EEG in Encephalopathy and Coma including Brain Death 이 향 운

2007 추계 간질학회 보수교육 강의
EEG in Encephalopathy and Coma
including Brain Death
이 향운
이화여자대학교 의학전문대학원 신경과
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 μV, 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
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
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
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
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
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 µV, 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
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
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)
Varying degree of EEG change
Profound coma and/or major convulsions with massive
Epileptogenic lesions are more likely hypo- than
Even complex partial seizures in insulinoma
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
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 Alzheimer’s
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
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
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 dépassé
Irreversible coma
Cerebral death syndrome
Irreversible breakdown of cerebral functions
For organ transplantation, donorship expanded to
anencephalic infants and to non-heart-beating
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
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
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 µV/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
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