1. TOPIC: STATUS EPILEPTICUS
SOURCES: -UNIVERSITY OF DEBRECEN (MHSC), DEBRECEN, HUNGARY
- MEDSCAPE
-NATIONAL CENTRE FOR BIOTECHNOLOGY INFORMATION (NCBI), NATIONAL
LIBRARY OF MEDICINE, MARYLAND.
BY: ONAZI ENE (4TH YEAR MEDICAL STUDENT)

2. DEFINITION
 STATUS:
SITUATION AT A PARTICULAR TIME DURING A PROCESS
 EPILEPSY:
- NEUROLOGICAL DISORDER
- RECURRENT EPISODES
- SENSORY DISTURBANCE
- CONVULSIONS, LOSS OF CONSCIOUSNESS
- ABNORMAL BRAIN ACTIVITY
 STATUS EPILEPTICUS (SE):
PROLONGED EPILEPTIC CRISIS, CONTINUOUS SEIZURE, >30 MINS OR 2 OR MORE,
NO RECOVERY OF CONSCIOUSNESS. BUT…

3. CLASSIFICATION OF SE
• NOT CLEAR CUT, CONVULSIVE AND NON-CONVULSIVE
• TONIC, CLONIC, TONIC-CLONIC, MYOCLONIC SE = CSE
• GENERALIZED TONIC-CLONIC IS MOST COMMON. MYOCLONIC HAS GOOD
PROGNOSIS EXCEPT INDUCED BY VIRAL ENCEPHALITIS, HYPOXIC ISHAEMIC INSULT,
AND PRION DISEASE.
• SEMIOLOGIC (BASED ON SIGNS AND SYMPTOMS) VERSUS SIMPLE AND FUNCTIONAL
• REFRACTORY STATUS EPILEPTICUS (RSE): FAILURE OF STANDARD TREATMENT
RESPONSE, CONTINUOUS OR REPETITIVE SEIZURES LASTING LONGER THAN 60 MIN
• MALIGNANT SE: RSE VARIANT.18-50 YRS. DESPITE AGGRESSIVE TREATMENT.
ENCEPHALITIS.
Luders & Rona Treiman
- Type of brain function
predominantly compromised
- Body part involved
- Evolution overtime
- Generalized convulsive SE
- Subtle SE
- Nonconvulsive SE (absence and
complex partial SE)
- Simple partial SE

4. GENERALIZED CONVULSIVE & SUBTLE SE
• GCSE- MOST FREQUENT & POTENTIALLY DANGEROUS. ABNORMAL EXCESSIVE
CORTICAL ACTIVITY AND MOTOR ACTIVITY OF A SEIZURE
• SSE- ABSENT/FRAGMENTARY MOTOR RESPONSES WITH ELECTRICAL SEIZURE
ACTIVITY IN THE BRAIN. SOMETIMES CATEGORIZED AS NCSE. MOST SEVERE OF
GCSE, POOR PROGNOSIS.

5. NONCONVULSIVE SE
• CLASSIFIED BY AGE OF OCCURRENCE: NEONATAL/INFANTILE, CHILDHOOD, CHILDHOOD&ADULT
LIFE, LATE ADULT LIFE
• TREATMENT, ETIOLOGY & PROGNOSIS
ABSENCE SE COMPLEX PARTIAL SE (CPSE)
- Clear change in level of consciousness
- Lethargy and confusion
- Reduced spontaneity & slow speech
- Low alertness
- 75% before 20 years
- Adult mean age of 51 years
- One continuous ictal episode of variable
intensity*
- Stereotyped automatisms*
- Anxiety, aggression, fear & irritability
- EEG* best way if differentiation
- No deaths/ long-term morbidities
- Differentiation is important due to
irreversible neuronal damage caused by
mimics.
-rare
- Limbic cortex (mesial temporal)- staring,
unresponsiveness, automatisms, atypical
anxiety, rising abdominal symptoms, déjà
vu, profound stupor.
- Frontal lobe as well.
- Isolated in temporal, CPSE is
extratemporal
- Manifests with recurring cycles of 2
separate phases: ictal and interictal*
- Richer Sterotyped automatisms*
- Anxiety, aggression, fear & irritability is
more common*

6. SIMPLE PARTIAL STATUS EPILEPTICUS (SPSE)
• LOCALIZED SEIZURES TO CEREBRAL CORTEX
• RARE
• FOCAL SE: ANY CORTICAL REGION, MOTOR REFLEX INVOLVED= EPILEPSIES
PARTIALIS CONTINUA (EPC) INVOLVES FOCAL TWITCHING OF LIMBS &/FACE AND
CONSCIOUSNESS.
• OTHER CORTICAL REGIONS: OCCIPITAL FOCAL CAUSES FOCAL VISUAL
SYMPTOMS E.G. FLASHING SPOTS OF LIGHT AND COLOURFUL VISUAL
HALLUCINATIONS.
• DIAGNOSIS: EEG, DIFFICULT.
• PROGNOSIS BASED ON AGE, ETIOLOGY, SE DURATION, COMPLICATIONS.
• TREATMENT IS SAME FOR CONVULSIVE SE BUT LESS AGGRESSIVE.

7. PATHOPHYSIOLOGY
 FAILURE OF INHIBITORY NEUROCHEMICAL PROCESSES (GABA)
 EXCESS EXCITATORY NEUROCHEMICAL PROCESSES (GLUTAMATE-NMDA)
 FAILED SPONTANEOUS TERMINATION
 CATECHOLAMINE SURGE: TACHYCARDIA, CARDIAC ARRHYTHMIAS, HYPERGLYCAEMIA
 INITIAL ELEVATION OF SYSTEMIC ARTERIAL PRESSURE AND DECREASE TO LEVELS BELOW
PREVIOUS BASELINE
 HYPERTHERMIA, REQUIRES AGGRESSIVE TREATMENT
 ACIDOSIS: RESPIRATORY AND METABOLIC, REQUIRES NO TREATMENT.
 BLOOD AND CSF DEMARGINATION
 AFFECTS BREATHING AND CAUSES PULMONARY EDEMA. INTUBATION ON BENZO. & BARB.
ADMINISTRATION
 INCREASED CEREBRAL AND METABOLIC DEMAND
 MOST VULNERABLE TO NEURONAL DAMAGE- THE HIPPOCAMPUS, CORTEX AND THALAMUS
 MORBIDITY AND MORTALITY CORRELATION WITH DURATION
 PHARMACORESISTANCE. NEURONAL DEATH. ADAPTIVE TOLERANCE. DRUG RESPONSE.

8. STAGES OF SE
1. GENERALIZED CONVULSIVE TONIC-CLONIC SEIZURES-
- INCREASED MUSCLE TONE ---- SPASMS OF MUSCLE CONTRACTION AND
RELAXATION
- INCREASED AUTONOMIC ACTIVITY LEADING TO HYPERTENSION,
HYPERGLYCAEMIA, SALIVATION, HYPERPYRREXIA. INCREASED CEREBRAL BLOOD
FLOW.
- AFTER 30 MINS OF ACTIVITY, PATIENTS ENTER THE 2ND PHASE
2. FAILURE OF CEREBRAL AUTOREGULATION, DECREASED CEREBRAL BLOOD FLOW,
INCREASED INTERCRANIAL PRESSURE (ICP) AND SYSTEMIC HYPOTENSION.
ELECTROCHEMICAL DISSOCIATION, CEREBRAL SEIZURE ACTIVITY CONTINUES,
MINOR TWITCHING.

9. ETIOLOGY
• EXACERBATION, INITIAL MANIFESTATION OR INSULT/TRAUMA
• EPILEPTICS: CHANGE IN MEDICATION
• TOXIC/METABOLIC PROCESSES: STROKE. HYPOXIA. TUMOR, SUBARACHNOID
HAEMORRHAGE, HEAD TRAUMA, DRUGS (COCAINE, THEOPHYLLINE, ISONIAZID-
VIT B6), ALCOHOL WITHDRAWAL, ELECTROLYTE ABNORMALITIES, NEOPLASMS,
CNS INFECTIONS, SYMPATHOMIMETICS.
• FEVER &/INFECTION < 16 YEARS & CEREBROVASCULAR DISEASE IN ADULTS.
• CEREBRAL TOXOPLASMOSIS, LYMPHOMA AND ANTICONVULSANT WITHDRAWAL
IN HIV

10. TREATMENT
• EARLY- BENZODIAZEPINES AND FOSPHENYTOIN
• INEFFECTIVE – AGGRESSIVE 2ND LINE TREATMENT E.G. PROPOFOL AND BARBITURATES
• DEVELOPING COUNTRIES- NON-SEDATIVE ANTEPILEPTICS E.G. VALPROIC ACID,
TOPIRAMATE & LEVETIRACETAM.
• AVOID REFRACTORY STATE
• GENERAL PATIENT CONDITION
• HAEMODYNAMIC STABILITY
• PROTECTION OF VITAL FUNCTIONS, EARLY AND ENERGETIC TREATMENT OF
CONVULSIONS FOLLOWED BY ETIOLOGICAL EVALUATION TO PREVENT
COMPLICATIONS AND REOCCURRENCE.

11. COMPLICATIONS OF PROLONGED SE
• CARDIAC DYSRHYTHMIA
• METABOLIC DERANGEMENTS
• AUTONOMIC DYSFUNCTION
• NEUROGENIC PULMONARY EDEMA
• HYPERTHERMIA, RHABDOMYOLYSIS, AND PULMONARY ASPIRATION.
• PERMANENT NEUROLOGIC DAMAGE

12. THANK YOU.