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Pre-existing White Matter Hyperintensity Lesion Burden and Diagnostic Certainty of Transient Ischemic Attack.

ABSTRACT: GOALS:There are no validated biomarkers that allow for reliable distinction between TIA and other transient neurological symptoms that mimic TIA. We sought to determine whether the degree of pre-existing white matter hyperintensity (WMH) lesion burden relates to the diagnostic certainty of TIA in a cohort of patients presenting with transient neurological symptoms. MATERIALS AND METHODS:We retrospectively analyzed 144 consecutive patients with available brain MRI to quantify and normalize the WMH volume for brain atrophy (adjusted white matter hyperintensity [aWMHV]). We first stratified subjects to probable (n?=?62) versus possible (n?=?82) TIA as per existing guidelines. Receiver-operating characteristic curves were used to determine a critical aWMHV-threshold (7.8 mL) that best differentiated probable from possible TIA. We then further stratified patients with possible TIA to likely (n?=?52) versus unlikely (n?=?30) TIA after independent chart review and adjudication. Finally, multivariable logistic and multinomial regression was used to determine whether the defined aWMHV independently related to probable and likely TIA after adjustment for pertinent confounders. FINDINGS:With the exception of age (P < .001) and use of antiplatelets (P?=?.017), baseline characteristics were similar between patients with probable, likely, and unlikely TIA. In the fully adjusted multinomial model, the aWMHV cut-off greater than 7.8 mL (odds ratio 3.8, 95% confidence interval 1.3-10.9, P?=?.012) was significantly more frequent in patients with a probable TIA as compared to those with an unlikely TIA diagnosis. CONCLUSIONS:We provide proof-of-principle that WMH may serve as a neuroimaging marker of diagnostic certainty of TIA after neurological workup has been completed.

SUBMITTER: Nagy M

PROVIDER: S-EPMC6441369 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Pre-existing White Matter Hyperintensity Lesion Burden and Diagnostic Certainty of Transient Ischemic Attack.

Nagy Muhammad M Azeem Muhammad U MU Soliman Youssef Y Nawab Sahil A SA Jun-O'Connell Adalia H AH Goddeau Richard P RP Moonis Majaz M Silver Brian B Henninger Nils N

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 20190107 4

<h4>Goals</h4>There are no validated biomarkers that allow for reliable distinction between TIA and other transient neurological symptoms that mimic TIA. We sought to determine whether the degree of pre-existing white matter hyperintensity (WMH) lesion burden relates to the diagnostic certainty of TIA in a cohort of patients presenting with transient neurological symptoms.<h4>Materials and methods</h4>We retrospectively analyzed 144 consecutive patients with available brain MRI to quantify and n ...[more]

PMID: 30630754

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Project description:White matter hyperintensities of presumed vascular origin (WMH) are a prevalent form of cerebral small-vessel disease and an important risk factor for post-stroke cognitive dysfunction. Despite this prevalence, it is not well understood how WMH contributes to post-stroke cognitive dysfunction. Preliminary findings suggest that increasing WMH volume is associated with total hippocampal volume in chronic stroke patients. The hippocampus, however, is a complex structure with distinct subfields that have varying roles in the function of the hippocampal circuitry and unique anatomical projections to different brain regions. For these reasons, an investigation into the relationship between WMH and hippocampal subfield volume may further delineate how WMH predispose to post-stroke cognitive dysfunction. In a prospective study of acute ischemic stroke patients with moderate/severe WMH burden, we assessed the relationship between quantitative WMH burden and hippocampal subfield volumes. Patients underwent a 3T MRI brain within 2-5 days of stroke onset. Total WMH volume was calculated in a semi-automated manner. Mean cortical thickness and hippocampal volumes were measured in the contralesional hemisphere. Total and subfield hippocampal volumes were measured using an automated, high-resolution, ex vivo computational atlas. Linear regression analyses were performed for predictors of total and subfield hippocampal volumes. Forty patients with acute ischemic stroke and moderate/severe white matter hyperintensity burden were included in this analysis. Median WMH volume was 9.0 cm3. Adjusting for intracranial volume and stroke laterality, age (β = -3.7, P < 0.001), hypertension (β = -44.7, P = 0.04), WMH volume (β = -0.89, P = 0.049), and mean cortical thickness (β = 286.2, P = 0.006) were associated with total hippocampal volume. In multivariable analysis, age (β = -3.3, P < 0.001) and cortical thickness (β = 205.2, P = 0.028) remained independently associated with total hippocampal volume. In linear regression for predictors of hippocampal subfield volume, increasing WMH volume was associated with decreased hippocampal-amygdala transition area volume (β = -0.04, P = 0.001). These finding suggest that in ischemic stroke patients, increased WMH burden is associated with selective hippocampal subfield degeneration in the hippocampal-amygdala transition area.

Project description:Background This study was conducted to compare frequencies of chronic brain infarctions (CBIs) and white matter hyperintensities (WMHs) as well as their associations with established early recurrence risk scores in patients with transient ischemic attack (TIA) and stroke mimics compared with ischemic stroke. Methods and Results Single-center cohort study including consecutive patients with TIA, stroke mimics, and acute ischemic stroke, with available magnetic resonance imaging from January 2015 to December 2017. Blinded raters adjudicated WMH (age-related white matter changes score) and CBI according to established definitions. A total of 2112 patients (median [Q1-Q3] age 71 [59-80] years, 43% women, National Institutes of Health Stroke Scale score of 2 [1-7], 80% ischemic stroke, 18% TIA, 2% stroke mimics) were included. While CBIs were present in only 10% of patients with stroke mimic, they were detected in 28% of TIAs and 38% of ischemic strokes (P<0.001). WMHs were less pronounced (0, 0-1) in patients with stroke mimic, but there was no difference between TIA (1, 1-2) and ischemic stroke (0, 1-2) patients. CBIs (adjusted odds ratio, 0.3; 95% CI, 0.1-0.9) were associated with a lower rate of stroke mimic as the final diagnosis, while WMHs were not (adjusted odds ratio per point, 1.3; 95% CI, 0.7-2.2). WMH (β per point, 0.4; 95% CI, 0.3-0.6) and presence of CBI (β, 0.6; 95% CI, 0.3-0.9) were associated with a higher cardiovascular risk profile according to the ABCD3-I score. The accuracy of prediction was good for high-risk TIA (cross-validated area under the receiver operating characteristic curve, 0.89; 95% CI, 0.79-0.93) on the basis of brain imaging, age, and sex. Conclusions CBI and WMH differ between patients with stroke mimic and patients with TIA/ischemic stroke and are closely associated with established recurrence risk scores. Prospective studies need to clarify whether including brain frailty markers may contribute to the refinement of current management algorithms and risk stratifications.

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Pre-existing White Matter Hyperintensity Lesion Burden and Diagnostic Certainty of Transient Ischemic Attack.

Publications

Pre-existing White Matter Hyperintensity Lesion Burden and Diagnostic Certainty of Transient Ischemic Attack.

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