Motor cortex excitability in vascular depression

Bella, Rita; Ferri, Raffaele; Cantone, Mariagiovanna; Pennisi, Manuela; Lanza, Giuseppe; Malaguarnera, Michele; Spampinato, Concetto; Giordano, Daniela; Raggi, Alberto; Pennisi, Giovanni

doi:10.1016/j.ijpsycho.2011.09.006

Cited by 46 publications

(39 citation statements)

References 59 publications

(57 reference statements)

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“…The main finding is the observation of potentially distinctive neurophysiological profiles elicited by TMS, adding support to the hypothesis that late onset VD is a different syndrome with respect to early onset recurrent MD. Despite the abundant literature on TMS and depression, only one study has been conducted in VD patients, where VD patients were compared with patients with SVD patients and controls [30]. The results of this study confirm previous findings on VD, and are consistent with most TMS reports investigating MD.…”

Section: Discussionsupporting

confidence: 88%

“…ICI and ICF interactions are likley related to the balance of GABAergic, dopaminergic, and glutamatergic transmissions [29]. In a single study evaluating inhibitory/facilitatory intracortical circuit changes, Bella et al [30] did not find significant differences between patients with VD and patients with subcortical vascular disease (SVD), suggesting that VD with or without depression might result in a similar neurophysiological profile of cortical excitability, probably as a consequence of cerebral small vessel disease.…”

Section: Introductionmentioning

confidence: 99%

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Different patterns of cortical excitability in major depression and vascular depression: a transcranial magnetic stimulation study

et al. 2013

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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.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Different patterns of cortical excitability in major depression and vascular depression: a transcranial magnetic stimulation study

et al. 2013

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“…Lack of ICF (at 10 and 12 ms) in our CADASIL partially contradicts a recent study where an enhanced ICF was observed in a sample of subcortical vascular disease (SVD) sample of patients 16. Those different results could be explained by the different clinical situations of two samples (SVD vs CADASIL) and by the experimental procedure used for assessment of ICF.…”

Section: Discussioncontrasting

confidence: 99%

Abnormal sensorimotor plasticity in CADASIL correlates with neuropsychological impairment

Palomar

Suárez

Franco

et al. 2013

Journal of Neurology, Neurosurgery & Psychiatry

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“…a) Post-ischemic encephalopathy with several types of predominant distribution pattern: (1) Recent neurophysiological studies using transcranial motor stimulation (TMS) have revealed distinct patterns of cortical excitability in VaD, possibly associated with disease process and progress [43,44]. However, the pathophysiological details of VCI/VaD and of vascular depression (VaDep -see consensus paper [45]) are beyond the scope of this mini-review.…”

Section: Other Pathological Substrates Of Vci Includementioning

confidence: 99%

Current Pathogenetic Concepts of Vascular Cognitive Impairment

Jellinger¹

2016

J Neurol Neurol Sci Disord

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The term vascular cognitive impairment designates a heterogenous group of disorders ranging from mild cognitive impairment to full-blown dementia -vascular dementia -resulting from cerebrovascular lesions involving various brain areas. Current clinical criteria show moderate sensitivity (50-56%) and variable specifi city (range 64-98%). The prevalence in autopsy series ranges from 0.03 to 58% (mean 8-15% in Western series, 22-35% in Japan). Major morphological types -multi-infarct and subcortical vascular encephalopathy, strategic infarct dementia, lacunar state, cortical granular atrophy (rare), and ischemic encephalopathy -are caused by atherosclerosis of major cerebral arteries and small vessel disease, resulting from systemic, cardiac and local vascular disease or cerebral amyloid angiopathy. Pathogenesis of vascular dementia is multifactorial, and pathophysiology affects brain areas and neurological networks involved in cognition, memory, behavior, and executive functions. Vascular brain injury in elderly persons often coexists with Alzheimer-type lesions and other pathologies resulting in mixed dementia. However, these lesions are also present in many non-demented elderly subjects. The heterogeneity of clinical manifestations, cerebrovascular pathology and their pathogenic factors result in limitations of the accuracy of diagnostic criteria for vascular dementia. Therefore, standardized and reproducible neuropathological criteria for the assessment of cerebrovascular lesions associated with cognitive impairment in order to elucidate contribution of cerebrovascular disease to cognitive impairment are urgently needed.

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Motor cortex excitability in vascular depression

Cited by 46 publications

References 59 publications

Different patterns of cortical excitability in major depression and vascular depression: a transcranial magnetic stimulation study

Different patterns of cortical excitability in major depression and vascular depression: a transcranial magnetic stimulation study

Abnormal sensorimotor plasticity in CADASIL correlates with neuropsychological impairment

Current Pathogenetic Concepts of Vascular Cognitive Impairment

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