Postinfectious Stroke

History and Physical

An 8-year-old boy arrived in the emergency department with sudden-onset dysarthria and right hemiparesis, which evolved over 6 hours to complete right hemiplegia. During the week prior to presentation, he experienced fever, odynophagia, and exanthema that improved within 48 hours. He denied antecedent headache, trauma, recent vaccinations, and travel. His prenatal and birth history were normal, with no developmental issues or other medical/family history. On neurological examination, he was fully oriented but dysarthric with 2/5 weakness throughout the right upper and lower extremities, and 3+ reflexes with upgoing toes on the right. Sensation was intact.

Diagnostic Workup

Head CT showed patchy hypodensity in the left basal ganglia, external and internal capsules, and frontal operculum (Broca area) ( Fig. 21.1 ). Brain MRI confirmed acute infarction with T2/fluid-attenuated inversion recovery (FLAIR) hyperintense cytotoxic edema and restricted diffusion ( Fig. 21.2 ). MR angiography (MRA) demonstrated irregular stenosis of the left internal carotid artery (ICA) terminus, M1, and A1 segments ( Fig. 21.3 ). Digital subtraction angiography showed corresponding luminal narrowing without obvious dissection flap or collateral vessels. Blood and CSF testing was normal with no signs of coagulopathy or infection. Echocardiogram was normal. The patient was treated with aspirin and steroids, with residual hemiparesis after 6 months. Follow-up MRA at 9 months showed improved but persistent mild stenosis of the involved vessels ( Fig. 21.4 ).

An X-ray showing brain CT scan with white arrows indicating dark areas representing acute infarct in left brain regions. An X-ray showing an axial head computed tomography scan displaying patchy hypodensity in the left frontal operculum, internal/external capsules and basal ganglia. Two white arrows pointing to areas of decreased density, indicating acute infarct. The brain structures are visible in grayscale with the ventricular system appearing darker in the center surrounded by brain tissue. The skull appears as a white circular border surrounding the brain parenchyma. — Fig. 21.1

A photo shows brain MRI scan displaying patchy cytotoxic edema in left middle carotid artery region, marked with white arrows. A photo shows a brain MRI axial scan displaying patchy cytotoxic edema in the left middle carotid artery distribution. Two white arrows are pointing to areas of abnormality in the brain tissue. The scan reveals distinct contrast between normal brain tissue and affected regions, showing characteristic brightness patterns indicating restricted diffusion. The image demonstrates the typical appearance of an ischemic stroke with white arrows highlighting the affected area. — Fig. 21.2

A diagram shows magnetic resonance angiography displaying blood vessels with arrows indicating irregular stenoses of left internal carotid artery terminus. A diagram shows a magnetic resonance angiography (MRA) image of cerebral blood vessels displaying the circle of Willis and surrounding vasculature. Two white arrows point to irregular stenoses (narrowings) in the left internal carotid artery terminus and adjacent vessels including the M1 and A1 segments. The image reveals the branching pattern of major cerebral arteries with the main trunks appearing bright against the dark background, highlighting the vascular architecture and pathological narrowings that could potentially restrict blood flow to brain tissue. — Fig. 21.3

An X-ray showing cerebral blood vessels with magnetic resonance angiography revealing mild stenosis in brain arteries following treatment. An X-ray angiography image showing the cerebral blood vessels at the base of the brain, displaying the Circle of Willis. The branching white vessels appear against a dark background, revealing the arterial network structure. The image demonstrates mild stenosis persisting in the distal internal carotid artery, M1, and A1 segments, though improved from previous studies. The vascular anatomy shows the characteristic circular connection between anterior and posterior cerebral circulation with visible arterial branches extending outward. — Fig. 21.4

Clinical Differential Diagnosis

Hemiplegic migraine (familial or sporadic): usually presents with aura of progressive visual and sensory disturbances and unilateral paresthesias, followed by language disturbances and hemiparesis. The deficit lasts from minutes to hours, followed by headache with nausea, vomiting, and photophobia.

Postictal hemiparesis (Todd phenomenon): occurs following seizure, with duration of less than 24 hours.

Hemorrhagic stroke or venous thrombosis: symptoms of intracranial hypertension or encephalopathy.

Central nervous system infection (meningoencephalitis): elevated CSF and blood inflammatory markers and positive cultures.

Imaging Differential Diagnosis

Post-varicella (varicella zoster virus, VZV) arteriopathy: Variant of focal cerebral arteriopathy (FCA) with a history of varicella infection in the last 12 months or positive PCR in CSF.

Intracranial arterial dissection: Rare but classically seen in young boys following trauma. Usually affects the internal carotid or vertebral artery with spiraling or tapered luminal narrowing, and can predispose to distal thromboembolism ( Figs. 21.5 and 21.6 ).