ArticlePsychiatry and clinical neurosciences2019
Cefepime-induced encephalopathy: Neural mass modeling of triphasic wave-like generalized periodic discharges with a high negative component (Tri-HNC).
Article in Psychiatry and clinical neurosciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Cefepime-Induced Encephalopathy in a Patient With Uncompromised Renal Function: A Case Report.Case reports in infectious diseases · 2025Article
- EEG and video documentation of benzodiazepine challenge in catatonic stupor: A case report.Neuropsychopharmacology reports · 2024Article
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Abstract
aimCefepime, a fourth-generation cephalosporin, acts as a GABA
methodsCIE cases documented by a single-center consultation-liaison team between April 2015 and March 2017 were retrospectively reviewed. For further investigation, neural mass modeling was performed in silico.
resultsThree patients with CIE refused medication/examination and showed overt pain, palilalia, and much greater deterioration of eye and verbal response than the motor response, which was possibly related to GABAergic dysfunction. Triphasic wave-like generalized periodic discharges with a high negative component (Tri-HNC) were identified on the EEG of all three cases. The simulation reproduced the characteristic feature of 2-3 Hz Tri-HNC and recovery course on EEG, and a possible involvement of individual differences in pharmacological intervention. It also suggested that auto-inhibition (synaptic inputs from interneuron to interneuron) dysregulation contributed to generating Tri-HNC in CIE.
conclusionAs CIE is iatrogenic and continues unless cefepime is stopped, early recognition is crucial. Physicians should be vigilant about altered mental status, pain, and verbal changes in patients taking cefepime. Tri-HNC on EEG can expedite the diagnosis of CIE, and the association between Tri-HNC and CIE suggests that an excitatory and inhibitory imbalance due to the dysfunction of GABAergic interneurons is the underlying mechanism. This modeling may offer a new method of investigating disorders related to GABAergic dysfunction.
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