1. Nonconvulsive status and long term EEG Monitoring
Maysaa M. Basha, MD Assistant Professor of Neurology
Comprehensive Epilepsy Program
WSU/DMC

2. Objectives Define nonconvulsive status epilepticus and its subsets
Identify the clinical presentation of NCSE
Describe the role of EEG AND its limitations

3. Definition of Status Epilepticus
Patient should be considered in SE if seizure persists for more than 5 minutes
Reasoning: Very few single seizures will last this long
Divided into convulsive and nonconvulsive
Dependent on presence or absence of rhythmic jerking of the extremities

4. Nonconvulsive Status Epilepticus: NCSE
Prolonged electrographic seizure activity that result in nonconvulsive clinical symptoms.
subtle symptoms
no symptoms

5. “SUBTLE SIGNS”
Aphasia/mutism
Amnesia
Catatonia
Staring
Automatisms
Blinking
Facial twitching
Nystagmus/eye deviation
Perseveration
Pyschosis
Important and challenging to differentiate between ictal and postictal semiology
Jirsch&Hirsch 2007, Kaplan PW. 1996

6. ? Classification of NONCONVULSIVE SE No LOC
Alteration of consciousness
COMA
No clinical signs/ “subtle” sign
ICU patients
Elementary SE/Focal seizures
Auditory, psychic, visual, SS, aphasic
“Absence” SE
Typical
Late onset
“complex partial” SE

7. ICTAL COMATOSE
NONCONVULSIVE SE IN THE COMATOSE PATIENT

8. ICTAL COMATOSE
NCSE should be suspected if a patient has seizures without recovery of consciousness in between attacks.
No improvement in ~ 20 minutes after seizure ends
Persistent unexplained mental status abnormalities ~ 1 hour after convulsion
Most seizures in the ICU setting are nonconvulsive and require continuous EEG monitoring

9. ICTAL COMATOSE Who? Unexplained depressed level of consciousness
“Subtle signs”
Comorbidities
Underlying Brain Pathology
History of prior epilepsy
History of recent convulsive seizures

10. ICTAL COMATOSE
Patients with unexplained depressed level of consciousness
Sick patients: infxn, SAH, stroke, head trauma, brain tumor, prior hx of epilepsy.
18-34% had NCSE
Claasen et al. 2004; Jirsch&Hirsch 2007

11. History of recent convulsive seizures
Patient with prior convulsive status, who go on to develop coma
Coma > 2 hours
13-48% of them had NCSE
Etiology of convulsive seizures is important:
Patients with underlying brain disease more likely to be in nonconvulsive status.
Patients less likely to be in nonconvulsive status were those who had their seizures due to:
AED discontinuation
Drug overdose
EtOH withdrawal
DeLorenzo et al. 1998; Treiman et al. 1998

12. Towne et al. 2000
Patient with unexplained depressed level of consciousness
Patient with prior seizures and those with “subtle” signs were excluded
8% were found to be in NCSE

13. How long should you record?
30-60 minutes of recording will capture ~50% of patients
Noncomatose:
95% will have seizure within the first 24 H
Comatose:
80% will have seizure within the first 24 H and an additional 7% within 48 H.
? Presence of certain patterns on EEG may prompt longer recording = better communication w/ your EEGer
Pandian et al. 2004; Jirsch &Hirsch 2007; Claassen et al. 2004

14. EEG patterns in Nonconvulsive SE

15. Purpose of EEG in ICU setting
ID of NCS or NCSE
Characterize clinical spells
Importance of video recording!!!
Detection of ischemia
Management of Burst Suppression Pattern
Monitoring treatment and Prognosis.

16. EEG Criteria for NCSE (1/3)
I. Frequent Nonconvulsive seizures (Electrographic seizures)
What is an Electrographic seizure?
Sequential rhythmic, periodic, or quasi-periodic waves of at least 1 Hz frequency, lasting > 10s with evolution (or devolution) in:
Frequency
Distribution
Morphology (not just change in sharpness)
Amplitude

17. Surface electrodes: top viewFz Cz Pz F3
Fp1 O1 P3 C3 P4 O2
Fp2 C4 F4 P8 T8 A2 F8 P7 A1 T7 F7 T3 T4 T5 T6

21. EEG criteria for NCSE (2/3)
II. Repetitive generalized or focal epileptiform complexes at ≥ 3 Hz

22. Repetitive Generalized epileptiform complexes

23. Repetitive Focal epileptiform discharges

24. EEG Criteria for NCSE (3/3)
III. Repetitive generalized or focal epileptiform complexes at < 3/s (slower)
AND
Improved clinical response and EEG “normalization” after administration of IV AED
Repeated 1mg midazolam doses
Disappearance of abnormal pattern w/o clinical improvement doesn’t count
Many patterns improve w/ benzo including triphasics
Fountain and Waldman, 2001

25. Commonly seen slow pattern that can be considered NCSE
Periodic patterns
PLEDs, Bi-PEDs
GPEDs
SIRPIDs
Stimulus-induced Rhythmic, Periodic, or Ictal Discharges

26. Periodic Pattern: PLEDs plus (clinically Lt facial twitch)
F4-C4

27. Same patient: 24 hours prior PLEDs with no visible jerkings

28. SIRPIDs, nurse checks pupils

29. Examples

30. Patient 1 Patient with right parieto-occipital mass s/p resection
Not waking up
Noted to have “subtle” left face and at times arm twitching by psychiatry rotator.

32. MRI

33. Patient # 2 Patient has cardiac event Undergoes CPR
Currently unresponsive and having generalized myoclonic jerks

35. Myoclonic status epilepticus
Burst suppression pattern with burst containing generalized epileptiform activity that generates clinical myoclonus.
Seen in post-anoxic encephalopathy
Myoclonic postanoxic status epilepticus (PSE)
Invariably leads to poor outcome and calls for w/d of care
Only 3 cases reported to survive beyond a vegetative state:
All received therapeutic hypothermia post-CPR
“reactive EEG Background” described
Rosetti, et al. 2009

36. Patient # 3 Patient found in NH pulseless Undergoes CPR
Currently unresponsive

37. EEG #1

38. EEG #2 (48-72 H later)

39. Patient # 4
Patient with ESRD
Febrile
Unresponsive

41. Referential Montage

42. Patient # 5
Patient with history of epilepsy who had several GTC on presentation
Currently arousable
No purposeful movement
Noted to have right arm jerks

44. Patient #6 46 year old with cryptococcal meningitis.
Had 2 generalized convulsions (new-onset).
Worsened in clinical state and is now unresponsive.
EEG for nonconvulsive status?

45. Day 1: Background – semirhythmic delta

46. Day 1: Nurse attempting to get iv

48. Day 1: Nurse care

49. SIRPID  Patient was monitored another 24 hours without seizures.

50. 2 Days later.. Patient still not waking up

51. Associated with movement

52. At bedside. Stimulus provided: Clap

53. At bedside. Stimulus provided: Clap cont.

54. At bedside. Stimulus provided: Clap cont.

55. Response to stimulus w/ NM blockade

56. TREATMENT

57. Treatment of NCSE. What is the evidence?
Seizures are bad for your brain!
Hippocampal , cortical, cerebellar atrophy.
Limitation: separating effects of NCSE from underlying cause/complications/clinical course.
Animal studies – severity of consequences largely depends on convulsive activity.
Association of development of ipsilateral hippcampal atrophy in posttraumatic patients within 6 months. (Vespa et al )
Small sample size (6 versus 10 control)
None of these patients developed epilepsy

58. Treatment – as with convulsive status
Reverse Underlying cause /ABC Benzo’s AED Drips ?? (controversial for NCSE)

59. Benzo’s: AED: Drips: Lorazepam 0.1mg/kg at 2mg/min; Max: 8mg
Fosphenytoin 20mg/kg PE at 150mg PE/min
VA: 20mg/kg over 5-10min, then ½ dose divided q6
Phenobarb; 20mg/kg; may repeat, max of 40mg/kg
Drips:
Midazoloam: 0.2mg/kg, then 0.1-2mg/kg/h
Propofol: 2mg/kg, then 2-15mg/kg/h
Pentobarb: 5-10mg/kg; then 5mg/kg/h and titrate by mg/kg/h
Ketamine: 1mg/kg; then 0.5mg/kg/h up to 3-5mg/kg/h