Human Metapneumovirus-Induced Acute Ischemic Stroke in a Pediatric Case Report

Introduction The relationship between viral infections and ischemic stroke has been studied for decades, with proposed mechanisms including virus‐induced hypercoagulability, vasculopathy, and hemodynamic instability. Varicella zoster virus, SARS‐CoV‐2, Parvovirus B19, and Mycobacteria are recognized culprits; however, less common viruses can cause cerebrovascular injury through either direct neuroinvasion or systemic inflammatory responses. Human metapneumovirus (hMPV) is a respiratory pathogen causing bronchiolitis and pneumonia in children. Neurological complications are rare, though cases of encephalitis, seizures, and, very infrequently, stroke have been reported. We present a case of lacunar stroke in a previously healthy 5‐year‐old girl with acute hMPV infection, highlighting diagnostic challenges and the need for further study. Case A 5‐year‐old girl developed acute right‐sided weakness, facial droop, and dysarthria, prompting activation of a stroke alert. Her NIHSS score was 9, consistent with moderate neurological impairment. A non‐contrast CT head was negative for acute infarction or hemorrhage but revealed pansinusitis. Vessel imaging showed focal narrowing of the left middle cerebral artery (M1 segment). Because of her history of headaches, hemiplegic migraine was initially suspected, and systemic thrombolysis was withheld. A respiratory viral panel was positive for hMPV, and symptomatic management was continued. Contrast‐enhanced MRI demonstrated an acute left basal ganglia infarct, raising suspicion for vasospasm or early moyamoya‐like changes (Fig. A and B). MR angiography confirmed LMCA irregularity with multiple perforator vessels, findings consistent with vasculopathy rather than migraine (Fig. C). She was treated with aspirin, corticosteroids, and empiric antibiotics given concerns for virus‐associated vasculitis or intracranial extension of infection. A hematologic and stroke workup was negative. She was discharged to rehabilitation and achieved significant recovery with an mRS score of 1 at three weeks. Conclusion This case suggests that hMPV can trigger a pediatric ischemic stroke. The hypothesized mechanism involves endothelial dysfunction, inflammatory vasculopathy, and activation of the coagulation cascade. While current evidence is limited to case reports, awareness of viral triggers in children is important, where stroke mimics like hemiplegic migraine complicate timely diagnosis and treatment. Future population‐based studies are needed to define the true burden of hMPV‐associated stroke and assess the risk of secondary vasculopathy or recurrence. Long‐term follow‐up may clarify neurocognitive outcomes, and advanced vessel wall imaging could help differentiate vasospasm, arteritis, or moyamoya‐like arteriopathy. This report adds to the limited but growing literature suggesting hMPV as an underrecognized contributor to pediatric stroke and emphasizes vigilance when evaluating viral illnesses in children with acute neurological symptoms.