--- title: "Post-stroke recrudescence vs new stroke: distinguishing features, causes, investigations, and mana" id: "cmaj-2-a-58-year-old-patient-with-right-sided-weakness-and-a-history-of-stroke-practice" canonical_url: "https://medichelpline.com/clinical-feed/cmaj-2-a-58-year-old-patient-with-right-sided-weakness-and-a-history-of-stroke-practice" content_type: "clinical_feed_article" specialty: "Neurology" source_name: "CMAJ" source_url: "http://www.cmaj.ca/cgi/content/short/198/29/E1156?rss=1" published_at: "2026-08-24T04:05:24.000Z" evidence_level: "Journal Feed" license: "CC-BY-NC-4.0 / Informational Use" --- # Post-stroke recrudescence vs new stroke: distinguishing features, causes, investigations, and mana ## Provenance & Clinical Metadata - **Canonical URL:** https://medichelpline.com/clinical-feed/cmaj-2-a-58-year-old-patient-with-right-sided-weakness-and-a-history-of-stroke-practice - **Specialty:** [Neurology](https://medichelpline.com/clinical-feed/neurology.md) - **Primary Source:** CMAJ - **Source URL:** [Original Journal Publication](http://www.cmaj.ca/cgi/content/short/198/29/E1156?rss=1) - **Published At:** 2026-08-24T04:05:24.000Z - **Evidence Rating:** Journal Feed ## Executive GIST (TL;DR) - A 58-year-old man with prior left M1 occlusion and endovascular thrombectomy presented with 2 days of fever, cough, headache and worsening of baseline right-sided weakness; infection was identified and white blood cell count was mildly elevated. - Brain MRI and chest x-ray showed no acute findings; diagnosis was **post-stroke recrudescence (PSR)** triggered by an upper respiratory tract infection and the patient was treated with azithromycin and discharged. - PSR is the transient recurrence of previous stroke deficits without new neurologic findings; symptoms mirror the original deficits and persist for the duration of the precipitant (hours to days). - PSR typically occurs a median of 4 years after the index event and has an estimated prevalence of about 10% among people with prior stroke or TIA. - Differential diagnoses include recurrent ischemic stroke, transient ischemic attack (TIA) and Todd paralysis; Todd paralysis was excluded in the case by normal EEG and no seizure history. - Common PSR triggers are systemic stressors: infection, sedative/analgesic medications, hypotension, electrolyte disturbance, hypoglycemia and dehydration. - Proposed mechanisms include altered pharmacokinetics/pharmacodynamics increasing vulnerability of injured brain tissue and post-stroke inflammatory responses with cytokine release and antigen reactivation; likely multifactorial. - Recommended investigations focus on excluding acute cerebrovascular events with neuroimaging (noncontrast CT or MRI); imaging in PSR typically shows chronic encephalomalacia/gliosis without new diffusion restriction or hemorrhage. - When deficits are strictly stereotyped and a clear trigger is present, observation and treatment of the trigger may be reasonable without immediate imaging; if ambiguous or not improving, maintain a low threshold for brain imaging. - Additional tests include serum electrolytes, complete blood count, urinalysis and chest radiography to identify metabolic derangements or infections. - Management targets the underlying trigger (e.g., treat infection), plus supportive care such as hydration and sleep; symptoms generally resolve with resolution of the precipitant. - Prognostically, within 90 days patients with PSR have fewer vascular events than those with TIA. - Recognition of PSR helps avoid unnecessary hospital admission, imaging, and potentially harmful treatments like thrombolysis. ## Clinical Analysis & Structured Key Points A 58-year-old patient with right-sided weakness and a history of stroke | CMAJ Skip to main content Log in Toggle navigation menu Open settings menu Open search Advanced Search Advanced Search Log in --> A 58-year-old patient with right-sided weakness and a history of stroke Abrar Ahmed Abrar Ahmed Schulich School of Medicine (Ahmed), University of Western Ontario, London, Ont.; Division of Neurology (Saposnik), Department of Medicine, University of Toronto; Stroke Outcomes Research Center (Saposnik), Li Ka Shing Knowledge Institute, Toronto, Ont. MD Find this author on Google Scholar Find this author on PubMed Search for this author on this site and Gustavo Saposnik Gustavo Saposnik Schulich School of Medicine (Ahmed), University of Western Ontario, London, Ont.; Division of Neurology (Saposnik), Department of Medicine, University of Toronto; Stroke Outcomes Research Center (Saposnik), Li Ka Shing Knowledge Institute, Toronto, Ont. MD PhD Find this author on Google Scholar Find this author on PubMed Search for this author on this site CMAJ August 24, 2026 198 (29) E1156-E1157; DOI: https://doi.org/10.1503/cmaj.251837 PDF Help Article Responses Metrics PDF A 58-year-old man presents to the emergency department with acute right-sided weakness. Fourteen months before this visit, he suffered a stroke caused by an occlusion of the M1 segment of the left middle cerebral artery. His National Institutes of Health Stroke Scale (NIHSS) score was 8 (range 0 to 42), making it a moderate stroke. 1 He underwent endovascular thrombectomy with stenting of the left M1 segment. Systemic thrombolytics were not administered. At discharge, the patient had a mild paretic gait (NIHSS score 1) and was given antihypertensive, lipid-lowering, and antithrombotic medications. At the 8-week follow-up, he was independent despite mild residual right-sided weakness. His medical history also includes hypertension and dyslipidemia. At this presentation, he describes a 2-day history of fever, cough, headache, and worsening of his baseline right-sided weakness. His blood pressure is 128/76 mm Hg, heart rate is 86 beats/min, and temperature is 38.1°C. Examination confirms increased right hemiparesis and gait impairment relative to post-stroke baseline. The patient’s bloodwork reveals an elevated white blood cell count of 11 (reference 4 to 11) × 10 9 /L with neutrophil predominance. Chest radiography and brain magnetic resonance imaging (MRI) reveal no acute abnormalities. He is diagnosed with post-stroke recrudescence (PSR) triggered by an upper respiratory tract infection (URTI) and given azithromycin. The patient is discharged after diagnosis and is not admitted. What features differentiate a new stroke from post-stroke recrudescence? The differential diagnosis of this patient’s worsening weakness included recurrent ischemic stroke, transient ischemic attack (TIA), PSR, and Todd paralysis. Todd paralysis was excluded because electroencephalography showed no epileptiform discharges and he had no history of seizures. Post-stroke recrudescence is the transient recurrence of stroke deficits after initial improvement. 2 It occurs at a median of 4 years after the event and has a prevalence of 10% among patients with prior stroke or TIA. 3 Distinguishing PSR from a new ischemic event relies on 2 features. 2 First, no novel deficits are seen as symptoms replicate the original deficits. Second, PSR persists for the duration of the precipitating stressor (hours to days). 2 This is unlike the clinical picture of TIAs, which typically last a few minutes, less commonly a few hours, and rarely up to 24 hours. 4 What causes post-stroke recrudescence? Episodes of PSR are triggered by systemic stressors such as infection, sedative or analgesic medications, hypotension, electrolyte disturbances, hypoglycemia, or dehydration. 2 The stroke incidence in Canada continues to rise with the aging population, resulting in a larger number of people at risk of PSR. Certain populations are more susceptible, including women and African American individuals. 2 Additional risk factors include tobacco use and greater initial stroke severity. 2 Several pathophysiological hypotheses have been proposed. Altered pharmacokinetics or pharmacodynamics may render previously injured brain tissue more sensitive to certain medications. 2 Animal studies suggest that a post-stroke inflammatory response can induce cytokine release, leading to the development of brain-specific antigens that are retriggered by infection. 5 These mechanisms likely interact in a multifactorial manner. What investigations are recommended? Neuroimaging (e.g., noncontrast computed tomography or MRI) is recommended to exclude acute cerebrovascular events. 2 Imaging usually shows chronic encephalomalacia or gliosis in the prior infarct territory without new diffusion restriction or hemorrhage. Observation and treatment of the trigger instead of imaging are reasonable when deficits are strictly stereotyped without new neurologic findings, and a clear stressor is present. If symptoms do not improve or if the clinical picture remains ambiguous, the threshold for brain imaging should remain low. Investigations may include serum electrolytes (to identify metabolic derangements), complete blood count (to identify infection or inflammation), and urinalysis and chest radiography (to identify common infections). Recognition helps avoid unnecessary hospital admission, imaging, and potentially harmful treatments such as thrombolysis. What should patients and families be told about management and prognosis? Management requires treating the underlying trigger. 6 Supportive measures include hydration and adequate sleep. Symptoms generally resolve once the trigger is treated. 2 Within 90 days, patients with PSR have fewer vascular events than those with TIA. 4 Case revisited The patient’s weakness returned to baseline as the infection resolved. Decisions is a series that focuses on practical evidence-based approaches to common presentations in primary care. The articles address key decisions that a clinician may encounter during initial assessment. The information presented can usually be covered in a typical primary care appointment. Articles should be no longer than 650 words, may include a box, figure or table and should begin with a very brief description (75 words or less) of the clinical situation. The decisions addressed should be presented in the form of questions. A box providing helpful resources for the patient or physician is encouraged. Footnotes Decisions articles include a brief, common clinical scenario that is either real or fictional as a starting point to discuss an evidence-based approach to a common presentation in primary care. The following article presents a real clinical scenario. Competing interests: Gustavo Saposnik is vice president of the World Stroke Organization. No other competing interests were declared. This article has been peer reviewed. The authors have obtained patient consent. Contributors: Abrar Ahmed conceived the article, conducted the literature review, and drafted the manuscript. Gustavo Saposnik contributed clinical expertise and the patient case, assisted with manuscript drafting, and critically revised the manuscript for important intellectual content. Gustavo Saposnik supervised the project. Both authors gave final approval of the version to be published and agreed to be accountable for all aspects of the work. This is an Open Access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY-NC-ND 4.0) licence, which permits use, distribution and reproduction in any medium, provided that the original publication is properly cited, the use is noncommercial (i.e., research or educational use), and no modifications or adaptations are made. See: https://creativecommons.org/licenses/by-nc-nd/4.0/ References 1 ↵ Kogan E Twyman K Heap J . Assessing stroke severity using electronic health record data: a machine learning approach . BMC Med Inform Decis Mak 2020 ; 20 : 8 . Google Scholar OpenURL CrossRef PubMed 2 ↵ Topcuoglu MA Saka E Silverman SB . Recrudescence of deficits after stroke: clinical and imaging phenotype, triggers, and risk factors . JAMA Neurol 2017 ; 74 : 1048 – 55 . Google Scholar OpenURL PubMed 3 ↵ Jun-O’connell AH Henninger N Moonis M . Recrudescence of old stroke deficits among transient neurological attacks . Neurohospitalist 2019 ; 9 : 183 – 9 . Google Scholar OpenURL PubMed 4 ↵ Weimar C Kraywinkel K Rödl J .; German Stroke Data Bank Collaborators . Etiology, duration, and prognosis of transient ischemic attacks: an analysis from the German Stroke Data Bank . Arch Neurol 2002 ; 59 : 1584 – 8 . Google Scholar OpenURL CrossRef PubMed Web of Science 5 ↵ Zierath D Hadwin J Savos A . Anamnestic recall of stroke-related deficits: an animal model . Stroke 2010 ; 41 : 2653 – 60 . Google Scholar OpenURL CrossRef Abstract / Full Text PubMed 6 ↵ Pu MJ Yu JL Hu X . Incidence, characteristics and outcome of post-stroke recrudescence in the Chinese population: a single-centre observational study . BMJ Open 2023 ; 13 : e068878 . 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Your Personal Message CAPTCHA Please verify that you are a real person Close Citation Tools Citation Tools A 58-year-old patient with right-sided weakness and a history of stroke Abrar Ahmed Abrar Ahmed and Gustavo Saposnik Gustavo Saposnik CMAJ Aug 2026, 198 (29) E1156-E1157; DOI: 10.1503/cmaj.251837 Citation Manager Formats BibTeX Bookends EasyBib EndNote (tagged) EndNote 8 (xml) Medlars Mendeley Papers RefWorks Tagged Ref Manager RIS Zotero Request Permissions Share Share This Article A 58-year-old patient with right-sided weakness and a history of stroke Abrar Ahmed Abrar Ahmed and Gustavo Saposnik Gustavo Saposnik CMAJ Aug 2026, 198 (29) E1156-E1157; DOI: 10.1503/cmaj.251837 Share This Article: Copy Post Like 0 Jump To Section What features differentiate a new stroke from post-stroke recrudescence? What causes post-stroke recrudescence? What investigations are recommended? What should patients and families be told about management and prognosis? Case revisited Footnotes References PDF Related Articles No related articles found. Google Scholar PubMed Cited By... No citing articles found. 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