DR SREEKRISHNA R

PG RESIDENT IN PAEDIATRICS

MGM MEDICAL COLLEGE INDORE

DIAGNOSTIC CHOICES ;Reliance on clinical v/s EEG seizures

ETIOLOGIC EXPLANATIONS; Multiple prenatal /neonatal conditions with variable time of onset and duration.

TREATMENT DECISIONS; WhICH,WhenAND HOW long

PROGNOSTIC QUESTIONS ;Mechanism of injury based on underlying disorder v/s vulnerability of

immature brain to seizures

Definition:-

A seizure is defined clinically as

a paroxysmal alteration in neurologic

function, i.e. motor, behavior and/or

autonomic function.

1.EPILEPTIC SEIZURE phenomena associated

with

corresponding EEG seizure activity e.g. clonic seizures

2. NON EPILEPTIC SEIZURE: clinical seizures

without corresponding EEG correlate e.g. subtle

and generalized tonic seizures

3. EEG SEIZURES: abnormal EEG activity with

no clinical correlation.

Immature CNS cannot sustain a synchronized, well orchestrated generalized seizure

Neurite outgrowth—dendritic and axonal ramifications—inprocess

Synaptogenesis not completeDeficient myelination in cortical efferent systems

CLINICAL CLASSIFICATION

SUBTLE SEIZURES;Clinical

manifestations are mild and often missed, most

common type

1. Ocular - Tonic horizontal deviation of eyes or

sustained opening with ocular fixation or cycled

fluttering

2. Oral–facial–lingual movements - Chewing,

tongue- thrusting, lip-smacking, etc.

3. Limb movements - Cycling, paddling, boxing-jabs,

4.Autonomic phenomena - Tachycardia or bradycardia

5. APNEA

CLONIC SEIZURESThey are rhythmic movements of muscle groups. They

have both fast and slow components, occur with a

frequency of 1-3 jerks per second

Tonic seizures:

refers to a sustained flexion or extension of axial

or

appendicular muscle group

MYOCLONIC SEIZUREsingle or multiple lightning fast jerks of limbs

Rapid speed

Absence of slow return and predilection for flexor muscle

groups

Myoclonic seizures carry the worst prognosis in

terms of neuro-developmental outcome and

seizure recurrence.

Focal clonic seizures have the best prognosis.

Jitteriness or tremors

Normal movements seen more commonly

in preterm infants

1. Benign neonatal sleep myoclonus

2. Fragmentary myoclonic jerks

3. Eye movements: Roving or dys-conjugate

eye movements

Jitteriness Versus Seizure

CLINICAL FEATURE JITTERINESS SEIZURE

Abnormality of gaze or ey O +

movement

Movements exquisitely stimulus + O

sensitive

Predominant movement Tremor Clonic jerking

Movements cease with passive + O

flexion

Autonomic changes O +------------------------------------------------------------------------------------------------------------------

Certain clinical seizures in the human newborn

originate deep cerebral structures (limbic

regions), or in diencephalic, or brain stem

structures and thereby are either not detected

by surface-recorded EEG or inconsistently

propagated to the surface

A. PERINATAL CAUSES

1. Neonatal encephalopathy

(hypoxic ishaemic) – 40 – 50 %

2. Intracranial hemorrhages- CNS

trauma, SAH, PVH,

Hypoglycemia Hypocalcemia – most common metabolic cause

for NNS Hypomagnesemia Hypo / Hypernatremia Pyridoxine dependency IEM - Disorders of amino acid metabolism

Intracranial

- Meningitis

- encephalitis – herpes, coxachie, echo, CMV,

- Toxoplasmosis,Rubella

Extracranial

– septicemia

- Tetanus

◦ Cerebral Dysgenesis

◦ Hydrocephalus

◦Microcephaly

◦ Neuronal migration defects-

Lissencephaly or pachygyria.

E.DRUGS-Narcotic withdrawal of mother

F.BENIGN FAMILIAL SEIZURE does not

continue after neonatal period

G.CEREBRO VASCULAR LESIONS

H.IDIOPATHIC 3- 25 %

DIAGNOSTIC

APPRAOACH

HISTORY EXAMINATION INVESTIGATION

HISTOR

Y

SEIZURE

(PATTERN AND

ONSET)

ANTEN

ATAL

PERIN

ATAL

FEEDI

NG

FAMIL

Y

INTRA UTERINE INFE

MATERNAL DIABETES

PREECLAMPSIA

NARCOTIC USE

H/O FOETAL DISTRESS

LOW APGAR

INSRUMENTAL DELIVERY

NEONATAL RESUCCTN

PUDENDAL BLOCK

EXAMINATI

ON

•GENERAL EXAMINATIONS•VITALS

•GESTATION

•DYSMORPHIC FEATURES

•NEURO CUT MARKERS

CNSTONE,REFLEXES ,AF,

FUNDUS,

CONSCIOUSNESS

SYSTEMICGIT

INVESTIGAT

IONS

MANDATORY

CBC

Blood – glucose, calcium, electrolytes, Mg,

bilirubin, ABG

CSF analysis

Blood C/S , urine C/S

Cranial USG

SPECIFIC

TORCH screening

IEM screening – urine organic acids

S. amino acid assay, CSF lactate,

pyruvate, ammonia

Imaging – CT scan

- MRI

- EEG brain

Major Etiologies of Neonatal Seizures in Relation to Time of

Seizure Onset and Relative Frequency

TIME OF ONSET* RELATIVE FREQUENCY†

0-3 DAYS >3DAYS PREMATURE FULL TERM

Hypoxic-ischemic + +++ +++

encephalopathy

Intracranial + + ++ +

hemorrhage‡

Intracranial infection + + ++ ++

Developmental + + ++ ++

defects

Hypoglycemia + + +

Hypocalcaemia + + + +

Other metabolic + +

Epileptic syndromes + + +

Aiims protocol:- identify and characterize seizure

Nurse the baby in TNZ( room temp 26’-28’ C)

Maintain airway ,breathing, circulation , start O2

Check blood glucose (<40mg) and give glucose @ 8mg/kg

(2ml/kg of D10 %)

Give 2ml/kg of 10% of ca gluconate over 10 minI(If s.ca

< 7)

0.25ml/kg of 50% mgso4 i/m

Phenobarbitone 20mg/kg over 20 min

Give phenobaritone again @ 10mg/kg

Give maintenance dose 3-5 mg/day

Phenytoin 20mg/kg over 20 min

Repeat phenytoin 10mg/kg

Benzodiazepines used

Lorazepam: 0.05 mg/kg IV bolus over 2-5 minutes or

Midazolam: 0.15 mg/kg IV bolus followed by infusion of 0.1 to 0.4 mg/kg/hour

In refractory seizurez second line drugs can be used

Lidocaine 4mg/kg iv followed by 2mg/kg/hr or

Sodium valproate 20-25mg/kg/day followed by 5-10mg/kg/day

Other drugs like vigabatrin. Topiramate, paraldehyde

Therapeutic trial of pyridoxine

1 ml of neurobion on both gluteus i/m

Weaning of anticonvulsant therapy

Newborn on anticonvulsant therapy

Wean all antiepileptic drugs except phenobarbitone

once seizure controlled

Perform neurological examination prior to discharge

normal Abnormal

Stop

phenobarbitone

prior to discharge

Continue

phenobarbitone for

1 month

Repeat neurological

examination at 1

month of age

Abnormal

examinationNormal examination

Taper drugs over

2 weekEvaluate EEG

Normal EEG

Taper drug over

2 weeks

Abnormal EEG

Continue drug

Reassess at 3

months

Outcome depends on1. Level of maturity

2. Etiology

3. Neurological examination

4. EEG / Imaging studies

Uncomplicated hypoglycemia

Narcotic withdrawal

SAH

Low APGAR score ≤ 6 at 5min

Onset o seizures within 24 hrs of life

Presence of myoclonic attacks

Abnormal EEG

3 or more days of uncontrolled seizures

Cerebral palsy

Hydrocephalus

Epilepsy

Spasticity

Feeding difficulties

CLOHERTY TEXT BOOK OF NEONATOLOGY

MEHARBAN TEXT BOOK OF NEONATOLOGY

AVERY TEXT BOOK OF NEONATOLOGY

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