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Adult hypoglycemic encephalopathy
Imbalance between glucose supply, utilization → brain injury
Hypoglycemia: Sudden decrease in serum glucose level < 50 mg/dL
Stroke/coma in adult diabetic on insulin replacement therapy (IRT)
Parietal/temporal/occipital lobes, basal ganglia, ± hippocampi
Hyperintensity in parietooccipital cortex and basal ganglia
Thalami, subcortical/deep white matter and cerebellum generally spared
Restricted diffusion, ↓ ADC (may be transient)
MRS shows ↓ NAA, ↑ lactate
Acute cerebral ischemia/infarction
Hypoxia, hypoperfusion
Acute hypertensive encephalopathy (PRES)
Caused by IRT either without adequate glucose intake or excessive glucose utilization
Ingestion of oral hypoglycemic medication, either accidental or intentional
Accumulation/release of excitatory neurotransmitters increases glucose utilization
Patchy or diffuse laminar necrosis
Varying severity, white matter generally spared
Often elderly diabetic, altered dietary glucose intake
Coma, depressed level of consciousness
May be preceded by seizures
, temporal and occipital cortex bilaterally
.
, temporal and occipital cortex
. Prognosis in adult hypoglycemic encephalopathy varies with severity and duration of hypoglycemia, as well as extent of brain injury.
and cerebral cortex
.
and a prominent lactate peak
. Using an intermediate TE inverts only lactate, allowing it to be distinguished from lipid. Lactate is a marker of anaerobic metabolism with no peak seen in normal spectra.
Adult hypoglycemic encephalopathy (AHE)
Hypoglycemic brain injury
Diabetic coma (nonspecific; term may include AHE)
Imbalance between glucose supply, utilization → brain injury
Hypoglycemia: Sudden decrease in serum glucose level < 50 mg/dL
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