Cortical Cerebral Microbleeds Research Articles

Microbleeds colocalize with enlarged juxtacortical perivascular spaces in amnestic mild cognitive impairment and early Alzheimer’s disease: A 7 Tesla MRI study

MRI-visible perivascular spaces (PVS) in the semioval centre are associated with cerebral amyloid angiopathy (CAA), but it is unknown if PVS co-localize with MRI markers of CAA. To examine this, we assessed the topographical association between cortical cerebral microbleeds (CMBs) – as an indirect marker of CAA – and dilatation of juxtacortical perivascular spaces (jPVS) in 46 patients with amnestic mild cognitive impairment (aMCI) or early Alzheimer’s disease (eAD). The degree of dilatation of jPVS <1 cm around each cortical CMBs was compared with a similar reference site (no CMB) in the contralateral hemisphere, using a 4-point scale. Also, jPVS dilatation was compared between patients with and without cortical CMBs. Eleven patients (24%) had cortical CMBs [total=35, median=1, range=1–14] of whom five had >1 cortical CMBs. The degree of jPVS dilatation was higher around CMBs than at the reference sites [Wilcoxon signed rank test, Z = 2.2, p = 0.03]. Patients with >1 cortical CMBs had a higher degree of jPVS dilation [median=2.2, IQR = 1.8–2.3] than patients without cortical CMBs [median=1.4, IQR = 1.0–1.8], p = 0.02. We found a topographical association between a high degree of jPVS dilatation and cortical CMBs, supporting a common underlying pathophysiology – most likely CAA.

P98. CSF NFL – A new biomarker for neurodegeneration in CSVD?

Background Cerebrospinal fluid (CSF) neurofilament light chain (NfL) has emerged as a putative biomarker of neuroaxonal injury in various neurodegenerative diseases. Particularly, patients suffering from amyotrophic lateral sclerosis (ALS) display significantly elevated levels. We here aimed to compare CSF NfL between patients diagnosed to have cerebral small vessel disease (CSVD) and those exhibiting ALS. Supposing there to be some shared mechanisms of white matter injury we suspected to find similarly increased CSF NfL levels across the diagnostic groups. Methods Our analysis comprised (i) n = 22 patients with CSVD, defined according to the detectability of subcortical and cortical cerebral microbleeds and/or intracerebral hemorrhages (ICH), (ii) n = 39 patients diagnosed to have definite, probable or probable laboratory-supported ALS according to the El Escorial criteria and (iii) n = 31 hospital- and community-based control subjects. All cases were matched for age and sex, and all of them had CSF NfL levels available. In CSVD, cerebral MRIs were rated for the number of (i) cerebral microbleeds, (ii) enlarged perivascular spaces, (iii) lacunes and, for the existence of (a) cortical superficial siderosis and (b) white matter hyperintensities (WMH). WMH have thereby been assessed in a semiquantitative manner according to the Fazeka’s visual rating scale ranging from 0 to 3 and according to the existence of different patterns (multiple subcortical spots, peri-basal ganglia WMH, anterior subcortical patches, posterior subcortical patches). ANOVA was conducted with CSF NfL as dependent variable and group as a fixed factor; for subgroup comparisons Bonferroni adjusted post hoc analysis was performed. In CSVD, bivariate correlations and Mann–Whitney U test were calculated to relate CSF NfL levels to the various MRI measures. P-values £ 0.05 were deemed to be statistically significant. Results When considering the whole cohort CSF NfL levels were not related to age or sex. Analysis revealed a significant group effect (F(2) = 10.5, p ρ = 0.4, p = 0.04, one-tailed). Higher CSF NfL concentrations were, moreover, related to the existence of peri-basal ganglia WMH (Z = 1.9, p = 0.06 [trend-level]). Discussion Our data demonstrate that CSF NfL could serve as a biomarker for neuroaxonal injury in CSVD subjects, revealing similarly elevated concentrations as those found in ALS. In CSVD CSF NfL thereby seems to reflect the extent and patterns of white matter damage, as expected.

Cerebral Microbleeds in Cerebrovascular and Neurodegenerative Diseases with Cognitive Impairments

Objectives. To identify the significance of cerebral microbleeds (CMB) in the diagnosis of the main cerebrovascular and neurodegenerative diseases with cognitive impairments (CI). Materials and methods. MRI scans (1.5 T, T2* regime, gradient echo) were performed in 120 patients with Alzheimer’s disease (AD), Lewy body dementia (LBD), and vascular dementia to study CMB, their influence on the state of cognitive functions, and links with signs of vascular and neurodegenerative brain lesions. Neuropsychological studies were performed using the Montreal and Addenbrooke scales, including assessment of speech activity, the clock drawing test, and the pictures test. Results and discussion. CMB were detected in more than 1/3 patients with neurodegenerative and cerebrovascular pathologies; cortical CMB were mostly seen in neurodegenerative pathology and subcortical in cerebrovascular pathology, and these locations can be used for differential diagnosis. Single subcortical CMB were seen in 48% of patients with LBD, and these were accompanied by smaller numbers of lacunar infarcts and a lower severity of leukoaraiosis. In AD with additional signs of LBD and cerebrovascular disease, CMB was encountered more frequently (60%) and was a criterion for mixed pathology. Conclusions. Leukoaraiosis has great clinical significance in neurodegenerative and cerebrovascular diseases with CI, if accompanied by CMB. The presence of CMB is a marker for severe CI and a predictor for mixed pathology in CMB located cortically-subcortical and the corresponding neuropsychological profile.

Are the cortical cerebral microbleeds (CMB) present in dementia with Lewy bodies?

Are the cortical cerebral microbleeds (CMB) present in dementia with Lewy bodies?

Brain MRI Findings in Neurologically Asymptomatic Patients with Infective Endocarditis

Neurologic complications in infective endocarditis are frequent and affect patient prognosis negatively. Additionally, detection of asymptomatic lesions by MR imaging could help early management of this condition. The objective of our study was to describe MR imaging characteristics of cerebral lesions in a neurologically asymptomatic population with infective endocarditis. One hundred nine patients at the acute phase of a definite or possible infective endocarditis according to the Duke modified criteria and without neurologic manifestations according to the NIHSS were prospectively included. Each patient underwent cerebral MR imaging and MRA within 7 days of admission. MR imaging showed abnormalities in 78 patients (71.5%). Acute ischemic lesions (40 patients, 37%) and cerebral microbleeds (62 patients, 57%) were the most frequent lesions. Eight patients had an acute SAH, 3 patients had brain microabscesses, 3 had a small cortical hemorrhage, and 3 had a mycotic aneurysm. Acute ischemic lesions mostly appeared as multiple small infarcts disseminated in watershed territories (25/40, 62.5%) and as lesions of different ages (21/40, 52.5%). Cerebral microbleeds were preferentially distributed in cortical areas (362/539 cerebral microbleeds, 67%). No significant correlation was found among lesions, in particular between acute ischemia and cerebral microbleeds. Occult cerebral lesions, in particular cerebral microbleeds and acute ischemic lesions, are frequent in infective endocarditis. The MR imaging pattern of acute small infarcts of different ages predominating in watershed territories and cortical cerebral microbleeds may represent a surrogate imaging marker of infective endocarditis.

Nicholas John Unsworth

<h3>BACKGROUND AND PURPOSE:</h3> Neurologic complications in infective endocarditis are frequent and affect patient prognosis negatively. Additionally, detection of asymptomatic lesions by MR imaging could help early management of this condition....