Download neonatal convulsions

NEONATAL
CONVULSIONS
DR. MUSTAFA BERBER
ÇOCUK SAĞLIĞI VE HASTALIKLARI A.D.
NEONATOLOJİ B.D.
• Neonatal seizures (NS) are the most frequent and distinctive clinical
manifestation of neurological dysfunction in the newborn infant.
• Neonatal period limited to :
- first 28 days for term infants
- 44 weeks gestational age for pre-term
• First sign of neurological dysfunction
• Powerful predictors of long-term cognitive and developmental impairment
Definition:
A seizure is defined clinically as a paroxysmal alteration in
neurologic function, i.e. motor, behavior and/or autonomic
function.
1. Epileptic seizures: phenomena associated with
corresponding EEG seizure activity e.g. clonic seizures.
2. Non-epileptic seizures: Clinical seizures without
corresponding EEG correlate e.g. subtle and
generalized tonic seizures.
3. EEG seizures: abnormal EEG activity with no clinical
correlation.
Pathophysiology
• Abnormal synchronous depolarization from large group of
neurons
• Excessive excitatory amino acid release (glutamate)
• Lack of inhibitory systems (GABA)
• Depolarization results from Na influx into cells;
repolarization from outflux of K+
• Disruption of Na/K ATP pump
Basic Mechanisms of Seizures
• Abnormal energy production (hypoxemia, hypoglycemia)
• Alteration in neuronal membrane (hypocalcemia,
hypomagnesemia)
• Relative excess of excitatory versus inhibitory
neurotransmitters (GABA)
Do Seizures Harm the Developing
Brain?
• Animal studies:
• Persistent neonatal seizures in rats induce neuronal death
and changes in hippocampus
• Chronic seizures in adults associated with memory
impairment and poor psychosocial outcome
• Permanent reduction in seizure threshold associated
with significant deficits in learning and memory
Biochemical Changes with Seizures
• ↓ ATP
• ↓ phosphocreatine
• Pyruvate converted to lactate
• ↓ brain glucose
• Increased production of pyruvate from ADP
Adverse Effects of Seizures
• Cell division and migration
• Formation and expression of receptors
• Synaptogenesis and apotosis
• Long term effects: seizure threshold, learning, and
cognition
Incidence
• Higher in neonates than any other age
group
• Incidence(overall):2 in 1000 to 14 in 1000
live births
• Most frequent in the first 10 days of life
Etiology
Convulsion
Neurological:
Metabolic:
HİE
Hypoglycemia
ICH
Hypocalcemia
CNS infection
Hyponatremia
Epileptic syndroms
Hypernatremia
Infarction
Hypomagnesemia
Malformation
ETIOLOGY
• HIE (45-50%)
• Intracranial hemorrhage (17%)
• CNS infection (10%)
• Infarction (7%)
• Metabolic disorders (5%)
• Inborn errors (3%)
• Unknown (10%)
• Drug withdrawal (1%)
ETIOLOGY
Hypoxic-ischemic encephalopathy
Intracranial Hemorrhage
subarachnoid haemorrhage
germinal matrix –intraventricular haemorrhage
subdural hemorrhage
Metabolic disorders(hypoglycemia/ hypocalcemia
/hypomagnesemia/hyponatremia)
Intracranial infections
bacterial meningitis
TORCH infections
Pyridoxine dependency
Benign neonatal seizures
Etyoloji-4
Time relation
ICH
HIE
Hypoglycemi a
Hypocalcemia
Inborn error of met.
CNS inf.
Malformation
Epileptic syndromes
1-2 days
X
Convulsion time
3-7 days
7-10 days
X
X
X
X (early)
X
X (late)
X
X
X
X
X
X
Classification:
Subtle seizures:
They are the most common type. More common in
premature infants. Typically have no electrographic correlate,
are likely primarily subcortical
1. Ocular - Tonic horizontal deviation of eyes or sustained eye
opening with ocular fixation or cycled fluttering
2. Oral–facial–lingual movements - Chewing, tonguethrusting, lip-smacking, etc.
4. Limb movements - Cycling, paddling, boxingjabs, etc
5. Autonomic phenomena - Tachycardia or
bradycardia
6. Apnea
may be a rare manifestation of seizures.
Apnea due to
seizure activity has an accelerated or
a normal heart rate when evaluated 20 seconds
after onset.
Clonic seizures:
• Primarily in term. Signals focal cerebral injury
• Focal or multifocal, rhythmic movements with slow return
movement
• rhythmic movements of muscle groups.
• May be associated with generalized or focal brain abnormality
• Most commonly associated with electrographic seizures
• occur with a frequency of 1-3 jerks per second
Tonic seizures:
• Primarily in Preterm
• Sustained flexion or extension of one extremity or the whole body
• Extensive neocortical damage with uninhibited subcortically
generated movements
• May or may not have electrographic correlate
• Signals severe ICH in preterm infants Generally poor prognosis
Myoclonic seizures:
• Rare
•
Focal, multifocal or generalized
•
Lightning fast contractions-like jerks of extremities
•
(upper > lower)
•
Signify diffuse –serious brain injury Rapid, isolated
jerks which lacks the slow return phase of clonic
movements
• Myoclonic movements may be normal in preterm or
term infants
• Myoclonic seizures carry the worst prognosis in
terms of neuro-developmental outcome and
seizure recurrence.
• Focal clonic seizures have the best prognosis.
Nonepileptic movements
• Benign sleep myoclonus
• jitteriness
• Stimulus evoked myoclonus from metabolic
encephalopathies, CNS malformation
• Apnoea
Benign Sleep Myoclonus
• Onset 1st week of life
• Synchronous jerks of upper and lower extremities
during sleep
• No EEG correlate
• Ceases upon arousal
• Resolves by 2 months
• Good prognosis
Jitteriness vs. Seizures
• No ocular phenomena
• Stimulus sensitive
• Tremor
• Movements cease with passive flexion
DIAGNOSIS
Seizure history
• eye movements
• restraint of episode by passive flexion of the affected
limb
• The day of life on which the seizure occurred
Antenatal history
• Intruterine infection, maternal diabetes and narcotic
addiction
Perinatal history
• Perinatal asphyxia
• fetal distress
• Need for resuscitation in the labor room, low Apgar scores (<3 at
1 and/ or 5 minutes) and
• abnormal cord pH (≤7) and base deficit (> 10 mEq/L) should be
obtained.
Feeding history:
• Appearance of clinical features AFTER initiation of breast-feeding may
be suggestive of inborn errors of metabolism.
• Late onset hypocalcemia should be considered in the presence of top
feeding with cows’ milk.
Family history
• consanguinity in parents,
• family history of seizures or mental retardation
• early fetal/neonatal deaths would be suggestive of inborn errors of
metabolism.
• History of seizures in either parent or sib(s) in the neonatal period may
suggest benign familial neonatal convulsions (BFNC).
• GENERAL EXAMINATION
• CNS EXAMINATION
• BLOOD INVESTIGATIONS
• ULTRASOUND CRANIUM
• EEG (ELECTROENCEPHALOGRAPHY)
• SPECIFIC INVESTIGATIONS
CT SCAN OR MRI
INVESTIGATIONS:
 Lab studies
-Blood count
-Blood, urine & CSF culture
-Blood biochem.->evaluation of Glu, Ca, Mg,
electrolytes
-Blood gas levels to detect acidosis AND hypoxia.
-Serum IgM & IgG-specific TORCH titres
-METABOLİC EVALUATİON (AMMONİA,LACTATE…)
EEG:
• Main tool for diagnosis
It is useful to confirm a clinically doubtful
convulsion , to locate an epileptic focus and
and to determine its anatomical basis
Ultrasonography and CT scan of head:
• To detect subarachnoid /intraventricular hemorrhage
Treatment
• More difficult to suppress than in older children
• Treatment is worthwhile because seizures:
• May cause hemodynamic or respiratory compromise
• Disrupt cerebral autoregulation
• May result in cerebral energy failure and further injury
Treatment
• Stabilize vital signs and treat underlying
hypotension
• Correct transient metabolic disturbances
• Phenobarbital is first line agent
Nelson Protocol:
Maintain ABC and temperature
Check blood glucose
Correct glucose and calcium
Administer IV, phenobarbitone 20mg/kg
Repeat in 5 -10mg/kg boluses till a maximum of 40 mg/kg,
IV phenytoin 15-20 mg/kg diluted in equal volume of normal saline at a
maximum rate of 1mg/kg/min over 35-40 minutes
IV lorazepam 0.05 mg/kg every 4-8 hourly
IV midazolam as a continuous infusion (as initial IV bolus of 0.05-0.1mg/kg,
followed by continuous infusion (0.5-1ug/kg/min ) increasing by 2 ug/kg/min
every 5 minutes to achieve seizure control
Primidone, lidocaine, carbamazepine, valproate, lamotrigine,
topiramate, and levetiracetam have been used.
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
Normal examination
Abnormal
examination
Taper drugs over 2
week
Normal EEG
Taper drug over 2
weeks
Evaluate EEG
Abnormal EEG
Continue drug
Reassess at 3
months
Prognosis
Prognosis based on etiology
• Cerebral dysgenesis has grave prognosis, almost
none are normal
• Prematurity and seizures associated with high risk
of death or very poor outcome
Prognosis based on type
• Subtle
Depends on cause,
other seizure types
• Clonic
• Generalized Tonic
• Myoclonic
Better prognosis
Poor
Poor
Prognosis by EEG
• Severe inter-ictal EEG background associated with adverse
outcome
• Normal EEG background at presentation associated with
good outcome
• Ictal features less reliable
• Better outcome when clinical and EEG seizures correlate
• Increased number and frequency may relate to worse outcome
Prognoz
Burst-suppression pattern
• https://www.youtube.com/watch?v=iM9fj4qw7CA
• https://www.youtube.com/watch?v=-McoJOeJ8B4
• https://www.youtube.com/watch?v=0j-pwZSKOpc
• https://www.youtube.com/watch?v=lNLAQX4dRQc