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In the case of suspicion of nonconvulsive status epilepticus (NCSE), reactivity on electroencephalograms (EEGs) can provide valuable diagnostic information. Reactivity refers to responses to auditory or somatosensory stimulation, with changes in amplitude and frequency of background activity. Because of self‐perpetuating processes and the failure of self‐terminating mechanisms, status epilepticus is unlikely to cease when patients spontaneously move, and it cannot typically be stopped by external stimulation (i.e., auditory and tactile stimuli). The defining EEG characteristic of absence status epilepticus is the presence of bilateral, synchronous, symmetric, rhythmic paroxysmal activity that shows little or no reactivity to sensory stimulation. On the other hand, in metabolic/toxic or multifactorial encephalopathies, triphasic waves (TWs) are influenced by the level of vigilance. TWs may be transiently abolished when patients increase their level of alertness from a drowsy/lethargic state to a state of wakefulness. This reactivity is only observed when patients can be aroused by a somatosensory or auditory stimulus. This reactivity tends to disappear with increasing severity of the disease and in comatose patients. In patients without preexisting developmental and epileptic encephalopathy, this pattern of stimulus‐induced wakefulness with transient improvement of the EEG is a major criterion in determining that the EEG patterns are not ictal. This criterion of reactivity on EEGs, beyond the classical clinical/EEG criteria of NCSE (Salzburg criteria), should now be systematically added. [ABSTRACT FROM AUTHOR]

Electroencephalography (EEG) is a useful adjunct to clinical neurological examination, particularly as it may detect subtle or subclinical disturbance of cerebral function and it allows monitoring of cerebral activity over time. Continuous EEG combined with quantitative analysis and machine learning may help identify changes in real time, before the emergence of clinical signs and response to interventions. EEG is rarely pathognomonic in encephalopathy/encephalitis but when interpreted correctly and within the clinical context, certain phenotypes may indicate a specific pathophysiology (eg, lateralised periodic discharges in HSV-1, generalised periodic discharges in sporadic Creutzfeldt-Jakob disease, and extreme delta brushes in anti-n-methyl-D-aspartate receptor autoimmune encephalitis). EEG is included in some specialist guidelines for disease assessment, monitoring and prognostication (ie, hepatic, cancer immunotherapy, viral, prion, autoimmune encephalitis and hypoxic ischaemic encephalopathy). EEG is invaluable for confirming or excluding non-convulsive seizures or status epilepticus, particularly in critically ill patients, and in understanding new concepts such as epileptic encephalopathy and the ictal-interictal continuum. [ABSTRACT FROM AUTHOR]

Objective: The Salzburg criteria for nonconvulsive status epilepticus (NCSE) and the American Clinical Neurophysiology Society (ACNS) Standardized Critical Care EEG Terminology 2021 include a diagnostic trial with intravenous (IV) antiseizure medications (ASMs) to assess electroencephalographic (EEG) and clinical response as a diagnostic criterion for definite NCSE and possible NCSE. However, how to perform this diagnostic test and assessing the EEG and clinical responses have not been operationally defined. Methods: We performed a Delphi process involving six experts to standardize the diagnostic administration of IV ASM and propose operational criteria for EEG and clinical response. Results: Either benzodiazepines (BZDs) or non‐BZD ASMs can be used as first choice for a diagnostic IV ASM trial. However, non‐BZDs should be considered in patients who already have impaired alertness or are at risk of respiratory depression. Levetiracetam, valproate, lacosamide, brivaracetam, or (if the only feasible drug) fosphenytoin or phenobarbital were deemed appropriate for a diagnostic IV trial. The starting dose should be approximately two thirds to three quarters of the full loading dose recommended for treatment of status epilepticus, with an additional smaller dose if needed. ASMs should be administered during EEG recording under supervision. A monitoring time of at least 15 min is recommended. If there is no response, a second trial with another non‐BDZ or BDZs may be considered. A positive EEG response is defined as the resolution of the ictal–interictal continuum pattern for at least three times the longest previously observed spontaneous interval of resolution (if any), but minimum of one continuous minute. For a clinical response, physicians should use a standardized examination before and after IV ASM administration. We suggest a definite time‐locked improvement in a focal deficit or at least one‐step improvement on a new dedicated one‐domain 10‐level NCSE response scale. Significance: The proposed standardized approach of a diagnostic IV ASM trial further refines the ACNS and Salzburg diagnostic criteria for NCSE. [ABSTRACT FROM AUTHOR]

Aims: Seizures and status epilepticus (SE) are detected in almost a third of the comatose cardiac arrest survivors. As the literature is quite exhaustive regarding SE with motor symptoms in those patients, little is known about nonconvulsive SE (NCSE). Our aim was to compile the evidence from the literature of the frequency and outcome of NCSE in adult patients remaining in coma after resuscitation. Methods: The medical search PubMed was screened for most relevant articles reporting the emergence and outcome of NCSE in comatose post-resuscitated adult patients. Results: We identified 11 cohort studies (four prospective observational, seven retrospective) including 1092 patients with SE in 29–96% and NCSE reported in 1–20%. EEG evaluation started at a median of 9.5 h (range 7.5–14.8) after cardiac arrest, during sedation and targeted temperature management (TTM). Favorable outcome after NCSE occurred in 24.5%. We found no study reporting EEG to detect or exclude NCSE in patients remaining in coma prior to the initiation of TTM and without sedation withing the first hours after ROSC. Discussion: Studies on NCSE after ROSC are scarce and unsystematic, reporting favorable outcome in every fourth patient experiencing NCSE after ROSC. This suggests that NCSE is often overlooked and outcome after NCSE is not always poor. The low data quality does not allow firm conclusions regarding the effects of NCSE on outcome calling for further investigation. In the meantime, clinicians should avoid equating NCSE after ROSC with poor prognosis. [ABSTRACT FROM AUTHOR]

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