Kwang Ki Kim

Department of Neurology
Dongguk University Ilsan Hospital

1.

Case

2.

NCSE criteria and diagnosis

3.

Role of cEEG monitoring

4.

Strategies of treatment of NCSE in the neuroICU

C.C) Altered mentality

BHx) Underlying alcoholic LC patient (child class C with
esophageal varix)
He had previous history of recurrent spontaneous bacterial
peritonitis and pleural effusion
One day before admission, he showed general weakness and
altered mentality. He was found half naked and staring.
He was transferred to emergency room.

V/S 110/62, 112BPM, RR 22 BT 37.8

Icteric sclera, pale conjunctiva

Decreased Rt lung sound

Regular heart beat without murmur

Soft abdomen

Normoactive bowel sound

Pretibial pitting edema (+/+)

CBC (4/15)

WBC 9.73x103/ul

Hb 10.5g/dL

RBC 2.98x106/ul

Platelet 45x103/ ul

Neutrophil 97.1%

ABGA (4/15)

7.507-38.6-77.1-30.8

BUN/Cr 23.0/0.97 BST 284mg/dL

PT INR 1.39 (4/16)

D-dimer 24.89 (4/17)

Blood culture (4/15 4/17)

K.pneumoniae

Chest AP

Stuporous mentality.
Normal pupillary light reflex, corneal reflex and doll's eye
reflex.
U/E- Grade I with painful stimuli
L/E- Grade II with painful stimuli
DTR - normal
No pathologic reflex



IV levetiracetam on admission
 add midazolam
 add fosphenytoin + phenobarbital

Current medication

Levetiracetam + oxcarbazepine

C.C) Sudden onset sensory aphasia

BHx) She could not understand caregiver's
words suddenly one hour before she
visited to the emergency room.
NIHSS :5

IV levetiracetam loading

Symptoms

Acute impairment or fluctuation of mental status

Impaired consciousness with facial twitching or nystagmus

Episodic aphasia, staring, automatisms

Episodic altered behavior without cause

Clinical Settings

Prolonged encephalopathy following surgery or a neurological

damage (head trauma, hypoxia,)

Post seizure with prolonged consciousness impairment
Encephalitis, meningoencephalitis
Severe metabolic encephalopathy
Stroke ( hemispheric, embolic)
Subarachnoid hemorrhage
Coma of unknown etiology

Nonconvulsive status epilepticus (NCSE) is a term used

to denote a range of conditions in which electrographic
seizure activity is prolonged and results in nonconvulsive
clinical symptoms.

Note:
1. NCSE can be most usefully viewed as a form of cerebral
response, which is dependant largely on the level of cerebral
development of the individual (age and cerebral
integrity/development/maturity), epilepsy syndrome, and the
anatomical location of the epileptic activity.
2.The electrographic activity can take various forms.

1. NCSE occurring in the neonatal and infantile

epilepsy syndromes
1a. West syndrome
1b. Ohtahara syndrome
1c. Severe myoclonic encephalopathy of infancy

(SMEI; Dravet syndrome)

1d. NCSE in other forms of neonatal or infantile

epilepsy

2. NCSE occurring only in childhood

2a. NCSE in Early-onset benign childhood occipital
epilepsy (Panayiotopoulos syndrome)
2b. NCSE in other forms of childhood epileptic
encephalopathies, syndromes and etiologies, e.g., Ring

chromosome X and other karyotype abnormalities,

Angelman syndrome, Rett syndrome, myoclonic-astatic
epilepsy, other childhood myoclonic encephalopathies.
2c. Electrical status epilepticus in slow wave sleep
(ESES)
2d. Landau-Kleffner syndrome

3. NCSE occurring in both childhood and adult life

With epileptic encephalopathy
3a. NCSE in the Lennox-Gastaut syndrome
i. Atypical absence status epilepticus
ii. Tonicstatus epilepticus

3b. Other forms of NCSE in patients with learning disability or disturbed

cerebral development (cryptogenic or symptomatic)
Without epileptic encephalopathy
3c. Typical absence status epilepticus in idiopathic generalized epilepsy
3d. Complex partial status epilepticus:
i. Limbic
ii. Nonlimbic

3e. NCSE in the postictal phase of tonicclonic seizures

3f. Subtle Status epilepticus (myoclonic SE occurring in the late stage of
convulsive SE)
3g. Aura continua (with: i. sensory, ii. special sensory, iii. autonomic, iv.
cognitive symptoms)

4. NCSE occurring in late adult life

4a. De novo absence status epilepticus of late onset

5. Boundary syndromes
5a. Some cases of epileptic encephalopathy.
5b. Some cases of coma due to acute brain injury with epileptiform
EEG changes.
5c. Some cases of epileptic behavioral disturbance or psychosis.
5d. Some cases of drug induced or metabolic confusional state with
epileptiform EEG changes.

PEDs

Surface-negative bi-, tri-, or polyphasic discharges with

spike, sharp, polyspike components, and/or slow-wave

complexes.
Complex duration: 60600 msec (mean 200 msec)
Amplitude: 50300 uV (usually up to 150 uV)
Frequency: 0.23 Hz (usually 0.52.0 Hz)
Persistence: minimum of 10 min in a recording.
Evolution: static with only minor variability (<50%) in the
above characteristics.

Triphasic waves

Surface negative, blunted triphasic complexes with a) low-

amplitude, blunted, negative first phase (often wide-based); b)

dominant, steep positive second phase; and c) slow rising third
slow-wave component. No polyspike component.
Complex duration: 400600 msec
Amplitude: 100300 uV on referential montage; smaller on
bipolar.
Frequency: 1.02.5 Hz (typically 1.8 Hz).
Persistence: wax and wane; occupy >10% of a standard
recording (20 min).
Evolution/reactivity: decrease with sleep, drowsiness or after
BZPs; increase and reappear with arousal or noxious stimulation.
May exhibit phase-lag best seen on referential montage

In patients without a known epileptic

encephalopathy

In patients with known epileptic

encephalopathy

1) Repetitive generalized or focal spikes, polyspike,

sharp waves, spike-and-wave or sharp-and-slow wave
complexes at >2.5/second.
2) Above, with discharges <2.5/second but with EEG
and clinical improvement after rapid onset antiepileptic
drugs, typically BZPs. Testing for patient responsiveness
and improvement in EEG; increases in EEG reactivity
and appearance of EEG background activity.
3) Above, with discharges < 2.5/sec with focal ictal
phenomena (e.g., facial twitching, gaze deviation,
nystagmus, limb myoclonus).

4) Rhythmic waves (theta-delta) at >0.5 Hz with

a) incrementing onset (increase in voltage with increase
or decrease in frequency),
b)evolution in pattern (increase or decrease in
frequency (>1 Hz), or location [changes in discharge
voltage (amplitude) or morphology are not sufficient], or
c) decrementing termination (voltage or frequency),
d) post-PEDs background slowing or attenuation.
a,b,c may be acutely abolished by IV BZPs.

1) Frequent or continuous generalized spike-wave

discharges, which show an increase in profusion or
frequency when compared to baseline
EEG with observable change in clinical state.
2) Regression (improvement) of clinical or EEG
features with IV BZPs.

Daniel Friedman and Lawrence J. Hirsch

Seizures in Critical Care: A Guide to Diagnosis and Therapeutics :
Current Clinical Neurology, 2010

Any pattern lasting at least 10s satisfying any

one of the following three primary criteria

1.
2.

3.

Repetitive generalized or focal spikes, sharp-waves,

spike-and-wave complexes at 3/s
Repetitive generalized or focal spikes, sharp-waves,
spike-and-wave, or sharp-and-slow wave complexes at
<3/s and the secondary criterion
Sequential rhythmic, periodic, or quasi-periodic waves
at 1/s and unequivocal evolution in frequency
(gradually increasing or decreasing by at least 1/s. e.g.,
2-3/s), morphology, or location (gradual spread into or
out of a region involving at least two electrodes).
Evolution in amplitude is not sufficient. Change in
sharpness without other change in morphology is not
enough to satisfy evolution in morphology.


Significant improvement in clinical state or

appearance of previously absent normal EEG patterns

(such as posterior-dominant alpha rhythm)
temporally coupled to acute administration of a rapidly
acting antiepileptic drug. Resolution of the
epileptiform discharges leaving diffuse slowing
without clinical improvement and without appearance
of previoulsy absent normal EEG patterns would not
satisfy the secondary criterion.

Appropriate patients have rhythmic or periodic focal or

generalized epileptiform discharges on electroencephalogram
(EEG) with unexplained altered level of consciousness or a level
of consciousness lower than expected given their level of
sedation. Patients who are heavily sedated/paralyzed are not
suitable as they would not be expected to demonstrate clinical
improvement.

Need to monitor EEG, pulse oximetry, arterial blood pressure,

electrocardiogram, respiratory rate with dedicated nurse as
patients are at risk for hypotension and respiratory depression

Antiepileptic drug trial

Sequential small doses of rapidly acting short-duration benzodiazepine such as

midazolam at 1 mg/dose
Between doses, repeated clinical and EEG assessment
Trial is stopped after any of the following:
1. Persistent resolution of the EEG pattern (and exam repeated)
2. Definite clinical improvement
3. Respiratory depression, hypotension, or other adverse effect
4. A maximum dose is reached (such as 0.2 mg/kg midazolam, although
higher may be needed if the patient is on chronic benzodiazepines)
Test is considered positive if there is resolution of the potentially ictal EEG pattern and
either an improvement in the clinical state or the appearance of previously absent
normal EEG patterns (e.g., posterior dominant alpha
rhythm). If EEG improves but patient does not, the result is equivocal.

Ativan

12% sz
56% sz

28% of all studies



Previous history of SAH

Strange feeling  unresponsiveness
Tf for possible IA thrombolysis
CT angiogram-normal
Rt Facial twitchingLt facial twichingleft
arm and both leg
Lorazepam and fosphenytoin 1.5g loading

Valproate loading
30mg/kg

Levetiracetam 1500mg IV
bolus

Complex partial seizures  phenytoin, valproate, levetiracetam

at outside hospital

cEEG on arrival PLEDs at 1-2Hz Rt hemisphere at times with

superimposed delta

Morning after admission EEG very frequent epilepfiform

discharges from the right temporal lobe that evolved in frequency
and were followed by right greater than left background slowing.
 NCSE (?)

Midazolam load 14mg and drip 0.4mg/kg/h

Persistent PLEDs with superimposed rhythmic slowing and

fast activity

 The midazolam drip was increased to 1mg/kg/h

Valproate tapering due to thrombocytopenia NCSE (facial

twitching) recur  add PB  weaning PB encehalopathic
with facial twitching  EEG-PLEDs at times stimulus
induced but without clear association with the facial
twtiching (below) benzodiazepine trial (MDZ 1mg to 4 mg)
showed equivocal (resolution of facial twitching and PLEDs
but no improvement of neurological examination)

Decreased right temporal metabolism

 Tapered PB

Subclassify EEG patterns of the IIC into those that are

1.

more (PLEDS plus) and those that are less frequently

associated with electrographic seizures during the
hospital course (PLEDs proper)
Benzodiazepine trials

2.

Imaging studies may be used

SPECT, CT perfusion, dynamic susceptibility MR iamging. PET
scanning

3.

Treatment intensity may be determined by quantifying

neuronal injury associated with specific EEG patterns
and determining the potential benefit of therapies by
studying these parameters over time.
1.

Serum markers (NSE, GFAP)

2.

Microdialysis

3.

Imaging studies (ADC quantification, MRS)

Chest Compression

cEEG as soon as possible for adequate

duration ( improvement of autodetection and
online monitoring?)

EEG categorization

Benzodiazepine trial if needed

Combine with imaging methods

Utilize surrogate markers to find neuronal injury