Abstract
BackgroundClinical and functional studies consider major depression (MD) and vascular depression (VD) as different neurobiological processes. Hypoexcitability of the left frontal cortex to transcranial magnetic stimulation (TMS) is frequently reported in MD, whereas little is known about the effects of TMS in VD. Thus, we aimed to assess and compare motor cortex excitability in patients with VD and MD.MethodsEleven VD patients, 11 recurrent drug-resistant MD patients, and 11 healthy controls underwent clinical, neuropsychological and neuroimaging evaluations in addition to bilateral resting motor threshold, cortical silent period, and paired-pulse TMS curves of intracortical excitability. All patients continued on psychotropic drugs, which were unchanged throughout the study.ResultsScores on one of the tests evaluating frontal lobe abilities (Stroop Color-Word interference test) were worse in patients compared with controls. The resting motor threshold in patients with MD was significantly higher in the left hemisphere compared with the right (p < 0.05), and compared with the VD patients and controls. The cortical silent period was bilaterally prolonged in MD patients compared with VD patients and controls, with a statistically significant difference in the left hemisphere (p < 0.01). No differences were observed in the paired-pulse curves between patients and controls.ConclusionsThis study showed distinctive patterns of motor cortex excitability between late-onset depression with subcortical vascular disease and early-onset recurrent drug resistant MD. The data provide a TMS model of the different processes underlying VD and MD. Additionally, our results support the “Vascular depression hypothesis” at the neurophysiological level, and confirm the inter-hemispheric asymmetry to TMS in patients with MD. We were unable to support previous findings of impaired intracortical inhibitory mechanisms to TMS in patients with MD, although a drug-induced effect on our results cannot be excluded. This study may aid the understanding of the pathogenetic differences underlying the clinical spectrum of depressive disorders.
Highlights
Clinical and functional studies consider major depression (MD) and vascular depression (VD) as different neurobiological processes
Recently, the finding that patients with late-onset depression had higher rates of brain magnetic resonance imaging (MRI) changes compared with patients with early onset major depression (MD), has led to the hypothesis that mood disorders in the elderly may be related to neurobiological abnormalities, such as cerebrovascular disease [1]
MD were younger than VD patients and controls
Summary
Clinical and functional studies consider major depression (MD) and vascular depression (VD) as different neurobiological processes. The finding that patients with late-onset depression had higher rates of brain magnetic resonance imaging (MRI) changes compared with patients with early onset major depression (MD), has led to the hypothesis that mood disorders in the elderly may be related to neurobiological abnormalities, such as cerebrovascular disease [1]. Patients with late-onset MD disorder showed specific deficits in attention and executive function [9,10], whereas patients with recurrent MD exhibited deficits in episodic memory [11,12] These neuropsychological differences are thought to be associated with prominent fronto-striatal dysfunction in late-onset MD, and with a reduction in hippocampal volume in recurrent geriatric MD. The rates of anhedonia and comorbid cardiovascular illness were higher in patients with lateonset MD [11]
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