We describe a 56-year-old woman with multiple comorbidities including myasthenia gravis, who developed an acute ischemic stroke shortly after initiation of IVIg. Despite timely administration of intravenous TNK, her course was marked by progression to a large middle cerebral artery infarct of the opposite hemisphere with hemorrhagic transformation. This may suggests a paradoxical interaction between IVIg-induced vascular vulnerability and the pro-inflammatory properties of plasmin, or other underlying pathogenesis.
While the incidence of IVIG-associated stroke remains low, the risk appears to increase in patients with multiple vascular comorbidities and risk factors such as hypertension. Our case underscores a potential interaction between IVIg and TNK, in which IVIg may prime the cerebrovascular environment for thrombosis through mechanisms such as hyperviscosity, endothelial dysfunction, or platelet activation. Furthermore, the proinflammatory properties of plasmin may amplify infarct size and augment stroke risk. Interestingly, in our patient, the absence of laboratory evidence of hyperviscosity coupled with the presence of newly noted vascular beading on repeat magnetic resonance angiography indicate the possibility of involvement of alternative or complementary pathogenic mechanisms.