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Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
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Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:
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Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
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Reversible splenial abnormality in hypoglycemic encephalopathy.

Ji Hyun Kim1, Jeong Yoon Choi, Seong-Beom Koh

  • 1Department of Neurology, Guro Hospital, Korea University School of Medicine, 80 Guro-Dong, Guro-Ku, Seoul, 152-703, South Korea. jhkim.merrf@gmail.com

Neuroradiology
|December 1, 2006
PubMed
Summary

Hypoglycemic encephalopathy can cause reversible signal abnormalities in the splenium of the corpus callosum (SCC). This finding suggests the SCC is vulnerable to low blood sugar and should be considered in diagnosing reversible SCC lesions.

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Area of Science:

  • Neurology
  • Radiology
  • Endocrinology

Background:

  • Splenium of the corpus callosum (SCC) lesions are infrequently reported in hypoglycemic brain injury.
  • Hypoglycemic encephalopathy can lead to neurological deficits.

Observation:

  • Three adult patients with hypoglycemic encephalopathy exhibited signal abnormalities in the SCC on diffusion-weighted imaging (DWI).
  • These abnormalities presented as high signals in the SCC with reduced apparent diffusion coefficients.

Findings:

  • The SCC signal abnormalities reversed completely within days after hypoglycemia correction.
  • Routine MRI and MR angiography showed no residual lesions or vascular abnormalities.
  • Medical history and lab tests excluded other causes for the SCC abnormalities.

Implications:

  • The splenium of the corpus callosum (SCC) is susceptible to hypoglycemia.
  • Hypoglycemia should be considered in the differential diagnosis for reversible SCC abnormalities.
  • DWI is a valuable tool for detecting and monitoring these reversible changes.