Non-convulsive status epilepticus

Definition

Non-convulsive status epilepticus (NCSE) is a form of status epilepticus characterized by continuous or recurrent epileptic activity lasting ≥10 minutes (or recurrent seizures without recovery) without prominent motor convulsions, presenting primarily with altered mental status and diagnosed electrographically on EEG.

 ILAE concept
NCSE = “Status epilepticus without major motor signs but with persistent electrographic seizure activity and clinical impairment.”


Why NCSE is Important

  • Commonly missed cause of unexplained coma/delirium in ICU
  • Associated with neuronal injury, worse outcomes, increased mortality
  • Requires EEG for diagnosis → clinical examination alone is insufficient


Clinical Presentation

NCSE manifests as altered consciousness with subtle or no motor signs.

Common Features

  • Confusion, delirium, agitation
  • Reduced responsiveness or coma
  • Aphasia
  • Memory impairment
  • Behavioral changes
  • Eye deviation, blinking
  • Subtle automatisms (lip smacking, facial twitching)

When to Suspect NCSE

  • Unexplained coma or delirium
  • Failure to wake after convulsive SE
  • ICU patient with fluctuating mental status
  • Post–cardiac arrest encephalopathy
  • Stroke, CNS infection, metabolic encephalopathy with worsening sensorium


Classification of NCSE

1. Absence Status Epilepticus

  • Seen in idiopathic generalized epilepsy
  • Clouding of consciousness
  • EEG: generalized 3-Hz spike-and-wave
  • Responds well to benzodiazepines


2. Focal NCSE (Complex Partial Status)

  • Most common in adults
  • Due to focal brain lesions
  • EEG: focal or lateralized epileptiform discharges
  • Often subtle clinical signs (aphasia, automatisms)


3. NCSE in Coma (Critical Care NCSE)

  • Seen in ICU patients
  • High mortality
  • EEG shows periodic or rhythmic patterns
  • Often overlaps with ictal–interictal continuum


EEG Patterns in NCSE 

Definite NCSE

  • Continuous epileptiform discharges ≥2.5 Hz
  • Evolution in frequency, amplitude, or morphology
  • Clinical improvement after antiepileptic drug (AED)

Ictal–Interictal Continuum (IIC)

  • Periodic discharges 1–2.5 Hz
  • Rhythmic delta activity with sharp waves
  • Needs clinical + EEG + treatment response correlation


Etiology of NCSE

Structural

  • Stroke (ischemic > hemorrhagic)
  • Traumatic brain injury
  • Brain tumors

Metabolic / Toxic

  • Hypoglycemia, hyponatremia
  • Hepatic or uremic encephalopathy
  • Drug intoxication or withdrawal

Infectious

  • Encephalitis
  • Meningitis
  • Sepsis-associated encephalopathy

Post-Anoxic

  • After cardiac arrest (poor prognosis subtype)


Diagnosis

Gold Standard: EEG

  • Continuous EEG (cEEG) preferred
  • Minimum 30–60 minutes, longer if suspicion remains

Ancillary

  • MRI brain (DWI for ictal changes)
  • CSF if infection suspected
  • Metabolic panel, drug levels


Management of NCSE (Guideline-Based, Exam-Oriented)

Step 1: Benzodiazepine

  • Lorazepam IV (preferred)
  • Diazepam IV if lorazepam unavailable


Step 2: IV Antiseizure Drug

Choose one:

  • Levetiracetam
  • Valproate
  • Fosphenytoin

Levetiracetam is preferred in ICU due to safety and minimal interactions.


Step 3: Refractory NCSE

  • Continuous IV anesthetic:
    • Midazolam infusion
    • Propofol infusion
    • Thiopentone (selected cases)

Target: EEG seizure suppression (not necessarily burst suppression unless refractory)


Prognosis

Depends on:

  • Underlying cause (best in absence status, worst in post-anoxic NCSE)
  • Duration before diagnosis
  • EEG background
  • Response to treatment


Key Exam Pearls 

  • Unexplained coma = NCSE until proven otherwise
  • Diagnosis requires EEG
  • Periodic discharges ≠ always interictal → consider IIC
  • Treat promptly even if clinical signs are subtle
  • Post-convulsive persistent coma → suspect NCSE