Case based discussion regarding the utility of EEG in the management of convulsive and non convulsive seizures, including status epilepticus in the intensive care unit

1. EEG in convulsive and
non-convulsive seizures in the
intensive care unit
Dr Pramod Krishnan
Consultant Neurologist and Epileptologist
HOD Neurology
Manipal Hospital, Bengaluru

2. Introduction
• Critically ill patients are predisposed to multiple neurological disorders
like seizures, ischemia, edema and raised intracranial pressure,
encephalopathy and neuroinfections.
• EEG is a sensitive test to identify and monitor cerebral dysfunction.
• Critical care continuous EEG (CCEEG) is increasingly available and
being used to monitor patients in the ICU.
• Understanding EEG patterns in various neurological disorders is
essential to provide timely intervention and for prognostication.

3. ACNS recommendations for the use of CCEEG in crtitically ill in adults and children
• Diagnosis of non-convulsive seizures (NCS), non-convulsive status epilepticus
(NCSE), and other paroxysmal events.
• Evaluate the efficacy of therapy for convulsive seizures (CS), non-convulsive status
epilepticus (NCSE) and generalised convulsive status epilepticus (GCSE).
• Early detection of cerebral ischemia.
• To assess severity of encephalopathy and prognostication.
CCEEG Task Force of the American Clinical Neurophysiology Society (ACNS)

4. When to suspect NCSE?
Patient profile in whom NCSE should be suspected.
Altered mental status with previous history of epilepsy.
Unexplained altered mental status.
Fluctuating level of consciousness.
Acute brain injury due to any cause.
Recent GCSE with persisting altered mental state or if the patient is sedated or paralysed.
Subtle clinical phenomenon like nystagmus, persistent or repeated eye deviation, hippus, face
and limb myoclonus, stereotyped chewing, episodic posturing, autonomic instability,

5. Case 1:
• 64 year old lady, no comorbidities.
• Developed fever, headache and altered sensorium.
• Developed right sided paucity followed by 2 episodes of GTCS.
• Was intubated subsequently and put on Fentanyl infusion.
• MRI showed multiple areas of hyperintensity and hemorrhages
involving both cerebral hemispheres.
• CSF showed lymphocytic pleocytosis.
• Features were suggestive of viral encephalitis.
• She was started on Levetiracetam, followed by Lacosamide.

6. CCEEG of the patient, bipolar montage showing seizure onset over the left hemispheric
region (arrow) evolving in frequency and amplitude over the entire left hemispheric
region. Diffuse slowing of the background is seen prior to the seizure onset.

7. EEG shows rhythmic spikes mainly over the left temporal region compared to the left
fronto-centro-parietal region. Patient had eye deviation to the right side along with subtle
jerks of right hand and fluctuations in her BP along with reduced pupillary reactivity.

8. Large amplitude rhythmic spikes are seen over the left temporal and fronto-central
regions. Changes begin to appear on the right hemispheric regions as well (blue arrows).

9. EEG shows generalised ictal pattern comprising fast spikes. The stage patient is E1M1Vt
with evident stiffening of the whole body with subtle jerks of the right face and right UL.

10. The ictal pattern subsided on the left side, due to neuronal exhaustion, while it continued
over the right hemispheric region. Clinical manifestations subsided at this point.

11. There is further exhaustion of the ictal pattern with slower rhythmic spikes on the right
side. There is no ictal pattern over the left side and it is replaced by diffuse slowness.

12. The right sided ictal pattern further evolves into polymorphic slower waves and the
seizure finally terminates. This is followed by diffuse slowing.

13. LALLU SINGH(2764693)
Bilateral Multifocal spikes.
Subsequent EEG Longitudinal bipolar montage of the same patient with refractory status
epilepticus due to viral encephalitis, showing frequent multifocal spikes.

14. “If a patient has clinical seizures and thereafter continues to be
encephalopathic, do CCEEG for 12-24 hours to look for any
evidence of NCSE”.

15. How to identify seizure patterns on EEG?
• Clear change from ongoing activity.
• Rhythmic fast (or slow waves).
• Evolving in amplitude and frequency.
• Involving adjacent channels and spreading to nearby brain areas or
becoming hemispheric or generalised.
• May be accompanied by subtle movements of eyes, face, limbs or with
BP, heart rate or pupillary changes.
• Resolving rapidly with AEDs or spontaneously.
• Usually stereotyped patterns.

16. Case 2:
• 36 year old gentleman with new onset generalised convulsive status
epilepticus due to substance abuse.
• Clinical seizures stopped after administration of Inj Midazolam and
Levetiracetam.
• Shifted to MICU, sedated and paralysed.
• MRI brain was normal. Metabolic work up normal.
• CSF normal.

17. Longitudinal bipolar montage showing diffuse slowing, followed by ictal onset over the right
hemispheric region. There were no clinical manifestations.

18. Subsequently there is also evolution over the left hemispheric region in the form of rhythmic
spikes, more than the right side. Pulse rate and BP fluctuations were noted.

19. After involving both hemispheres, there were some jerks of the whole body and then the seizure
subsided and was followed by diffuse low amplitude slowing and intermittent bursts.

20. Follow up
• Multiple subclinical seizures and NCSE were recorded.
• Required Inj Lacosamide and a short period of Midazolam infusion.
• Patient recovered well.

21. “Always do CCEEG for atleast 24 hours after admission for
GCSE, if patient is sedated and paralysed, or if patient
sensorium is not normal”.

22. Case 3:
• 56 year old male patient presenting with urosepsis, mild hyponatremia
and deranged LFT.
• In view of altered sensorium he was shifted in the MICU.
• MRI brain showed age related atrophy and small vessel ischemic
changes.
• CSF was unremarkable.
• EEG was requested in view of persistently poor sensorium despite
improvement in sepsis and metabolic abnormalities.
• No features to suggest seizures.

23. Triphasic NCSE was noted in this patient, rhythmic, 2Hz, waxing and waning pattern,
maximum frontal, with subtle eye movements. Diffuse background slowing is noted.
LF 1Hz, HF 70Hz, Sen 7 uv

24. Triphasic NCSE: initial component is small and of short duration. This pattern was abolished
by Inj Midazolam, with partial improvement in responsiveness.
LF 1Hz, HF 70Hz, Sen 7 uv

25. Triphasic NCSE in a 57 year old patient with metabolic encephalopathy without history of
seizures. This pattern resolved with Inj Midazolam 2 mg, with improvement in his alertness.

26. NCSE with triphasic morphology Non-epileptiform rhythmic
triphasic waves
Higher frequency Lower frequency
Phase one is shorter (spiky) Relatively longer
Extra spike components Absent
Background slowing is less prominent and
often not generalised.
Prominent generalised slowing
Not affected by noxious or auditory stimuli Becomes more prominent.
Abolished by BZDs May or may not be abolished.
Can be seen in deeply comatose patients. Not seen.
Boulanger JM, et al. Can J Neurol Sci 2006;33:175-180.

27. Intravenous benzodiazepine trial for the diagnosis of NCSE
Clinical setting: Patients with altered mental status with suspected diagnosis of NCSE and with
an EEG showing epileptiform discharges ≤ 2.5 Hz or rhythmic delta/ theta activity (>0.5 Hz).
NICU/ ICU: Need to monitor EEG, pulse oximetry, ECG, BP and respiratory rate.
Test procedure: Sequential dosing of rapidly acting short duration midazolam 1 mg/dose and
repeated clinical and EEG evaluation in between the doses.
Test result: Test is considered positive when there is persistent resolution of epileptiform
discharges along with definite clinical improvement. If EEG improves but patient does not, the
result is considered equivocal.

28. Case 4:
• 52 year old male patient with DM2, HTN, previous stroke admitted
with altered sensorium since 2 days. GCS was E2VTM5
• He had mild fever at onset, which resolved in a day.
• He had mild hyponatremia (127), creatinine of 1.5 mg/dl.
• MRI brain showed multiple chronic lacunar infarcts.
• CSF analysis was normal.
• Initial EEG showed mild diffuse slowing.
• CCEEG was done in view of poor sensorium

29. EEG showed mild diffuse slowing. Multiple brief seizures were recorded over the right
hemispheric region lasting 20-25 s, without any clinical manifestations.

30. The seizures became generalised and subsided after initiation of anti seizure medications:
Levetiracetam and Fosphenytoin.

31. EEG showing resolution of the seizure spontaneously, followed by diffuse slowing suggestive of
bihemispheric dysfunction.

32. “CCEEG should be requested in all patients with
encephalopathy not explained by or disproportionate to the
identified causes of encephalopathy”.

33. Case 5:
• 48 year old lady, with DM 2 and urosepsis was shifted from ward to
MICU due to acute onset altered sensorium.
• She improved in the MICU but continued to have episodes of reduced
responsiveness lasting 10-20 minutes. Fluctuations in BP and heart rate
were noted during these episodes.
• During the episode she would not speak or obey, no eye contact, and
would respond only to pain. At other times she would obey and move
limbs spontaneously.
• EEG was requested to evaluate these episodes.

34. Longitudinal bipolar montage shows diffuse slowing of the background, followed by evolving
seizure in the right hemispheric region.

35. Seizure becomes generalised in the form of generalised rhythmic spikes. At this time the
patient is unresponsive to commands and only to pain.

36. Susequently the seizure resolves spontaneously, followed by severe bihemispheric slowing.
Several such seizures were recorded and were eventually controlled with AEDs.

37. Case 6:
• 36 year old lady with CKD, hyponatremia and diabetes was admitted for
evaluation of altered sensorium.
• Her sensorium improved in the first 2 days of MICU stay.
• Subsequently, she was noted to have variable levels of responsiveness
though the fever had resolved and metabolic parameters had improved.
• MRI brain showed chronic ischemic changes.
• EEG for 2 hours showed intermittent mild diffuse slowing.
• As she continued to have fluctuating sensorium, 24 hour CCEEG was
done.

38. Longitudinal bipolar montage showed seizure onset post-hyperventilation. It starts over the
right fronto central region in the form of rhythmic theta activity, evolving into delta range
activity. She had repetitive eye blinking during the seizure.

39. The seizure continued for 40 seconds and was characterised by blank look, unresponsiveness
and unawareness. Repetitive eye blinking was noted.

40. Subsequently the seizure resolved spontaneously, followed by bihemispheric slowing.

41. “CCEEG is indicated in all patients with unexplained
fluctuation in sensorium and responsiveness”

42. Case 7:
• 34 year old lady, with herpes encephalitis, was treated in the MICU for
altered sensorium and few episodes of seizures.
• MRI brain showed bilateral asymmetric medial temporal
hyperintensities.

43. REKHA MADHURI(4840651)
PLEDs
Longitudinal bipolar montage showing frequent right anterior temporal periodic lateralising
epileptiform discharges (PLEDs).

44. REKHA MADHURI(4840651)
PLEDs
Lack of evolution in frequency or amplitude differentiates this from an ictal pattern. The same
PLEDs pattern continued for several days and gradually subsided.

45. EEG Longitudinal bipolar montage of a 42 year old lady with HSV encephalitis showing left
fronto-temporal periodic lateralising epileptiform discharges (PLEDs).

46. PLEDs and BIPLEDs
• The EEG pattern shows complexes which consist of a di or multiphasic
spike and may include a slow wave.
• Complexes usually last for only a fraction of a second, and recur every
1-2 seconds, separated by low amplitude slow waves or no detectable
activity at regular gain.
• They appear in a wide distribution on one side of the head.
• The background in regions not showing PLEDs is often abnormal.
• PLEDs may also occur independently over both hemispheres a pattern
referred to as BIPLEDs.

47. “PLEDs and BIPLEDs indicate an increased risk of seizures
and warrant CCEEG to detect subclinical seizures.
However, they are not necessarily an ictal pattern and
abolishing it with anti-seizure medications should not be the
target of therapy”

48. Definition of NCSE
Diagnostic criteria for NCSE
Classification of NCSE

49. Salzburg consensus criteria for non-convulsive status epilepticus
Patients without known epileptic encephalopathy
EDs > 2.5 Hz, or
EDs ≤ 2.5 Hz or rhythmic delta/ theta activity (>0.5 Hz) AND one of the following:
• EEG and clinical improvement after IV AED, or
• Subtle clinical ictal phenomenon during the EEG patterns mentioned above, or
• Typical spatiotemporal evolution.
If EEG improvement occurs without clinical improvement, or if fluctuation occurs without
definite evolution, this should be considered possible NCSE.
Salzburg consensus criteria for non-convulsive status epilepticus
Patients with known epileptic encephalopathy
• Increase in prominence or frequency of the features mentioned above, when compared to
baseline with observable change in clinical state.
• Improvement of clinical and EEG features with IV AEDs.
ED: epileptiform discharges. IV AED: intravenous antiepileptic drugs.

50. Classification of non-convulsive status epilepticus (NCSE)
1. NCSE with coma/ stupor (including ‘subtle’ SE)
2. NCSE without coma/ stupor
Generalised (absence SE, typical, atypical and myoclonic absence)
Focal
• Without impairment of consciousness (aura continua, with autonomic, sensory, visual,
olfactory, gustatory, emotional/ psychic/ experiential, or auditory symptoms)
• Aphasic status
• With impaired consciousness
Unknown whether focal or generalised (eg, autonomic SE)
NCSE is defined as a continuous state of seizures without convulsions, or
multiple nonconvulsive seizures for more than 30 minutes without interictal full
recovery. To qualify for diagnosis of NCSE, the whole EEG recording should
be abnormal during this period (EEG criteria have to be continuously present
for atleast 10 seconds).

51. Altered mental state: clinical
suspicion of NCSE
Continuous rhythmic theta/
delta >0.5
Epileptiform discharges ≤2 Hz
Epileptiform discharges >2 Hz
IV Antiepileptic
drug
Subtle clinical signs
during EEG recording
Typical spatiotemporal
evolution
Persistent EEG resolution
and clinical improvement
NCSE Possible NCSE
Fluctuation without definite
evolution and EEG without clinical
improvement after IV AED

52. How long to monitor?
• No consensus.
• Minimum 1 hour. Ideally 24 hours.
• In one study, routine 30 min EEG identified seizures in 11% of patients,
while CCEEG detected seizures in another 28% of patients. (Pandian JD, et
al. Arch Neurol 2004; 61: 1090-4)
• In a study from India, 60 min EEG detected NCSE in 5.7% of 200
patients, while CCEEG for 12-48 hours identified NCSE in 4.8% of the
remaining patients. (Narayanan JT, et al. Epilepsia 2007; 48: 900-6)
• Monitoring should be longer in patients with definite clinical or
subclinical seizures identified on CCEEG.

53. Monitoring treatment of
status epilepticus

54. CCEEG to monitor treatment efficacy in seizures
and status epilepticus
• To identify seizure suppression, burst suppression or complete EEG
suppression, especially in patients on IV anesthetic agents.
• To ensure adequacy of burst suppression or complete suppression,
especially in the treatment of status epilepticus.
• It is unclear whether clinical seizure suppression, burst suppression or
complete EEG suppression better predicts outcome in SE.
• Adequate period of burst suppression ? (between 4s to 10-15s).
• Maintain Burst suppression for 12-48 hours.
• Timely review of the entire EEG is crucial.

55. Burst suppression pattern in a 28 year old lady with status epilepticus on IV anesthetic agents.
Burst Suppression
LF 1Hz, HF 70Hz, Sen 7 uv

56. Definition
• Electrographic bursts containing theta and/or delta waves, spikes,
sharp waves or any other morphology.
• Intervening periods of low amplitude (below 10 µV).
• Isoelectric or low-amplitude inter-burst interval of at least 1 second.
• Bilateral synchronous.
• Inter-ictal phenomenon.
• No stimulus sensitivity.
• May be associated with myoclonus, subtle eye movements.

57. Case 6:
• 62 year old lady, with viral encephalitis, cerebral venous sinus
thrombosis, hyponatremia and Klebsiella sepsis, requiring ventilator,
sedation and inotropes.
• She had repeated generalised convulsive seizures.
• She was started on Levetiracetam, followed by Fosphenytoin.
• In view of refractory status epilepticus, she was started on propofol
infusion followed by additional midazolam infusion.
• Clinical seizures stopped.
• CCEEG was used to titrate medications and achieve burst suppression.

58. CCEEG showed bursts of polymorphic activity with reduced interburst activity. This is not
true burst suppression as the amplitude of the suppressed area is not <10uv.

59. CCEEG showed bursts of polymorphic activity comprising spikes superimposed on delta
waves lasting around 2 seconds with periods of suppression lasting around 2 seconds.

60. Further treatment produced true burst suppression with large amplitude bursts of
polymorphic delta with superimposed fast activity with periods of very low activity in between

61. Further treatment produced true burst suppression with large amplitude bursts of
polymorphic delta with superimposed fast activity with periods of very low activity in between

62. Increasing the dose of IV anesthetic agents produced more sustained burst suppression
which was maintained for 16 hours and the IV anesthetic agents were withdrawn.

63. Refractory status epilepticus
Use IV anesthetic agents under
CCEEG monitoring
Complete EEG
suppression
Burst suppression of
4-10 seconds
Clinical seizure
suppression
Maintain burst suppression
for 12-48 hours
Wean IV anesthetics under
CCEEG monitoring
Recurrence of seizures
Reintroduce IV
anesthetic agents.
Continue CCEEG for 24
hours after stopping IV
anesthetic agents.
No seizures

64. Rare scenarios

65. Case 7:
• 15 year old girl, with epilepsy due to left parietal gliosis.
• Recurrent seizures, multiple attacks in a day, with reduced
responsiveness.
• Admitted at a local hospital, Levetiracetam and Lacosamide added to
Oxcarbazepine, Clobazam. Subsequently Valproate was added, but
continued to have seizures.
• Shifted to our hospital MICU. Midazolam infusion was started.
• CCEEG was requested.
• It was noted that her current semiology was different from her usual
semiology.

66. Follow up
• CCEEG was normal even during the paroxysmal events.
• All the recently added medications were withdrawn.
• Evaluation revealed recent stressors.
• Diagnosis: recurrent non-epileptic events.

67. “All paroxysmal events are not seizures, even in an epilepsy
patient. New semiology, unexplained increase in frequency and
inconsistent clinical manifestations should alert one to the
possibility of PNES”.

68. SIRPIDs
• First described in 2004 using continuous EEG in critically ill patients.
Hirsch LJ, et al. Epilepsia 2004;45:109-123.
• Striking EEG patterns were noted when stuporous or comatose patients
were stimulated and noted that many of these patterns appeared ictal,
but were consistently elicited by stimulation.
• Definition: periodic, rhythmic or ictal appearing discharges consistently
induced by alerting stimuli (eg. auditory, sternal rub, examination,
suctioning, turning, other patient-care activity).

69. Patient 1: 86 year old with Alzheimers disease and recent anoxic episode.

70. Patient 1: Sternal rub results in generalised periodic epileptiform discharges.

71. Patient 1: GPEDs continue for several seconds.

72. Patient 2: 76 year old with Hunt and Hess Grade III SAH and b/l medial frontal lobe injury.
Stimulation- someone at bedside

73. Patient 2: Stimulation consistently generated left hemispheric ictal appearing discharges.

74. Patient 2: Discharges continue for several seconds.
Discharges subside

75. Patient 3: A 61-year-old with recurrent right frontal GBM. Stimulation consistently elicited
PLEDs, maximal at C4, with some underlying rhythmic delta and bilateral spread.
PLEDs

76. Patient 3: After vigorous or repetitive stimulation, this pattern often became a focal
ictal-appearing pattern.

77. SIRPIDs
• Some patients have clinical seizures with SIRPIDs, especially focal
motor seizures, but this pattern is usually a purely electrographic
change, with no obvious clinical manifestations.
• Pathophysiology, clinical, therapeutic and prognostic significance of
SIRPIDs is still undefined.
Hirsch LJ, et al. Epilepsia 2004;45:109-123.
Chong DJ, et al. J Clin Neurophysiol 2005;22:79-91.

78. THANK YOU