Vascular Cognitive Impairment through the Looking Glass of Transcranial Magnetic Stimulation

Abstract

In the last years, there has been a significant growth in the literature exploiting transcranial magnetic stimulation (TMS) with the aim at gaining further insights into the electrophysiological and neurochemical basis underlying vascular cognitive impairment (VCI). Overall, TMS points at enhanced brain cortical excitability and synaptic plasticity in VCI, especially in patients with overt dementia, and neurophysiological changes seem to correlate with disease process and progress. These findings have been interpreted as part of a glutamate-mediated compensatory effect in response to vascular lesions. Although a single TMS parameter owns low specificity, a panel of measures can support the VCI diagnosis, predict progression, and possibly identify early markers of “brain at risk” for future dementia, thus making VCI a potentially preventable cause of both vascular and degenerative dementia in late life. Moreover, TMS can be also exploited to select and evaluate the responders to specific drugs, as well as to become an innovative rehabilitative tool in the attempt to restore impaired neural plasticity. The present review provides a perspective of the different TMS techniques by further understanding the cortical electrophysiology and the role of distinctive neurotransmission pathways and networks involved in the pathogenesis and pathophysiology of VCI and its subtypes.

<b><i>Valeriana officinalis</i></b> Root Extract Modulates Cortical Excitatory Circuits in Humans

“…We should acknowledge that calcium-channel agonists consistently increase ICF [30]; nonetheless, the assumption of a top-down regulation of ICF induced by the NE brain concentration is speculative at the moment. Furthermore, previous TMS studies carried out in a clinical context highlighted the electrophysiological role of ICF changes as potential markers of a glutamate-mediated adaptive response or compensatory neuroplastic phenomena [42,43,44,45,46,47]. Thus, we cannot rule out an indirect (adaptive) modulatory effect on ICF.…”

Towards the concept of disease-modifier in post-stroke or vascular cognitive impairment: a consensus report

“…Several studies, although methodologically heterogeneous and most of them open-label in design, have shown that specific paradigms of stimulation might improve cognitive performance, thus possibly becoming an alternative to conventional neuroleptic therapy for psychiatric symptoms of dementia [79]. In AD, these effects are probably mediated by compensatory mechanisms supporting the residual abilities [80], and the efficacy can be maximized by selecting patients on the basis of putative neurophysiological markers [78].…”

Cortical Plasticity in Depression

“…Moreover, the normality of CSP and SICI in VD patients indicates that the mechanisms regulating GABAergic intracortical inhibitory circuits are not involved in these individuals. These data provide a new and intriguing neurophysiological explanation for the differences in the neurobiological processes that underlie nonvascular early onset major depression and late-onset VD (Bella et al., 2011; Concerto et al., 2013; Lanza et al., 2017). Furthermore, a longitudinal study evaluated the electrophysiological changes and progression of cognitive decline in patients with subcortical cerebrovascular lesions, and the results showed that glutamate-related neuroplasticity was differentially enhanced between patients with and without VD.…”

“…These symptoms may even present in the preclinical or early stages of these diseases (Bella et al., 2011a, 2011b, 2013; Lanza et al., 2013; Pennisi et al., 2016; Lanza et al., 2017). …”