Thalamus L-Sign: A Potential Biomarker of Neonatal Partial, Prolonged Hypoxic-Ischemic Brain Injury or Hypoglycemic Encephalopathy?

Abstract

Considerable overlap exists in the MR imaging features of hypoglycemic injury and hypoxic-ischemic brain injury, with similar predilections for the occipital and parietal lobes. In partial, prolonged hypoxia-ischemia, there is cortical destruction at the interarterial watershed zones, and in concomitant hypoglycemia and hypoxia-ischemia, an exaggerated final common pathway injury occurs. We interrogated secondary white matter tract-based thalamic injury as a tool to separate pure injuries in each group. A retrospective observational study of the MRIs of 320 children with a history of hypoxia-ischemia and/or hypoglycemia was undertaken with 3 major subgroups: 1) watershed-type hypoxic-ischemic injury, 2) neonatal hypoglycemia, and 3) both perinatal hypoxia-ischemia and proved hypoglycemia. Cerebral and thalamic injuries were assessed, particularly hyperintensity of the posterolateral margin of the thalami. A modified Poisson regression model was used to assess factors associated with such thalamic injury. Parieto-occipital injuries occurred commonly in patients with hypoglycemia and/or hypoxia-ischemia. Eighty-five of 99 (86%) patients with partial, prolonged hypoxia-ischemia exhibited the thalamus L-sign. This sign was also observed in patients who had both hypoglycemia and hypoxia-ischemia, predominantly attributable to the latter. Notably, the risk of a thalamus L-sign injury was 2.79 times higher when both the parietal and occipital lobes were injured compared with when they were not involved (95% CI, 1.25-6.23; P = .012). The thalamus L-sign was not depicted in patients with pure hypoglycemia. We propose the thalamus L-sign as a biomarker of partial, prolonged hypoxia-ischemia, which is exaggerated in combined hypoglycemic/hypoxic-ischemic injury.