학술논문

White matter hyperintensity volume predicts persistent cognitive impairment in transient ischemic attack and minor stroke.
Document Type
Article
Source
International Journal of Stroke. Apr2017, Vol. 12 Issue 3, p264-272. 9p.
Subject
*COGNITION disorders
*STROKE
*WHITE matter (Nerve tissue)
*TRANSIENT ischemic attack
*CEREBROVASCULAR disease
Language
ISSN
1747-4930
Abstract
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. [ABSTRACT FROM AUTHOR]