1. Non-Epileptiform Patterns
Dr Lim Shih Hui
Senior Consultant Neurologist
Singapore General Hospital

2. EEG Interpretation Normal Abnormal Lack of Abnormality
Non-epileptiform Patterns
Epileptiform Patterns

3. Non-Epileptiform Patterns
Special Patterns
Excessive fast
Asymmetry
Periodic pattern
Triphasic waves
Periodic lateralized epileptiform discharges (PLEDs)
Burst suppression
Background suppression
Sleep-onset rapid eye movement
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

4. Background Slow

5. 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

6. 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

7. Background Slow Activity Interpretation
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

8. Intermittent Slow, Generalized

9. 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

10. 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)

11. Intermittent Rhythmic Slow, Generalized (FIRDA)

12. Intermittent Rhythmic Slow, Regional, Bi-occipital (OIRDA)

13. 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

14. Continuous Slow, Generalized

15. 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

16. Continuous Slow, Lateralized, Left Hemisphere

17. 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

18. Alpha Coma

19. Theta Coma Predominant theta activity in patient in coma
Due to severe diffuse encephalopathy
Potentially reversible; prognosis depends on underlying condition

20. Theta Coma

21. Other Coma Patterns Spindle Coma Beta Coma Delta 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

22. Sleep Coma

23. Excessive Fast Beta activity of > 50 uV
Present during at least 50% of awake recording
Frequently due to sedative medication

24. Excessive Beta Activity

25. 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

26. Asymmetry, Decreased Background, left

27. 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

28. Periodic Pattern, Generalized (CJD)

29. Periodic Pattern, Generalized

30. Periodic Pattern, Generalized (Post-Hypoxic)

31. 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

32. Triphasic Waves

33. 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

34. PLEDs, Regional, Left Posterior

35. PLEDs, Regional, Left Frontal

36. 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

37. Burst-Suppression

38. Burst-Suppression

39. Burst-Suppression

40. Sleep-Onset-REM-Period

41. 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