encephalopathy and cma

8/3/2019 Encephalopathy and Cma

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EEG in Encephalopathy and Coma

including Brain Death

2007200720072007


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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


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EEG Changes & Severity of Encephalopathy In mild encephalopathy

Slowing of posterior alpha rhythm in mild clouding ofconsciousness 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 drugintoxication

If due to drug intoxication, severely abnormalpatterns are quite reversible with high potential for

full recovery


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Diffuse Slowing & Intermittent Delta

Diffuse slowing In early phase of coma, gradual dissolution of alpha

rhythm interspersed theta frequency, mimickingnormal drowsiness

Diffuse continuous slowing, theta or delta range

Intermittent delta rhythms In initial phase of coma, intermittent rhythmic

bilaterally synchronous delta with subcortical, deepfrontal, other supratentorial lesions, or metabolic andhypoxic encephalopathy

Frontal maximum in adult (FIRDA), or occipitaldominance in children (OIRDA)

However, TIRDA (temporal) is epileptogenic pattern


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Frontal Intermittent Rhythmic Delta Activity

(FIRDA)


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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 brainsteminvolvement

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 low-voltage 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


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Prolonged Bursts of Delta Waves and

EEG Reactivity

Prolonged bursts of bilateral high-voltage delta forseveral seconds or minutes, in various intracranial

conditions, mainly with head injuries Delta bursts either spontaneous or secondary to

exogenous stimuli, considered as exaggerated Kcomplex, 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 thetaactivity, mulscle artifacts without EEG changes


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Prolonged Delta Bursts by painful stimulation


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Epileptiform Activity and Periodic LateralizedEpileptiform 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 trueunconsciousness

Periodic lateralized epileptiform discharges (PLEDs);

With coma or without alterations in vigilance (50%)

Acute convulsions in vascular structural lesions, or awide variety of conditions

Sometimes with nonconvulsive status epilepticuswithout effects of IV antiepileptic drugs


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Periodic Lateralized Epileptiform Discharges

(PLEDs) - 1


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Periodic Lateralized Epileptiform Discharges

(PLEDs) - 2


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Suppression-Burst Activity and Periodic

Spiking

Suppression-burst activity

High-voltage bursts of slow waves with intermingled sharp

transients or spikes against depressed background orcomplete flatness

Quasi periodically repeated and frequently with diffusemyoclonic jerks

Remnants between bursts frequently consist of nonreactiverhythmic 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 higherrepetition rate and less prominent or lacking slow waves

Periodic spikes accompanied by myoclonic jerks, but nodefinite one-to-one relation to spikes


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Burst-Suppression Pattern


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Suppression-Burst Pattern


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Monorhythmic Activity

Monorhythmic activity in coma patients Normal-looking rhythmical activities in alpha range in

deep coma

Encountered in unresponsive conditions after brainstemlesions 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 comawith unfavorable prognosis

In a traditional narrow definition, transient epilepticantemortem stage following burst-suppression pattern

Should be differentiated from spindle-like activities, from10 to 18 cycles/sec rhythms due to intoxication, or normalalpha rhythm in locked-in syndrome


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Alpha Coma in Anoxic Encephalopathy


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Alpha Coma in Phenobarbital Intoxication


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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 affectedhemisphere

For correct lateralization, differentiation between

consistent unilateral accentuated slowing and asymmetricalalerting response is crucial However, localized EEG abnormalities area not uncommon

with diffuse encephalopathy, especially nonketotic diabeticcoma, apt to produce focal neurological deficits, partialseizures and corresponding EEG signs


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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 encephalopathywith fatal prognosis

Periodic discharges Suppression-burst pattern

Alpha coma pattern

Electrocerebral inactivity


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Periodic Discharges and Myoclonic Status

Epilepticus in Anoxic Encephalopathy


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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


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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 massiveEEG 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 and6 Hz positive spikes

Renal encephalopathy or Uremia In acute uremia, irregular low-voltage activity with posterior

background slowing (theta), and prolonged bursts of bilateralsynchronous mixed slow and sharp or spikes with or withoutwidespread myoclonic jerks, grand mals, exceptionally focal seizures;epileptic seizures in 1/3 patients usually due to water-electrolyteimbalance

In chronic uremia, usually stable EEG and mental function due toprolonged dialysis, occasional deterioration with seizures and diffusedelta and theta activity, correlated best with BUN fluctuations;generalized spike-wave bursts in 8-9% of uremia, with heightenedsensitivity to photic stimulation

In children with renal failure, commonly diffuse slowing andgeneralized bursts of spikes or spike-wave-like activity


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Triphasic Waves

Typical triphasic waves;

Medium- to high-voltage triphasic waves in rhythmical trainsat 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 ofnonconvulsive status epilepticus in hepatic coma

Also in hypoxic states, intoxication, other metabolic orsepsis-associated encephalopathy, subdural

hematoma/brainstem infarction, cerebralcarcinomatosis, preserved consciousness in Alzheimersdisease, prion disease, unspecified demented states

Confused with sharp and slow waves with absence status

of Lennox-Gastaut syndrome


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Triphasic Waves


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Lennox-Gastaut Syndrome


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EEG and Other Etiologies of Coma (I)

EEG in supratentorial lesions Always markedly abnormal

Focal slowing in lesion site, whereas diffuse slowingparallel to degree of herniation

Detailed electroclinical correlation in acute secondarymidbrain syndromes

EEG in infratentorial lesions Disproportional to neurological signs and EEG

abnormalities (e.g. normal looking EEG in apparentcomatose behavior)

In brainstem infarction with predominant alphafrequency, locked-in syndrome should bedifferentiated; the only clue is reactive alpha rhythm


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EEG and Other Etiologies of Coma (II)

Infectious diseases Exceptionally prominent diffuse slowing, often rhythmic

or quasiperiodic, superimposed theta or alpha areascarce

Characteristic EEG patternsGeneralized 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, othertypes of nonconvulsive status epilepticus Prominent seizure activity, but EEG without spikes does

not exclude epileptic nature and complicated byinterspersed epileptic seizures in many coma patients


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Periodic Epileptiform Discharges in Right Temporal Area

in Herpes Simplex Encephalitis


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Subacute Sclerosing Panencephalitis


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Creutzfeldt-Jakob Disease


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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 tothe 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 bulbarbrain 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


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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-beatingpatients

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


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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 thenerve 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 orcomplex 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 ruledout by giving a short-acting neuromuscular blockingagent (succinylcholine 20-40 mg IV)


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EEG in Brain Death (III)

Electrocerebral silence (ECS) In adult, single EEG and 6-to 12-hour clinical

observation after acute cerebral insult are minimumrequirements 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 beexcluded

However, ECS can be found with complete apallic

syndrome, with intoxication and full recovery, withhypothermia, with transient decorticate statesfollowed by varying degrees of recovery


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Brain Death (IV)

Technical standards for EEG recording in braindeath Minimum of 8 scalp electrodes and reference electrodes

to cover major brain areas

Interelectrode impedances under 10,000 ohms but over100 ohms

Testing the integrity of the entire recording system

Interelectrode distances of at least 10 cm to enlarge theamplitudes and to pick up electrical fields originating indeep structures

Sensitivity increase up to 2 V/mm during most of therecording 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 ECGrecording to be mandatory

Testing EEG reactivity to exogenous stimuli

Recording time ofat least 30 minutes

Recording to be made only by a qualified technologist


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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


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Electrocerebral Silence (ECS) &

Double-Distance Montage

FP1-T3

F7-T5

T3-O1

FP2-T4

F8-T6

T4-O2

Fz-Pz

Cz-Oz


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