ArticleCureus2021
A Case of Valproic-Acid Induced Hyperammonemic Encephalopathy.
Article in Cureus, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Article
- Hyperammonemia associated with low doses and concentrations of valproic acid in older adults with neurocognitive disorder.The mental health clinician · 2026Article
- Valproate-induced hyperammonemic encephalopathy after aneurysm clipping surgery: a case report with literature review.Frontiers in medicine · 2026Article
- Valproate-related hyperammonemic encephalopathy with generalized suppression EEG: a case report.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Valproic acid (VPA), an antiepileptic medication, is known to cause hyperammonemia, which may be asymptomatic or can present with encephalopathy. VPA-induced hyperammonemic encephalopathy (VHE) is a serious but reversible condition, which requires high clinical suspicion for diagnosis. It may occur acutely or after chronic use of VPA. We present the case of a 44-year-old male who was on long-term VPA therapy for a seizure disorder. He presented to the emergency department with the complaint of two episodes of seizures two days before admission. On arrival, the patient was confused and tearful and was unable to recollect the events leading to the seizure. The initial complete metabolic panel, liver function tests, urinalysis, and serum VPA levels were observed to be normal. However, there was a marked elevation in ammonia levels. VPA was suspected to be the inciting agent of hyperammonemic encephalopathy, and, therefore, it was discontinued. The patient was started on oral lactulose and prescribed a different anti-seizure medication (i.e., lamotrigine). His ammonia levels decreased gradually, and his condition improved. Thus, it was concluded that the patient had developed VHE. At the time of discharge, he was stable and had no confusion or seizures. This case report evaluates his presentation and discusses the possible pathogenesis of VHE.
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