ممانتین در پیشگیری و یا کاهش الکتروشوک درمانی باعث اختلالات شناختی می شود: یک کارآزمایی کنترل شده با پلاسبو
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34520||2015||5 صفحه PDF||سفارش دهید||3727 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Asian Journal of Psychiatry, Available online 21 April 2015
The purpose of this study was to evaluate the effect of memantine administration on the adverse cognitive effects of electroconvulsive therapy (ECT). Forty patients diagnosed with a major depressive disorder for which ECT was indicated as a treatment for their current episode were randomly allocated to either the memantine (5 mg/day) group or the placebo group. All patients underwent the same protocol for anaesthesia and ECT procedures. The patients received memantine or the placebo for the whole period of ECT treatment, starting the day before ECT and continuing until the fourth session of ECT. The Modified Mental State Examination (MMSE) was used for the assessment of cognition before and after the trial. Regarding MMSE and item 3 MMSE (related to recent memory), the memantine group scored significantly higher at the end of ECT sessions than the control group (P = 0.02, P < 0.001, respectively). Our data support the hypothesis that memantine may reduce cognitive impairment following ECT. Memantine could be both a safe and well-tolerated treatment for use with ECT.
Electroconvulsive therapy (ECT) is an effective method for the treatment of a variety of psychiatric disorders, especially depression (McCall et al., 2014). However, the cognitive abnormality induced by ECT is the major factor limiting its use in practice (Sackeim et al., 2007). ECT is associated with retrograde amnesia (reduced ability to recall recent events), anterograde amnesia (reduced ability for new learning) and prolonged postictal delirium and confusion (John et al., 2008). The exact mechanisms contributing to ECT-induced cognitive deficits are not well determined. It has been shown that the cognitive deficits associated with ECT are directly related to the treatment and are not an adverse side effect of the anaesthesia that accompanies the treatment (Frith et al., 1983). It seems that ECT indiscriminately stimulates extensive parts of the brain and thereby induces changes in a wide range of molecular systems. Systems involved in learning and memory and for which ECT-related data are available include glutamatergic neurotransmission and N-methyl-d-aspartate (NMDA) receptor functioning, intracellular calcium, inflammatory processes and cholinergic transmission ( Pigot et al., 2008). The neuroprotective effects of a number of pharmacological agents have been studied in previous animal and clinical studies (Pigot et al., 2008). However, as yet, no pharmacological treatments have been proven to consistently attenuate ECT-induced memory impairment. Chamberlain and Tsai proposed a hypothesis involving glutamate and the NMDA receptor in ECT-induced memory impairment (Chamberlin and Tsai, 1998). Glutamate and NMDA receptors are involved in long-term potentiation (LTP), a fundamental process for memory consolidation, whereby brief high-frequency stimulation leads to an increased response after subsequent activation (Rita et al., 2008). This hypothesis explains the cascade of events that follow NMDA receptor depolarization. Magnesium antagonizes the NMDA receptor to calcium, and after removal of the blockade (during a seizure), calcium and water enter the cell, causing it to swell. This swelling temporarily impedes neurotransmission. There is also associated hyperactivity in reverberating pathways centring around the NMDA receptor and implicating cyclooxygenase 2, platelet activating factor, endogenous cannabinoids and prostaglandins; this hyperactivity results in a reversible oxidative stress. The net result of all these mechanisms is a transient cognition dysfunction (Andrade et al., 2008). The well-documented ability of NMDA antagonists to slow the cognitive dysfunction in patients with Alzheimer's disease (AD) (Corbett et al., 2010) suggests that they may have the potential to alleviate or prevent cognitive abnormality secondary to ECT. Also combination of cholinergic agents with memantine would be better than either alone in alleviation of cognition disorders. For example Atri et al. have shown that combination treatment with memantine added to donepezil in patients with moderate to severe Alzheimer's disease is associated with significant benefits in reducing 24 weeks decline in cognition, function and global status (Atri et al., 2013). In another study, the combination of galantamine and memantine was effective in schizophrenia in order to increase the selective cognition enhancement produced by either medication alone (Koola et al., 2014). Ketamine is an NMDA antagonist that has attracted attention for the induction of anaesthesia during ECT in recent years. Yoosefi et al. evaluated the effect of ketamine and thiopental in patients undergoing ECT. They used Mini-Mental State Examination (MMSE) scores for the evaluation of memory dysfunction. They reported that despite a significant decline in MMSE scores in both groups after the first ECT, cognitive function improved afterwards, but the difference was significant only in the ketamine group (Yoosefi et al., 2014). Memantine is a non-competitive NMDA receptor antagonist that is approved by the United States Food and Drug Administration for the treatment of moderate to severe Alzheimer's disease. It has shown modest benefits in cognition, function, global and behavioural measures and has shown a low potential for drug interactions (Herrmann et al., 2011). The aim of this pilot study was to evaluate the potential use of memantine in the alleviation or prevention of cognition impairment in patients undergoing ECT. We were also interested in exploring the safety and tolerability of memantine in patients receiving ECT.