BJA Education, 19(3): 74e82 (2019)

doi: 10.1016/j.bjae.2018.11.002
Advance Access Publication Date: 17 December 2018

Matrix codes: 1A01,

2C01, 3F00

Introduction to interpretation of the EEG in intensive

care
L. Sewell1 A. Abbas2 and N. Kane1,*
1
North Bristol NHS Trust, Bristol, UK and 2Queen Elizabeth Hospital, Birmingham, UK
*Corresponding author: [email protected]

Learning objectives Key points

By reading this article, you should be able to:  EEG and somatosensory evoked potentials (SSEP)
 Describe the basic principles of EEG, including can provide objective measures of cerebral
waveforms seen in the healthy adult population. activity.
 Summarise the common causes of encephalopa-  EEG is a sensitive measure of cerebral distur-
thy and their associated features on the bance, although it is not specific to particular
electroencephalograph. aetiologies.
 Discuss the neurophysiological features associ-  Diagnostic uses of EEG in critical care include the
ated with favourable and unfavourable outcomes identification and grading of encephalopathy,
in critically ill patients. and the identification and guidance for manage-
ment of patients with non-convulsive epileptic
EEG is an investigation often used in critical care, but the seizures.
application of the EEG findings in clinical care by ICU physi-  Therapeutic indications of EEG include assess-
cians can prove challenging. ment of the depth of sedation in induced coma.
Common conditions in which EEG can inform diagnosis  EEG and SSEP, in combination with neuroimaging
and neurological prognosis include encephalopathy, seizure and biochemical measurements, can provide
disorders, hypoxic and traumatic brain injuries, cerebral valuable prognostic information after cardiac ar-
structural abnormalities, and coma. EEG also has therapeutic rest or traumatic brain injury.
indications, such as determining the depth of anaesthesia in
induced coma and the cessation of non-convulsive status
epilepticus by anticonvulsant or anaesthetic agents. the internationally agreed recently revised glossary of terms
Patterns that are frequently encountered in critical care most commonly used by clinical electroencephalographers.1
include slow (wave) activity, frontal intermittent rhythmic This overview discusses the basic principles of EEG,
delta activity (FIRDA), triphasic waves, epileptiform patterns recording and interpretation, followed by EEG patterns pre-
and periodic discharges (PDs), suppression, and burst sup- sent in the aforementioned pathologies, as illustrated in
pression. Detailed definitions of these patterns can be found in Figures 1e8 (also see additional details in Supplementary
data).

Basic principles
Laura Sewell MRCP is a specialty trainee in clinical neurophysiology
and neurology at North Bristol NHS Trust. The EEG records electrical activity generated by cerebral
neurones, in the form of potential differences between elec-
Ahmed Abbas MRCP FHEA is a specialty trainee in clinical neuro- trodes positioned over the scalp. The EEG is digitised, ampli-
physiology at Queen Elizabeth Hospital, Birmingham. fied (as in a healthy adult it is typically 20e100 mV), filtered to
Nick Kane MSc, MD (Hons), FRCS, FRCP (by election), is a consul- remove or reduce noise (usually from 0.3 to 70 Hz), and dis-
tant in clinical neurophysiology at Southmead Hospital, North played as waveforms of varying morphologies and fre-
Bristol NHS Trust. quencies (Table 1). Interpretation of these waveforms is

Accepted: 12 November 2018

© 2019 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.
For Permissions, please email: [email protected]

74
 Introduction to interpretation of EEG

Fig 1 Normal adult EEG demonstrating alpha rhythm (highlighted in box), with blocking on eye opening (vertical line).

usually by visual inspection, but can be performed by quan- propofol, benzodiazepines).3 However, in simplified terms,
titative analysis of the frequency, amplitude, topographical increasing depth of anaesthesia results in progressive in-
distribution, cross correlation, and reactivity; these analyses crease of slower frequencies, although different agents can
enable an objective assessment of cerebral activity.2 induce several effects.4 In the case of propofol, the beta ac-
Standard recording typically uses 21 electrodes, applied tivity decreases first with an increase in coherent alpha ac-
according to the international 10e20 classification system, tivity, which becomes more prominent over the anterior part
over the frontal (F), temporal (T), central (C), parietal (P), and of the head (‘anteriorisation’), before slower incoherent fre-
occipital (O) regions. Even-numbered electrodes relate to the quencies emerge, followed by burst suppression and finally
right hemisphere and odd ones to the left, whilst a post-fixed z suppression of all cortical activity.5
refers to the midline. A standard recording is usually 20e30 While epileptiform activity can be assessed in the presence
min in duration. of pharmacological sedation, temporary weaning of such
agents should produce a more reliable EEG for interpretation
of the ongoing background activity.
Normal adult EEG
Alpha activity is usually evident over posterior cortical regions
and is ‘reactive’ to arousal stimulation, which means it at-
EEG in encephalopathy
tenuates (or blocks) on eye opening or mental activity. Beta Encephalopathy, or global cerebral dysfunction, is a common
activity is present over anterior regions. complication in the critically ill and its aetiology is wide ranging.
A few examples of common causes include metabolic derange-
ment, hepatic or renal failure, systemic infection, toxins, and
Effect of drugs on EEG patterns traumatic and hypoxic ischaemic encephalopathies.
Beta activity is initially increased by several sedative, anaes- While the EEG is generally not specific to aetiology, it is a
thetic, and anticonvulsant medications (e.g. barbiturates, very sensitive measure of cerebral dysfunction and can give

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Introduction to interpretation of EEG

Fig 2 Frontal intermittent rhythmic delta activity (highlighted in box) appears as intermittent symmetrical rhythmic delta activity over frontal regions. It is non-
specific and can arise secondary to structural or non-structural pathologies, but is most often associated with metabolic disturbances, for example uraemia or
hyperglycaemia, commonly in combination with cerebrovascular insufficiency.6

information regarding the severity of encephalopathy.6 The Triphasic waves

earliest changes of encephalopathy are usually ‘slowing’, or
Triphasic waves arise as a result of toxic, metabolic, and
fall out of the alpha rhythm. With an advancing clinical pic-
hypoxic ischaemic encephalopathies, and prion disease
ture, patterns visualised include slow (wave) activity, FIRDA,
(CreutzfeldteJakob disease).7 Triphasic waves can occur in
triphasic waves, PDs, intermittent suppression, and burst
overdose of several drugs including sodium valproate, bac-
suppression.
lofen, lithium, levodopa, barbiturates, and serotonergic
drugs.3
Slow wave activity
Slow waves are theta and delta frequency activity and should
Periodic discharges
be present for a significant proportion (i.e. approximately
>50%) of a recording in an awake patient to be deemed path- PDs are repeating waveforms of relatively uniform
ological. Common neuropsychiatric drugs associated with morphology, duration, and quantifiable inter-discharge in-
diffuse slow wave activity include tricyclic antidepressants, terval, occupying the majority of the recording.8 PDs are
lithium, and clozapine.3 Structural cerebral abnormali- described by their topography and inter-discharge interval,
tiesdsuch as tumour; gliosis; encephalitis; and cerebrovas- usually 0.3 s to several seconds, which can provide clues to
cular insults caused by infarction, subdural haematoma, and their aetiology.7 Topographic descriptions include lateralised
subarachnoid haemorrhagedgenerally produce asymmet- periodic discharges (LPDs), bilateral independent periodic
rical slow-wave activity. discharges (BIPDs), and generalised periodic discharges
(GPDs).1 In response to an alerting event, stimulus-induced
rhythmic ictal or periodic discharges (SIRPIDs) have been
Frontal intermittent rhythmic delta activity described in comatose patients. The significance of PDs
FIRDA is fairly regular, approximately sinusoidal or should be interpreted within the clinical context in which they
sawtooth waves, occurring in intermittent bursts at 1.5-2.5 occur, as there is no formal standard of care, but a prophy-
Hz synchronously over the frontal regions (occasionally lactic anticonvulsant may be warranted because of their
unilaterally). FIRDA is most commonly associated with mild frequent association with seizures.1 For example, in a patient
to moderate unspecified encephalopathy in responsive pa- with fever, delirium, and an EEG revealing LPDs over the left
tients, often with metabolic derangement and cerebrovas- hemisphere, there should be a strong suspicion of herpes
cular disease. simplex encephalitis (HSE). The same EEG from a patient with

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 Introduction to interpretation of EEG

Fig 3 Triphasic waves (highlighted in box) occurring with a periodicity of 1e2 Hz in a 63 yr old male as a result of hepatic encephalopathy. Triphasic waves are
symmetrical positive sharp transients (downward deflection) preceded and followed by relatively low amplitude negative waves (upward deflection), dominant
over frontal cortex with an anterio-posterior lag.

acute right-sided hemiparesis would suggest significant left both response and reversibility of the underlying cause, but is
hemispheric dysfunction and structural damage secondary to generally poor.
a stroke.
Stimulus-induced rhythmic periodic or ictal discharges
Lateralised periodic discharges In comatose patients, rhythmic periodic or ictal discharges can
LPDs can be seen in acute destructive lesions such as cere- arise in the context of alerting stimuli. SIRPIDs may not corre-
brovascular insults, space-occupying lesions, and encepha- late with any obvious clinical change, but on occasions clinical
litides, including HSE.9 The literature suggests that up to 90% seizures do occur. Discrimination between ictal and non-ictal
of patients with LPDs will experience seizures during the activity can prove difficult. Clinical significance of SIRPIDs is
course of their illness.10 therefore uncertain and should be assessed in the clinical
context, but are often associated with a poor prognosis.12

Bilateral independent periodic discharges

BIPDs refers to the presence of two independent, asyn- Suppression
chronous, lateralised discharges in both hemispheres.11
Suppression implies a low amplitude recording, defined as
Common pathologies include hypoxic ischaemic encepha-
voltage <10 mV throughout all channels.8 As previously noted,
lopathy (HIE), severe hypoglycaemia, central nervous sys-
intermittent suppression can occur as a result of deeper states of
tem (CNS) infections, and HSE.10 BIPDs are also frequently
anaesthesia, which are reversible. In pathological states, sup-
associated with seizures, and often a poor neurological
pression is suggestive of gross cerebral disturbance and gener-
prognosis.
ally indicates a poor prognosis. Although not aetiology-specific,
possibilities include cerebral intoxication, post-ictal suppres-
Generalised periodic discharges sion, brainstem haemorrhage, cerebral ischaemia, and oedema.
GPDs are commonly seen in toxic, metabolic, and hypoxic Electrocerebral inactivity (ECI) represents extreme sup-
ischaemic encephalopathies, but can occur in NCS and NCSE. pression caused by the global loss of electrical activity, defined
Discrimination between these conditions based on the GPD as <2 mV. Profound hypothermia, severe hypotension, and
appearance alone is unreliable, and must be interpreted CNS depressant intoxication are potentially reversible causes
within the clinical context.12 Management should be focused of ECI, which must be excluded before ascribing this pattern to
on treatment of the underlying cause and prognosis guided by irreversible coma.11

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Introduction to interpretation of EEG

Fig 4 Lateralised periodic discharges over the left hemisphere (highlighted in box), consisting of sharp waves at a frequency of 1 Hz, in a 74 yr old female patient
recorded 24 h after an episode of complex partial status epilepticus. LPDs are confined to one hemisphere and can suggest ictal activity; however, they are most
often considered interictal.11

Burst suppression infection. Intensivists should also be vigilant for the possi-
bility of ongoing subclinical seizures after convulsive status
As the EEG becomes discontinuous, bursts of sharp and slow
epilepticus appears to have terminated, and in the setting of
wave activity of variable duration alternate with variable
hypoxiceischaemic encephalopathy.
periods of attenuation or suppression below 10 mV. When
To confirm a diagnosis of NCS or NCSE, a repetitive pattern
more than 50% of the record consists of attenuation or
of focal or generalised epileptiform discharges at a frequency
suppression, this pattern has recently been defined as burst
>2.5 Hz should be present for 10 s or 30 min, respectively.14
suppression.8 An alternative definition, sometimes used
Where repetitive epileptiform discharges at a frequency <2.5
clinically, describes burst suppression as a state of uncon-
Hz or rhythmic activity at a frequency of >0.5 Hz are present, a
sciousness and profound brain inactivation in which the EEG
diagnosis of NCS or NCSE may also be appropriate if spatio-
shows periods of electrical activity alternating with periods
temporal EEG evolution is evident or if a trial of rapidly
of isoelectricity or electrical silence.5 Common causes of this
acting intravenous anticonvulsant therapy results in both
pattern include sedative and general anaesthetic agents,
clinical and EEG improvement.14
status epilepticus, and hypoxic ischemic encephalopathy.13
There is considerable debate as to the best treatment of
Consideration should be given to a trial period of sedation
subclinical (or electrographic only) NCSE, as there is a
hold, unless being used for therapeutic purposes, as this
riskebenefit equation which must be considered on an indi-
pattern can be seen accompanying myoclonic status epi-
vidual basis.
lepticus after a profound hypoxic ischaemic insult and
carries a grave prognosis.

Continuous EEG
EEG in epileptiform disorders Continuous EEG (cEEG), with or without video, is a relatively
recent innovation in the ICU, whereby cerebral activity
Non-convulsive seizures and non-convulsive status
alongside clinical behaviour is recorded over a period ranging
epilepticus
from hours to weeks. It can be used to identify NCS and NCSE
Non-convulsive seizures and status epilepticus (NCS and and hence is increasing in clinical application. In cases of re-
NCSE, respectively) should be considered in patients with fractory status epilepticus it is also used to guide depth of
disordered consciousness, particularly those in coma with a anaesthesia, with evidence of burst suppression acting as a
history of epilepsy; after neurosurgery, stroke, or cerebral surrogate marker for adequate depth of anaesthesia. It is also

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 Introduction to interpretation of EEG

Fig 5 Generalised periodic discharges (highlighted in box, but seen throughout the image) at a frequency of 2.5 Hz in a 70 yr old male, secondary to hypoxic
ischaemic encephalopathy, after in-hospital cardiac arrest. Generalised periodic discharges (GPDs) are generalised, synchronous, periodic, or quasi-periodic
complexes that occupy at least 50% of a recording, with a repetition rate of 0.5e1.5 Hz.

used to distinguish non-epileptic events that may closely been precisely quantified. Unfavourable outcomes are
mimic epileptic seizures, and to detect early, real-time generally seen in patients with a non-reactive, discontin-
changes in brain function such as might occur in cerebral uous, or suppressed EEG, and with the presence of epilepti-
ischaemia complicating subarachnoid haemorrhage. form discharges, GPDs, or both.20
The use of cEEG in critically ill patients has been endorsed
in recommendations by both the American Clinical Neuro-
physiological Society and European Society of Intensive Care Somatosensory evoked potentials
Medicine, and guidelines for its use have been recently pro-
Somatosensory evoked potentials (SSEPs), which record elec-
posed.15,16 However, cEEG is still a field of active clinical
trical activity from myelinated peripheral and central (sen-
research, and more evidence is required to establish its cost-
sory) neurones, have been used in the ICU setting to aid
effectiveness. cEEG is also resource-intensive and often re-
neurological prognosis, particularly after HIE and TBI. Elec-
quires real-time expert interpretation, which may not always
trical stimulation is usually applied to the median nerve at the
be readily available.
wrist, and responses are recorded at the brachial plexus,
cervical spine, and ipsilateral and contralateral sensory
cortices.
Prognostication in coma The principle component of interest for neurological
Coma is defined as ‘an eyes-closed state of unresponsiveness prognosis is the N20 response, which by electrophysiological
with severely impaired arousal and cognition’.17 In comatose convention is denoted by an upward deflection. The nomen-
patients the EEG can be used to assess for evidence of clature is derived as a result of the polarity of the potential, in
potentially reversible causes, such as intoxication with sed- this case negative (N), and the typical peak latency in milli-
atives, NCS, and NCSE. The EEG can also aid neuro- seconds of approximately 20 ms from wrist to sensory cortex.
prognostication in coma, particularly after cardiorespiratory It is generated in the primary sensory cortex and can be
arrest and traumatic brain injury (TBI).18 Favourable out- dichotomised into either present or absent.
comes are seen when continuous rhythmic EEG activities are In comparison with EEG waveforms, muscle activity,
present, which are reactive to alerting stimuli.19 Reactivity is movement, and electromagnetic artefacts, the amplitudes of
a reproducible EEG change in response to external alerting, SSEP responses are typically low. In order to eliminate or
noxious stimuli, or both. This can manifest as a change in attenuate such artefacts and the background ‘noise’ computer
amplitude or frequency or both, although this has not yet averaging of the individual responses is performed, whereby

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Introduction to interpretation of EEG

Fig 6 Diffuse slow wave activity (highlighted in black box) and left hemisphere suppression (highlighted in blue box), in a 62 yr old male secondary to traumatic
brain injury with associated subarachnoid and bilateral subdural haemorrhage. Where suppression is unilateral (or bilateral) and CT or MRI has not yet taken
place, urgent neuroimaging should be considered to assess for evidence of subdural haemorrhage or cerebral infarction.

Fig 7 Interictal discharges (highlighted in box) in a 31 yr old female with primary generalised epilepsy.

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 Introduction to interpretation of EEG

Fig 8 Median nerve somatosensory evoked potentials (SSEPs) (left and right, respectively), demonstrating bilateral presence of cortical responses (N20, black
arrowheads), after electrical stimulation at the wrist. Stimulus was applied at the start of each trace. Negative potentials are shown as an upward deflection.

indeterminate in HIE, but is more favourable in TBI. SSEPs can

Table 1 EEG waveforms in the healthy adult population. (Not evolve during the first 24 h after cardiac arrest, and are
to scale, in general terms lower frequency activity is higher in therefore best performed after this time when the patient is
amplitude and vice versa.). under light sedation and normothermic.21

Wave Frequency Location Morphology (1s)

form (Hz) Conclusion
Gamma >30 Somatosensory EEG is a real-time objective measure of cerebral activity
cortex available to clinicians in the ICU, particularly where clinical
neurological examination is difficult or unreliable. EEG can
Beta 13e30 Frontal indicate cortical, subcortical, or arousal disturbance and
detect epileptiform activity, which can inform diagnosis and
management. It is complimentary to neuroimaging and can
Alpha 8e13 Occipital be used in conjunction with other neurophysiological tech-
niques such as SSEPs in neuroprognostication for patients in
coma.
Theta 4e8 Diffuse

Declaration of interest
Delta <4 Diffuse The authors declare that they have no conflicts of interest.

MCQs
The associated MCQs (to support CME/CPD activity) will be
accessible at www.bjaed.org/cme/home by subscribers to BJA
hundreds of responses in relation to a time-locked stimulus Education.
are summated and random background noise is subtracted
out by phase cancellation.
The bilateral absence of N20 confers an unfavourable
Supplementary data
neurological prognosis, with specificity nearing 100% mortal- Supplementary data to this article can be found online at
ity in HIE. The presence of N20 renders prognosis https://doi.org/10.1016/j.bjae.2018.11.002.

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Introduction to interpretation of EEG

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