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Hepatic Encephalopathy01:29

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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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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Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
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Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
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Updated: Jun 17, 2026

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats
06:39

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats

Published on: October 17, 2018

Asymmetrical delayed encephalopathy after acute CO intoxication: a case report.

Pi-Shan Sung1, Chin-Yin Yu, Thy-Sheng Lin

  • 1Department of Neurology, National Cheng Kung University Hospital, Tainan, Taiwan. Small_33.tw@yahoo.com.tw

Neurotoxicology
|December 26, 2009
PubMed
Summary

Delayed encephalopathy after carbon monoxide (CO) intoxication may involve ischemic components. Magnetic resonance imaging revealed prominent changes in the right middle cerebral artery territory, suggesting a link between CO exposure and stroke-like brain injury.

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Last Updated: Jun 17, 2026

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats
06:39

Sub-acute Cerebral Microhemorrhages Induced by Lipopolysaccharide Injection in Rats

Published on: October 17, 2018

Area of Science:

  • Neurology
  • Toxicology
  • Radiology

Background:

  • Carbon monoxide (CO) intoxication can lead to delayed neurological sequelae.
  • The pathophysiology of delayed CO encephalopathy is not fully understood.
  • Ischemic mechanisms are being investigated as a potential contributor.

Observation:

  • A patient presented with delayed encephalopathy 21 days post-acute CO intoxication.
  • Initial MRI showed a right middle cerebral artery (MCA) stenosis with an acute infarct.
  • Follow-up MRI demonstrated significant delayed encephalopathy changes.

Findings:

  • Delayed encephalopathy changes were most pronounced in the right MCA territory.
  • The observed pattern suggests an ischemic component in CO-related brain injury.
  • MRI findings correlated infarcts and MCA territory with encephalopathy severity.

Implications:

  • This case highlights the potential for ischemic injury in delayed CO encephalopathy.
  • Findings suggest that vascular factors, such as MCA stenosis, may exacerbate CO toxicity.
  • Further research into the ischemic contribution to CO-induced brain damage is warranted.