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ECT and Memantine.


- candidate number14102
- NTR NumberNTR3753
- ISRCTNISRCTN wordt niet meer aangevraagd.
- Date ISRCTN created
- date ISRCTN requested
- Date Registered NTR15-dec-2012
- Secondary IDsNL33782.097.10 CCMO
- Public TitleECT and Memantine.
- Scientific TitleECT and Memantine.
- ACRONYMECT and Memantine
- hypothesisThe efficacy of ECT for the treatment of mood disorders requires the induction of generalized seizures (Nobler et al., 1993). Following the repeated induction of generalized seizures through ECT, enhanced excitability and altered histologic characteristics of the hippocampus have been well demonstrated (Gombos et al., 1999; Perera et al., 2007). Although hippocampal excitotoxicity is mediated in part by excessive calcium influx through over-activation of NMDA receptors, physiological NMDA receptor activation is essential for normal neuronal function. Therefore, potential neuroprotective agents that block virtually all NMDA receptor activity will very likely have unacceptable side effects. In contrast to other clinically-available NMDA receptor antagonists, memantine has been demonstrated to substantially reduce excitotoxic neuronal inury, as well as being clinically well-tolerated in humans. The superior efficacy and clinical safety of memantine result from its highly advantageous pharmacological properties (Chen et al., 1998). Memantine has the unique attributes of being an open-channel blocker, as well as having a relatively fast dissociation rate, compared with other NMDAantagonists such as ketamine. Therefore, memantine will only block NMDAreceptors that are excessively stimulated (open-channel blockade) without disrupting normal synaptic transmission (fast dissociation rate). Together, memantine represents a novel, low-affinity, open-channel NMDA antagonist that appears to enter the channel preferentially when pathologically activated without interfering with normal synaptic transmission, yielding the potential to provide neuroprotection.
- Healt Condition(s) or Problem(s) studiedDepression, Electroconvulsive therapy, Memantine, Cognitive side effects
- Inclusion criteriaDSM-IV criteria for unipolar or bipolar depression and a clinical indication for electroconvulsive treatment (ECT).
- Exclusion criteriaPatients with organic brain syndrome, Mini-Mental State Exam score lower than 24, schizophrenia, schizoaffective disorder, use of lithium or inadequate command of the Dutch language will be excluded.
- mec approval receivedyes
- multicenter trialno
- randomisedyes
- masking/blindingDouble
- controlPlacebo
- groupParallel
- Type2 or more arms, randomized
- Studytypeintervention
- planned startdate 1-dec-2012
- planned closingdate1-dec-2015
- Target number of participants30
- Interventions1. The experimental group will receive once daily 20 mg/d memantine during ECT. This will be titrated before commencing ECT;
2. The control group will receive an identical placbo once daily.
- Primary outcomeScores on a standard cognitive testbattery. This test is administered before, during and after ECT and at follow-up. This testbattery has been proven to be sensitive to cognitive side-effects of depression and also for the ECT effects in depression.
- Secondary outcomeN/A
- TimepointsDuring the course of ECT treatment and at 2 months follow-up.
- Trial web siteN/A
- statusopen: patient inclusion
- CONTACT FOR PUBLIC QUERIESDr. R.M. Kok
- CONTACT for SCIENTIFIC QUERIES
- Sponsor/Initiator Parnassia, psycho-medische zorg, Erasmus Medical Center
- Funding
(Source(s) of Monetary or Material Support)
Lundbeck
- PublicationsN/A
- Brief summaryN/A
- Main changes (audit trail)
- RECORD15-dec-2012 - 4-jan-2013


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