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Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks.

ABSTRACT: Background:Recrudescence of old stroke deficits (ROSD) is a reported cause of transient neurological symptoms, but it is not well characterized. Objective:We sought to determine the prevalence, potential triggers, and clinical outcome of ROSD in a cohort of patients presenting with acute transient neurological attack (TNA) and absent acute pathology on brain imaging. Methods:We retrospectively analyzed 340 consecutive patients who presented with TNA and no acute pathology on brain imaging that were included in an institutional stroke registry between February 2013 and April 2015. The presumed TNA cause was categorized as transient ischemic attack (TIA), ROSD, and other cause. Baseline characteristics, triggers, cardiovascular complications within 90 days, and death were recorded. Results:The prevalence of ROSD in the studied cohort was 10% (34/340). Infectious stressors and acute metabolite derangements were more common in ROSD compared to TIA (P < .05, each). Compared to TIA and the other TNA, ROSD was more likely to have more than 1 acute stressor (P < .001). Patients with ROSD had similar vascular risk factors compared to TIA (P > .05), including hypertension, diabetes mellitus, peripheral vascular disease, hyperlipidemia, and similarly used HMG-CoA reductase inhibitor, antihypertensive, and antiplatelet medications. Among the patients with an available 90-day follow-up (n = 233), cardiovascular events were more frequent in the TIA group as compared to other TNA (P < .05). Conclusion:ROSD is common and distinct from TIA and is associated with a triggering physiologic reaction leading to transient reemergence of prior neurologic deficits. Further study of the mechanism of this phenomenon is needed to help better identify these patients.

SUBMITTER: Jun-O'connell AH

PROVIDER: S-EPMC6739667 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks.

Jun-O'connell Adalia H AH Henninger Nils N Moonis Majaz M Silver Brian B Ionete Carolina C Goddeau Richard P RP

The Neurohospitalist 20190221 4

<h4>Background</h4>Recrudescence of old stroke deficits (ROSD) is a reported cause of transient neurological symptoms, but it is not well characterized.<h4>Objective</h4>We sought to determine the prevalence, potential triggers, and clinical outcome of ROSD in a cohort of patients presenting with acute transient neurological attack (TNA) and absent acute pathology on brain imaging.<h4>Methods</h4>We retrospectively analyzed 340 consecutive patients who presented with TNA and no acute pathology o ...[more]

PMID: 31534606

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Project description:IntroductionNonfocal transient neurological attacks (TNAs) are associated with an increased risk of future dementia, but it is unclear whether TNAs are also associated with concurrent cognitive impairment. We hypothesized that recent TNAs are related to worse cognitive functioning. We tested our hypothesis in patients with heart failure, as these patients are at risk of cerebral hypoperfusion, which might play a role in the etiology of TNAs.MethodsWe performed neuropsychological testing in all patients with heart failure enrolled in the Heart Brain Connection study. We assessed global cognition, attention-psychomotor speed, executive functioning, memory and language. All patients were interviewed with a standardized questionnaire on the occurrence of TNAs in the preceding 6 months. We studied associations between TNAs and cognitive functioning with linear and logistic regression analyses, adjusted for age, sex and education. We performed additional analyses in patients without previous stroke or TIA and in patients without brain infarction on MRI.ResultsThirty-seven (23%) of 158 patients (mean age 70 years, 67% men) experienced one or more TNAs. Patients with a recent TNA were more likely to be impaired on ≥ 1 cognitive domains than patients without TNAs [41% vs. 18%, adjusted odds ratio 4.6, 95% confidence interval (CI) 1.8-11.8]. Patients with TNAs performed worse than patients without TNAs on global cognition (mean difference in z scores - 0.36, 95% CI - 0.54 to - 0.18), and on the cognitive domains attention-psychomotor speed (mean difference - 0.40, 95% CI - 0.66 to - 0.14), memory (mean difference - 0.57, 95% CI - 0.98 to - 0.15) and language (mean difference - 0.47, 95% CI - 0.79 to - 0.16). These associations were independent of cardiac output and volume of white matter hyperintensities. Subgroup analyses in patients without previous stroke or TIA or brain infarction on MRI (n = 78) yielded comparable results, with the exception of the cognitive domain language, which was no longer different between patients with and without TNAs.ConclusionAmong patients with heart failure, TNAs are associated with cognitive impairment, which warrants the need for more clinical awareness of this problem.

Project description:Perforin-mediated cytotoxicity plays a crucial role in microbial defense, tumor surveillance, and primary autoimmune disorders. However, the contribution of the cytolytic protein perforin to ischemia-induced secondary tissue damage in the brain has not been fully investigated. Here, we examined the kinetics and subpopulations of perforin-positive cells and then evaluated the direct effects of perforin-mediated cytotoxicity on outcomes after ischemic stroke. Using flow cytometry, we showed that perforin+CD45+ immune cells could be detected at 12 h and that the percentage of these cells increased largely until on day 3 and then significantly declined on day 7. Surprisingly, the percentage of Perforin+CD45+ cells also unexpectedly increased from day 7 to day 14 after ischemic stroke in Perforin1-EGFP transgenic mice. Our results suggested that Perforin+CD45+ cells play vital roles in the ischemic brain at early and late stages and further suggested that Perforin+CD45+ cells are a heterogeneous population. Surprisingly, in addition to CD8+ T cells, NK cells, and NKT cells, central nervous system (CNS)-resident immune microglia, which are first triggered and activated within minutes after ischemic stroke in mice, also secreted perforin during ischemic brain injury. In our study, the percentage of perforin+ microglia increased from 12 h after ischemic stroke, increased largely until on day 3 after ischemic stroke, and then moderately declined from days 3 to 7. Intriguingly, the percentage of perforin+ microglia also dramatically increased from days 7 to 14 after ischemic stroke. Furthermore, compared with wild-type littermates, Perforin 1-/- mice exhibited significant increases in the cerebral infarct volume, neurological deficits, and neurogenesis and inhibition of neurotoxic astrogliosis. Interestingly, the number of CD45+CD3+ T cells was significantly decreased in Perforin 1-/- mice compared with their wild-type littermates, especially the number of γδ T cells. In addition, Perforin 1-/- mice had lower levels of IL-17 than their wild-type littermates. Our results identified a critical function of perforin-mediated neurotoxicity in the ischemic brain, suggesting that targeting perforin-mediated neurotoxicity in brain-resident microglia and invading perforin+CD45+ immune cells may be a potential strategy for the treatment of ischemic stroke.

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Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks.

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Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks.

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