Recrudescence of Old Stroke Deficits Among Transient Neurological Attacks

Neurohospitalist. 2019 Oct;9(4):183-189. doi: 10.1177/1941874419829288. Epub 2019 Feb 21.


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.

Keywords: diagnosis; exacerbation of focal neurological deficits; locus minoris resistantiae; poststroke recrudescence; reactivation of prior deficits; stroke; transient neurological symptoms.