Post-stroke recrudescence (PSR) is the transient return of previously resolved stroke deficits. The defining clinical clues that distinguish PSR from a new ischemic event are twofold. First, deficits in PSR are stereotyped and replicate the original deficits rather than producing new focal neurologic findings. Second, PSR persists for the duration of an identifiable precipitating stressor and typically resolves over hours to days once the trigger is treated or abates.
By contrast, a recurrent ischemic stroke commonly produces new neurologic deficits referable to a different vascular territory, and transient ischemic attacks (TIA) tend to be short-lived — most TIAs last minutes and only rarely persist up to 24 hours. Todd paralysis related to seizure can mimic focal weakness but should be suspected when electroencephalography (EEG) demonstrates epileptiform activity or when there is a history of seizures; in the presented case Todd paralysis was excluded by a normal EEG and absence of seizure history.
Recognizing that symptoms are anamnestic reproductions of prior deficits and temporally linked to an acute systemic stressor is central to diagnosing PSR and differentiating it from new cerebrovascular events.
PSR episodes are commonly precipitated by systemic stressors that transiently worsen the function of previously injured brain tissue. Reported triggers include:
Population-level observations note that PSR has a median onset of about 4 years after the index stroke and a prevalence of roughly 10% among people with prior stroke or TIA. Certain groups may be more susceptible, including women and African American individuals, with tobacco use and greater initial stroke severity also identified as risk factors.
Pathophysiologically, several hypotheses exist. Changes in pharmacokinetics or pharmacodynamics after stroke may render injured tissue more sensitive to medications. Animal and translational studies suggest that a post-stroke inflammatory response can prime brain-specific immune reactions; subsequent systemic infection may retrigger cytokine-mediated processes and lead to recurrence of deficits. These mechanisms are not mutually exclusive and likely interact to produce PSR in susceptible patients.
The primary clinical aim when deficits recur after a prior stroke is to exclude an acute cerebrovascular event. Recommended investigations include neuroimaging (noncontrast CT or MRI) to rule out new infarction or hemorrhage. In PSR, imaging typically demonstrates chronic encephalomalacia or gliosis in the territory of the previous infarct without new diffusion restriction or acute hemorrhage.
When the clinical picture shows strictly stereotyped recurrence of prior deficits and there is a clear precipitating stressor, observation and directed treatment of the trigger may be reasonable without immediate imaging. However, if new neurologic findings are present, the presentation is ambiguous, or symptoms do not improve with treatment of the trigger, clinicians should maintain a low threshold for neuroimaging.
Ancillary laboratory and bedside investigations that help identify precipitants include:
Appropriate investigation reduces unnecessary hospital admission, imaging, and potentially harmful interventions, such as inappropriate thrombolysis.
Management centers on identifying and treating the underlying trigger rather than initiating stroke-directed reperfusion therapies when PSR is confidently diagnosed. For example, infection should be treated according to usual clinical indications. Supportive measures include ensuring adequate hydration and sleep and avoiding precipitants such as unnecessary sedative medications when possible.
Symptoms of PSR generally resolve once the precipitant is controlled. Observational data indicate that within 90 days patients with PSR have fewer subsequent vascular events than patients with TIA, although vigilance for recurrent stroke remains important. Clear communication with patients and caregivers about the nature of PSR, the need to treat the trigger, and signs that should prompt urgent reassessment is essential.
In the reported case, the 58-year-old man with prior left M1 occlusion and endovascular thrombectomy presented with fever, respiratory symptoms and worsening of his baseline right-sided weakness. Chest radiography and brain MRI showed no acute abnormalities; white blood cell count was mildly elevated. The clinical picture — recurrence of prior deficits temporally linked to an upper respiratory tract infection — supported a diagnosis of post-stroke recrudescence. He received azithromycin for the infection, was not admitted, and his neurologic status returned to baseline as the infection resolved.
This case illustrates the practical approach: confirm that deficits replicate the prior stroke phenotype, seek an identifiable precipitant, perform targeted investigations to exclude new stroke when indicated, treat the trigger, and monitor for recovery. Recognition of PSR can avoid unnecessary interventions while ensuring patient safety.