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[Adverse cognitive effects and ECT].

Abstract

Electroconvulsive therapy (ECT) is a rapidly acting and highly effective treatment for severe and life threatening conditions seen in affective and schizophrenic diseases. Notwithstanding its therapeutic benefits, ECT remains controversial because of seizure induction, cognitive side effects, memory dysfunction and effects on cerebral physiology. These factors have raised the concern that ECT produces structural and functional brain damages. This issue continues to have a major impact on the acceptance of ECT as a therapeutic modality, both within the medical community and in public opinion. A close look at incidence, type, severity, neurofunctional and -anatomical correlates, aetiology and therapeutic approaches of the adverse cognitive effects attributed to ECT may contribute to rational and objective handling of this topic. The final chapter deals with the issue of whether ECT causes brain damage.

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BibTeXRIS

Michael Prapotnik, Roger Pycha, Csaba Nemes, Peter König, Armand Hausmann, Andreas Conca. 2006. [Adverse cognitive effects and ECT].. https://doi.org/10.1007/s10354-005-0237-6

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Glucocorticoid mechanisms may contribute to ECT-induced retrograde amnesia.

RATIONALE: Cortisol levels rise sharply immediately after electroconvulsive therapy (ECT); the resultant stimulation of steroid receptors in the hippocampus may be beneficial or harmful to cognition, depending on the magnitude of the stimulation. Steroid mechanisms may therefore modulate ECT-induced amnesia. OBJECTIVES: Using mifepristone (a glucocorticoid receptor antagonist) as a chemical probe, we sought to examine steroid mechanisms in an animal model of ECT-induced retrograde amnesia. MATERIALS AND METHODS: Adult, male Wistar rats (n = 68) trained in a step-through passive-avoidance task were randomized to receive mifepristone (20 or 40 mg kg(-1) day(-1)) or vehicle (control). These treatments were administered 1 day before the electroconvulsive shock (ECS) course and, again, 1 h before each of five once-daily true (30 mC) or sham ECS. Recall of pre-ECS learning was tested 1 day after the last ECS. RESULTS: Relative to sham ECS, true ECS resulted in significant retrograde amnesia in the vehicle group but not in either of the mifepristone groups. In sham ECS-treated animals, mifepristone did not significantly influence recall. In ECS-treated rats, the higher but not the lower dose of mifepristone was associated with significant protection against the retrograde amnesia evident in the vehicle group. CONCLUSION: Mifepristone administered before the ECT seizure may attenuate ECT-induced retrograde amnesia. This suggests that glucocorticoid mechanisms may contribute to ECT-induced retrograde amnesia.

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[Comparison of retrograde amnesia changes within different injury levels of cerebral concussion in rats].

OBJECTIVE: To investigate the retrograde amnesia changes within different injury levels of cerebral concussion in rats. METHODS: A metallic pendulum striker device of brain injury was deployed to duplicate CC models of different injury levels within Sprague-Dawley (S-D) rats. The investigated animals were divided into two groups according to classification standard, that is, Pure Cerebral Concussion (PCC) group and Complicated Cerebral Concussion (CCC) group. One control group was used, and each group included 8 animals. The retrograde amnesia of each group was assessed by Morris Water Maze (MWM) Test from 3 days preinjury to 7 days postconcussion. RESULTS: Compared with the control group, the retrograde amnesia was detected within 3 days in PCC group, and 5 days in CCC group after injury. At the same time, the two groups both manifested space recognition deficit. CONCLUSION: The retrograde amnesia existed in both pure cerebral concussion group and complicated cerebral concussion. Furthermore, the lasting time of retrograde amnesia in animals correlates to the injury level of brain concussion.

Amnesia, Retrograde↗