Neonatal hypoglycemia is a common occurrence, in up to 15% of infants born near or at term. It is the most common metabolic problem in neonates, and not only is it important because of the immediate health of the child, but neonatal hypoglycemia is also associated with long-term neurologic sequelae. As the child transitions from a continuous supply of maternal glucose via the placenta to an intermittent supply via milk, there is a normal physiologic nadir that occurs for blood glucose; however, this process may become pathologic due to various reasons.
It is very challenging to provide a definition of exactly when neonatal hypoglycemia occurs, as many infants with hypoglycemia may be asymptomatic; also, some patients may be symptomatic at higher glucose levels than others. Hypoglycemic newborns may present with either neuroglycopenic symptoms, such as poor feeding, lethargy, seizures, and hypotonia among others, or neurogenic symptoms resulting from sympathetic activity due to hypoglycemia. These neurogenic symptoms include tremors, sweating, tachypnea, irritability and pallor.
Generally, on T1 imaging, the lesions would show decreased intensity, T2 with increased intensity and DWI would show reduced restriction diffusion in the affected regions. On T2 and FLAIR imaging, there may be a bilateral increased signal involving the insula and the parieto-occipital part of the cerebral cortex, the posterior limb of the internal capsule, the hippocampus and basal ganglia. In neonates, the corpus callosum may be involved, along with the cerebellum, brainstem and the thalami. Some studies show that the specific lesions in the bilateral basal ganglia, cerebral cortex, substantia nigra and hippocampus suggest that these areas are susceptible to hypoglycemia in the brain. On DWI, there may be evidence of transient cerebral edema and hemorrhage.
References:
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