Joseph Junewick, MD FACR
over 7 years ago
Please choose a workflow. A standard workflow allows you to browse the repository with full case detail; the academic workflow allows you to browse the repository with limited case detail revealed. Double click on the images to launch image viewer.
Joseph Junewick, MD FACR
|Diagnostic Category: Metabolic
|Created: over 5 years ago
|Updated: over 5 years ago
Newborn with seizure-like activity and hypoglycemia.
MR – Junctional blurring and restricted diffusion in the parieto-occipital regions bilaterally; restricted diffusion is also present in the splenium of the corpus callosum.
Symptoms of neonatal hypoglycemia are non-specific and include stupor, jitterieness and seizure. Hypoglycemia is defined by a blood glucose level below 45 mg/dL although lower levels are tolerated in the immediate newborn period and by premature infants. The pathophysiology of hypoglycemic encephalopathy still remains unclear but may be related to 1) energy failure, 2) excitotoxic edema, and/or 3) asymmetric cerebral blood flow. In general, hypoglycemia is better tolerated than hypoxia.
While neurons can use lactate as an alternative energy source, glucose deprivation leads to arrest of protein synthesis in many regions, incomplete energy failure and loss of ion homeostasis, cellular calcium influx, and intracellular alkalosis. Consequently, release iof neuroactive amino acids into the extracellular space occurs and results in selective neuronal necrosis, predominantly in the cerebral cortex, caudoputamen, and hippocampus. However, protein synthesis in the cerebellum, brain stem, and hypothalamus remains unaffected because of the greater activity of the glucose transport mechanisms.
Increased extracellular glutamate leads to excitotoxic edema. The presence of glutamate leads to calcium and sodium entry into the cell and induces apoptosis. Excitotoxic edema does not imply neuronal damage. Glutamate reuptake systems are not impaired in hypoglycemia. Consequently, cell injury may be transitory and DWI abnormalities normalize with time. Lack of autoregulation in the posterior circulation may make the parietal and occipital regions more vulenerable. The prognosis or neurologic sequelae of hypoglycemic encephalopathy depends on the severity and duration of hypoglycemia. DWI may be useful to predict outcome. White matter may recover better than cortical, basal ganglial and hippocampal locations.
Kanga EG, Jeona SJ, Choia CJ, et al. Diffusion MR Imaging of Hypoglycemic Encephalopathy. American Journal of Neuroradiology (2010); 31:559-564.
Barkovich AJ. Pediatric Neuroimaging, 4th Ed. Lippincott, Williams and Wilkins (2005).