Brain Atrophy Is Related to Lacunar Lesions and Tissue Microstructural Changes in CADASIL

Jouvent, Éric; Viswanathan, Anand; Mangin, Jean‐François; O'Sullivan, Michael J.; Guichard, Jean‐Pierre; Gschwendtner, Andreas; Cumurciuc, R.; Buffon, Frédérique; Peters, Nils; Pachaï, Chahin; Bousser, Marie‐Germaine; Dichgans, Martin; Chabriat, Hugues

doi:10.1161/strokeaha.106.478263

Cited by 96 publications

(116 citation statements)

References 26 publications

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“…Volume of lacunes (LL V ) and that of white matter hyperintensities of presumed vascular origin (WMH V ) as well as number of microbleeds (MB N ) were measured in all participants from 3D T1, fluid-attenuated inversion recovery, and T2* sequences, respectively, using validated methods detailed previously and in agreement with the STRIVE criteria. 12,13 Brain parenchymal fraction (BPF) was defined as the ratio of brain tissue volume to the intracranial cavity volume. 12 Statistical analyses.…”

Section: 9-11mentioning

confidence: 99%

Prediction of 3-year clinical course in CADASIL

et al. 2016

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Objective: To obtain simple models predicting disease evolution at 3 years for a given patient with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).Methods: Based on data obtained in a prospective study of 236 patients, we built and validated models predicting, at the individual level, 3-year changes in Mini-Mental State Examination (MMSE), Mattis Dementia Rating Scale (MDRS), Trail Making Test version B (TMTB), and modified Rankin Scale (mRS). These models were based on different sets of predictors obtained at baseline, including either clinical data (epidemiologic data and cardiovascular risk factors) or clinical data and quantitative MRI markers (volume of lacunes [LL V ], volume of white matter hyperintensities, normalized brain volume [BPF], number of microbleeds). The Bayesian information criterion (BIC) and the coefficient of determination (R 2 ) were used to determine models with the highest predictive ability and the lowest numbers of predictors. Results:We obtained validated models with a demonstrated ability to predict, for a given patient, 3-year changes in MMSE, MDRS, TMTB, and mRS (R 2 on independent samples: 0.22, 0.12, 0.09, and 0.17, respectively). In all cases, the best models according to R 2 and BIC values included only the baseline values of the outcome, of BPF, and of LL V . Inclusion of other potential predictors always led to a loss of generalizability. Conclusions:The prediction of 3-year changes in MMSE, MDRS, TMTB, and mRS for a given patient with CADASIL can be obtained using simple models relying only on the initial values of the considered score, BPF, and LL V . Neurology ® 2016;87:1787-1795 GLOSSARY BIC 5 Bayesian Information Criterion; BPF 5 brain parenchymal fraction; CADASIL 5 cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; CI 5 confidence interval; LLV 5 volume of lacunes; MBN 5 number of microbleeds; MDRS 5 Mattis Dementia Rating Scale; MMSE 5 Mini-Mental State Examination; mRS 5 modified Rankin Scale; MSPE 5 mean squared prediction error; SVD 5 small vessel disease; TMTB 5 Trail Making Test part B; WMHV 5 white matter hyperintensities of presumed vascular origin.Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most frequent hereditary cerebral small vessel disease (SVD), caused by mutations of the NOTCH3 gene.1 In CADASIL, the clinical course appears highly variable. Some patients develop dementia and become heavily disabled around their 50s while others live independently during their 80s.2 Age, male sex, active smoking, brain atrophy, and volume of lacunes are associated with clinical severity and with further clinical worsening, 3-5 while associations between other factors, such as blood pressure, number of microbleeds, or volume of white matter hyperintensities, and clinical severity have been inconsistently observed. 6,7 Among all these factors, those that actually predict disease evolution for a given patient...

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Section: 9-11mentioning

confidence: 99%

Prediction of 3-year clinical course in CADASIL

et al. 2016

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“…Atrophy is usually considered as a marker of Alzheimer's disease 27 , although it has been also reported as the consequence of pure vascular lesions 28 . There is actual evidence that global brain atrophy 29,30 and medial temporal lobe atrophy can also be the consequence of pure vascular disorders 28 .…”

Section: Mechanisms Of Pre-existing Cognitive Impairmentmentioning

confidence: 99%

Stroke occurring in patients with cognitive impairment or dementia

Moulin

Leys

2017

Arq. Neuro-Psiquiatr.

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Stroke survivors are at risk for (i) new vascular events such as recurrent stroke 1 , myocardial infarction 2 or vascular death 3 ; (ii) complications of treatments 4 ; and (iii) delayed neurological complications, such as epileptic seizures 5,6 , cognitive impairment 7,8 , depression 9 , and pain 10 . Cognitive impairment is one of the major causes of dependency after stroke 7,8 .It is quite frequent that cognitive impairment, or even dementia, was already present before the stroke 7,8 . Stroke and cognitive impairment are both common, occur in the same age category, and share similar risk factors 11 . Moreover, stroke lesions can lead to cognitive impairment, alone or in association with Alzheimer pathology 11 . Most studies on the relationship between stroke and cognitive impairment have focused on cognitive impairment occurring after stroke, or on patients with cognitive impairment who have "apparently silent" brain lesions of vascular origin. However, although one patient in six admitted for a stroke was already demented before the stroke 7,12,13,14 , and probably many more were cognitively impaired, little is known about the characteristics of stroke occurring in patients with pre-existing cognitive decline, and about the optimal management of stroke in these patients. ABSTRACTOne in six patients admitted for stroke was previously demented. These patients have less access to appropriate stroke care, although little is known about their optimal management. Objective: To determine how pre-stroke cognitive impairment can be detected, its mechanism, and influence on outcome and management. Methods: Literature search. Results: (i) A systematic approach with the Informant Questionnaire of Cognitive Decline in the Elderly is recommended; (ii) Pre-stroke cognitive impairment may be due to brain lesions of vascular, degenerative, or mixed origin; (iii) Patients with pre-stroke dementia, have worse outcomes, more seizures, delirium, and depression, and higher mortality rates; they often need to be institutionalised after their stroke; (iv) Although the safety profile of treatment is not as good as that of cognitively normal patients, the risk:benefit ratio is in favour of treating these patients like others. Conclusion: Patients with cognitive impairment who develop a stroke have worse outcomes, but should be treated like others.Keywords: stroke; cerebral infarction; cerebral hemorrhage; dementia; mild cognitive impairment. RESUMOUm em cada seis pacientes internados em decorrência de acidente vascular cerebral (AVC) apresenta diagnóstico prévio de demência. Estes indivíduos têm menor acesso à assistência recomendada para pacientes com AVC, mas pouco ainda se sabe em relação aos cuidados médicos ideais que devem receber. (ii) O comprometimento cognitivo preexistente pode ser devido a lesões cerebrais de origem vascular, degenerativa ou mista; (iii) Pacientes com demência prévia ao AVC têm pior prognóstico, maior frequência de crises epilépticas, de delirium e depressão, além de taxas de mortalidade mais altas; eles ...

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“…6,7 Image Processing 3D T1-weighted images were segmented to obtain brain masks for GM and WM by using the Morphologist pipeline of BrainVISA (http://www.brainvisa.info), which relies on a histogram analysis algorithm performed after a first step consisting of field inhomogeneity bias correction. 12 Lacunar lesions were defined on T1-weighted images as hypointense lesions with a signal identical to that of CSF, a diameter of Ͼ3 mm, and a distinct shape from that of enlarged perivascular spaces. 13 Microhemorrhages were defined as rounded foci of signal loss with a diameter inferior to 5 mm on gradient-echo sequences and distinct from vascular flow voids, leptomeningeal hemosiderosis, or nonhemorrhagic mineralization.…”

Section: Mr Imaging Protocolmentioning

confidence: 99%

Decreased T1 Contrast between Gray Matter and Normal-Appearing White Matter in CADASIL

Guio

Reyes

Duering

et al. 2013

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:CADASIL is the most frequent hereditary small-vessel disease of the brain. The clinical impact of various MR imaging markers has been repeatedly studied in this disorder, but alterations of contrast between gray matter and normal-appearing white matter remain unknown. The aim of this study was to evaluate the contrast alterations between gray matter and normal-appearing white matter on T1-weighted images in patients with CADASIL compared with healthy subjects.

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Brain Atrophy Is Related to Lacunar Lesions and Tissue Microstructural Changes in CADASIL

Cited by 96 publications

References 26 publications

Prediction of 3-year clinical course in CADASIL

Prediction of 3-year clinical course in CADASIL

Stroke occurring in patients with cognitive impairment or dementia

Decreased T1 Contrast between Gray Matter and Normal-Appearing White Matter in CADASIL

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