Incident lacunes influence cognitive decline

Jokinen, Hanna; Gouw, Alida A.; Madureira, Sofia; Ylikoski, Raija; Straaten, E.C.W. van; Flier, Wiesje M. van der; Barkhof, Frederik; Scheltens, Philip; Fazekas, Franz; Schmidt, Reinhold; Verdelho, Ana; Ferro, José M.; Pantoni, Leonardo; Inzitari, Domenico; Erkinjuntti, Timo

doi:10.1212/wnl.0b013e31821d752f

Cited by 183 publications

(160 citation statements)

References 34 publications

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“…26 In the LADIS study, a relationship between incident lacunes at 3-year followup and steeper decline in executive functions and psychomotor speed was reported. 57 According to the previously published data on the rate of incident lacunes, 12,26,30,53,54 detection of a 20% treatment effect in a 3-year trial with 80% power would require samples sizes in the range between 1,540 and 3,678 patients. All calculations assumed a power of 80% at a two-sided significance level of 5%.…”

Section: Lacunesmentioning

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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Section: Lacunesmentioning

confidence: 99%

Longitudinal change of small-vessel disease-related brain abnormalities

Schmidt

Seiler

Loitfelder

2015

J Cereb Blood Flow Metab

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“…Lacunar infarcts: Are rounded, < 20 mm diameter lesions, founded more frequently in the basal ganglia, associated with SVD and a strong predictor of VCI [11]. They are caused by acute occlusion of small perforating cerebral arteries or embolism from upstream vessels [12].…”

Section: Neuropathological Alterations Caused By Cerebral Svd Linked mentioning

confidence: 99%

Cardiovascular Alterations in Patients with Dementia

2017

JCCR

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Submit Manuscript | http://medcraveonline.com one of the most susceptible being the brain [1]. Hypertension is a major risk factor for vascular cognitive impairment (VCI) and for Alzheimer disease (AD), the most frequent causes of dementia in the elderly [3]. Continuous elevation in blood pressure has progressive effects on the structure and function of cerebral arteries determining adaptive changes like remodeling, aiming to decrease the mechanical stress on the arterial wall [4]. Remodeling could be hypertrophic or eutrophic and reduces the vesselsˈ lumen increasing the vascular resistance and represents a potential risk factor for cardiovascular and cerebrovascular disease [5].Old hypertension also induces an increase in the stiffness of large arteries which is a good predictor of cognitive decline and stroke and is associated with silent brain lesions [3,6]. HTN is a major risk factor for atherosclerosis. Increase in BP increases the odds of complex aortic atherosclerosis, predictive of ischemic strokes [7]. Atherosclerotic lesions are localised at the site of turbulence of the flow like the carotid bifurcation and the vertebrobasilar system and less frequently in intracranial arteries. Stroke can be produced by releasing fragments from atherosclerotic plaques (artery-to-artery embolism) or by rupture and hemorrhage with acute cerebrovascular occlusions.HTN also provokes small vessel disease (SVD) in which the most frequent pathological substrate is arteriolosclerosis [8], affecting the deep hemispheric white matter and basal ganglia. One of the pathological features of arteriosclerosis is lipohyalinosis [8] and in advanced lesions rupture of the vessel with microscopic or macroscopic hemorrhages disposed typically in basal ganglia or thalamus. Capillary rarefaction induces lesions in the periventricular white matter. Brain alterations underlying VCIVCI includes a spectrum of cognitive alterations due to cerebrovascular factors, ranging from mild to full blown vascular dementia impairing the daily lifeˈs activities [3]. A major cause of cognitive impairment is stroke. Having a stroke doubles the risk of dementia (poststroke dementia) [3]. The risk of VCI is incresed in patients with no history of stroke but with brain infarcts (silent infarcts) at imagistic investigations. Strategic-infarct dementia is produced by a single stroke affecting a region important for cognition like the frontal lobe or the thalamus [3]. Multi-infarct dementia can also results from multiple strokes destroying large amounts of brain tissue [3]. SVD is a major cause of VCI, being responsible for up to 45 % of dementia cases [3]. Neuropathological alterations caused by cerebral SVD linked with VCILacunar infarcts: Are rounded, < 20 mm diameter lesions, founded more frequently in the basal ganglia, associated with SVD and a strong predictor of VCI [11]. They are caused by acute occlusion of small perforating cerebral arteries or embolism from upstream vessels [12]. Recent studies show the possibility that blood-brain barrier (BBB) alte...

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“…The Leukoaraiosis and Disability Study (LADIS) 28 Asymptomatic progression of small-artery disease was a characteristic feature. The individual contribution of silent lacunes on cognition was modest, but the asymptomatic lacunes found on MRI should not be considered a benign vascular condition, but rather a potentially severe disease as a risk indicating progressive cognitive decline requiring adequate and rigorous therapeutic control and medical follow up.…”

Section: -27mentioning

confidence: 99%

“…The individual contribution of silent lacunes on cognition was modest, but the asymptomatic lacunes found on MRI should not be considered a benign vascular condition, but rather a potentially severe disease as a risk indicating progressive cognitive decline requiring adequate and rigorous therapeutic control and medical follow up. 28 However, this clinical and neuropsychological aspect is still poorly studied. Long-term follow-up studies with large samples should be carried out to assess the outcome of patients with silent lacunes and to determine clinical and neuroimaging predictors of cognitive decline.…”

Section: -27mentioning

confidence: 99%

Cognitive Impairment in Ischaemic Lacunar Stroke

Arboix¹,

Blanco-Rojas²

2013

European Neurological Review

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Ischaemic cerebral small-vessel disease (SVD) can be visualised on brain magnetic resonance imaging (MRI) scans as lacunar infarcts, white matter hyperintensities and cerebral microbleeds, and has been recognised as the most frequent cause of cognitive impairment of vascular origin. Lacunar infarction is the most common manifestation of SVD and accounts for approximately 25 % of all brain infarctions. In patients with first-ever lacunar infarction, more than half of cases show impairment of the executive functions and meet criteria of mild vascular cognitive impairment. Lacunar stroke is an important predictor of post-stroke cognitive decline and vascular dementia. In the wellcharacterised cohort of 1,636 lacunar stroke patients of the Secondary Prevention of Small Subcortical Strokes (SPS3) trial, mild cognitive impairment was present in nearly half of participants and was an important complication of lacunar stroke more prevalent than physical disability. The cognitive profile identified to be associated with ischaemic cerebral SVD includes preserved memory with attention deficits and executive functioning impairment. However, in a recent systematic review of cognitive impairment in lacunar ischaemic stroke, impaired cognition appears less selective than previously thought, involving episodic memory and all major cognitive domains. Brain atrophy is also a feature of ischaemic cerebral SVD. Cognitive dysfunction in lacunar stroke sufferers is frequently overlooked in routine clinical practice and may be as common and clinically relevant as motor and sensory sequelae. KeywordsLacunar infarct, brain atrophy, prognosis, cognitive impairment, neuropsychology, cerebral small-vessel disease, brain atrophy Disclosure: The authors have no conflicts of interest to declare. Acknowledgements:The authors thank Marta Grau-Olivares for her contribution in searching the literature and helpful constructive comments and Marta Pulido for editing the manuscript and editorial assistance.

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Incident lacunes influence cognitive decline

Cited by 183 publications

References 34 publications

Longitudinal change of small-vessel disease-related brain abnormalities

Longitudinal change of small-vessel disease-related brain abnormalities

Cardiovascular Alterations in Patients with Dementia

Cognitive Impairment in Ischaemic Lacunar Stroke

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