Hypoglycemic encephalopathy

Case contributed by Anar Kazimov
Diagnosis almost certain


Decreased conscious state. Patient previously well. No history of diabetes or medications other than Prozac.

Patient Data

Age: 30 years
Gender: Female

Diffusion restriction in splenium corpus callosum, bilateral posterior limb of internal capsule is noted. 


Exactly 1 month later we see that the restricted diffusion in splenium corpus callosum and posterior limb of internal capsules is totally resolved. 

Case Discussion

On biochemical examination, blood glucose level was 32 mg/dL and T3, T4 and anti-TSH were high. The only medication the patient was on was Prozac, which has been associated with hypoglycemia. 

Hypoglycemia is the sudden decrease in serum glucose level <50 mg/dL. In severe cases of hypoglycemia, the commonly affected sites are cerebral cortex, hippocampus and basal ganglia. In evaluating severe hypoglycemic encephalopathy, DWI should be used. Undiagnosed insulinoma, sepsis, renal or hepatic failure can also induce hypoglycemia. Hypoglycemia can cause several neurologic symptoms including memory loss, transient motor deficits, a persistent vegetative state, and in rare cases death. In hypoglycemic encephalopathy cases, the lesions show reversible cytotoxic edema at the cerebral cortex, hippocampus, splenium of the corpus callosum (boomerang sign), internal capsule, and cerebral white matter.

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