Markers of lacunar stroke in patients with moderate internal carotid artery stenosis

Silvestrini, Mauro; Pasqualetti, Patrizio; Baruffaldi, Roberto; Catani, Sheila; Tibuzzi, Francesco; Altamura, Claudia; Bartolini, Marco; Provinciali, Leandro; Vernieri, Fabrizio

doi:10.1007/s00415-005-0989-3

Cited by 9 publications

(13 citation statements)

References 39 publications

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“…18 Similarly, lacunar strokes were included as endpoint as they had been associated with a poor hemodynamic response in patients with carotid stenosis. 11 Another point to discuss is the relatively high incidence of stroke in our cohort compared with more recent studies. 31,32 One explanation is that our study population might have been at particularly high risk, as we included subjects with a mean age above 70 years undergoing ultrasonographic evaluation of neck vessels for the presence of multiple vascular risk factors.…”

Section: Discussionmentioning

confidence: 76%

Ultrasonographic Markers of Vascular Risk in Patients with Asymptomatic Carotid Stenosis

Silvestrini

Altamura

Cerqua

et al. 2013

J Cereb Blood Flow Metab

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Six-hundred twenty-one subjects with unilateral asymptomatic severe internal carotid artery (ICA) stenosis were prospectively evaluated with a median follow-up of 27 months (min ¼ 6, max ¼ 68). Vascular risk profile, plaque characteristic, stenosis progression, and common carotid artery intima-media thickness (IMT) were investigated in all patients. Outcome measures were occurrence of ischemic stroke ipsilateral to ICA stenosis and vascular death, while myocardial infarction, contralateral strokes, and transient ischemic attack were considered as competing events. A total of 99 subjects (15.9%) suffered from a vascular event. Among them, 39 were strokes ipsilateral to the stenosis (6.3%). Degree of stenosis, stenosis progression, and common carotid artery IMT resulted as independent predictive factors of ipsilateral stroke. Considering a stenosis of 60% to 70% as reference, a degree between 71% and 90% increased the risk by 2.45, while a degree between 91% and 99% increased the risk by 3.26. The progression of stenosis was a strong risk factor (hazard ratio ¼ 4.32). Finally, the role of carotid IMT was confirmed as crucial additional measure, with an increased risk by 25% for each 0.1 mm IMT increase. Our data suggest that IMT, stenosis progression and severity should be considered as risk factors for cerebrovascular events in asymptomatic subjects with severe ICA stenosis.

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Section: Discussionmentioning

confidence: 76%

Ultrasonographic Markers of Vascular Risk in Patients with Asymptomatic Carotid Stenosis

Silvestrini

Altamura

Cerqua

et al. 2013

J Cereb Blood Flow Metab

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“…Of these, about 10–15 % patients fulfil criteria for behavioural variant frontotemporal dementia (bvFTD) [ 13 , 28 ]. In keeping with the pattern of cognitive change, frontal lobe abnormalities have been demonstrated in MND both on structural [ 2 , 17 ] and functional [ 1 , 18 ] imaging. bvFTD may precede, follow or coincide with the onset of motor symptoms [ 24 ], reinforcing the inter-relationship between the two disorders.…”

Section: Introductionmentioning

confidence: 86%

Pathological tau deposition in Motor Neurone Disease and frontotemporal lobar degeneration associated with TDP-43 proteinopathy

Behrouzi

et al. 2016

acta neuropathol commun

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It has been suggested that patients with motor neurone disease (MND) and those with MND combined with behavioural variant frontotemporal dementia (bvFTD) (ie FTD + MND) or with FTD alone might exist on a continuum based on commonalities of neuropathology and/or genetic risk. Moreover, it has been reported that both a neuronal and a glial cell tauopathy can accompany the TDP-43 proteinopathy in patients with motor neurone disease (MND) with cognitive changes, and that the tauopathy may be fundamental to disease pathogenesis and clinical phenotype. In the present study, we sought to substantiate these latter findings, and test this concept of a pathological continuum, in a consecutive series of 41 patients with MND, 16 with FTD + MND and 23 with FTD without MND. Paraffin sections of frontal, entorhinal, temporal and occipital cortex and hippocampus were immunostained for tau pathology using anti-tau antibodies, AT8, pThr175 and pThr217, and for amyloid β protein (Aβ) using 4G8 antibody. Twenty four (59 %) patients with MND, 7 (44 %) patients with FTD + MND and 10 (43 %) patients with FTD showed ‘significant’ tau pathology (ie more than just an isolated neurofibrillary tangle or a few neuropil threads in one or more brain regions examined). In most instances, this bore the histological characteristics of an Alzheimer’s disease process involving entorhinal cortex, hippocampus, temporal cortex, frontal cortex and occipital cortex in decreasing frequency, accompanied by a deposition of Aβ up to Thal phase 3, though 2 patients with MND, and 1 with FTD did show tau pathology beyond Braak stage III. Four other patients with MND showed novel neuronal tau pathology, within the frontal cortex alone, specifically detected by pThr175 antibody, which was characterised by a fine granular or more clumped aggregation of tau without neurofibrillary tangles or neuropil threads. However, none of these 4 patients had clinically evident cognitive disorder, and this type of tau pathology was not seen in any of the FTD + MND or FTD patients. Finally, two patients, one with MND and one with FTD, showed a tau pathology consistent with Argyrophilic Grain Disease (AGD). Western blotting and use of 3- and 4-repeat tau antibodies confirmed the histological interpretation of Alzheimer’s disease type pathology in all instances except for those patients with accompanying AGD where a banding pattern on western blot, and immunohistochemistry, confirmed 4-repeat tauopathy. In all 3 patient groups, amyloid pathology was more likely to be present in patients dying after 65 years of age, and in the presence of APOE ε4 allele. We conclude that tau pathological changes are equally common amongst patients with MND, FTD + MND and FTD though, in most instances, these are limited in extent. In patients with MND, when cognitive impairment is present this is most likely due to an accompanying/evolving (coincidental) Alzheimer’s disease process or, as in a single case, Dementia with Lewy bodies, within the cerebral cortex rather than as a result of TDP-43 prote...

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“…Patients with arterial stenosis >50% ipsilateral to an SDI are often classified as having a nonlacunar infarction. 29,30 However, whether the arterial disease is the actual cause of the SDI or a coincidental disease occurring in a patient with symptomatic small vessel disease remains unclear. 31 Symptomatic carotid stenosis derives greater benefit from vascular intervention compared to asymptomatic carotid stenosis.…”

Section: Arterial Small Deep Infarctsmentioning

confidence: 99%

“…32,33 Other studies also suggest that arterial disease is the cause of some SDIs, with the degree of vascular stenosis, intima medial thickness, and arterial stiffness all having been reported as predictors of nonlacunar stroke. 7,18,29,30,[34][35][36][37][38][39][40][41][42] Additionally, Tejada et al reported a 7% absolute increase in ipsilateral compared to contralateral carotid stenosis in patients with SDIs, suggesting that carotid disease contributes to some SDIs. 43 However, this finding has not been demonstrated by others.…”

Section: Arterial Small Deep Infarctsmentioning

confidence: 99%

Profiles of lacunar and nonlacunar stroke

Jickling¹,

Stamova²,

Ander³

et al. 2011

Annals of Neurology

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Objective Determining which small deep infarcts (SDI) are of lacunar, arterial or cardioembolic etiology is challenging, but important in order to deliver optimal stroke prevention therapy. We sought to distinguish lacunar from non-lacunar causes of SDI using a gene expression profile. Methods A total of 184 ischemic strokes were analyzed. Lacunar stroke was defined as a lacunar syndrome with infarction <15mm in a region supplied by penetrating arteries. RNA from blood was processed on whole genome microarrays. Genes differentially expressed between lacunar (n=30) and non-lacunar strokes (n=86) were identified (false discovery rate ≤0.05, fold change>|1.5|) and used to develop a prediction model. The model was evaluated by cross-validation and in a second test cohort (n=36). The etiology of SDI of unclear cause (SDI≥15mm or SDI with potential embolic source) (n=32) was predicted using the derived model. Results A 41 gene profile discriminated lacunar from non-lacunar stroke with greater than 90% sensitivity and specificity. Of the 32 SDI of unclear cause, 15 were predicted to be lacunar and 17 were predicted to be non-lacunar. The identified profile represents differences in immune response between lacunar and non-lacunar stroke. Interpretation Profiles of differentially expressed genes can distinguish lacunar from non-lacunar stroke. SDIs of unclear cause were frequently predicted to be of non-lacunar etiology, suggesting comprehensive workup of SDI is important to identify potential cardioembolic and arterial causes. Further study is required to evaluate the gene profile in an independent cohort and determine the clinical and treatment implications of SDI of predicted non-lacunar etiology.

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Markers of lacunar stroke in patients with moderate internal carotid artery stenosis

Cited by 9 publications

References 39 publications

Ultrasonographic Markers of Vascular Risk in Patients with Asymptomatic Carotid Stenosis

Ultrasonographic Markers of Vascular Risk in Patients with Asymptomatic Carotid Stenosis

Pathological tau deposition in Motor Neurone Disease and frontotemporal lobar degeneration associated with TDP-43 proteinopathy

Profiles of lacunar and nonlacunar stroke

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