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NEONATAL SEIZURE

Dr. Siti Lintang Kawuryan SpA(K)

I.

Introduction
Seizure are the most distinctive manifestation of neurologic disfunction in NB Potensially devastating forms of brain injury It is well known that most of the seizures in NB is difference with seizures in older patiens

Seizure should be treated as emergencies because often occurs in neonates. They can lead to hypoxia which can endanger live. The sequale have serious consequences longterm : lowering of seizure thresholds learning and memory disabilities

Incidence
USA: 0.8 to 1.2/ 1000 neonates / year about 1 5% of newborn experience seizure in their first moth premature, and is 1.4% in at term ones. However in between 70 - 80%neonates there are no clinical sign of seizures except on EEG

The decrease seizure threshold in the newborn reflects the developmental events active in immature brain The NB brain has overdevelopment of exitatory systems The immature brain has transient overexpresion in the density of excitatory amino acid reseptors and relative paucity(kekurangan) of glutamate reuptake transport -- more prolonged and intensive contact of glutamate with post synaptic receptors

Immature glutamate receptors as far more premissive of cationic influx - membran depolarization and seizure activation Inhibitory GABA ion chanels are relatively underexpressed in immature brain - depolarization( excitatory ) rather than hyprpolarization ( inhibitory) These celluler factors, deffertial development of neural systems may enchance the excitatory state seizure

Clinically
changes in the paroximal from neurological functions Sensoric motoric, Behavior autonomous nerve system, that occur during the neonatal period

Diagnosis
The clinical manifestions of neonatal seizure differ in many ways from those in older patiens: the behavioral features may be very Subtle

The peculiar(aneh) clinical characteristics of seizure in NB likely reflect the immature state of brain development

In late gestation & early post natal life, active but incomplete development processes ( cortical organization,axonal and dendritic branching, development of synaptic connection) Myelination commences around term but largely confined on the deep subcortical Generalized seizure in NB are very rare ec the relatively underdeveloped organizatition of the the cortex and undermyelination of axons

A. Clinical diagnosis of neonatal seizure


1. Clinical seizure subtypes seizure may defined as paroxysmal alteration of neurologic function , including behaviour, motor and aotonomic changes. EEG monitoring is important fact about seizure in NB categorized into four group:
1. 2. 3. 4. Subtle Clonic Tonic Myoclonic

Subtle
Most common type ( half of all seizure in term and preterm NB) Rarely isolated will almost always have other seizure Occuler phenomena: tonic eye deviation Nystagmus sustained eye opening with appearent visual fixation

Oro-bucco-lingual movements
Chewing Sucking Lip-smaking movements Drooling

Limb movements
Pedaling Boxing Rowing Swimming movement

Autonomic phenomena Sudden changes in skin color Capilary size Tachycardia Bradycardia Apnea Most subtle seizure are not associated with EEG seizure

Clonic
Stereotype and repitive biphasic(2bentuk) movements with a fast contraction phase and slower relaxation phase The rhythm slower that older patient Unifocal (not associated with lost conciousness),multifocal,generalized Causes unifocal : neonatal stroke,focal traumatic,subarachnoid hemorrhage, metabolic disturbances

Tonic
Have sustained periode of muscle contraction without repetitive Generalized
most common in premature infants with difuse neorologic dysfunction or mayor IVH Associated with motor automatism,clonis Letargic Abbolished by repositioning, restrint(terbatas)

focal Prognosis : very poor

Myoclonic
Fast contraction and non rythmic Multifocal, general Elicited by tactile auditory stimulation Suppressed by restraint Associated with diffuse and usullay serious brain dysfunction Etiologi: asphysia, inborn errors metabolism, cerebral disgenesis. Mayor brain trauma Poor longterm outcome

Seizure mimics
In the NB it may be difficult to distinguish between normal immature behaviour ( non nutritive sucking) abnormal but non epileptic behaviors ( jitterinness(gelisah)) and true epileptic manifestation These guilelines are most reliable with suspected clonic seizure: 1. True epileptic are rarely stimulus sensitive 2. Cannot be abolished(dihentikan) by pasive restrain or repositioning of the infant 3. Often associated with autonomic change or occular phenomena

1. Epileptic apnea
1. Is not uncommon,but reraly the only manifestation 2. Difficult to distinguish from apnea due to; neurologic depression,prematurity,sedative medications, respiratory illness 3. Several helpful to distnguishing: neonatal epileptic apnea rarely last longer than 2030 sec 4. Tachycardia --- bradycardia 5. EEG changes

2. Benign neonatatal sleep myoclonus


1. A relatively common 2. First week of life and resolved spontaneously 3. Presipitated by gentle rhythmic, rocking , tactile stimuli 4. The even never occure during wakefulnss 5. Neurlogic examination is normal

B. EEG diagnostic of neoantal seizures


Electrographic seizure: is a repetitive series of electrical discharges that involves in frequency,amplitude and topographic field EEG study should be recorded as soon as a seizure is first suspected, not later than 24 hours after

C. Etiologic diagnosis of neonatal seizure


1. Cerebral hypoxic ischemia 1. Global ( asphyxia) 2. Focal infection 2. Intracranial hemorrhage 3. CNS infection 4. Metabolic disease 5. Cerebral dysgenesis 6. Neonatal epileptic syndromes 7. Neoanatal abstensia syndromes 8. unknown

c. Etiologis diagnosis of neonatal seizures


1. Spesific etiologies
1. Hypoxic-ichaemic encephalopathy 2. Focal ischamic injury 3. Focal ischamic injury
1. Neonatal arterial stroke 2. Cerebral vein thrombosis

4. Intracranial hemorrhage 5. CNS infections 6. Metabolic disturbances

2. Inborn errors of metabolism


1. Pyridoxine dependency 2. Nonketotik hyperglycemia 3. Folinic acid responsive seizure

3. Epileptic syndromes in the NB


1. Benign familial neonatal seizure 2. Benign idiopathic neonatal seizure

III.

Treatment of neonatal seizure

A. Reversing rapidly correctable causes B. Specific anticonvulsant agents

Acute Management of Neonatal Seizure Step 1:stabilize vital function Step 2:correct transient metabolic disturbances Step 3: phenobarbital Step 4: phenytoin Step 5: lorazepam Step 6: pyridoxine Step 1: other

Anticonvulsant Manual in Neonates, Dose, and The Side effect


Phenobarbital

Phenytoin

Drug of choice Theraupetic target : 20 -40g/ml Initial dose10 20mg/kg. Added 5 mg/kg until maximum dose 30-40 mg/kgMaintenance dose : 3-5 mg/kg/dose HypotensionApnea Give in seizure uncontrolled by phenobarbital Initial dose :20 mg/kg/ IV in normal salineMaintenance dose :3 -5 mg/kg/day Cardiac arrhythmiaCerebellum damage Use for epileptic stateRepeated every 15 minutes for 2 -3 timesLorazepam :0.05 0.1 mg/kgDiazepam0.1 0.3 mg.kg Respiratory emergencyAffect bilrubin bindings to albumin

Benzodiazepin

IV. Prognosis after neonatal seizure


1. Etiology as prognostic factor 2. EEG 3. Gestational age has prognostic significance

IV: Prognosis after neonatal seizure


Etiology Hypoxic- ischemic Meningitis Hyoglycemia Subarachnoid hemorrhage Early hypocalcemia Late IVH Dysgenesis unknown Normal outcome(%) 50 50 50 90 50 100 10 0 75