Nocturnal Hypoxemia Is Associated with White Matter Hyperintensities in Patients with a Minor Stroke or Transient Ischemic Attack

Background Temporary and permanent cognitive changes following transient ischemic attack/minor stroke have been described previously. It is unknown if persisting cognitive deficits in these patients are correlated with acute infarction identified using magnetic resonance imaging. Aims We tested the hypothesis that persistent cognitive impairment after transient ischemic attack/minor stroke can be predicted by the volume of diffusion-weighted imaging lesions. Methods Acute transient ischemic attack/minor stroke (NIH stroke scale score ≤ 3) patients were prospectively recruited within 72 h of onset. Patients underwent Montreal cognitive assessment and magnetic resonance imaging, including diffusion-weighted imaging and Fluid-Attenuated Inverse Recovery sequences, at baseline, days 7 and 30. Cognitive testing was repeated at day 90. Diffusion-weighted imaging lesion and Fluid-Attenuated Inverse Recovery chronic white matter hyperintensity volumes were measured planimetrically. Cognitive impairment was defined a priori as Montreal cognitive assessment score < 26. Results One hundred fifteen patients were imaged at a median (inter-quartile range) of 24.0 (16.6) h after onset. Acute ischemic lesions were present in 91 (79%) patients. Cognitive impairment rates were similar in patients with (47/91, 52%) and without diffusion-weighted imaging lesions (13/24, 54%; p = 0.83). Although linear regression indicated no relationship between acute diffusion-weighted imaging lesion volume and day 30 Montreal cognitive assessment scores (β = −0.163, [−2.243, 0.334], p = 0.144), white matter hyperintensity volumes at baseline were predictive of persistent cognitive deficits after 30 days (β = 2.24, [1.956, 45.369], p = 0.005). Conclusions In most transient ischemic attack/minor stroke patients who suffer acute cognitive impairment post event, deficits are temporary. Deficits after 30 days of onset are correlated with chronic white matter hyperintensity, suggesting subclinical cognitive impairment and/or impaired ability to compensate for the effects of acute ischemic infarcts.

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Cognition in the First Year After a Minor Stroke, Transient Ischemic Attack, or Mimic Event and the Role of Vascular Risk Factors

Frontiers in Neurology ◽

10.3389/fneur.2020.00216 ◽

2020 ◽

Vol 11 ◽

Author(s):

Korinne Nicolas ◽

Christopher Levi ◽

Tiffany-Jane Evans ◽

Patricia T. Michie ◽

Parker Magin ◽

...

Keyword(s):

Risk Factors ◽

Transient Ischemic Attack ◽

Vascular Risk Factors ◽

Minor Stroke ◽

First Year ◽

Vascular Risk ◽

Ischemic Attack ◽

A Minor

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Abstract WP56: Refinement of imaging predictors of recurrent events following Transient Ischemic Attack and Minor Stroke.

Stroke ◽

10.1161/str.44.suppl_1.awp56 ◽

2013 ◽

Vol 44 (suppl_1) ◽

Author(s):

Myles Horton

Keyword(s):

White Matter ◽

Transient Ischemic Attack ◽

Recurrent Events ◽

Recurrent Stroke ◽

Initial Assessment ◽

Minor Stroke ◽

White Matter Disease ◽

Ischemic Attack ◽

Symptom Progression ◽

Prior Stroke

Background: Transient ischemic attack (TIA) and minor stroke have a high risk of recurrent stroke. We recently showed in the CATCH study that predefined radiographic abnormalities on CT/CTA and MRI predicted recurrent events after TIA and minor stroke. Specifically, the study recognized the predictive value of CT/CTA abnormalities that were defined apriori: acute ischemia on CT, intracranial or extracranial occlusion or stenosis > 50% (the CT/CTA positive metric), and diffusion-weighted imaging positivity on MRI. Aims: To improve upon the CT, CTA, MRI and clinical parameters that predict recurrent events after TIA and minor stroke. Our secondary aim was to explore predictors of stroke progression versus recurrence. Methods: 510 consecutive TIA and minor stroke patients (NIHSS score of <4) had CT/CTA and most had MRI. Primary outcome was recurrent events (combined outcome of stroke progression or distinct recurrent stroke) within 90 days. Imaging parameters not included in the original CATCH imaging (CT/CTA and MRI) metrics were assessed for prediction of recurrent events. We also completed an exploratory analysis comparing predictors of symptom progression versus recurrence. Results: There were 36 recurrent events (36/510, 7.1% (95%CI: 5.0-9.6)) including 19 progression and 17 recurrent strokes. On CT/CTA: white matter disease, prior stroke, aortic arch focal plaque≥4mm, or intraluminal thrombus did not predict recurrent events. On MRI: white matter disease, prior stroke, and microbleeds did not predict recurrent events. The only additional clinical predictor was symptom fluctuation (hazard ratio 2.3; 95% CI: 1.05-5.0). Parameters predicting symptom progression included: ongoing symptoms at initial assessment, symptom fluctuation, intracranial occlusion, intracranial occlusion or stenosis, and the CT/CTA metric. No parameter was strongly predictive of recurrent stroke. Conclusions: There was no imaging parameter that could improve upon our original CT/CTA or MRI metrics to predict recurrent events after TIA and minor stroke. Only the addition of symptom fluctuation to the CT/CTA metric improved the prediction of recurrent events. Imaging was more predictive of symptom progression than distinct recurrent events.

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White Matter Imaging Correlates of Early Cognitive Impairment Detected by the Montreal Cognitive Assessment After Transient Ischemic Attack and Minor Stroke

Stroke ◽

10.1161/strokeaha.116.016044 ◽

2017 ◽

Vol 48 (6) ◽

pp. 1539-1547 ◽

Cited By ~ 16

Author(s):

Giovanna Zamboni ◽

Ludovica Griffanti ◽

Mark Jenkinson ◽

Sara Mazzucco ◽

Linxin Li ◽

...

Keyword(s):

Cognitive Impairment ◽

White Matter ◽

Transient Ischemic Attack ◽

Cognitive Assessment ◽

Montreal Cognitive Assessment ◽

Minor Stroke ◽

Ischemic Attack

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Altered Functional Connectivity and Cognition Persists 4 Years After a Transient Ischemic Attack or Minor Stroke

Frontiers in Neurology ◽

10.3389/fneur.2021.612177 ◽

2021 ◽

Vol 12 ◽

Author(s):

Korinne Nicolas ◽

Peter Goodin ◽

Milanka M. Visser ◽

Patricia T. Michie ◽

Andrew Bivard ◽

...

Keyword(s):

Functional Connectivity ◽

Transient Ischemic Attack ◽

Resting State ◽

Minor Stroke ◽

Cerebrovascular Event ◽

Resting State Functional Connectivity ◽

Cognitive Differences ◽

Stroke Group ◽

Ischemic Attack ◽

A Minor

Background and Purpose: Altered executive functions and resting-state functional connectivity (rsFC) are common following a minor stroke or transient ischemic attack (TIA). However, the long-term persistence of these abnormalities is not well-studied. We investigated whether there were cognitive and rsFC differences between (a) controls and minor cerebrovascular event (CVE) patients and (b) between CVE patients with and without an imaging confirmed infarct (i.e., minor stroke and TIA, respectively) at an average of 3.8 years following their event.Methods: Structural and resting-state imaging and cognitive assessments including the Montreal Cognitive Assessment, the Trail Making Task and the National Institute of Health (NIH) Cognition Toolbox were conducted on 42 patients (minor stroke = 17, TIA = 25) and 20 healthy controls (total N = 62).Results: Controls performed better than patients on two measures of executive functioning (both p < 0.046) and had reduced rsFC between the frontoparietal and default mode networks (FPN and DMN, respectively; p = 0.035). No cognitive differences were found between minor stroke and TIA patients, however, rsFC differences were found within the FPN and the DMN (both p < 0.013). Specifically, increased connectivity within the FPN was associated with faster performance in the minor stroke group but not the TIA group (p = 0.047).Conclusions: These findings suggest that transient or relatively minor cerebrovascular events are associated with persistent disruption of functional connectivity of neural networks and cognitive performance. These findings suggest a need for novel interventions beyond secondary prevention to reduce the risk of persistent cognitive deficits.

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Abstract TMP96: Automated Segmentation of White Matter Hyperintensities and Enlarged Perivascular Spaces in a Cohort of Patients With Acute Ischemic Stroke or Transient Ischemic Attack

Stroke ◽

10.1161/str.51.suppl_1.tmp96 ◽

2020 ◽

Vol 51 (Suppl_1) ◽

Author(s):

Kimerly A Powell ◽

Katie M Gallagher ◽

Yousef Hannawi

Keyword(s):

Ischemic Stroke ◽

White Matter ◽

Basal Ganglia ◽

Acute Ischemic Stroke ◽

Transient Ischemic Attack ◽

White Matter Hyperintensities ◽

Perivascular Spaces ◽

Manual Segmentation ◽

Mri Sequences ◽

Ischemic Attack

Introduction: Cerebral Small Vessel Disease (CSVD) is a major cause of acute ischemic stroke (AIS), intracerebral hemorrhage and cognitive impairment. Methods to quantify the disease burden have been largely limited to white matter hyperintensities (WMH) as the disease surrogate and focused mainly on MRI sequences acquired for research purposes. We develop here novel methods to quantify WMH and enlarged perivascular spaces (EPVs) based on clinically acquired MRI sequences in patients with transient ischemic attack (TIA) or AIS. Methods: Subjects presenting with TIA or AIS and had brain MRI within 24 hour of hospital admission were selected for this study. Preprocessing pipeline was developed locally that included bias correction, image rescaling, rigid body registration to the Montreal Neurological Institute (MNI) space, skull stripping and intensity normalization. WMH segmentation was performed using a combination of global thresholding of FLAIR sequences that was spatially restricted to the white matter regions which were defined using a population-based atlas of age matched controls. EPVs in the basal ganglia were segmented on T2 sequences using adaptive thresholding of basal ganglia mask that was created from the ICBM template image and age-matched population average atlas. Segmented objects less than 3 mm in diameter were labelled as EPVs. Validation of the accuracy of EPVs segmentation was performed by expert counting of EPVs and WMH was validated using volume similarity against expert manual segmentation of WMH. Results: 41 patients (age 61.2±16.1, 65% males, 19.5% had TIAs, and 79.5% had AIS) were included. WMH volume was (manual: 21.34±20.48 mls vs automated: 15.74±14.56 mls) achieving a volume similarity of 0.92±0.01. EPVs in the basal ganglia counts were 16.32±5.4 using the automated method. Validation through comparison with manual segmentation of the axial slice with the highest EPVs (Doubal Method) showed significant correlation (Spearman’s rho=0.53, P = 0.0004). Conclusions: We describe successful segmentation of WMH and EPVs on clinically acquired MRI sequences in patients with TIA or AIS. This method will have applications to quantify CSVD burden in large clinical trials and clinical practice.

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