Objectives: Brain function depends on a continuous supply of glucose from blood, and oxidative
metabolism is the only source of energy except in extreme starvation. This is the
basis of the high frequency of cerebral dysfunction in cases of transient hypoglycemia.
Neuronal death can occur when plasma glucose levels fall below 18 mg/dL. Typically, MRI in hypoglycemic encephalopathy demonstrates T2 white matter
lesions in the cortex, hippocampus, and basal ganglia. Prolonged, severe hypoglycemia
can cause permanent neurologic damage. Complications include permanent brain damage
leading to persistent vegetative state and death. This is usually seen in diabetic
patients and rarely in prolonged starvation. This case is presented with the goal
of alert for a common pathology, somethimes not considered. Material and method: Retrospective analysis of the patient chart, blood analysis and image exams. Case report: A 31-year-old male was admitted after three days of no food ingestion, just alcohool
abuse. He was admitted in the emergency room for seizures. He had no past history
of diabetes, epilepsy or any other neurologic problems. A finger stick glucometer
reading showed a serum glucose level of 11 mg/dL. At entrance he scored 6 at Glasgow coma score. He had no extra-ocular movement
abnormalities or pyramidal signs at examination. A CT scan performed at D1 showed
diffuse cerebral edema and no focal lesions. An electroencephalogram (EEG) was done
at D3 and showed diffuse large theta–delta waves. The MRI scan at D18 revealed T2
white matter lesion of the caudate nucleus, hippocampus and putamina, and diffuse
global parenchyma atrophy but no evidence of cortical laminar necrosis. The analytic
workup was unremarkable, namely for hepatic function, thyroid function, viral serologies,
auto-immune research and CSF studies. There was no evidence of insulinoma. No other
metabolic disorder was found during admission. There were no other records of severe
hypoglycemia. The clinical findings were admitted to be related to hypoglycemic encephalopathy.
He was discharged at D25, maintaining language and gait disturbance. Discussion/conclusions: Hypoglycemic encephalopathy is a serious condition that can lead to death and permanent
severe neurologic deficits. Prompt recognition and adequate treatment carry the only
chance of good recovery. Diabetes and poor nutritional status are the more prevalent
risk factors but other causes must be excluded. Awareness of the presenting features
and typical EEG and MRI findings of this entity are of critical importance.
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© 2013 Published by Elsevier Inc.