scholarly journals Correlation between Motor Cortex Excitability Changes and Cognitive Impairment in Vascular Depression: Pathophysiological Insights from a Longitudinal TMS Study

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Manuela Pennisi ◽  
Giuseppe Lanza ◽  
Mariagiovanna Cantone ◽  
Riccardo Ricceri ◽  
Concetto Spampinato ◽  
...  

Background. Transcranial magnetic stimulation (TMS) highlighted functional changes in dementia, whereas there are few data in patients with vascular cognitive impairment-no dementia (VCI-ND). Similarly, little is known about the neurophysiological impact of vascular depression (VD) on deterioration of cognitive functions. We test whether depression might affect not only cognition but also specific cortical circuits in subcortical vascular disease. Methods. Sixteen VCI-ND and 11 VD patients, age-matched with 15 controls, underwent a clinical-cognitive, neuroimaging, and TMS assessment. After approximately two years, all participants were prospectively reevaluated. Results. At baseline, a significant more pronounced intracortical facilitation (ICF) was found in VCI-ND patients. Reevaluation revealed an increase of the global excitability in both VCI-ND and VD subjects. At follow-up, the ICF of VCI-ND becomes similar to the other groups. Only VD patients showed cognitive deterioration. Conclusions. Unlike VD, the hyperfacilitation found at baseline in VCI-ND patients suggests enhanced glutamatergic neurotransmission that might contribute to the preservation of cognitive functioning. The hyperexcitability observed at follow-up in both groups of patients also indicates functional changes in glutamatergic neurotransmission. The mechanisms enhancing the risk of dementia in VD might be related either to subcortical vascular lesions or to the lack of compensatory functional cortical changes.

2013 ◽  
Vol 534 ◽  
pp. 155-159 ◽  
Author(s):  
Rita Bella ◽  
Raffaele Ferri ◽  
Giuseppe Lanza ◽  
Mariagiovanna Cantone ◽  
Manuela Pennisi ◽  
...  

2016 ◽  
Vol 23 (6) ◽  
pp. 848-854 ◽  
Author(s):  
Marco Pitteri ◽  
Chiara Romualdi ◽  
Roberta Magliozzi ◽  
Salvatore Monaco ◽  
Massimiliano Calabrese

Background: Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system (CNS). Although cognitive impairment (CI) affects a large proportion of MS patients, only few data are available about its prognostic value associated with advanced magnetic resonance imaging (MRI) metrics. Objectives: We aimed at investigating the relationship between the early CI and the disease progression over 8-year follow-up in MS patients. Methods: We conducted a retrospective 8-year longitudinal study involving 78 patients with relapsing-remitting MS, who completed neuropsychological examination and structural MRI at the time of diagnosis. Each patient was clinically evaluated every 6 months, and cortical thickness was quantified at baseline and at the end of the follow-up. Patients were classified as having normal cognition and mild or severe CI. Results: The results show that CI at the time of diagnosis is a good predictor of conversion to definite MS ( p < 0.001), disability progression ( p < 0.001), as well as of transition to secondary progressive phase ( p < 0.001) and of cortical thinning ( p < 0.001). Conclusion: We confirmed and extended the evidence that early CI might be helpful in the identification of MS patients at high risk of disability progression and poor clinical outcome and should be considered as a marker of most aggressive pathology.


2007 ◽  
Vol 17 (1) ◽  
pp. 39-44
Author(s):  
J Birns ◽  
L Kalra

Vascular cognitive impairment (V.C.I.) encompasses all forms of cognitive loss associated with cerebrovascular disease and ischaemic brain injury. It includes cognitive impairment related to stroke, cortical and subcortical infarcts, silent infarcts and strategic infarcts, white matter lesions associated with small vessel disease, and specific arteriopathies such as CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leucoencephalopathy). Recent studies have demonstrated that VCI is most commonly of a subcortical aetiology with small vessel disease being the major cause. VCI plays an important part in patients with other forms of dementia, such as Alzheimer's disease, who have coexisting vascular lesions and it has been proposed that VCI may be the most common form of cognitive impairment in older people, with a prevalence of 5% in people over the age of 65. In view of the aging population and the growing magnitude of vascular disease in western society, the prevalence of subcortical VCI is likely to increase, with a greater impact on patients and health care providers. In this article, we will review the cerebrovascular pathology underlying subcortical VCI and its role in mediating the characteristic cognitive deficits.


2017 ◽  
Vol 7 (3) ◽  
pp. 140-152 ◽  
Author(s):  
Astrid M. Hooghiemstra ◽  
Anne Suzanne Bertens ◽  
Anna E. Leeuwis ◽  
Esther E. Bron ◽  
Michiel L. Bots ◽  
...  

Background: Hemodynamic balance in the heart-brain axis is increasingly recognized as a crucial factor in maintaining functional and structural integrity of the brain and thereby cognitive functioning. Patients with heart failure (HF), carotid occlusive disease (COD), and vascular cognitive impairment (VCI) present themselves with complaints attributed to specific parts of the heart-brain axis, but hemodynamic changes often go beyond the part of the axis for which they primarily seek medical advice. The Heart-Brain Study hypothesizes that the hemodynamic status of the heart and the brain is an important but underestimated cause of VCI. We investigate this by studying to what extent hemodynamic changes contribute to VCI and what the mechanisms involved are. Here, we provide an overview of the design and protocol. Methods: The Heart-Brain Study is a multicenter cohort study with a follow-up measurement after 2 years among 645 participants (175 VCI, 175 COD, 175 HF, and 120 controls). Enrollment criteria are the following: 1 of the 3 diseases diagnosed according to current guidelines, age ≥50 years, no magnetic resonance contraindications, ability to undergo cognitive testing, and independence in daily life. A core clinical dataset is collected including sociodemographic factors, cardiovascular risk factors, detailed neurologic, cardiac, and medical history, medication, and a physical examination. In addition, we perform standardized neuropsychological testing, cardiac, vascular and brain MRI, and blood sampling. In subsets of participants we assess Alz­heimer biomarkers in cerebrospinal fluid, and assess echocardiography and 24-hour blood pressure monitoring. Follow-up measurements after 2 years include neuropsychological testing, brain MRI, and blood samples for all participants. We use centralized state-of-the-art storage platforms for clinical and imaging data. Imaging data are processed centrally with automated standardized pipelines. Results and Conclusions: The Heart-Brain Study investigates relationships between (cardio-)vascular factors, the hemodynamic status of the heart and the brain, and cognitive impairment. By studying the complete heart-brain axis in patient groups that represent components of this axis, we have the opportunity to assess a combination of clinical and subclinical manifestations of disorders of the heart, vascular system and brain, with hemodynamic status as a possible binding factor.


2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Maria Luca ◽  
Antonina Luca

Oxidative stress- (OS-) related endothelial damage is involved in the occurrence and progression of several disorders, such as vascular depression and dementia. It has been reported that moderate, aerobic, physical exercise could reduce OS and inflammation, thus limiting the cardiovascular risk factors while improving endothelial homeostasis, mood, and cognition. In this review, we will discuss about the role of OS and OS-related endothelial damage in vascular depression and vascular cognitive impairment. Then, we will comment on the effects of physical exercise on both disorders.


2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Giuseppe Lanza ◽  
Placido Bramanti ◽  
Mariagiovanna Cantone ◽  
Manuela Pennisi ◽  
Giovanni Pennisi ◽  
...  

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.


2017 ◽  
Vol 11 (4) ◽  
pp. 381-388 ◽  
Author(s):  
Nilton Custodio ◽  
Rosa Montesinos ◽  
David Lira ◽  
Eder Herrera-Perez ◽  
Yadira Bardales ◽  
...  

ABSTRACT. There is limited evidence about the progression of cognitive performance during the post-stroke stage. Objective: To assess the evolution of cognitive performance in stroke patients without vascular cognitive impairment (VCI), patients with vascular mild cognitive impairment (MCI), and patients with vascular dementia (VD). Methods: A prospective cohort of stroke outpatients from two secondary medical centers in Lima, Peru was studied. We performed standardized evaluations at definitive diagnosis (baseline evaluation), and control follow-ups at 6 and 12 months, including a battery of short cognitive tests: Clinical Dementia Rating (CDR), Addenbrooke's Cognitive Examination (ACE), and INECO Frontal Screening (IFS). Results: 152 outpatients completed the follow-up, showing progressive increase in mean score on the CDR(0.34 to 0.46), contrary to the pattern observed on the ACE and IFS (78.18 to 76.48 and 23.63 to 22.24). The box plot for the CDR test showed that VCI patients had progressive worsening (0.79 to 0.16). Conversely, this trend was not observed in subjects without VCI. The box plot for the ACE and IFS showed that, for the majority of the differentiated stroke types, both non-VCI and VCI patients had progressive worsening. Conclusion: According to both ACE and IFS results during a 1-year follow-up, the cognitive performance of stroke patients worsened, a trend which was particularly consistent in infarction-type stroke patients.


2021 ◽  
pp. 1-5
Author(s):  
Calum A. Hamilton ◽  
Julia Schumacher ◽  
Fiona Matthews ◽  
John-Paul Taylor ◽  
Louise Allan ◽  
...  

ABSTRACT Electroencephalographic (EEG) abnormalities are greater in mild cognitive impairment (MCI) with Lewy bodies (MCI-LB) than in MCI due to Alzheimer’s disease (MCI-AD) and may anticipate the onset of dementia. We aimed to assess whether quantitative EEG (qEEG) slowing would predict a higher annual hazard of dementia in MCI across these etiologies. MCI patients (n = 92) and healthy comparators (n = 31) provided qEEG recording and underwent longitudinal clinical and cognitive follow-up. Associations between qEEG slowing, measured by increased theta/alpha ratio, and clinical progression from MCI to dementia were estimated with a multistate transition model to account for death as a competing risk, while controlling for age, cognitive function, and etiology classified by an expert consensus panel. Over a mean follow-up of 1.5 years (SD = 0.5), 14 cases of incident dementia and 5 deaths were observed. Increased theta/alpha ratio on qEEG was associated with increased annual hazard of dementia (hazard ratio = 1.84, 95% CI: 1.01–3.35). This extends previous findings that MCI-LB features early functional changes, showing that qEEG slowing may anticipate the onset of dementia in prospectively identified MCI.


GeroScience ◽  
2021 ◽  
Author(s):  
Ki Jung Kim ◽  
Juan Ramiro Diaz ◽  
Jessica L. Presa ◽  
P. Robinson Muller ◽  
Michael W. Brands ◽  
...  

AbstractChronic hypoperfusion is a key contributor to cognitive decline and neurodegenerative conditions, but the cellular mechanisms remain ill-defined. Using a multidisciplinary approach, we sought to elucidate chronic hypoperfusion-evoked functional changes at the neurovascular unit. We used bilateral common carotid artery stenosis (BCAS), a well-established model of vascular cognitive impairment, combined with an ex vivo preparation that allows pressurization of parenchymal arterioles in a brain slice. Our results demonstrate that mild (~ 30%), chronic hypoperfusion significantly altered the functional integrity of the cortical neurovascular unit. Although pial cerebral perfusion recovered over time, parenchymal arterioles progressively lost tone, exhibiting significant reductions by day 28 post-surgery. We provide supportive evidence for reduced adenosine 1 receptor-mediated vasoconstriction as a potential mechanism in the adaptive response underlying the reduced baseline tone in parenchymal arterioles. In addition, we show that in response to the neuromodulator adenosine, the action potential frequency of cortical pyramidal neurons was significantly reduced in all groups. However, a significant decrease in adenosine-induced hyperpolarization was observed in BCAS 14 days. At the microvascular level, constriction-induced inhibition of pyramidal neurons was significantly compromised in BCAS mice. Collectively, these results suggest that BCAS uncouples vessel-to-neuron communication—vasculo-neuronal coupling—a potential early event in cognitive decline.


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