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Non-Convulsive Status Epilepticus (NCSE):

Non-Convulsive Status Epilepticus (NCSE):. Our Experience at a Tertiary Care Center Brennen Bittel, DO Clinical Neurophysiology Fellow. Background information: Epidemiology Clinical features Electrographic definition EDX pitfalls Treatment Pathology Outcomes. KU Data 2009-2013.

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Non-Convulsive Status Epilepticus (NCSE):

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  1. Non-Convulsive Status Epilepticus (NCSE): Our Experience at a Tertiary Care Center Brennen Bittel, DO Clinical Neurophysiology Fellow

  2. Background information: Epidemiology Clinical features Electrographic definition EDX pitfalls Treatment Pathology Outcomes KU Data 2009-2013 Overview

  3. 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 coma Celesia 1976, Tomson 1992, Drislane 2000, Towne 2000

  4. Definition Diminished level of consciousness, confusion Epileptiform EEG (continuous or discrete) Response to treatment??

  5. 1. Change in mental status- Semiology Ambulatory confused patients, mildly confused hospitalized patients Lethargic and comatose patients in intensive care units

  6. Diminished Level of Consciousness, Confusion

  7. Clinical presentations

  8. NCSE ASE (absence SE) CPSE (complex partial SE) ESE (electrographic SE) SPSE (Simple partial SE) Intermittent Continuous 35-40% 20-40% Krumholz 1999, Meierkord 2007

  9. Stuporous Comatose GTC at onset Medical illness • Confused • Bizarre behavior • Fluctuations • +/- automatisms • Aphasia

  10. Agitation Lethargy Mutism Disruptive behavior Staring Laughter Crying Rigidity Perseveration Subtle motor movements Hallucinations Other sxs/signs

  11. DDx Metabolic/toxic encephalopathy Complicated migraine/aura Prolonged post-ictal state Psychiatric disorders Substance abuse/withdrawal/intoxication DTs TIA Transient global amnesia

  12. 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

  13. Epileptiform EEG

  14. 2. Epileptiform EEG Frequency Morphology Evolution Rhythmicity

  15. Treiman criteria- GCSE Five characteristic stages: • Discrete seizures • Merging seizures • Continuous seizures • Continuous seizures with brief "flat" periods on the EEG -- (usually no convulsions) • Prolonged flat periods with periodic discharges -- (usually no convulsions)

  16. Young 1996- NCSE • Primary Criteria • Repetitive generalized or focal spikes, sharp waves, spike-wave or sharp-slow wave complexes at >3/sec • Repetitive generalized or focal spikes, sharp waves, spike-wave or sharp-slow wave complexes at >3/sec AND #4 • Sequential rhythmic waves and 1-3, +/- 4 • Secondary Criteria • Incrementing onset: voltage or slowing • Decrementing offset: voltage or frequency • Post-discharge slowing or voltage attenuation • Significant improvement in clinical state or baseline EEG after AED***

  17. 1. 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. Walker 2005

  18. EEG Diagnosis Inevitably subjective

  19. Which tracing shows NCSE?

  20. PLEDS

  21. Triphasic waves

  22. GPEDS

  23. L Temp/parietal CPSE

  24. Diagnostic pitfalls PLEDs, BiPLEDs, GPEDs, SIRPIDs Encephalopathy Status myoclonus CJD

  25. 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

  26. 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

  27. 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

  28. PLEDs

  29. PLEDs regression- 1 week later

  30. 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

  31. 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

  32. CJD – EEG progression

  33. Patients at risk Following seizures or GCSE -- Up to 50% in NCSE after convulsions cease AMS with subtle motor signs AMS in epileptic w/ acute medical illness Post-stroke pt faring worse or recovery halted Elderly pt with AMS (post BZD withdrawal) DeLorenzo 1998, Drislane 2000

  34. Risk factors Mental status changes ICH SAH Large vessel CVA Meningoencephalitis CHI/TBI Tumor Post-surgical Drislane 2000

  35. 3. Treatment Response Treatment response less often considered diagnostic Clinical response may be delayed hours to days Shneker 2003

  36. 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

  37. 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

  38. Anesthesia No consensus on NCSE More harm than good? Hypotension Sepsis/line infection DVT Ultimate effect on brain? Outcomes…

  39. 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

  40. 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

  41. 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

  42. 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

  43. 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

  44. 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?

  45. KU Data

  46. KU Cohort Objective: Review and describe non-convulsive status epilepticus (NCSE) cases Etiology Co-morbidities Medical treatment Clinical outcomes

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