Sep;39(3):487-502. doi: 10.1016/j.psc.2016.04.009. Epub 2016 Jun 24. Review.
- Duncan WC, Sarasso S, Ferrarelli F, Selter J, Riedner BA, Hejazi NS, Yuan P, Brutsche N, Manji HK, Tononi G, Zarate CA. Concomitant BDNF and sleep slow wave changes indicate ketamine-induced plasticity in major depressive disorder. Int J Neuropsychopharmacol. 2013 Mar;16(2):301-11. doi: 10.1017/S1461145712000545. Epub 2012 Jun 7.
- Murphy MJ, Peterson MJ. Sleep Disturbances in Depression. Sleep Med Clin. 2015 Mar;10(1):17-23. doi: 10.1016/j.jsmc.2014.11.009. Epub 2014 Dec 12. Review.
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