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Related Concept Videos

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...
Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

Antiepileptic Drugs: GABAergic Pathway Potentiators

γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
The key GABA pathway potentiators used in epilepsy management are as follows.
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Antiepileptic Drugs: Glutamate Antagonists

Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...
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Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
Encephalitis l: Introduction01:19

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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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Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
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Published on: November 8, 2018

Valproate-induced hyperammonemic encephalopathy.

Hsiao-Feng Chou1, Rei-Cheng Yang, Cheng Ying Chen

  • 1Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan.

Pediatrics and Neonatology
|January 13, 2009
PubMed
Summary

Valproate can cause serious hyperammonemic encephalopathy, even with normal liver enzymes and valproate levels. This case highlights carnitine deficiency as a factor in valproate-induced encephalopathy.

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Published on: May 16, 2019

Area of Science:

  • Neurology
  • Toxicology
  • Metabolic Disorders

Background:

  • Valproate is a common antiepileptic drug.
  • Valproate-induced hyperammonemic encephalopathy (VHE) is a rare but severe complication.
  • VHE can occur despite normal liver function and therapeutic valproate serum levels.

Purpose of the Study:

  • To describe a case of VHE in an adolescent with absence seizures.
  • To highlight the association with carnitine deficiency.
  • To discuss potential mechanisms, risk factors, and treatment of VHE.

Main Methods:

  • Case report of an adolescent female treated with valproate for absence seizures.
  • Clinical monitoring for neurological symptoms, including dizziness, malaise, vomiting, and decreased consciousness.
  • Laboratory investigations including serum ammonia, liver-associated enzymes, valproate levels, and tandem mass spectrometry for carnitine levels.
  • Electroencephalography (EEG) for brain activity assessment.
  • Intervention with emergent hemodialysis.

Main Results:

  • The patient developed symptoms of VHE after restarting valproate.
  • Elevated serum ammonia levels (five times the upper normal limit) and a supra-therapeutic valproate level were observed.
  • Normal liver-associated enzyme levels were noted.
  • EEG showed continuous generalized slowing.
  • Carnitine deficiency was identified via tandem mass spectrometry.
  • Hemodialysis led to improvement in consciousness, ammonia levels, and EEG findings.

Conclusions:

  • VHE is a critical diagnosis to consider in patients on valproate presenting with altered consciousness.
  • Carnitine deficiency may be a predisposing factor for VHE.
  • Prompt recognition and intervention, such as hemodialysis, can be effective in managing VHE.