16 neonatal seizures
TRANSCRIPT
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NEONATAL SEIZURES
Seizures are the most frequent manifestaon of neonatal neurological diseases.It is important to recognize seizures, determine their aeology and treat thembecause:
1. the seizures may be related to signicant diseases that require specic treatment
2. the seizures may interfere with supporve measures e.g. feeding and assisted
respiraon for associated disorders
3. the seizures per se may lead to brain injury.
Table 1. Classicaon of neonatal seizures
Clinical seizure
Subtle
Clonic
Focal
Mulfocal
Tonic
Focal
Generalized
Myoclonic
Focal,Mulfocal
Generalized
EEG seizures
common
common
common
common
uncommon
common
Manifestaon
ocular phenomena
- tonic horizontal deviaon of eyes common in term infants- sustained eye opening with xaon common in preterm infants
- blinkingoral-buccal-lingual movements
- chewing common in preterm infants- lip smacking, cry-grimace
limb movements
- pedaling, stepping, rotary arm movements
apnoeic spells common in term infants
well localized clonic jerking, infant usually not unconscious
mulfocal clonic movements; simultaneous or in sequenceor non-ordered ( non-Jacksonian) migraon
sustained posturing of a limb, asymmetrical posturing of trunkor neck
tonic extension of upper and lower limbs (mimic decerebrateposturing)
tonic exion of upper limbs and extension of lower limbs( mimicdecorcate posturing)
those with EEG correlates; autonomic phenomenae.g. increased blood pressure are prominent features.
well localized, single or mulple, migrang jerks usually of limbs
single or several bilateral synchronous jerks or exionmovement occurring more in upper than lower limbs.
Aeology
Hypoxic ischaemic encephalopathy- usually secondary to perinatal asphyxia.
- most common cause of neonatal seizures (preterm and term)
- seizures occur in the rst day of life (DOL)
- presents with subtle seizures; mulfocal clonic or focal clonic seizures
- if focal clonic seizures may indicate associated focal cerebral infarcon
NEON
ATALOGY
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NEONATO
LOGY
Intracranial hemorrhage (ICH)
- principally germinal matrix-intraventricular (GM-IVH), oen with periventricularhaemorrhagic (PVH) infarcon in the premature infant
- in term infants ICH are principally (may occur with HIE) and subdural(associatedwith a trauma , presenng with focal seizures in the rst 2 DOL)
Intracranial Infecon
- common organisms are group B streptococci, E. coli., toxoplasmosis, herpes simplex,coxsackie B, rubella and cytomegalovirus
Malformaons of corcal development- neuronal migraon disorder resulng in cerebral corcal dysgenesis
e.g. lissencephaly, pachygyria and polymicrogyria
Metabolic disorder
- hypoglycemia common in SGA infants and infants of diabec mothers (IDM)
(see protocol on Neonatal Hypoglycemia
- hypocalcaemia has 2 major peaks of incidences: rst 2 to 3 DOL, in low birth weight infants, IDM and history of perinatal asphyxia. later-onset of hypocalcaemia associated with endocrinopathy (maternal
hypoparathyroidism, neonatal hypoparathyroidism) and heart disease (with orwithout Di George Syndrome), rarely with nutrional type (cows milk, highphosphorus synthec milk). Hypomagnesemia is a frequent accompaniment.
- inborn errors of metabolism: represent 3days
+
+
+
+
+
Premature
+++
++
++
++
+
+
Full term
+++
+
++
++
+
+
+
+
Time of onset Relave frequency
footnote: 1. postnatal age2. relave frequency of seizures among all eologies:
+++ most common, ++ less common, +least commonAbbreviaons. IEM, inborn errors of metabolism
Table 2. Major aeology in relaon to me of seizure onset and relave frequency
Eology
Hypoxic ischemic encephalopathy
Intracranial hemorrhage
Intracranial infecons
Developmental defects
Hypoglycaemia
Hypocalcaemia
Other metabolic disturbances & IEM
Epilepc Syndromes
Table 3. Inborn errors of metabolism presenng with neonatal seizures
Treatable
Pyridoxine-dependent epilepsy
Pyridoxal phosphate responsive epilepsyFolinic acid-responsive seizures
Bionidase deciency
Glucose transporter 1 deciency
Serine deciency syndromes
Creane deciency syndromes
Phenylketonuria
Non-treatable
Nonketoc hyperglycinemia
(poor outcome though seizure may be beercontrolled with dextromethorphan)
Sulphite oxidase deciency/Molybdenum cofactor deciency
Mitochondrial disorders
Peroxisomal disorder
Neuronal ceroid lipofuscinoses
Adenylosuccinate lyase deciency(purine disorder)
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Seizures versus Jieriness and Other Non-epilepc Movements
Some movements e.g. jieriness and other normal movement during sleep(Myoclonic jerks or generalized myoclonic jerks as infant wakes from sleep) or whenawake/ drowsy (roving somemes dysconjugate eye movements, sucking not accom-panied by ocular xaon or deviaon) in newborn may be mistaken for seizures.
Management
consensus is lacking on necessity for treatment of minimal or absent clinicalmanifestaons.
treatment with anconvulsant is to prevent potenal adverse eects onvenlatory funcon, circulaon and cerebral metabolism ( threat of brain injury)
controversy regarding idencaon of adequacy of treatment, eliminaon ofclinical seizures or electrophysiology seizures. Generally majority aempt to
eliminate all or nearly all clinical seizures.
Duraon of Anconvulsant Therapy - Guidelines
Duraon of therapy depends on the probability of recurrence of seizures if the drugsare disconnued and the risk of subsequent epilepsy. This can be determined byconsidering the neonatal neurological examinaon, cause of the seizure and the EEG.
Neonatal Period
if neonatal neurological examinaon becomes normal, disconnue therapy
if neonatal neurological examinaon is persistently abnormal,
- consider eology and obtain electroencephalogram(EEG)- in most cases connue phenobarbitone, disconnue phenytoin
- and reevaluate in a month
One Month aer Discharge
if neurological examinaon has become normal, disconnue phenobarbitone over2 weeks
if neurological examinaon is persistently abnormal, obtain EEG
if no seizure acvity or not overtly paroxysmal on EEG, disconnue
phenobarbitone over 2 weeks if seizure acvity is overtly paroxysmal connue phenobarbitone unl 3 months of
age and reassess in the same manner
Table 3. Dierenang seizures form non-epilpec events, e.g. jierinessClinical Features
Abnormality of gaze or eye movement
Movements exquisitely smulus sensive
Predominant movement
Movements cease with passive exion of aected limb
Autonomic changes ( tachycardia, BP, apnoea,salivaon, cutaneous vasomotor phenomena)
Jieriness
0
+
tremors
+
0
Seizure
+
0
clonic, jerking
0
+
footnote: 1. alternang movements are rhythmical and of equal rate and amplitude
2. clonic, jerking movements with a fast and slow component
NEON
ATALOGY
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footnote. 1. Prognosis is based on those cases with the stated neurological disease when seizures area manifestaon. This will dier from overall prognosis of the disease.
Table 4. Prognosis according to aeology of neonatal seizures
Neurological Disorder
Hypoxic Ischemic Encephalopathy
Severe Intraventricular Haemorrhage with PVH infarcon
Hypocalcaemia
Early onset (depends on the prognosis of complicang illness, if
no neurological illness present prognosis approaches later onset )Later onset (nutrional type)
Hypoglycemia
Bacterial Meningis
Developmental defect
Normal Development (%)
50
10
50
100
50
50
0
infant withclinical seizures
Ensure venlaon
perfusion adequate (ABCs)
DEXTROSTIX
Invesgaons to consider
blood sugar, calcium, magnesium, electrolytes
sepc screen: FBC, Blood C&S, LP, TORCHES
metabolic screen: blood gas, ammoniaamino acids, organic acids
neuroimaging: US, CT Scan brain electroencephalography (EEG)
Figure 1. Approach to neonatal seizures
IV 10% Dextrose 2 ml/kg (200mg/kg)then IV glucose infusionat 8 mg/kg/min
Maintenance therapy
IV or Oral 3-4mg/kg/d in 2 divided dosesgiven 12-24 h aer loading
adverse eects:respiratory depression, hypotension
IV Phenobarbitone 20mg/kg
over 10 -15 minutes
A repeat loading dose of20mg/kg may be necessary
IV Phenytoin 20mg/kg loading dose
via infusion at 1mg/kg/min
- with cardiac rate, rhythm monitoring
- repeat a 2nd loading dose if ts recur
Maintenance therapy
IV 3-4mg/kg/d q12h
given 12-24 h aer loading
adverse eect: heart block
Benzodiazepine:
IV Diazepam 0.3 mg/kg/h infusion
or
IV Midazolam:1-4 mcg/kg/min infusion
consider
IV Calcium Gluconate, 10% soluon: 0.5 ml/kg slow bolusIV Magnesium sulfate, 50% soluon: 0.2 ml/kg
Oral Pyridoxine: 50-100mgPyrodoxal phosphate/Folinic acid *
Maintenance therapy
Midazolamadverse eects: hypotension,respiratory depression, urinary retenon
hypoglycaemia
no
hypoglycaemia
sll seizures
sll seizures
sll seizures
NEONATO
LOGY
* consult a neurologist ora metabolic clinician