ReviewCureus2026
Post-Stroke Recrudescence During the Perioperative Period: Potential Roles of Anesthetic and Sedative Agents.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-stroke recrudescence (PSR) is the transient reappearance of previously recovered focal neurologic deficits after a systemic or pharmacologic stressor, without evidence of a new cerebral infarction. In the perioperative setting, PSR can closely resemble acute ischemic stroke, residual anesthetic effects, seizure, or delirium, creating a significant diagnostic challenge. This narrative review examines the proposed mechanisms of PSR and evaluates the available evidence regarding anesthetic, sedative, and analgesic agents as potential triggers. Previously injured neural networks may remain vulnerable to disruptions in excitatory-inhibitory balance despite apparent clinical recovery. Human evidence is strongest for midazolam and broader benzodiazepine exposure, while evidence involving opioids, propofol, volatile anesthetics, and dexmedetomidine remains limited or indirect. Determining the independent effect of any single medication is difficult because surgery frequently involves simultaneous stressors, including hypotension, hypoxemia, infection, electrolyte abnormalities, pain, and sleep disruption. PSR typically reproduces the pattern of a patient's prior stroke deficits, is not associated with new diffusion-weighted imaging abnormalities, and improves after correction of the underlying trigger or resolution of medication effects. However, PSR remains a diagnosis of exclusion, and its consideration should not delay prompt evaluation for acute stroke. Recognition may be improved through clear preoperative documentation of baseline neurologic findings, comparison of postoperative deficits with the previous stroke syndrome, and early communication among anesthesiology, surgical, and neurology teams. Current evidence does not establish most anesthetic agents as independent causes of PSR, highlighting the need for prospective studies that document specific agents, doses, timing, concurrent perioperative stressors, and neurologic outcomes.
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