Hypoglycemic brain injury
History of sulfonylurea abuse presenting with hypoglycemic coma.
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Diffuse damage of the cortex and bilateral basal ganglia (caudate, globus pallidus and putamen), with sparing of the cerebellum, subcortical white matter, thalami and the stem.
The neurological manifestations complicated by profound hypoglycemia range from reversible focal deficits to irreversible coma. The cortex, basal ganglia, and hippocampus seem to be the brain tissues most vulnerable to hypoglycemia The thalami, cerebellum, and hypothalamus are typically unaffected. Involvement of the caudoputamen and basal ganglia may portend a poor prognosis.
The localized lesions represent tissue degeneration, including some combination of selective neuronal death, proliferation of astrocytic glial cells, paramagnetic substance deposition, and/or lipid accumulation.
- 1. Fujioka M, Okuchi K, Hiramatsu KI et-al. Specific changes in human brain after hypoglycemic injury. Stroke. 1997;28 (3): 584-7. Pubmed citation