New cerebral microbleeds in ischemic stroke patients on warfarin treatment: Two-year follow-up

Örken, Dilek Neci̇oğlu; Uysal, Ender; Timer, Emin; Kuloglu-Pazarcı, N.; Mumcu, S.; Forta, Hulki

doi:10.1016/j.clineuro.2013.03.004

Cited by 37 publications

(19 citation statements)

References 19 publications

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“…A recent longitudinal study has shown that the frequency of new MBs was increased in warfarin-treated patients with ischemic stroke during follow-up of 2 years. 31 Other studies reported previously that warfarin treatment had no significant effects on MBs frequency. 32,33 Rotterdam Scan study described that antiplatelet medication increased significantly the presence of MBs in nondemented population of more than 60 years of age.…”

Section: Discussionmentioning

confidence: 98%

Prevalence and Clinicoradiological Analyses of Patients with Alzheimer Disease Coexisting Multiple Microbleeds

Nagasawa¹,

Kiyozaka²,

Ikeda³

2014

Journal of Stroke and Cerebrovascular Diseases

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Section: Discussionmentioning

confidence: 98%

Prevalence and Clinicoradiological Analyses of Patients with Alzheimer Disease Coexisting Multiple Microbleeds

Nagasawa¹,

Kiyozaka²,

Ikeda³

2014

Journal of Stroke and Cerebrovascular Diseases

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“…There are only a few longitudinal studies available. [61][62][63][64] Although Gregoire et al 64 report on the predictive value of baseline microbleeds considering executive functions over 5.7 years, Meier et al 62 report on decreasing executive functions if at least two microbleeds are present. Liem et al 61 identified increasing cognitive decline with increasing number of incident microbleeds in CADASIL patients over 7 years of follow-up.…”

Section: Microbleedsmentioning

confidence: 99%

“…Moreover, patients with warfarin therapy and baseline microbleeds had an increased risk for additional microbleeds. 63 Because of the lack of clinical correlative data the validation status of these lesions as a possible surrogate marker in vascular cognitive impairment trials has to be considered incomplete and sample size calculations are thus not provided.…”

Section: Microbleedsmentioning

confidence: 99%

Longitudinal change of small-vessel disease-related brain abnormalities

Schmidt

Seiler

Loitfelder

2015

J Cereb Blood Flow Metab

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Knowledge about the longitudinal change of cerebral small-vessel disease-related magnetic resonance imaging abnormalities increases our pathophysiologic understanding of cerebral microangiopathy. The change of specific lesion types may also serve as secondary surrogate endpoint in clinical trials. A surrogate endpoint needs to progress fast enough to allow monitoring of treatment effects within a reasonable time period, and change of the brain abnormality needs to be correlated with clinical change. Confluent white matter lesions show fast progression and correlations with cognitive decline. Thus, the change of confluent white matter lesions may be used as a surrogate marker in proof-of-concept trials with small patient numbers needed to show treatment effects on lesion progression. Nonetheless if the expected change in cognitive performance resulting from treatment effects on lesion progression is used as outcome, the sample size needed to show small to moderate treatment effects becomes very large. Lacunes may also fulfill the prerequisites of a surrogate marker, but in the general population the incidence of lacunes over short observational periods is small. For other small-vessel disease-related brain abnormalities including microbleeds and microstructural changes in normalappearing white matter longitudinal change and correlations with clinical decline is not yet fully determined.

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“…CMBs have also been implicated as a risk factor for intracerebral hemorrhage following anticoagulant or antiplatelet therapy. 21,22 Tightly controlling vascular risk factors reduces the progression of hCSVD, which might prevent new-onset CMBs and the rate of hemorrhagic complications in patients with combined amyloid and hCSVD.…”

Section: Increased Overallmentioning

confidence: 99%

Synergistic effects of longitudinal amyloid and vascular changes on lobar microbleeds

Kim

Park

et al. 2016

Neurology

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Objective: To determine whether amyloid and hypertensive cerebral small vessel disease (hCSVD) changes synergistically affect the progression of lobar microbleeds in patients with subcortical vascular mild cognitive impairment (svMCI).Methods: Among 72 patients with svMCI who underwent brain MRI and [11 C] Pittsburgh compound B (PiB)-PET, 52 (72.2%) completed the third year of follow-up. These patients were evaluated by annual neuropsychological testing, brain MRI, and follow-up PiB-PET.Results: Over 3 years, 31 of 52 patients (59.6%) had incident cerebral microbleeds (CMBs) in the lobar and deep regions. Both baseline and longitudinal changes in lacune numbers were associated with increased numbers of lobar and deep microbleeds, while baseline and longitudinal changes in PiB uptake ratio were associated only with the progression of lobar microbleeds, especially in the temporal, parietal, and occipital areas. Regional white matter hyperintensity severity was also associated with regional lobar CMBs in the parietal and occipital regions. There were interactive effects between baseline and longitudinal lacune number and PiB retention on lobar microbleed progression. Increased lobar, but not deep, CMBs were associated with decreased scores in the digit span backward task and Rey-Osterrieth Complex Figure Alzheimer disease (AD) and hypertensive cerebral small vessel disease (hCSVD) are major causes of cognitive impairment in the elderly.1,2 There is increasing evidence that AD pathologies and hCSVD coexist and interact in individuals with cognitive impairment.3 Recent amyloid PET studies suggested that approximately 30% of patients with extensive hCSVD also had amyloid lesions of the brain, showing a relationship between amyloid and hCSVD and their clinical relevance. 4,5 Cerebral microbleeds (CMBs) have generated a great deal of interest, since they are thought to result from 2 key age-related small vessel pathologies, cerebral amyloid angiopathy (CAA) and hCSVD, which may have different underlying causes and mechanisms. 6,7 The topography of

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New cerebral microbleeds in ischemic stroke patients on warfarin treatment: Two-year follow-up

Cited by 37 publications

References 19 publications

Prevalence and Clinicoradiological Analyses of Patients with Alzheimer Disease Coexisting Multiple Microbleeds

Prevalence and Clinicoradiological Analyses of Patients with Alzheimer Disease Coexisting Multiple Microbleeds

Longitudinal change of small-vessel disease-related brain abnormalities

Synergistic effects of longitudinal amyloid and vascular changes on lobar microbleeds

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