Clinical diagnosis
Case 248
【Discussion】
Bilateral diffuse cerebral cortex necrosis (BDCCN) can occur in various situations. Traumatic brain contusion, hanging, post-total radiation therapy, hypoxia, carbon monoxide intoxication, hypoglycemia and Creutzfeldt Jakob disease (Jakob disease). Most patients with BDCCN might trace the causes based on their present illness and/or past personal history. Jakob disease is reported to occur as one of family members or crazy cow disease (who ate meats or received cow dura containing prion). Jakob disease causes monthly atrophy of cerebrum.
Natural hypoglycemia such as starvation or practice fasting does not occur brain necrosis. However, artificial hypoglycemia during insulin or medicine for lowering blood sugar sometimes causes severe hypoglycemia. When blood sugar lowers below 50mg/dL, decreased cognition, seizure, or coma appears (1, 2). These symptoms are most functional or reversible. However, when blood sugar lowers below 20mg/dL, it leads to brain necrosis (1). Diffusion MRI is available to check brain disorder by hypoglycemia; in an early stage, high signal intensity is found on posterior limb of internal capsule, putamen, caudate nucleus and splenium of corpus callosum which are functional and reversible: in a delayed phase, high signal intensity on cerebral cortex indicates irreversible and necrotic (3-5).
In our case, he had loss of consciousness and his blood sugar was 36mg/dL. DWIMRI showed high signal intensity cerebral cortex at posterior lobe, parietal lobe, temporal lobe including insula and frontal lobe. Of these, high signal intensity was predominantly found in posterior lobe and lateral geniculate body. Additionally, centrum semiovale and splenium of corpus callosum with high signal intensity were demonstrated. The damages of bilateral diffuse high signal intensity indicate brain necrosis and poor prognosis. The mechanism of artificial hypoglycemia into brain necrosis is yet to be clarified.
Hypoxia or carbon monoxide intoxication causes high signal intensity on globus pallidus at first where it spares in transient hypoglycemia (6-8). It might indicate different findings of brain damage on DWIMRI between hypoxia and hypoglycemia.
When bilateral diffuse cerebral cortex is found on DWIMRI, it indicates brain necrosis. The causes are hidden under the medical or life history of patients, such as hypoxia, hypoglycemia and carbon monoxide intoxication. When the remarkable event is not found, Jakob disease is listed to be suspected.
【Summary】
We presented a seventy nine-year-old male with coma. His blood sugar was 32mg/dL. DWIMRI showed high signal intensity of cerebral cortex in whole lobes, lateral geniculate body and splenium of corpus callosum, indicative of diffuse brain necrosis. Brain necrosis occurs following drop of blood sugar below 20mg/dL. It is borne in mind that in an early stage of hypoglycemia, high signal intensity is found on posterior limb of internal capsule, putamen, caudate nucleus and splenium of corpus callosum which are functional and reversible, meanwhile in a delayed phase, high signal intensity on cerebral cortex indicates irreversible and necrotic. Further, when bilateral diffuse high signal intensity are demonstrated on DWIMRI, hypoxia, hypoglycemia, carbon monoxide intoxication and Jakob disease are listed to be suspected.
【References】
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3.Kang EG, et al. Diffusion MR Imaging of Hypoglycemic Encephalopathy. American Journal of Neuroradiology March 2010, 31 (3) 559-564;
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6.Kim DM, et al. Acute carbon monoxide poisoning: MR imaging findings with clinical correlation. Neuroradiology. 2017; 98: 299-306
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2021.11.1