Commentary: Newly Diagnosed Hepatic Encephalopathy Presenting as Non-convulsive Status Epilepticus: A Case Report and Literature Review

Philippe Gelisse^1,2*Arielle Crespel^2,3

• ¹Hopital Gui de Chauliac Service de Neurologie, Montpellier, France
• ²Centre Hospitalier Universitaire de Montpellier, Montpellier, France
• ³Hopital Gui de Chauliac, Montpellier, France

Olivero et al. (2022) described a case of hepatic encephalopathy (HE) presenting as nonconvulsive status epilepticus (NCSE), asserting that this was the first reported instance of NCSE as the initial manifestation of HE [1]. It is a typical HE case without any ictal activity on the EEG. Indeed, their diagnosis of NCSE based on EEG findings is very questionable. The authors interpreted the EEG as demonstrating "fast paroxysmal bilateral sharp-wave activity" that resolved after diazepam administration. Yet, the provided EEG recordings are more consistent with metabolic encephalopathy, characterized by runs of triphasic waves (TWs) (Fig. 1) associated with slow-wave activity. This strictly corresponds to the HE pattern described by Bickford and Butt 70 years ago [2].The observed EEG improvement following diazepam does not confirm NCSE, as diazepam is a hypnotic agent. There is a common false syllogism in the case of TWs: "Intravenous benzodiazepines suppress the ictal activity in NCSE, TWs are suppressed by intravenous benzodiazepines. Therefore, these patients have NCSE" [3]. In the case report of Olivero et al, the resolution of TWs simply reflects sleep induction rather than seizure termination. Older studies have shown that TWs and rhythmic delta waves in metabolic encephalopathy either decrease or disappear entirely during NREM sleep [4]. In his famous Textbook of Electroencephalography, Niedermeyer (1999), wrote of HE that ''when such patients are allowed to fall asleep, normalization of the record takes place for the duration of sleep" [5]. Authors should incorporate EEG reactivity testing into their clinical protocols for patients with suspected NCSE, as it offers critical diagnostic insights beyond conventional criteria. This simple, cost-effective test is a safer alternative to empirical trials of antiseizure medications.In true NCSE, epileptiform activity is self-sustaining and typically unresponsive to external stimuli. In contrast, TWs or generalized periodic discharges in metabolic/toxic encephalopathies often exhibit vigilance-dependent reactivity. This resolves transiently when patients are aroused from drowsiness to full wakefulness, although reactivity tends to disappear with the increasing severity of the disease and in comatose patients. In patients without preexisting epileptic encephalopathy, stimulus-induced wakefulness with transient EEG improvement strongly favors a non-ictal (encephalopathic) pattern over NCSE. (Table 1) [6].Moreover, the authors reported unremarkable CT perfusion findings, whereas MRI revealed changes consistent with hepatic encephalopathy but no evidence of status epilepticus (SE). Nevertheless, seizures can occur in HE as well. We report a 66-year-old male with alcoholinduced cirrhosis who was hospitalized in coma. His EEG demonstrated independent rightand left-hemispheric focal subclinical seizures, and a CT scan showed cerebral edema.Because the seizures were not recognized, his course progressed to a pattern consistent with anoxic encephalopathy [12].In conclusion, sometimes the EEGs of patients with metabolic/toxic encephalopathy are striking, and NCSE may be part of the differential diagnosis. In addition to the Salzburg criteria for diagnosing NCSE, six key questions should be routinely considered in such cases (Table 1). Now, neuroimaging findings have become an essential component in refining the diagnostics of NCSE.. However, it demonstrates bilateral runs of triphasic waves (TWs), a pattern characteristic of metabolic encephalopathy-specifically hepatic encephalopathy in this case. The shaded (grey) areas include zoomed-in segments to highlight the three distinct phases of the waves, which are annotated for clarity. In the first panel, the TWs appear continuously, with no discernible intervals between successive waveforms. Nonconvulsive status epilepticus versus metabolic/toxic encephalopathies with generalized periodic activity. The six key questions. Is it a confusional state or only a problem of vigilance? Question 2Is there a fluctuation of symptoms or a change in consciousness from somnolence to coma? Question 3Is the EEG activity rhythmic or periodic? Question 4Is the EEG activity dynamic, showing spatiotemporal evolution, or relatively monomorphic? Question 5Is the EEG reactive to stimuli, wakefulness, sleep, arousal, or antiseizure drugs*? Question 6Neuroimaging results*Only consider an IV benzodiazepine test positive if both EEG and consciousness normalize.