Download Non-Epileptiform Pattern

Non-Epileptiform Patterns
Dr Lim Shih Hui
Senior Consultant Neurologist
Singapore General Hospital
EEG Interpretation
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Normal
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Lack of Abnormality
Abnormal
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Non-epileptiform Patterns
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Epileptiform Patterns
Non-Epileptiform Patterns
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Slow Activity
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Background slow
Intermittent slow
Continuous slow
Special Patterns Used Only In
Stupor & Coma
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Alpha coma
Spindle coma
Beta coma
Theta coma
Delta coma
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Special Patterns
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Excessive fast
Asymmetry
Periodic pattern
Triphasic waves
Periodic lateralized epileptiform
discharges (PLEDs)
Burst suppression
Background suppression
Sleep-onset rapid eye movement
Background Slow
Slow Waves
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Indicates underlying cortical dysfunction,
?deafferentation of the cortex
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Location indicates a focal, lateralized or generalized
cortical dysfunction
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Degree, persistence and reactivity roughly correlate
with severity of dysfunction
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Rhythmic slowing: more likely to be electrophysiological disturbances
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Polymorphic slowing: more likely to have structural
abnormality
Background Slow Activity
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Frequency of the background rhythm is
lower than normal value for the age.
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1 yr: <5 Hz
4 yr: <6 Hz
5 yr: <7 Hz
>8yr: <8 Hz
Must be verified that slowing is not due to
drowsiness
Background Slow Activity
Interpretation
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Cortical or subcortical mechanism involved in the
generation of the background rhythm are disturbed 
synchronization of background rhythms of abnormally slow
frequency
A manifestation of a diffuse dysfunction of the cortex, or
subcortical gray structures
A non-specific EEG finding that have different causes
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Adult: usually disorders of cerebral perfusion; metabolic and toxic
cause
Childhood: perinatal sequelae
Intermittent Slow, Generalized
Intermittent Slow, Generalized
Intermittent Slow Activity
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Occurs intermittently and is not caused by drowsiness
Rhythmic or irregular
Generalized, regional or lateralized
Background rhythm is generally well preserved; indicating that
cortical and subcortical mechanism involved in its generation
are functionally normal
A non-specific functional cerebral dysfunction
Has diverse cause
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Can be an early manifestation of continuous slow activity or
epileptiform changes
Generalized Intermittent Slow Activity
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Can be caused by infra-tentorial or supratentorial lesions
Unprovoked intermittent slow
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diffuse cortical dysfunction
generalized epilepsy
Adult: predominantly frontal (Frontal
Intermittent Rhythmic Delta Activity FIRDA)
Children: predominantly occipital (OIRDA)
Intermittent Rhythmic Slow,
Generalized (FIRDA)
Intermittent Rhythmic Slow,
Regional, Bi-occipital (OIRDA)
Intermittent Rhythmic Slow (IRS)
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More specific subclass of intermittent slow
Appeared grouped in bursts
Relatively rhythmic
Generalized IRS:
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Diffuse involvement of cortical and subcortical grey
structures (e.g. diffuse encephalopathy or generalized
non-focal epilepsy)
Mesial cortical lesion
Focal subcortical grey matter lesion; infra- or supratentorial destructive process e.g. tumors or raised
intracranial pressure
Continuous Slow, Generalized
Continuous Slow Activity
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Occurs continuously
Irregular (polymorphic)
Lies within frequency range of delta/theta waves
Non-responsive to external stimuli
Clearly exceeds the amount considered
physiologically normal for the patient’s age
Severe disturbances of interneuronal connections
or of the biochemical environment of cortical
neurons  continuous slow activity
Continuous Slow, Lateralized, Left Hemisphere
Continuous Slow, Lateralized,
Left Hemisphere
Alpha Coma
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Predominant alpha activity in a patient with
a clinical state of coma
Due to :
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Discrete lesion of the ponto-mesencephalic
level
Severe anoxic encephalopathies
Drug intoxication
Alpha Coma
Theta Coma
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Predominant theta activity in patient
in coma
Due to severe diffuse encephalopathy
Potentially reversible; prognosis
depends on underlying condition
Theta Coma
Other Coma Patterns
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Spindle Coma
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Beta Coma
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Due to lesion at high mesencephaic level
If not due to progressive lesion  good prognosis
Most frequently due to drug intoxication; potentially
reversible
Delta Coma
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Severe diffuse encephalopathy
Reversibility depends on underlying condition
Sleep Coma
Excessive Fast
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Beta activity of > 50 uV
Present during at least 50% of awake
recording
Frequently due to sedative medication
Excessive Beta Activity
Asymmetry
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Asymmetries of amplitude of background rhythms
Asymmetries of frequency are included under focal
slow
Asymmetries are considered significant when
amplitude in one hemisphere with the lower
amplitude is <50%
A reliable sign of focal structural lesions on the side
that has lower amplitude
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e.g. Porencephalic cyst, subdural hematoma
Asymmetry, Decreased Background, left
Periodic Pattern
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Relatively stereotyped waveforms
Frequently sharp waves
Appear in a periodic or quasiperiodic fashion
Generalized
Indicative of an acute or sub-acute, severe and
diffuse encephalopathy
Repetition rate
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1-2 every 1-2 seconds: CJD, post-hypoxic
1 every > 4 seconds: SSPE
Periodic Pattern, Generalized (CJD)
Periodic Pattern, Generalized
Periodic Pattern, Generalized
(Post-Hypoxic)
Triphasic Waves
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High voltage (>70 uV)
Triphasic, predominantly postive
Generalized, maximum anterior
Tend to be periodic, 1-2 Hz
Due to metabolic encephalopathy (e.g hepatic
encephalopathy) or any condition that produce
intermittent
Usually associated with alteration of consiousness
but not as severe as stupor or coma
Triphasic Waves
Periodic Lateralized Epileptiform
Discharges (PLEDs)
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Sharp transients including sharp wave or spikes
Appear in a periodic or semi-periodic fasion
Lateralized or focal
Seen in
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Acute or subacute, severe, focal destructive lesions
(e.g CVA, fast growing tumors)
Focal epileptogenic lesion not necessary associated
with can acute or subacute underlying structural
pathology
PLEDs, Regional, Left Posterior
PLEDs, Regional, Left Frontal
Burst Suppression
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A subgroup of periodic patterns in which
activity between complexes is suppressed
Generalized
Seen in extremely severe toxic or anoxic
encephalopathy; may precede
electrocerebral inactivity
Patients always in stupor or coma
Burst-Suppression
Burst-Suppression
Burst-Suppression
Sleep-Onset-REM-Period
Sleep Onset Rapid Eye Movement
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Occurrence of REM sleep <15 min after falling asleep
Dysfunction of subcortical mechanism that induce
sleep
Occur in
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Narcolepsy
Severe sleep deprivation with consequent REM rebound
Withdrawal of MAO inhibitors or TAD
Neonates  normal