Case 9: Pregnant? Who's Pregnant?: Memory Loss in a Young Woman

Constance Smith-Hicks, MD, PhD

Disclosures

May 26, 2005

Case Discussion

The neurologist believes that the patient's symptoms are multifactorial — primarily due to profound hypoglycemia along with some component of osmotic demyelination.

Cerebral dysfunction is known to occur when the arterial blood glucose concentrations fall below 40 mg/dL. Primary hyperinsulinism (resulting from pancreatic islet cell carcinoma) or functional hyperinsulinism (seen in patients on insulin pumps) is the usual cause of profound hypoglycemia. The clinical presentation may include seizures; coma; strokelike episodes; or, as in this patient, profound cognitive deficits. Animal and human studies of profound hypoglycemia demonstrate selective neuronal necrosis of the cerebral cortex, the pyramidal neurons of Sommer sector (CA1 region), and the dentate gyrus. The damage is thought to occur via NMDA receptor activation by endogenous aspartate, in the case of hypoglycemia, and via the glutamine pathway during hypoxia. In this case, the patient's inability to learn new information as well as her difficulty with both visual and verbal information are supported by signal changes in both mesial temporal lobes. Of interest, the blood glucose concentration at which neurologic dysfunction becomes apparent is patient-dependent and may occur at levels as high as 55 mg/dL.

Case series and reports that address long-term outcome suggest that the natural history is varied and depends not only on the duration of hypoglycemia but also on the presence or absence of confounders, such as hypoxia or hypertension. In general, patients with shorter downtime and no other confounders experienced full recoveries that are associated with resolution of signal abnormalities seen on MRI.

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