This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Electroconvulsive therapy (ECT) is the most efficacious treatment for major depressive episodes in unipolar and bipolar disorders currently available. Because of the cost, requirements for anesthesia and its attendant risks including cognitive and memory deficits associated with ECT, it is usually reserved for the most severely ill, and most refractory mood disordered patients.Cognitive impairment associated with ECT includes disturbance of memory, executive function and visual spatial processing speed. ECT is known to cause the release of glutamate, which may initiate a cascade of events leading to neuronal endangerment and dysfunction. Presumably such a mechanism may underlie the observed cognitive disturbance following treatment with ECT. Consistent with this are results showing that cortisol elevations during ECT are correlated with cognitive impairment. The authors hypothesized that glucocorticoids increase excitatory amino acids (such as glutamate), and mobilize intracellular calcium thus exacerbating cell endangerment due to excitotoxicity.The primary objective of this study is to determine whether the novel NMDA antagonist Memantine, now FDA-approved for use in moderate to severe Alzheimer's dementia, may reduce the neurocognitive deficits associated with ECT treatments in patients receiving unilateral ECT for a severe and relatively refractory major depressive episode.
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