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Elsevier, Brain Stimulation, 3(6), p. 346-354, 2013

DOI: 10.1016/j.brs.2012.06.006

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An Investigation of Medial Temporal Lobe Changes and Cognition Following Antidepressant Response: A Prospective rTMS Study

This paper is available in a repository.
This paper is available in a repository.

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Data provided by SHERPA/RoMEO

Abstract

BACKGROUND: Major depressive disorder (MDD) is often resistant to treatment with standard approaches. Repetitive transcranial magnetic stimulation (rTMS) is a new treatment that has proven antidepressant efficacy in treatment resistant MDD (TRD). Preliminary evidence also raises the possibility of rTMS enhancing neuronal plasticity; with demonstrated increases in serum levels of brain derived neurotrophic factor (BDNF) found. This is of most relevance to volumetric reductions associated with MDD, particularly in the hippocampus and related structures. Extensive preclinical literature suggests that hippocampal volume reductions from MDD induced suppression of adult neurogenesis can be reversed by different types of classical antidepressant treatments which increase expression of BDNF. OBJECTIVE: The aims of this study were to investigate whether antidepressant response to rTMS has similar therapeutic potential as antidepressant pharmacotherapy in promoting neurogenesis in the HC and surrounding structures and facilitating related neurocognitive improvements. METHODS: Magnetic resonance imaging and neurocognitive assessments were conducted on 29 patients prior to rTMS treatment (baseline) and at three months post baseline (endpoint). RESULTS: Over time, antidepressant response was associated with a near significant increase in left amygdala volume (6.58%), whilst treatment non-responders showed significant declines in left hippocampus volumes (-2.64%) from baseline. Functionally, there was no cognitive deterioration following rTMS treatment. The results are limited, however, by sample size. CONCLUSIONS: These preliminary findings suggest that rTMS may promote neurogenesis or other effects that favour neuronal plasticity and may also be neuroprotective for patients with TRD but these findings need replication in a larger sample.