Non-Epileptiform Patterns

Dr Lim Shih Hui

Senior Consultant Neurologist

Singapore General Hospital

EEG Interpretation

Normal Lack of Abnormality

Abnormal Non-epileptiform Patterns

Epileptiform Patterns

Non-Epileptiform Patterns

Slow Activity Background slow Intermittent slow Continuous slow

Special Patterns Used Only In Stupor & Coma Alpha coma Spindle coma Beta coma Theta coma Delta coma

Special Patterns 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

Indicates underlying cortical dysfunction, ?deafferentation of the cortex

Location indicates a focal, lateralized or generalized cortical dysfunction

Degree, persistence and reactivity roughly correlate with severity of dysfunction

Rhythmic slowing: more likely to be electro-physiological disturbances

Polymorphic slowing: more likely to have structural abnormality

Background Slow Activity

Frequency of the background rhythm is lower than normal value for the age. 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 ActivityInterpretation

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 Adult: usually disorders of cerebral perfusion; metabolic and toxic

cause Childhood: perinatal sequelae

Intermittent Slow, Generalized

Intermittent Slow, Generalized

Intermittent Slow Activity

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

Can be an early manifestation of continuous slow activity or epileptiform changes

Generalized Intermittent Slow Activity

Can be caused by infra-tentorial or supra-tentorial lesions

Unprovoked intermittent slow 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) More specific subclass of intermittent slow Appeared grouped in bursts Relatively rhythmic Generalized IRS:

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 supra-

tentorial destructive process e.g. tumors or raised intracranial pressure

Continuous Slow, Generalized

Continuous Slow Activity

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

Predominant alpha activity in a patient with a clinical state of coma

Due to : Discrete lesion of the ponto-mesencephalic

level Severe anoxic encephalopathies Drug intoxication

Alpha Coma

Theta Coma

Predominant theta activity in patient in coma

Due to severe diffuse encephalopathy Potentially reversible; prognosis

depends on underlying condition

Theta Coma

Other Coma Patterns

Spindle Coma Due to lesion at high mesencephaic level If not due to progressive lesion good prognosis

Beta Coma Most frequently due to drug intoxication; potentially

reversible

Delta Coma Severe diffuse encephalopathy Reversibility depends on underlying condition

Sleep Coma

Excessive Fast

Beta activity of > 50 uV Present during at least 50% of awake

recording Frequently due to sedative medication

Excessive Beta Activity

Asymmetry

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 e.g. Porencephalic cyst, subdural hematoma

Asymmetry, Decreased Background, left

Periodic Pattern

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

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

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)

Sharp transients including sharp wave or spikes Appear in a periodic or semi-periodic fasion Lateralized or focal Seen in

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

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 Occurrence of REM sleep <15 min after falling asleep Dysfunction of subcortical mechanism that induce

sleep Occur in

Narcolepsy Severe sleep deprivation with consequent REM rebound Withdrawal of MAO inhibitors or TAD Neonates normal