HPA axis normalization, estimated by DEX/CRH test, but less alteration on cerebral glucose metabolism in depressed patients receiving ECT after medication treatment failures.
Yuuki N, Ida I, Oshima A, Kumano H, Takahashi K, et al. ;
Commented by , 23 Oct 2005
Background
In randomised controlled trials approximately 60 % of patients respond to antidepressant agents, and 80 to 90 % respond to electroconvulsive stimulation (ECT). Is has not been investigated how ECT affects the hypothalamic-pituitary-adrenocortical (HPA) axis and the cerebral glucose metabolism as reflected in PET scans.
Method
A total of seven Japanese patients who were non-responders to two or more antidepressant treatments and who were referred for ECT underwent an investigation with the combined dexamethasone/corticotrophin-releasing hormone (DEX/CRH) test and with a PET scan before and after ECT.
Results
The number of ECT sessions was 6-20. All patients remitted sufficiently with ECT presenting a Hamilton-21 item below 7 after ECT. Before ECT, two patients were dexamethasone suppression (DST) non-suppressors and seven were DEX/CRH non-suppressors.
After ECT, 0 were DST non-suppressors and two were DEX/CRH non-suppressors. Before ECT, patients presented with a significant hypometabolism in various frontal regions and hypermetabolism in parietal regions compared with normal controls. These findings did not change after ECT.
Professor Kessing's comments
Since the DEX/CRH test has been reported to be more sensitive to depression than the DST, investigations of the HPA-axis in depression have had a renaissance. Similarly, ECT is having a renaissance in many countries as it has become increasingly evident that ECT is superior in efficacy compared with drugs.
Recent studies from e.g. the Department of Psychiatry, Rigshospitalet, Copenhagen (ref. 1) have suggested that ECT may induce neurogenesis in sensitive brain areas, especially the hippocampus.
Hippocampus is crucially involved in the regulation of the HPA axis. The present preliminary study showed that remission with ECT was accompanied by resolution of HPA dysregulation whereas measures of cerebral brain metabolism did not resolve.
As long as we have no methods to detect neurogenesis in living human beings the association between neurogenesis the HPA axis and the cerebral glucose metabolism will remain unclear.
There is a huge need for identifying endophenotypes for depression such as dysfunction of the HPA axis and the cerebral glucose metabolism and their relation to antidepressive treatment if we shall ever understand the biology of depression.
References
1. Madsen TM, Treschow A, Bengzon J, Bolwig TG, Lindvall O and Tingstrom A. Increased neurogenesis in a model of electroconvulsive therapy. Biological Psychiatry 2000; 47(12); 1043-1049