🔍 Definition
📊 Incidence
&
🔍 Subtypes
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* Primary generalized NCSE * Secondary generalized NCSE
⚠️ Risk Factors for NCSE
I* Sepsis (esp. in patients with pre-existing seizure disorder)
II* Severe traumatic brain injury (TBI) III* Subarachnoid hemorrhage (SAH) / intracerebral hemorrhage IV* Ischemic stroke V* Encephalitis VI* Post-cardiac arrest VII* Dementia (particularly advanced-stage) VIII* Drug withdrawal (e.g. benzodiazepines, antiepileptics) IX* Excessive use of psychotropic medications
🔍 Diagnosis – When to Suspect NCSE- give 3 scenarios
I* Postictal confusion lasting >20 minutes after a GTCS
- NCSE complicates ~10–40% of convulsive SE
II* Persistent altered sensorium:
- Especially when not explained by imaging or labs
III* Fluctuating GCS in a patient with seizure risk
IV* Unexplained delirium or encephalopathy (especially in elderly)
V* Paradoxical improvement after:
- AED administration
- Benzodiazepines or propofol trial
🧠 6 Clinical Features of NCSE
🧠 Clinical Features:
1* Altered sensorium (unexplained) 2* Behavioral changes, such as: - Delusions, hallucinations 3* Subtle motor signs: * Eye deviation * Nystagmus * Myoclonus 4* Autonomic dysregulation 5* Catatonia-like features 6* Speech disturbances
No prominent convulsive activity
* Often underdiagnosed due to subtlety.
* Requires EEG monitoring to confirm.
🧪 Investigations
🧪 Investigations
I. Routine labs:
* CBC, CRP (sepsis screen)
* Electrolytes: Na, K, Ca, Mg, glucose
* LFTs, RFTs (hepatic/renal dysfunction)
* Coagulation panel, TTP screen
* Urine toxicology
* Infection workup:
- Blood cultures
⸻
⸻
⚡ EEG Features Suggestive of NCSE
1* Periodic epileptiform discharges
2* Rhythmic discharges + clinical signs (e.g., altered awareness) 3* Rhythmic discharge ± clinical signs but with EEG response to AEDs
⚠️ Challenges in Diagnosis
⚠️ Challenges in Diagnosis
I. Requires high clinical suspicion- no obvious clinical signs-delayed diagnosis
II. Lack of consensus: * * Clinical definitions * * Diagnostic criteria * * EEG thresholds * * Management
III. Difficulty predicting if EEG findings reflect persistent seizure activity vs. postictal or non-ictal phenomena.
IV. Low GCS may result from:
* * Postictal state
* * Metabolic or septic encephalopathy
* * Sedative drug effects
* * NCSE itself
V. Limited availability of continuous EEG monitoring in many centers. VI. EEG findings are not 100% specific - Can occur in other conditions like epilepsy or encephalitis.
VII. Treatment strategies are poorly defined
🔍 Differential Diagnosis for NCSE
🧠 Management Priorities in NCSE
🧠 Management Priorities in NCSE
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🟢 Early Diagnosis & Treatment
* Paramount to preserve neurologic and systemic function.
* Delay increases risk of permanent sequelae.
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🛑 Immediate Threats to Address
* Secure airway as needed.
* Correct:
* Hypoglycemia
* Hyperthermia
⸻
🔍 Investigate & Treat Underlying Cause
* Reversible triggers:
* Missed AED doses
* Drug withdrawal
* Infection/sepsis
* Check and correct:
* Glucose, sodium, calcium, magnesium
* Optimize AED regimen in known epileptics
Tt of seizures
->Ist line- Benzodiazepines
->2nd line- Valproate/Levetiracetam/Phenytoin
->4th line:
* Barbiturates
* Ketamine (may be used in refractory cases)
Mx cont
🧠 EEG Monitoring
* Used to:
- Detect & diagnose NCSE
- Monitor response to treatment
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⚠️ Sedation Weaning Practice
* Continue anesthetic agents for 24–48 hrs
* Allow a period of seizure-free EEG before tapering
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🧠 Neurology Consult
* Should be obtained early in refractory or unclear cases
🚨 Complication Management