Pure Insular Cortex Infarct in Sepsis-Induced Hypoxic Ischemic Encephalopathy.

Each year there are an estimated 1.7 million adults in the United States that develop sepsis and nearly 16% of these adult patients die because of this disease process. Sepsis, however, can impact patients of all ages. Neonatal sepsis is currently one of the leading causes of morbidity and mortality among neonates. There are many complications of neonatal sepsis including meningitis, seizures, and hypoxic ischemic encephalopathy (HIE). HIE is estimated to impact one to five in 1000 live births worldwide, primarily impacting neonates. It is more commonly seen in premature infants and infants with low birth weights due to immature organ systems and a lack of adequate auto-regulatory mechanisms that would otherwise manage brain perfusion. In premature neonates, the most commonly recognized pathological pattern found on MRI is focal non-cystic white matter injury. HIE can also impact term infants as well. In these neonates, there exist two common MRI patterns that include either basal ganglia-thalamus ischemia, most often involving deep gray nuclei and perirolandic cortex, or watershed predominant ischemic changes that involve cortical gray matter.  We report a 38-week-old male neonate born at gestation diagnosed with HIE secondary to neonatal sepsis with an MRI finding of isolated insular cortex hypersensitivity on fluid-attenuated inversion recovery (FLAIR) and T1-weighted imaging. Isolated insular cortex hypersensitivity can be seen in non-lacunar ischemic middle cerebral artery (MCA) territory strokes but it is not common for it to present as a sole finding. In our case, these findings persisted for several weeks without evidence of any common patterns of hypoxia-induced cerebrovascular insult on MRI imaging.