1. EEG monitoring in childhood Status Epilepticus
بسم الله الرحمن الرحیم
EEG monitoring in childhood Status Epilepticus

2. EEG monitoring in childhood Status Epilepticus
As there are No clinical or radiographic findings specific to NCS/NCSE, diagnosis may often rely on EEG findings.
EEG: gold standard for making diagnosis
In critically ill patients, there may be No clinical manifestations of seizure activity at all, and a high degree of suspicion is required to detect NCSE.
A standard EEG may not detect NCSE and continuous EEG monitoring may be required.

3. Convulsive SE: overt clinical signs tonic, tonic-clonic, or clonic motor movements.
Nonconvulsive status epilepticus (NCSE):
electrographic SE is associated with:
altered awareness without overt clinical signs
altered awareness with subtle motor signs, such as minimal eyelid blinking

4. A variety of term in the literature to denote NCSE
minor status epilepticus
spike–wave stupor
epileptic twilight state
epilepsia minores continua
petit mal
impulsive-petit mal status
dialeptic status epilepticus
Arzimanoglou A, Guerrini R, Aicardi J. Aicardi’s epilepsy in children. Baltimore: Lippincott Williams & Wilkins; 2004.

5. There are no current universally accepted definitions of NCSE.
The definition of NCSE can not rely on clinical symptoms alone because they may range from subtle encephalopathy and subtle clinical signs to a frank comatose state.

6. CSE is more common than NCSE, occurring in as much as 86% of patients.
Nishiyama I, Ohtsuka Y, Tsuda T, et al.: An epidemiological study of children with status epilepticus in Okayama, Japan. Epilepsia 2007, 48:1133–1137.
This is the first report of the incidence of SE in Japan, where the incidence is much higher than that reported in whites.

7. Seventy-six percent of patients had a history of a clinical seizure preceding NCSE, and 25% were de novo.
Mortality of NCSE in this combined adult–pediatric study was 57% and was strongly linked to duration of NCSE and delay of diagnosis of NCSE.
Young GB, Jordan KG, Doig GS: An assessment of nonconvulsive seizures in the intensive care unit using continuous EEG monitoring. Neurology 1996, 47:83–89.

8. The overall mortality rate of NCSE was 26%.
The incidence of NCSE in pediatric patients undergoing long-term monitoring in the intensive care setting ranges from 16% to 32%.
The overall mortality rate of NCSE was 26%.
Tay SK, Hirsch LJ, Leary L, et al.: Nonconvulsive status epilepticus in children: clinical and EEG characteristics. Epilepsia 2006, 47:1503–1509.
Abend NS, Dlugos DJ: Nonconvulsive status epilepticus in a pediatric intensive care unit. Pediatr Neurol 2007, 37:165–170.
Saengpattrachai M, Sharma R, Hunjan A, et al.: Nonconvulsive seizures in the pediatric intensive care unit: etiology, EEG, and brain imaging fi ndings. Epilepsia 2006, 47:1510–1518.

9. Studies have revealed NCSE in 23% to 34% of children who underwent long-term EEG monitoring due to altered mental status in pediatric intensive care units or emergency departments [Class IV].
In retrospective studies of children selected for the presence of NCSE, 20% to 26% of cases occurred after convulsive SE, 60% after convulsive seizures, and 10% to 20% with no proceeding convulsions [Class IV].

10. In a study by DeLorenzo and colleagues, 14% of patients treated successfully for convulsive SE were in NCSE when EEG was begun; of the patients who underwent continuous EEG monitoring (cEEG) after convulsive SE was controlled, 48% had nonconvulsive seizures.
DeLorenzo RJ, Waterhouse EJ, Towne AR, et al. Persistent nonconvulsive status epilepticus after the control of convulsive status epilepticus. Epilepsia 1998;39:833–840

11. Nonconvulsive status epilepticus (NCSE) represents a diagnostic dilemma, and so far several different definitions and diagnostic criteria have been proposed in the literature order to address and try to solve the diagnostic problems related to this condition.
The diagnosis of NCSE is electro-clinical

12. An EEG done at the time of SE (ictal EEG) can determine if the electrographic discharge is focal or generalized, demonstrate NCSE, or may also distinguish an epileptic event from a nonepileptic event (pseudoseizures).
Privitera MD, Strawsurg RH. Electroencephalographic monitoring in the emergency department. Emerg Med Clin North Am 1994;12:1089–1101.
Thomas P. Status epileptics: Indications for emergency EEG. Neurophysiol Clin 1997;27:398–405.

13. EBM
Six class III studies, report 413 EEG findings in 358 children who presented in SE and had an EEG.

14. Data revealed generalized or focal epileptiform activity in 43
Data revealed generalized or focal epileptiform activity in 43.1% of the EEGs done for SE.
Abnormalities on EEG occur in 62% of children with SE compared to
41% of children with a first FUS less than 30 minute.
Sufficient data on the prevalence of NCSE in children who presented with SE are not available.
reported that 21% of children initially thought to be in SE had pseudostatus.

15. Recommendations:
1. An EEG may be considered in a child presenting with new onset SE as it may determine whether there are focal or generalized abnormalities that may influence diagnostic and treatment decisions (Level C, class III evidence). 2. Although NCSE occurs in children who present with SE, there are insufficient data to support or refute recommendations regarding whether an EEG should be obtained to establish this diagnosis (Level U). 3. An EEG may be considered in a child presenting with SE if the diagnosis of pseudostatus epilepticus is suspected (Level C, class III evidence).

16. A new diagnostic classification system of SE
There are four axes:
Semiology
(2) Etiology
(3) Electroencephalography (EEG) correlates
(4) Age
A definition and classification of status epilepticus – Report of the ILAE Task Force on Classification of Status Epilepticus
Eugen Trinka, §Hannah Cock, ¶Dale Hesdorffer, #Andrea O. Rossetti, **Ingrid E. Scheffer, ††Shlomo Shinnar, ‡‡Simon Shorvon, and §§Daniel H. Lowenstein Epilepsia, 56(10):1515–1523, 2015

17. ILAE Task Force on Classification
None of the ictal EEG patterns of any type of SE is specific.
Epileptiform discharges are regarded as the hallmark, but with increasing duration of SE, the EEG changes and rhythmic nonepileptiform patterns may prevail.
Similar EEG patterns, such as triphasic waves, can be recorded in various pathologic conditions, leading to substantial confusion in the
literature.

18. ILAE Task Force on Classification
Currently indeterminate conditions (or “boundary syndromes”): Epileptic encephalopathies Coma with non evolving epileptiform EEG pattern Behavioral disturbance (e.g., psychosis) in patients with epilepsy Acute confusional states, (e.g., delirium) with epileptiform EEG patterns

19. Although the EEG is overloaded with movement and muscle artifact in the CSE and thus of limited clinical value, it is indispensable in the diagnosis of NCSE, as the clinical signs (if any) are often subtle and nonspecific.
Shorvon S. Clinical forms of status epilepticus. In Shorvon S (Ed) Status epilepticus. Ist clinical features and treatment in children and adults. Cambridge,UnitedKingdom:Cambridge University Press; 1994:34–137.
Sutter R, Kaplan PW. The neurophysiologic types of nonconvulsive status epilepticus: EEG patterns of different phenotypes. Epilepsia 2013;54(Suppl. 6):23–27.

20. Advances in electrophysiologic techniques may provide us with increased capability to utilize EEG in the emergency setting and allow better delineation of the highly dynamic changes of EEG patterns in the near future.
Currently there are NO evidence-based EEG criteria for SE.

21. Definition and criteria for NCSE
Non-convulsive status epilepticus is a term that covers a range
of disparate conditions, denoting prolonged electrographic seizure
activity (set arbitrarily at 30 minutes) with resultant non-convulsive clinical symptoms (Walker et al., 2005).

22. Nonconvulsive status epilepticus was defined as continuous ictal appearing patterns lasting more than 30 min or ictal patterns present more than 50% of 1 h of EEG with subtle movements (facial twitching and eye deviation) observed in the video or reported in the chart.
Foreman B, Claassen J, Abou Khaled K, Jirsch J, Alschuler DM, Wittman J, et al. Generalized periodic discharges in the critically ill: a case–control study of 200 patients. Neurology 2012;79(19):1951–60.

23. Hypothesis
abnormal periodic discharges as epiphenomena in severely injured brains or as harmful epileptiform discharges that could lead to additional brain injury.
periodic discharges and seizures in the acutely-injured brain lead to secondary neuronal injury via excessive metabolic demand, excitotoxicity, or other mechanisms (Claassen, 2009).

24. Chong and Hirsch (2005) proposed an ictal-interictal injury continuum to put into context the likelihood of neuronal injury for each type of discharge in a given clinical setting in order to guide management (Chong and Hirsch, 2005).

25. EEG Findings in Status Epilepticus:
Treiman et al. initially described five identifiable EEG patterns that occurred in a predictable sequence during the course of secondarily generalized CSE in adults.
Treiman DM, Walton NY, Kendrick C: A progressive sequence of electroencephalographic changes during generalized convulsive status epilepticus. Epilepsy Res 1990, 5:49–60

26. The stages were: 1) EEG changes of discrete seizures with interictal slowing 2) merging seizures with waxing and waning ictal discharges 3) continuous ictal discharges 4) Continuous ictal discharges with “flat” periods 5) Periodic epileptiform discharges on a “flat” background

27. EEG patterns
In ambulatory patients, the most common EEG patterns associated with NCSE are generalized spike-and-wave or generalized polyspike- and-wave discharges (in the case of ASE), or rhythmic focal discharges (in the case of CPSE).
Brenner RP. EEG in convulsive and nonconvulsive status epilepticus. J Clin Neurophysiol 2004;21:319–31.

28. In contrast, in obtunded or comatose patients, the EEG patterns are more complex and controversial.
Electrographic seizures have been defined as generalized spike-and-wave discharges at 3 Hz and clearly evolving discharges of any type that reach a frequency of 4 Hz.
Hirsch LJ, Brenner RP, Drislane FW, et alfor the ACNS Subcommittee on Research Terminology for Continuous EEG Monitoring. Proposed standardized terminology for rhythmic and periodic EEG patterns encountered in critically ill patients. J Clin Neurophysiol 2005;22:128–35

29. Periodic lateralizing epileptiform discharges (PLEDs)
Chatrian et al. first described PLEDs as an EEG finding associated with an acute unilateral forebrain lesion.
Next, studies have shown that PLEDs can be associated with lesions of the cortical gray matter, subcortical white matter, subcortical gray matter, or a combination of these.
Lateralized periodic discharges (LPDs)

30. PLEDs-plus: with superimposed faster activity
In addition, PLEDs reported in patients with NO focal lesion at all or with chronic brain lesions.
PLEDs: PLEDs-proper
PLEDs-plus: with superimposed faster activity
Brenner RP, Schaul N. Periodic EEG patterns: classification, clinical correlation, and pathophysiology. J Clin Neurophysiol 1990;7:249–67.
Reiher J, Rivest J, Grand’Maison F, Leduc CP. Periodic lateralized epileptiform discharges with transitional rhythmic discharges: association with seizures. Electroencephalogr Clin Neurophysiol 1991;78:12–7.

31. The incidence of clinical seizures in the acute setting of PLEDs ranges from 58 to 100%; most commonly these are focal motor seizures or epilepsia partialis continua.
Pohlmann-Eden B, Hoch DB, Cochuis JL, Chiappa KH. Periodic lateralized epileptiform discharges: a critical review. J Clin Neurophysiol 1996;13:519–30.

32. Whether PLEDs represents a definitively ictal pattern is debated in the literature.
PLEDs have been reported to be ‘‘time-locked” with focal motor movements.
also been reported to be associated with a reversible confusional state.
Jirsch J, Hirsch LJ. Nonconvulsive seizures: developing a rational approach to the diagnosis and management in the critically ill population. Clin Neurophysiol 2007;118:1660–70.

33. However, longstanding PLEDs in ambulatory patients without apparent sequelae have been reported, so that they can sometimes not be ictal.
Reiher et al. suggested that PLEDs exist on an ictal–interictal continuum between PLEDs-proper (PLEDs without associated low-amplitude rhythmic discharges), PLEDs-plus (PLEDs with associated low-amplitude rhythmic discharges), and electrographic seizure activity.
Neuroimaging studies (PET and SPECT) argue for the ictal nature of some forms of LPDs.

34. Generalized periodic epileptiform discharges (GPEDs)
are periodic complexes that are bilaterally synchronous, and can have a variety of morphologies.
OR relatively uniform morphology
Husain et al. included ‘‘sharp, slow, and triphasic-like waves,” but excluded suppression–
burst patterns and continuous triphasic waves, in their series of 25 patients with GPEDs.
Generalized periodic discharges (GPDs)
Husain AM, Mebust KA, Radtke RA. Generalized periodic epileptiform discharges: etiologies, relationship to status epilepticus, and prognosis. J Clin Neurophysiol 1999;16:51–8.

35. GPEDs: periodic short-interval diffuse discharges
periodic long-interval diffuse discharges
Brenner RP, Schaul N. Periodic EEG patterns: classification, clinical correlation, and pathophysiology. J Clin Neurophysiol 1990;7:249–67.
Reiher J, Rivest J, Grand’Maison F, Leduc CP. Periodic lateralized epileptiform discharges with transitional rhythmic discharges: association with seizures. Electroencephalogr Clin Neurophysiol 1991;78:12–7.

36. Triphasic waves (TWs)
consist of an initial small negative phase, a larger positive phase (usually with the largest amplitude of the three), followed by a final negative phase.
typically duration of 0.25 to 0.5 second
A phase lag, either anterior to posterior or posterior to anterior, can be seen in the longitudinal bipolar montage.
Continuous 2/s GPDs with triphasic morphology

37. TWs occurring in rhythmical trains at 1.5–2.5 Hz.
TWs can appear in a periodic or quasiperiodic pattern at 0.5- to 1- second intervals.
‘‘Typical” TWs have been distinguished as bilaterally synchronous, symmetric, medium- to high-voltage.
TWs occurring in rhythmical trains at 1.5–2.5 Hz.
Fisch BJ. Electrographic seizure patterns, pseudoperiodic patterns, and pseudoepileptiform patterns. In: Fisch and Spehlmann’s EEG primer: basic principles of digital and analog EEG. Amsterdam: Elsevier; p. 307–48
Bauer G. Coma and brain death. In: Niedermayer E, Da Silva FL, editors. Electroencephalography: basic principles, clinical applications and related fields. Baltimore: Lippincott Williams and Wilkins; p. 471–87

38. Although TWs is the term usually used to imply a pattern of metabolic encephalopathy, this pattern can be indistinguishable from electrographic NCSE, and both NCSE and triphasic waves have been shown to clear with intravenous benzodiazepines.
Brenner RP. EEG in convulsive and nonconvulsive status epilepticus. J Clin Neurophysiol 2004;21:319–31
Chong DJ, Hirsch LJ. Which EEG patterns warrant treatment in the critically ill? Reviewing the evidence for treatment of periodic epileptiform discharges and related patterns. J Clin Neurophysiol 2005;22:79–91

39. Occasionally, TWs are very difficult to differentiate from NCSE, especially when they appear with a frequency exceeding 1.0/sec.
They may therefore straddle the border zone between epilepsy and
encephalopathy.

40. It is not clear from the literature when TWs should be considered epileptiform as they may be indistinguishable from GPEDs sometimes.
Some authors consider blunted peaks, antero-posterior amplitude gradient, and a time lag as features consistent with TWs, and use these criteria to make the distinction.
Kaplan PW, Birbeck G. Lithium-induced confusional states: nonconvulsive status epilepticus or triphasic encephalopathy, Epilepsia2006;47:2071–4

41. Boulanger et al. reported that TWs associated with metabolic encephalopathies (as opposed to epileptiform discharges in NCSE) tend to have a lower frequency, a dominant phase 2 wave, an anterior–posterior lag, and associated diffuse background slowing.

42. Burst suppression patterns
deep stages of coma
some rare childhood encephalopathies (e.g., Ohtahara syndrome)
deep anesthesia
poor prognosis in cerebral hypoxia/anoxia after cardiopulmonary arrest
various etiologies (structural, toxic, and metabolic)
hypothermia

43. The pattern consists of periodic high voltage, sharply contoured waveforms, including spikes and polyspikes, at times with a buildup or salvos of spikes alternating with periods of severe suppression or even isoelectricity.
The bursts last from less than a second to 10 s or more, and the period of suppression may be a second to 10 s or much longer.
The suppression period may have a variable degree of residual activity of low voltage or is completely isoelectric.

44. Various patterns of transitions to or from diffuse slow activity, alpha coma, theta coma, low output voltage, isoelectric EEG, LPD, or GPD have been described.

45. Some indications for cEEG in SE:
Recent clinical seizure or SE without return to baseline >10 min
Coma, including post-cardiac arrest
Epileptiform activity or periodic discharges on initial 30 min EEG
Intracranial hemorrhage including TBI, SAH, ICH
Suspected non-convulsive seizures in patients with altered mental status

46. Non convulsive status epilepticus after replacement of valproate with lamotrigine
J Neurol (2002) 249 : 1417–1422
Eugen Trinka
Erika Dilitz
Iris Unterberger
Gerhard Luef
Florian Deisenhammer
Ulrike Niedermüller
Claudia Thaler
Gerhard Bauer

47. Non-convulsive status epilepticus associated with tiagabine therapy in children
ANGELIKI SKARDOUTSOU, KONSTANTINOS A. VOUDRIS & ELENI A. VAGIAKOU
Second Department of Paediatrics-University of Athens, “P & A Kyriakou” Children’s Hospital,
Athens, Greece
Correspondence to: Dr A. Skardoutsou, M.D., Second Department of Paediatrics-University of Athens, “P & A Kyriakou” Children’s Hospital, Thivon & Levadeias St, , Athens, Greece.