Non-Convulsive Status Epilepticus

Consultant: dr. Slamet Trijono, Sp.S

Presented By: Jocelyn Judian 11.2014.249

Department of Neurology
Fakultas Kedokteran Universitas Kristen Krida Wacana
August 3rd 2015 September 5th 2015
Rumah Sakit Mardi Rahayu Kudus

Introduction
NCSE: a change in behaviour and/or mental processes from
baseline associated with continuous epileptiform discharges
in the EEG.
Basis of the definition: alterations in the clinical state
and associated plausible EEG changes.
The definition must not exclusively rely on EEG changes
because no single pattern can be regarded as
pathognomonic.

Definition : based on duration

NCSE
Complex
Subtle
Late
Typical
onset
absence
Partial
absence
Focal
Generalized
Simple
Atypical
Partial
absence
Convulsive or Non-convulsive?

Subtypes

Subtypes : Focal
Simple Partial

Subtypes : Generalized
Absence

Problems

1. Epileptic nature of the clinical features is not usually readily recognized.

Epidemiology

Strong age-dependency (> 60 years old

Etiology

Etiology is the most reliable factor in predicting the

prognosis of each SE types but there is a paucity of reliable
published causal data on the different subtypes.

Glutaminergic

Pathophysiology
1. Abnormal persistence of excessive excitation

Pathophysiology

Neuronal and Clinical Consequences

Prognosis in NCSE with pre-existing epilepsy vs NCSE post
acute neurological / systemic disorders? Worse in?
In experimental animals the severity of functional &
structural
neuron
damage
depends
on the
extent of
A flaw
in the experiment
of excitatory
seizure
activity compared
to human?
convulsive activity. (How about NCSE in human?)
Most clinical forms of NCSE except subtle SE are benign in
terms of morbidity and mortality.

Treatment

Depends on the subtype.

Most clinical forms of NCSE (except subtle SE ) are not
associated with acute systemic and chronic neurological
complications less aggressive pharmacological management.
A European survey indicated that neurologists are more
reluctant to administer anaesthetics in CPSE than in GCSE.
If CPSE cannot be terminated, consider GA in patients who are
young and do not have additional medical problems
Midazolam (0,2 mg/kg bolus, 0,10,4 mg/kg per hour infusion),
Propofol (2 mg/kg bolus, 510 mg/kg per hour infusion).

Treatment
SPSE & CPSE

Treatment
Late

Conclusion
The diagnosis of NCSE should be based on clinical+ EEG findings
(to confirm).
Most clinical forms of NCSE seem to be less harmful than SE with
generalized convulsive phenomenology.
Treatment aims to terminate NCSE to prevent serious injuries,
especially in impaired conciousness.
In refractory cases, a less aggressive management is preferred
except subtle SE.
Future clinical research should focus on randomised controlled
treatment trials that rely on strict definitions and diagnostic
criteria for NCSE and its subtypes.

Thank You