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Ketamine has recently become an agent of interest as an acute treatment for severe depression and as the anaesthetic for electroconvulsive therapy (ECT). Subanaesthetic doses result in an acute reduction in depression severity while evidence is equivocal for this antidepressant effect with anaesthetic or adjuvant doses. Recent systematic reviews call for high-quality evidence from further randomised controlled trials (RCTs).
To establish if ketamine as the anaesthetic for ECT results in fewer ECT treatments, improvements in depression severity ratings and less memory impairment than the standard anaesthetic.
Double-blind, parallel-design, RCT of intravenous ketamine (up to 2 mg/kg) with an active comparator, intravenous propofol (up to 2.5 mg/kg), as the anaesthetic for ECT in patients receiving ECT for major depression on an informal basis. (Trial registration: European Clinical Trials Database (EudraCT): 2011-000396-14 and clinicalTrials.gov: NCT01306760.)
No significant differences were found on any outcome measure during, at the end of or 1 month following the ECT course.
Ketamine as an anaesthetic does not enhance the efficacy of ECT.
Anzac Battlefield: A Gallipoli Landscape of War and Memory explores the transformation of Gallipoli's landscape in antiquity, during the famed battles of the First World War and in the present day. Drawing on archival, archaeological and cartographic material, this book unearths the deep history of the Gallipoli peninsula, setting the Gallipoli campaign in a broader cultural and historical context. The book presents the results of an original archaeological survey, the research for which was supported by the Australian, New Zealand and Turkish Governments. The survey examines materials from both sides of the battlefield, and sheds new light on the environment in which Anzac and Turkish soldiers endured the conflict. Richly illustrated with both Ottoman and Anzac archival images and maps, as well as original maps and photographs of the landscape and archaeological findings, Anzac Battlefield is an important contribution to our understanding of Gallipoli and its landscape of war and memory.
To determine whether exercise is effective as an adjunct to antidepressant therapy in reducing depressive symptoms in older people.
Patients were randomised to attend either exercise classes or health education talks for 10 weeks. Assessments were made ‘blind’ at baseline, and at 10 and 34 weeks. The primary outcome was seen with the 17-item Hamilton Rating Scale for Depression (HRSD). Secondary outcomes were seen with the Geriatric Depression Scale, Clinical Global Impression and Patient Global Impression.
At 10 weeks a significantly higher proportion of the exercise group (55% v. 33%) experienced a greater than 30% decline in depression according to HRSD (OR=2.51, P=0.05, 95% Cl 1.00–6.38).
Because exercise was associated with a modest improvement in depressive symptoms at 10 weeks, older people with poorly responsive depressive disorder should be encouraged to attend group exercise activities.
New research in animals is beginning to change radically our understanding of the biology of stress and the effects of antidepressant agents.
To relate recent findings from the basic neurosciences to the pathophysiology of depressive disorder.
Drawing together findings from molecular and physiological studies in rats, social studies in primates and neuropsychological studies in humans, we review the neurotrophic and neuroplastic effects of antidepressants and stress.
Stress and antidepressants have reciprocal actions on neuronal growth and vulnerability (mediated by the expression of neurotrophins) and synaptic plasticity (mediated by excitatory amino acid neurotransmission) in the hippocampus and other brain structures. Stressors have the capacity to progressively disrupt both the activities of individual cells and the operating characteristics of networks of neurons throughout the life cycle, while antidepressant treatments act to reverse such injurious effects.
We propose a central role for the regulation of synaptic connectivity in the pathophysiology of depressive disorder.
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