Possible synergism of tissue plasminogen activator and neurocysticercosis leading to intracranial hemorrhage

Abstract

Neurocysticercosis (NCC) remains the most common helminth infection of the human central nervous system worldwide. Patients with NCC are especially predisposed to cerebrovascular events such as acute ischemic stroke (AIS), intracerebral hemorrhage (ICH), and subarachnoid hemorrhage due to an immune-mediated process in which infiltration of inflammatory cells into blood vessel walls leads to endothelial hyperplasia and endarteritis, known as cysticercotic angiitis. Additionally, the oncosphere of the parasite causing NCC produces T. solium enolase, an enzyme which binds and activates human plasminogen receptor proteins to plasmin, leading to a hypercoagulable state. Currently, NCC is not a contraindication to administration of tissue plasminogen activator (tPA) for a suspected AIS. However, to our knowledge, it has not been assessed whether the presence of NCC increases the likelihood of hemorrhagic conversion of an AIS after tPA administration. We present the case of an 83-year-old lady with NCC who developed multifocal right-sided ICH involving the temporal, parietal, and frontal lobes six and a half hours after tPA administration for a suspected AIS. Given this event and the cellular mechanisms provided, we recommend a safety surveillance study to further determine the potential risks of hemorrhagic conversion in this population.