Non-Convulsive Status Epilepticus (NCSE):
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Transcript of Non-Convulsive Status Epilepticus (NCSE):
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Non-Convulsive Status Epilepticus (NCSE):Our Experience at a Tertiary Care Center
Brennen Bittel, DOClinical Neurophysiology Fellow
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Overview Background
information: Epidemiology Clinical features Electrographic definition
EDX pitfalls Treatment Pathology Outcomes
KU Data 2009-2013
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Incidence/prevalence SE* in emergency room or intensive care
units ~ 150,000/yr NCSE:
25 % of all SE 1.5 – 60/100,000/yr
34% of all SE in a tertiary care center 27% of ICU pts w/ altered mental status 8% of pts in comaCelesia 1976, Tomson 1992, Drislane 2000, Towne 2000
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Definition1. Diminished level of consciousness,
confusion
2. Epileptiform EEG (continuous or discrete)
3. Response to treatment??
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1. Change in mental status- Semiology Ambulatory confused patients, mildly
confused hospitalized patients
Lethargic and comatose patients in intensive care units
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Diminished Level of Consciousness, Confusion
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Clinical presentations
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NCSE
CPSE(complex partial SE)
ESE(electrographic SE)
SPSE(Simple partial SE)
ASE(absence SE)
Intermittent Continuous
20-40%
35-40%
Krumholz 1999, Meierkord 2007
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NCSE
ASE(absence SE)
CPSE(complex partial SE)
ESE(electrographic SE) SPSE
(Simple partial SE)
Continuous Intermittent
• Confused• Bizarre behavior• Fluctuations• +/- automatisms• Aphasia
Stuporous Comatose GTC at onset Medical illness
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Other sxs/signs Agitation Lethargy Mutism Disruptive behavior Staring Laughter Crying Rigidity Perseveration
Subtle motor movements
Hallucinations
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DDx Metabolic/toxic encephalopathy Complicated migraine/aura Prolonged post-ictal state Psychiatric disorders Substance abuse/withdrawal/intoxication
DTs TIA Transient global amnesia
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Husain 2003 12 in the NCSE group and 36 in the non-
NCSE group 100% sensitivity Ocular movements
Rhythmic blinking, deviation, nystagmus, rhythmic hippus Recent or remote risk factor for seizure
Previous stroke, tumor, previous neurosurgery, dementia, epilepsy, and meningitis
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Epileptiform EEG
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2. Epileptiform EEG Frequency Morphology Evolution Rhythmicity
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Treiman criteria- GCSE
Five characteristic stages:1. Discrete seizures2. Merging seizures3. Continuous seizures4. Continuous seizures with brief "flat" periods on the
EEG -- (usually no convulsions)
5. Prolonged flat periods with periodic discharges -- (usually no convulsions)
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Young 1996- NCSE Primary Criteria
1. Repetitive generalized or focal spikes, sharp waves, spike-wave or sharp-slow wave complexes at >3/sec
2. Repetitive generalized or focal spikes, sharp waves, spike-wave or sharp-slow wave complexes at >3/sec AND #4
3. Sequential rhythmic waves and 1-3, +/- 4
Secondary Criteria1. Incrementing onset: voltage
or slowing2. Decrementing offset:
voltage or frequency3. Post-discharge slowing or
voltage attenuation4. Significant improvement in
clinical state or baseline EEG after AED***
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Walker 20051. Frequent/continuous focal
electrographic szs, with ictal patterns that wax and wane with change in amplitude, frequency, and/or spatial distribution.
2. Frequent/continuous generalized spike-wave discharges in pts without a previous history of epileptic encephalopathy or epilepsy syndrome.
3. Frequent/continuous generalized spike-wave discharges, which showed significant changes in intensity or frequency (usually a faster frequency) when compared to baseline EEG, in patients with an epileptic encephalopathy or epilepsy syndrome
4. PLEDs/ BIPEDs in patients in coma in the aftermath of a generalized tonic–clonic status epilepticus (subtle status epilepticus).
5. EEG patterns that were less easy to interpret included:Frequent/continuous EEG abnormalities (spikes, sharp-waves, rhythmic slow activity, PLEDs, BIPEDs, GPEDs, triphasic waves) in patients whose EEGs showed no previous similar abnormalities, in the context of acute cerebral damage (e.g., anoxic brain damage, infection, trauma).
6. Frequent/continuous generalized EEG abnormalities in pts w/ epileptic encephalopathies in whom similar interictal EEG patterns were seen, but in whom clinical symptoms were suggestive of NCSE.
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EEG Diagnosis
Inevitably subjective
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Which tracing shows NCSE?
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PLEDS
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Triphasic waves
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GPEDS
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L Temp/parietal CPSE
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Diagnostic pitfalls PLEDs, BiPLEDs, GPEDs, SIRPIDs Encephalopathy Status myoclonus CJD
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PLEDs
No absolute frequency criterion can be used to distinguish PLEDs from seizures
Frequency 1 - 4 seconds (short periodicity) >4 seconds (long periodicity)
Acute, serious neurologic illness Mortality is high—up to 50% within 2 months
Walsh 1987
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PLEDs Associated with:
• Stroke (the most common cause in many reports)• Tumors• Infections- Viral (acute and chronic)• Metabolic disturbances• Head injury• SDH• Anoxia• Brain abscess• Congenital lesions• Tuberous sclerosis• Multiple sclerosis• Creutzfeld–Jakob disease
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PLEDs 80-90% of pts had recent clinical seizures
66% had some form of SE Risk for more seizures
Half patients without prior epilepsy developed subsequent epilepsy
Most PLEDs will resolve after days to weeks
Part of an ictal-interictal spectrum
Snodgrass 1989, Kaplan 2007, Chong 2005, Walsh 1987
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PLEDs
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PLEDs regression- 1 week later
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Triphasic waves Seen commonly in metabolic encephalopathies
Classically in renal or hepatic failure Bursts 1-2Hz
Blunted, low-moderate amplitude Dominant positive second phase, slow rise
Phase lag not seen in NCSE
Increased with stimulation not seen in NCSE
Sometimes suppressed with BZDs (40-60%) Kaplan 2006
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Encephalopathies w/Epileptic Features
Reversible Usually no hx of epilepsy Medication related
BZD withdrawal Cephalosporin Abx Ifosfamide Baclofen Psychotropics
Rhythmic, semirhythmic delta
Drislane 2000
Irreversible Post-anoxic Creutzfeld-Jacob
Importance of c-VEEG Look for subtle clinical
changes a/w rhythmicity
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CJD – EEG progression
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Patients at risk1. Following seizures or GCSE
-- Up to 50% in NCSE after convulsions cease
2. AMS with subtle motor signs3. AMS in epileptic w/ acute medical illness4. Post-stroke pt faring worse or recovery
halted5. Elderly pt with AMS (post BZD withdrawal)DeLorenzo 1998, Drislane 2000
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Risk factors Mental status changes
ICH SAH Large vessel CVA Meningoencephalitis CHI/TBI Tumor Post-surgical
Drislane 2000
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3. Treatment Response Treatment response less often considered
diagnostic Clinical response may be delayed hours to days
Shneker 2003
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Treatment CPSE
BZDs IV AEDs Usually recurs
ESE 60% respond to initial BZD (clinical delay) 15% resistant to BZD Require IV AEDs
+/- Anesthesia Granner 1994, Shneker 2003
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Anesthesia- Claassen 2002 193 pts w/ refractory SE
Tx with midazolam vs propofol vs pentobarbitol Midazolam
Increased breakthrough seizures Less hypotension
Pentobarbitol Lowest treatment failure/recurrence More hypotension
Refractory NCSE- more common with propofol and midazolam
No standardized treatment regimen for use of anesthesia in SE
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Anesthesia No consensus on NCSE
More harm than good? Hypotension Sepsis/line infection DVT
Ultimate effect on brain? Outcomes…
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Pathologic changes Animal models
Induced GCSE, up to 5 hours, in baboons Hippocampal volume loss
↑ with frequent, prolonged seizures ↓ if paralytic used to abolish convulsions
Hyperpyrexia, hypotension, hypoxia, acidosis, and hypoglycemia
Changes in high-frequency (10Hz) vs low frequency (1Hz) discharges
Bertram 1990
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Pathologic changes Human autopsy studies
GCSE > epilepsy w/o SE > normal Synergistic damage
Increase in excitatory neurotransmitters Metabolic changes (lactate, pyruvate)
Earnest 1992, Kruhmholz 1995
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Outcomes: Mortality Vary highly based on the underlying etiology of the
condition Brain tumors (30-40%) Acute stroke (35%) Epilepsy (3%)
Duration of seizures 43 ICU pts in NCSE on VEEG
<10h = death in 10% >20h = death in 85%
Age > 60y Rarely fatal in isolation
Young 1996, Meierkord 2007, Towne 1994
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Outcomes: Morbidity CPSE
No difference between continuous and intermittent electrographic sz activity Return to baseline cognitive status (n=20) Cognitive decline, memory issues (n=10)
ESE Determined by primary etiology Tend to have poorer prognosis
Drislane 1999, Cockerell 1994, Krumholz 1995
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Outcomes: MICU vs NICU 168 visits over 3 yrs
27% NICU More pts w/ stroke More CPSE Avg age: 59 Alert/somnolent pts Fewer pts intubated,
more tracheostomized
Varelas 2013
73% MICU More toxic/metabolic enceph More GCSE Avg age: 51 Obtunded/comatose pts Higher APACHE 2 scores
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MICU vs NICU No difference in outcomes
Length of ICU/hospital stay Functional status at discharge (mRS)
Limitations: Smaller NICU population Neuro illness with longer recovery period?
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KU Data
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KU Cohort Objective:
Review and describe non-convulsive status epilepticus (NCSE) cases Etiology Co-morbidities Medical treatment Clinical outcomes
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KU Cohort Methods:
Medical records reviewed from Jan 2009-2013 ICD9 for status epilepticus, at discharge CPT code for video-EEG monitoring ICU room charge during hospital stay
Patients selected based on the following inclusion criteria: Age: 10- 110 years of age Diagnosis made utilizing routine or continuous video
electroencephalogram Patients with hypoxic-ischemic brain injury were excluded
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DataDemographics 56 charts reviewed 23 cases identified
M: 9 F: 14
Average age: 54
Presentation 30% (7):
GTC, tonic seizure(s) 48% (11):
confusion, lethargy, somnolent 22% (5):
obtunded, stuporus, comatose
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Data 35% (8): Automatism, subtle motor mvts
Head turning Subtle limb, facial, tongue movements Eyelid flutter
22% (5): eye deviation
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Data CPSE (74%)
LOS: 19.2 d ICU: 11.1 d VEEG: 6.1 d
# AEDs: 2.6 Anesthesia: 4.6 d
ESE (13%) LOS: 45.7 d ICU: 20.7 d VEEG: 8 d
# AEDs: 3 Anesthesia: 7.5 d
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Data- CPSE (17)
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Data- ESE (3)
Etiology Severe sepsis
OLT, ESRD on HD (2) CJD
+14-3-3 Characteristic MRI (2)
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DataCPSE
AEDs: 1st: PHT (73%) Increase dose of AED Sedation VPA or Vimpat
Anesthesia: Propofol (9/13)
2pt + Versed Ketamine, pentobarb
Versed (3/13)* Pentobarb (1/13)*
ESE AEDs:
1st: PHT (3) 2nd: Keppra (3) Vimpat, PHB, topiramate (1)
Anesthesia: 1st: Propofol (2)
Transition to Pentobarb = Versed
1pt: no tx
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EEG diagnosis not reported/unclear (3)
Pt#1: OLT on prograf L facial movements
Pt#2: Brain tumor 3 GTC szs prolonged
postictal
Pt#3: Hx of epilepsy, liver failure Poor responsiveness,
eye flutter
Age 56
LOS 23.7 d
ICU 10 d
VEEG 6.5 d
AEDs 2
Sedation 4.5 d
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Data CSF:
46% abnormal (6/13) 5/13: ≤ 15 WBCs
(lymph) Meningoencephalitis (3) Inflamm WMD CJD
+14-3-3 (1)
Imaging 22/23*
5 CT 17 MRI
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Data CPSE ESE
Time to resolution: Refractory (2) Transition to PLEDs (1)*
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Data CPSE
Outcome: Death - 41% LTACH/SNF - 18% Home – 29% Rehab – 12%
One death within 30d
ESE Outcome:
Death or hospice – 100%
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CPSE Outcomes Home (29%): 51.2 y
Epilepsy (2) Remote stroke (1) Autoimmune enceph/SDH (1) Tumor (1)
Rehab (12%): 57.5 y Post-stroke epilepsy Autoimmune enceph
LTACH/SNF (18%): 44 y Epilepsy + illness or NC (3)
Death (41%): 55.6 y Peritumoral stroke Remote stroke + sepsis Inflam WM lesions* CJD* MS + sepsis Meningoencephalitis (2)*
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CPSE
5/17 (29%): Sepsis Death or hospice- 4pts
CJD MS Peritumoral stroke Inflammatory WM lesions
LTACH- 1pt Hx of epilepsy
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Clinical outcome- CPSE
Follow-up in 5/10 2 pt: no new cognitive deficits
Epilepsy + NC <8 hr, <24h
3 pt: memory impairment, assistance w/ ADLs, cognitive decline Tumor, AIE, menignoencephalitis <96h, unknown (2)
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Limitations Limited number of patients
Majority from 2012, only 3 from 2009, 1 from 2010
Inclusion of patients with CJD 100% mortality Encephalopathy with epileptic features
Documentation, access to archived studies Lack of clinical follow-up information No cases of NCSE in acute stroke
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Conclusions Outcomes worse is ESE
Worse if underlying dx is CJD
Underlying epilepsy portends better outcome
Longer duration of uncontrolled NCSE adverse cognitive impact
Pt’s treated with Versed as initial agent, worse outcomes (2/3) death
Outcomes worse when pt diagnosed with sepsis
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Thanks
Nancy Hammond, MD Utku Uysal, MD Ivan Osorio, MD William Nowack, MD Rhonda Reliford
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References Celesia CG. Modern concepts of status epilepticus. JAMA 1976: 235:1771-4. Tomson T, Svanbog, E, Wedlund J.E. Nonconvulsive status epilepticus: high incidence of
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