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Review
. 2022 Oct;48(10):1443-1462.
doi: 10.1007/s00134-022-06854-3. Epub 2022 Aug 23.

Electroencephalogram in the intensive care unit: a focused look at acute brain injury

Affiliations
Review

Electroencephalogram in the intensive care unit: a focused look at acute brain injury

Ayham Alkhachroum et al. Intensive Care Med. 2022 Oct.

Abstract

Over the past decades, electroencephalography (EEG) has become a widely applied and highly sophisticated brain monitoring tool in a variety of intensive care unit (ICU) settings. The most common indication for EEG monitoring currently is the management of refractory status epilepticus. In addition, a number of studies have associated frequent seizures, including nonconvulsive status epilepticus (NCSE), with worsening secondary brain injury and with worse outcomes. With the widespread utilization of EEG (spot and continuous EEG), rhythmic and periodic patterns that do not fulfill strict seizure criteria have been identified, epidemiologically quantified, and linked to pathophysiological events across a wide spectrum of critical and acute illnesses, including acute brain injury. Increasingly, EEG is not just qualitatively described, but also quantitatively analyzed together with other modalities to generate innovative measurements with possible clinical relevance. In this review, we discuss the current knowledge and emerging applications of EEG in the ICU, including seizure detection, ischemia monitoring, detection of cortical spreading depolarizations, assessment of consciousness and prognostication. We also review some technical aspects and challenges of using EEG in the ICU including the logistics of setting up ICU EEG monitoring in resource-limited settings.

Keywords: Cortical spreading depolarization; Disorders of consciousness; Electroencephalogram; Intensive care unit; Ischemia; Nonconvulsive seizures; Status epilepticus.

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Conflict of interest statement

Conflict of interest

AA, BA, and SE report no disclosures. BF is supported by grant funding from the DOD (JW200215 and W81XWH1920013). He received additional support for research through the NIH/NINDS, NIH/NIBIB, and NSF. He receives speaking fees and consulting fees from UCB Pharma, and serves on the scientific advisory boards of Marinus, Inc and Sage Therapeutics. NG reports no disclosures. EJG is supported by grant funding from the NIH R01NS117904–01, is a consultant for UCB and co-founder (no financial relationship) of Intracranial Bioanalytics (IBA). LJH has received consultation fees for advising from Accure, Aquestive, Ceribell, Eisai, Marinus, Medtronic, Neurelis, Neuropace and UCB; royalties from Wolters-Kluwer for authoring chapters for UpToDate-Neurology, and from Wiley for co-authoring the book “Atlas of EEG in Critical Care”; and honoraria for speaking or running webinars from Neuropace, Natus, and UCB. PK reports no disclosures. VL reports no disclosures. JK is supported by grant funding through the University of Calgary, Office of Health and Medical Education Scholarship. PV is supported by grants from NIH and the State of California PV has received compensation for consultancy and speaker fees and expenses from Ceribell and consultancy and speaker fees from UCB Pharma. SFZ is supported by grant funding from the NIH K23NS114201 and the American Epilepsy Society (Infrastructure grant). She is a clinical neurophysiologist for Corticare. BR reports no disclosures. JC is a minority shareholder at iCE Neurosystems.

Figures

Fig. 1
Fig. 1
In a term infant undergoing extracorporeal membrane oxygenation, there is a gradual loss of power of frequencies in the 1–12 Hz range over the left hemisphere observed on the color dense spectral array (top panel), with an increase in power over the right hemisphere (red) as evidenced by the relative asymmetry spectrogram. Subsequent neuroimaging demonstrates a left posterior circulation infarction with cerebral edema
Fig. 2
Fig. 2
Cyclical seizures over the right posterior region can be observed on raw electroencephalography (left) and are demonstrated with the flame sign on color-dense spectral array panels
Fig. 3
Fig. 3
Recurrent multifocal seizures are in a term neonate, which are appreciated on raw EEG (left) in addition to the identification of the ‘fame sign’ on color dense spectral array (right, middle panels) and increase in amplitude on the aEEG panel (right, bottom panel)
Fig. 4
Fig. 4
Generalized periodic sharp waves are observed with triphasic morphology in a patient with hepatic encephalopathy
Fig. 5
Fig. 5
Example of sleep spindles observed over the bilateral hemispheres (arrow), indicative of corticothalamic function
Fig. 6
Fig. 6
An alpha coma pattern is observed in a 2-year-old female after a submersion injury and hypoxic-ischemic brain injury
Fig. 7
Fig. 7
Diagram describing different paradigms for evaluating event-related potentials with local and global effects to evaluate unconscious or conscious detection of novel auditory stimuli, in addition to the “motor command protocol” utilized for assessing motor command following using electroencephalographic power spectral density [7]
Fig. 8
Fig. 8
Clusters of spreading depolarizations on depth electrode monitoring after severe traumatic brain injury. A 76 year old man was admitted after a fall. His initial Glasgow Coma Scale score was 7 and he had bilaterally reactive pupils. A right frontal multimodality monitoring bolt was placed at the bedside in the intensive care unit which included a depth electrode. Hours later, he developed a worsening of his neurological exam. A Post-bolt non-contrast head CT demonstrates widespread contusions, traumatic subarachnoid hemorrhage, and intraventricular hemorrhage. The location of the bolt within the right frontal cortex is shown. B An example of spreading depolarization (SD) using referential electrocorticography (ECoG). The black band represents high-frequency EEG and the red band represents DC-centered signal. A negative DC potential is observed in channel 4 initially, followed by spread (red arrows) to channels 2 and 1. The depolarization in channel 4 occurred despite low voltage activity in the high-frequency band, defining an isoelectric spreading depolarization. The region of cortex recorded in channels 2 and 1 in contrast exhibits higher amplitude high-frequency activity that subsequently becomes depressed for approximately 10 min. C Using bipolar recording and near-DC low pass filtering (0.005 Hz), the same spreading depolarization can be visualized which displays the negative potential with an artificial ‘triphasic’ appearing morphology. Note the enhanced clarity of the focal regions of high-frequency depression. D Over a 6-h window, a cluster of spreading depolarizations occurs (denoted by white arrowheads), defined as 3 or more SD within a 2 h window. The restoration of high-frequency activity after each SD becomes progressively lower in amplitude until finally, the SDs become isoelectric
Fig. 9
Fig. 9
Example of normal awake background in an adult patient with a posterior dominant rhythm in the alpha (8–13 Hz) range
Fig. 10
Fig. 10
Example of an electrographic seizure manifesting with definitive spatiotemporal evolution over 10 s in duration
Fig. 11
Fig. 11
Bilateral independent periodic discharges with embedded polyspikes (BiLPDs+, arrow) are observed in a patient with posterior reversible encephalopathy syndrome
Fig. 12
Fig. 12
Lateralized rhythmic delta activity with embedded spikes (LRDA + S) observed in a patient with meningoencephalitis with acute symptomatic seizures

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