Abstract
The exact relationship between cognitive functioning, cortical excitability, and synaptic plasticity in dementia is not completely understood. Vascular cognitive impairment (VCI) is deemed to be the most common cognitive disorder in the elderly since it encompasses any degree of vascular-based cognitive decline. In different cognitive disorders, including VCI, transcranial magnetic stimulation (TMS) can be exploited as a noninvasive tool able to evaluate in vivo the cortical excitability, the propension to undergo neural plastic phenomena, and the underlying transmission pathways. Overall, TMS in VCI revealed enhanced cortical excitability and synaptic plasticity that seem to correlate with the disease process and progression. In some patients, such plasticity may be considered as an adaptive response to disease progression, thus allowing the preservation of motor programming and execution. Recent findings also point out the possibility to employ TMS to predict cognitive deterioration in the so-called “brains at risk” for dementia, which may be those patients who benefit more of disease-modifying drugs and rehabilitative or neuromodulatory approaches, such as those based on repetitive TMS (rTMS). Finally, TMS can be exploited to select the responders to specific drugs in the attempt to maximize the response and to restore maladaptive plasticity. While no single TMS index owns enough specificity, a panel of TMS-derived measures can support VCI diagnosis and identify early markers of progression into dementia. This work reviews all TMS and rTMS studies on VCI. The aim is to evaluate how cortical excitability, plasticity, and connectivity interact in the pathophysiology of the impairment and to provide a translational perspective towards novel treatments of these patients. Current pitfalls and limitations of both studies and techniques are also discussed, together with possible solutions and future research agenda.
Highlights
We review all the transcranial magnetic stimulation (TMS) and repetitive TMS (rTMS) studies related to vascular cognitive impairment (VCI) to provide a timely translational perspective on how cortical excitability and network connectivity interact to determine the pathophysiology and plastic changes in VCI and its subtypes, and how these findings may be exploited by experimental treatments
We included in the TMS group 6 studies on mild VCI [30, 31, 83,84,85,86], 6 on vascular dementia (VaD) [87,88,89,90,91,92], 3 on vascular depression [93,94,95], and 4 on Records identified through database searching (n = 77)
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) [96,97,98,99], while the rTMS studies group consisted of 2 articles in mild VCI [100, 101] and 4 in vascular depression [102,103,104,105]
Summary
Vascular cognitive impairment (VCI) is defined as a decline in cognition due to cerebrovascular injury. It is currently viewed as an “umbrella term” encompassing mild VCI, vascular dementia (VaD), and mixed dementia [1,2,3]. Vascular-derived impairment has a great prevalence in all types of cognitive decline, where its contribution to the deficits is considerable. Of note, this is the only contribution that can be, at least in part, treatable and preventable [7, 8]
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