2007

EEG in Encephalopathy and Coma

including Brain Death

EEG Patterns in Encephalopathy and Coma

Diffuse slowing
Intermittent delta rhythms
EEG patterns usually seen during sleep
Alternating pattern
Prolonged bursts of delta waves & EEG reactivity
Epileptiform activity
Triphasic waves
Suppression-burst activity
Periodic spiking
Monorhythmic activity
Low-voltage waves
Focal abnormalities in coma

EEG Changes & Severity of Encephalopathy

In mild encephalopathy


Slowing of posterior alpha rhythm in mild clouding of

consciousness and confusion; alpha to theta range

In severe encephalopathy





First, high-amplitude irregular delta

Lower amplitude below 20 V, invariant delta activity
Suppression-burst pattern
Electrocerebral inactivity (ECI)

Prognosis from EEG patterns



Grave prognosis if invariant low-amplitude delta,

suppression-burst, ECI, in the absence of drug
intoxication
If due to drug intoxication, severely abnormal
patterns are quite reversible with high potential for
full recovery

Diffuse Slowing & Intermittent Delta

Diffuse slowing


In early phase of coma, gradual dissolution of alpha

rhythm interspersed theta frequency, mimicking
normal drowsiness
Diffuse continuous slowing, theta or delta range

Intermittent delta rhythms



In initial phase of coma, intermittent rhythmic

bilaterally synchronous delta with subcortical, deep
frontal, other supratentorial lesions, or metabolic and
hypoxic encephalopathy
Frontal maximum in adult (FIRDA), or occipital
dominance in children (OIRDA)
However, TIRDA (temporal) is epileptogenic pattern

Frontal Intermittent Rhythmic Delta Activity

(FIRDA)

Sleep-like EEGs & Alternating Pattern

EEG patterns usually seen during sleep


Similar to sleep EEG in some types of coma (e.g. sleep

spindles or K complexes) with cyclic appearance,
influencing sleep-inducing systems
Gradual abolition of sleep structures with deepening coma,
due to increasing cortical dysfunction or direct brainstem
involvement

Alternating pattern


Cyclic alteration of low-voltage irregular & high-voltage

slow waves in coma with Cheyne-Stokes respiration
Induce high-voltage slowing with stimulus during lowvoltage period, more aroused during slow-wave period
May be due to pacemaker function of arousal system,
temporarily released by cortical inhibition, or blood gas
changes from respiratory center itself

Prolonged Bursts of Delta Waves and

EEG Reactivity

Prolonged bursts of bilateral high-voltage delta for
several seconds or minutes, in various intracranial
conditions, mainly with head injuries

Delta bursts either spontaneous or secondary to
exogenous stimuli, considered as exaggerated K
complex, associated with greater muscle activity,
restlessness, and attempts to communicate

Reactions to stimuli is essential
 Alerting type (paradoxical activation); increased
slow-wave response
 Blocking type; voltage reduction, or filtering
remnants of basic rhythm

No response even to repetitive stimulation in deep coma,
voltage flattening with or without blocking slow waves,
delta wave filtering with nonrhythmical alpha and theta
activity, mulscle artifacts without EEG changes

Prolonged Delta Bursts by painful stimulation

Epileptiform Activity and Periodic Lateralized

Epileptiform Discharges (PLEDs)

Predominant spikes and/or sharp waves, frequently and
not invariably with seizures

Generalized paroxysmal activities with myoclonic status
epilepticus, or no visible motor phenomena

Unilateral continuous spiking can be associated with
aphasia or inability to react adequately rather than true
unconsciousness

Periodic lateralized epileptiform discharges (PLEDs);




With coma or without alterations in vigilance (50%)

Acute convulsions in vascular structural lesions, or a
wide variety of conditions
Sometimes with nonconvulsive status epilepticus
without effects of IV antiepileptic drugs

Periodic Lateralized Epileptiform Discharges

(PLEDs) - 1

Periodic Lateralized Epileptiform Discharges

(PLEDs) - 2

Suppression-Burst Activity and Periodic

Spiking

Suppression-burst activity


High-voltage bursts of slow waves with intermingled sharp

transients or spikes against depressed background or
complete flatness
Quasi periodically repeated and frequently with diffuse
myoclonic jerks
Remnants between bursts frequently consist of nonreactive
rhythmic activity in alpha and theta ranges

Periodic spiking


Single or multiple spikes on a flat background activity,

closely related to suppression-burst activity, but with higher
repetition rate and less prominent or lacking slow waves
Periodic spikes accompanied by myoclonic jerks, but no
definite one-to-one relation to spikes

Burst-Suppression Pattern

Suppression-Burst Pattern

Monorhythmic Activity

Monorhythmic activity in coma patients


Normal-looking rhythmical activities in alpha range in

deep coma
Encountered in unresponsive conditions after brainstem
lesions and in severe anoxic encephalopathy

Differentiation from normal alpha rhythm



Steadily throughout the whole record and diffusely spread

or accentuated over anterior regions
No reaction to any stimulus

Alpha coma with unfavorable prognosis



In a traditional narrow definition, transient epileptic

antemortem stage following burst-suppression pattern
Should be differentiated from spindle-like activities, from
10 to 18 cycles/sec rhythms due to intoxication, or normal
alpha rhythm in locked-in syndrome

Alpha Coma in Anoxic Encephalopathy

Alpha Coma in Phenobarbital Intoxication

Low-Voltage EEG or Focal Abnormality

Low-voltage output EEG



Remnants of cerebral activity less than 20 V, a precursor

of electrocerebral silence (ECS)
Should not be confused with low-voltage records of
conscious subjects

Focal abnormalities in coma







Associated with focal EEG signs, but blurred or abolished

lateralizing signs with deepening coma
Localized or unilateral slowing, asymmetrical depression of
slow or fast activities, especially of sleep spindles,
asymmetric response to exogenous stimuli
Depressed prolonged delta bursts over the more affected
hemisphere
For correct lateralization, differentiation between
consistent unilateral accentuated slowing and asymmetrical
alerting response is crucial
However, localized EEG abnormalities area not uncommon
with diffuse encephalopathy, especially nonketotic diabetic
coma, apt to produce focal neurological deficits, partial
seizures and corresponding EEG signs

Anoxic Encephalopathy

EEG in anoxic encephalopathy


EEG should be obtained at least 5 or 6 hours after

cardiopulmonary resuscitation after stabilization
To assess the severity of cerebral insult and for
prognosis
Normal or almost normal EEG after a short episode of
cerebral anoxia

Unique EEG patterns in anoxic encephalopathy

with fatal prognosis





Periodic discharges
Suppression-burst pattern
Alpha coma pattern
Electrocerebral inactivity

Periodic Discharges and Myoclonic Status

Epilepticus in Anoxic Encephalopathy

EEG in Metabolic Encephalopathy (I)

Hypoglycemia



Varying degree of EEG change

Profound coma and/or major convulsions with massive
spikes
Epileptogenic lesions are more likely hypo- than
hyperglycemia
Even complex partial seizures in insulinoma

Hyperglycemia



EEG with mixed slow and fast frequency

In advanced diabetic coma, pronounced slowing,
indistinguishable from hypoglycemic state
Focal epileptic seizures are more common in non-ketotic
hyperglycemia, but possible in ketotic hyperglycemia

EEG in Metabolic Encephalopathy (II)

Hepatic encephalopathy



Degree of slowing often parallel to ammonia level

Posterior alpha rhythm may be preserved during early stage of
enhanced slowing, sudden shift and slow substitutes, then massive
EEG slowing with or without triphasic waves
Triphasic waves are highly indicative of hepatic coma (about 25%),
although not specific
Replaced by delta slowing and general flattening in profound coma in
impending death, often slow delta activity mixed with trains of 14 and
6 Hz positive spikes

Renal encephalopathy or Uremia



In acute uremia, irregular low-voltage activity with posterior

background slowing (theta), and prolonged bursts of bilateral
synchronous mixed slow and sharp or spikes with or without
widespread myoclonic jerks, grand mals, exceptionally focal seizures;
epileptic seizures in 1/3 patients usually due to water-electrolyte
imbalance
In chronic uremia, usually stable EEG and mental function due to
prolonged dialysis, occasional deterioration with seizures and diffuse
delta and theta activity, correlated best with BUN fluctuations;
generalized spike-wave bursts in 8-9% of uremia, with heightened
sensitivity to photic stimulation
In children with renal failure, commonly diffuse slowing and
generalized bursts of spikes or spike-wave-like activity

Triphasic Waves

Typical triphasic waves;


Medium- to high-voltage triphasic waves in rhythmical trains

at 1.5 to 2.5 cycles/sec with sharp transients, bilaterally
synchronous and symmetrical over both hemispheres
Anterior-posterior time delay as an important criterion but
observed with referential or transverse montages

Fairly characteristic of hepatic coma, but not specific

 Continuous triphasic waves considered a type of
nonconvulsive status epilepticus in hepatic coma
 Also in hypoxic states, intoxication, other metabolic or
sepsis-associated encephalopathy, subdural
hematoma/brainstem infarction, cerebral
carcinomatosis, preserved consciousness in Alzheimers
disease, prion disease, unspecified demented states

Confused with sharp and slow waves with absence status
of Lennox-Gastaut syndrome

Triphasic Waves

Lennox-Gastaut Syndrome

EEG and Other Etiologies of Coma (I)

EEG in supratentorial lesions



Always markedly abnormal

Focal slowing in lesion site, whereas diffuse slowing
parallel to degree of herniation
Detailed electroclinical correlation in acute secondary
midbrain syndromes

EEG in infratentorial lesions



Disproportional to neurological signs and EEG

abnormalities (e.g. normal looking EEG in apparent
comatose behavior)
In brainstem infarction with predominant alpha
frequency, locked-in syndrome should be
differentiated; the only clue is reactive alpha rhythm

EEG and Other Etiologies of Coma (II)

Infectious diseases


Exceptionally prominent diffuse slowing, often rhythmic

or quasiperiodic, superimposed theta or alpha area
scarce
Characteristic EEG patterns
 Generalized periodic pattern; highly suggestive for
SSPE, CJD, or diffuse encephalitis
 Lateralized periodic complexes; diagnostic
importance in herpes simplex encephalitis

Epileptic conditions


Prolonged coma in convulsive status epilepticus, in

postictal states with lingering subclinical paroxysmal
activity, in typical and atypical absence status, other
types of nonconvulsive status epilepticus
Prominent seizure activity, but EEG without spikes does
not exclude epileptic nature and complicated by
interspersed epileptic seizures in many coma patients

Periodic Epileptiform Discharges in Right Temporal Area

in Herpes Simplex Encephalitis

Subacute Sclerosing Panencephalitis

Creutzfeldt-Jakob Disease

EEG in Relation to the Depth of Coma

Degree and generalization of slowing




Related to the level of unresponsiveness

Exceptionally prolonged bursts of delta waves secondary to
exogenous stimuli
In children, degree of slowing is frequently disproportionate to
the clinical state

Effect of stimulation



Good information about coma depth

Blocking type of response is replaced by alerting type, and
finally unreactive EEG even to repeated stimulation

Potentials seen during sleep



Progressively scarcer finally disappear with deepening coma

Patterns highly suggestive of late midbrain or initial bulbar

brain syndrome






Progressive voltage depression

Extreme slowing with extinction of superimposed fast
activities
Intermittent isoelectric periods
Periodic spiking or burst-suppression activity
Monorhythmic unreactive alpha and theta frequency

Brain Death (I)

Definition and terms for the same clinical entity









Aperceptive, areactive, apathic, atonic syndrome

Brain death
Stage IV coma
Coma dpass
Irreversible coma
Cerebral death syndrome
Irreversible breakdown of cerebral functions
For organ transplantation, donorship expanded to
anencephalic infants and to non-heart-beating
patients

Pathophysiology


Crucial mechanism is elevation of intracranial pressure,

common final pathway, whatever the cause of coma
Intensity of pathological changes depends on
development of intracranial circulatory arrest

Brain Death (II)

Neurological signs


Absent cortical functions and brainstem activity

Fixed pupils with strong light stimulus with exclusion of
peripheral third nerve injury
 Muscle artifacts in EEG have been considered evidence of
brainstem functions, but due to hyperexcitability of the
nerve membrane caused by artificial hyperventilation





Absent spontaneous respiration, no respiration

movements after removal from the respirator
Apnea testing is necessary to confirm
Absent spinal reflexes by Harvard criteria, but simple or
complex spinal reflexes after initial phase of spinal
shock due to total brain infarction down to C1 level
Obscured EEG by very-low-amplitude fast activity due to
sustained contraction of scalp muscles should be ruled
out by giving a short-acting neuromuscular blocking
agent (succinylcholine 20-40 mg IV)

EEG in Brain Death (III)

Electrocerebral silence (ECS)





In adult, single EEG and 6-to 12-hour clinical

observation after acute cerebral insult are minimum
requirements for brain death
Isoelectric EEG to confirm cerebral death
Sign of brain death only if neurological signs of
cortical and brainstem functions are lacking,
intoxication and marked hypothermia should be
excluded
However, ECS can be found with complete apallic
syndrome, with intoxication and full recovery, with
hypothermia, with transient decorticate states
followed by varying degrees of recovery

Brain Death (IV)

Technical standards for EEG recording in brain
death












Minimum of 8 scalp electrodes and reference electrodes

to cover major brain areas
Interelectrode impedances under 10,000 ohms but over
100 ohms
Testing the integrity of the entire recording system
Interelectrode distances of at least 10 cm to enlarge the
amplitudes and to pick up electrical fields originating in
deep structures
Sensitivity increase up to 2 V/mm during most of the
recording to distinguish ECS from low-voltage output EEG
Use of time constants of 0.3 to 0.4 second
Use of monitoring techniques, with simultaneous ECG
recording to be mandatory
Testing EEG reactivity to exogenous stimuli
Recording time of at least 30 minutes
Recording to be made only by a qualified technologist

Brain Death (V)

Recommended guideline by a special task force
for confirming brain death in young children


Brain death should not be determined until at least 7

days of age
Seven days to 2 months: two examinations and two
EEGs separated by at least 48 hours
Two months to one year: two examinations and two
EEGs separated by at least 24 hours
Older than one year: similar criteria as an adult, one
EEG and at least 12 hours of clinical observation

Electrocerebral Silence (ECS) &

Double-Distance Montage
FP1-T3
F7-T5
T3-O1

FP2-T4

F8-T6
T4-O2
Fz-Pz

Cz-Oz

Thank you for your attention!