Battisti Nnconvulsions en

Professeur Oreste Battisti
Facult de Mdecine
Universit de Lige
Battisti: Convulsions nonatales 1

Summary
Seizures in the newborn period constitute a medical
emergency.
Subtle seizures are the commonest type of seizures occurring
in the neonatal period.
Other types include clonic, tonic, and myoclonic seizures.
Myoclonic seizures carry the worst prognosis in terms of long-
term neurodevelopmental outcome.
Hypoxic-ischemic encephalopathy is the most common cause
of neonatal seizures.
Multiple etiologies often co-exist in neonates and hence it is
essential to rule out common causes such as hypoglycemia
,hypocalcemia , meningitis before initiating specific therapy.
A comprehensive approach for management of neonatal
seizures is the best way for management.

Structure of
presentation
Introduction and epidemiology
Definitions and patterns of convulsions
or neonatal seizures
Classification: clinical and EEG
Etiology
Physiopathology
Treatment and follow-up

Epidmiologie
prvalence:80-120 /100,000 naissances

Incidence:1-5/1000
La priode nonatale est particulirement
cible

Causes of Neonatal Seizures and Outcomes
Percent of
Patients Who
Have Normal
Cause Development
Hypoxic-ischemic encephalopathy 50
Intraventricular hemorrhage 10
Subarachnoid hemorrhage 90
Hypocalcemia
Early-onset 50
Later-onset 100
Hypoglycemia 50
Bacterial meningitis 50
Developmental malformations 0
Benign familial neonatal convulsions ~100
Fifth-day fits ~100

Prognosis of Neonatal Seizures:
Relation to Neurological Diseases
Neurological Disease Normal Development
Hypoxic-ischemic encephalopathy 50%

Intraventricular hemorrhage 10%
Primary subarachnoid hemorrhage 90%
Hypocalcemia
Early-onset 50%
Later-onset 100%
Hypoglycemia 50%
Bacterial meningitis 50%
Developmental defect 0%

Prognosis in general
Myoclonic seizures carry the worst prognosis in terms of
neuro-developmental outcome and seizure recurrence.
Focal clonic seizures have the best prognosis.
Seizures due to Subarachnoid Hemorrhage and late
onset hypocalcemia carry a good prognosis for long term
neuro-developmental outcome while seizures related to
hypoglycemia, cerebral malformations and meningitis
have a high risk for adverse outcome.
A background abnormality in both term and preterm
neonates indicates a high risk for neurological sequelae.
These changes include burstsuppression pattern, low
voltage invariant pattern and electro-cerebral inactivity

1. Definition, classification
and patterns of
neonatal:
seizures
convulsions
epilepsy

The Definition of a
Seizure
paroxysmal discharge of cerebral

neurons sufficient to cause
clinically detectable events that
are apparent either to the subject or
to an observer

clinical patterns of seizures
in newborns (Fenichel)
Apnea with tonic stiffening of body

Focal clonic movements of one limb or both limbs on one
side
Multifocal clonic limb movements
Myoclonic jerking
Paroxysmal laughing
Tonic deviation of the eyes upward or to one side
Tonic stiffening of the body

Why do neonatal seizures have
such unusual presentations?
Immature CNS cannot sustain a

synchronized, well orchestrated
generalized seizure
Normal Neonatal Motor Activity Commonly
Mistaken for Seizure Activity
AWAKE OR DROWSY
Roving, sometimes dysconjugate eye movements, with
occasional nonsustained nystagmoid
jerks at the extremes of horizontal movement (contrast with
fixed, tonic horizontal deviation of eyes with or without jerking
characteristic of subtle seizure
Sucking, puckering movements not accompanied by ocular
fixation or deviation
SLEEP
Fragmentary myoclonic jerksmay be multiple
Isolated, generalized myoclonic jerk as infant wakes from sleep
Volpe Neurology of the Newborn..

Classification of Neonatal
Seizures
Clinical
Electroencephalographic

Classification
I. Clinical Seizure
Subtle
Tonic
Clonic
Myoclonic
Classification
II. Electroencephalographic seizure
Epileptic
Non-epileptic
Seizures
ELECTROENCEPHALOGRAPHIC SEIZURE
CLINICAL SEIZURE COMMON UNCOMMON
Subtle +*
Clonic
Focal +
Multifocal +
Tonic
Focal +
Generalized +
Myoclonic
Focal, multifocal +
Generalized +
---------------------------------------------------------------------------------------------------------------
*Only specific varieties of subtle seizures are commonly associate with simultaneous
Electroencephalographic seizure activity.
Volpe JJ.Neonatal Seizures:Neurology of the Newborn.4th ed.

Classification of neonatal
seizures
Seizure type Occurs in Clinical signs EEG changes
Subtle Preterm and Term Eye deviation (Term) Usually No

Blinking, fixed stare (Preterm)
Repetitive mouth & tongue movements Apnea
Pedaling, tonic posturing of limbs
Tonic Primarily preterm May be focal or generalized Usually No

Tonic extension or flexion of limbs (often signals
severe IVH in preterm infants)
Clonic Primarily term May be focal or multifocal Yes

Clonic limb movements (synchronous or
asynchronous, localized or often with no
anatomic order to progression) Consciousness
may be preserved
Often signals focal cerebral injury.
Myoclonic Rare Focal, multifocal, or generalized Lightning-like jerks +

of extremities (upper>lower)

Seizures
Clinical

Neonatal Seizures
Tonic Seizures
focal or generalized,
may mimic decorticate or decerebrate posturing, primarilyseen in preterms with
intracranial hemorrhage & generally have poor prognosis
Subtle seizures
Consist of chewing motion, excessive salivation and alteration
in respiratory rate including apnea, blinking, nystagmus,
bicycling and pedaling movements, changes in color

Clonic- focal (repetitive movements localized
to a single limb) or multifocal (random
migration of movements from limb to limb),
consciousness may be preserved, primarily
seen in term infants
Myoclonic- sudden flexor movements (lightning-like

jerks), may be focal, multifocal or generalized, may
occuring singly or in clusters, if due to early myoclonic
encephalopathy it carries a poor prognosis. Brief focal
or generalized jerks of the extremities or body that
tend to involve distal muscle groups

Clinical Classification
Focal/Multifocal Clonic
Not generalized
Migratory
Focal Tonic
Generalized Myoclonic

Neonatal seizures
The most common presentation is focal clonic or multifocal clonic movments.
The rhythmic jerking is well-localized to a limb, may migrate to other limbs, not
necessarily in a contiguous fashion with the infant usually not conscious.
Neonatal seizures do not manifest with generalized clonic activity.
Neonatal seizures may present with focal tonic, so persistently increased tone in a
limb.
Generalized tonic activity, of the whole body, usually is not associated with
seizure activity on EEG, but may be posturing.
Then there are myoclonic seizures; myoclonus being more rapid, more erratic
and non-rhythmic than clonic movements. Focal or multifocal myoclonus is
usually not associated with sz activity, but bilateral synchronous generalized
myoclonic more likely to be seizures with the kids more likely to be sicker, and
we can talk about the difference in mechanism there later as well.
Other than descriptive terminology, theres this funny classification thats used,
called subtle seizures, because they are.
Some also classify these as hypomotor seizures, which may present with
activity arrest, apnea, or eye deviation. The art in diagnosing these as true
seizures, and not just diagnosing every bowel movement as a seizure is in
looking for any associated signs, such as autonomic changes like BP or HR
increase. Autonomic sx may be an isolated finding in preemies, but usually
accompanies szs in term. The most common subtle manifestation is tonic
horizontal eye deviation.

Clinical Classification
Subtile (Hypomotor)
Motor activity arrest
Apnea
Eye deviation
Autonomic changes
Motor automatisms
Oral-buccal-lingual movements
Swimming
Bicycling

Subtle seizures
More in preterm than in term
Eye deviation (term)
Blinking, fixed stare (preterm)
Repetitive mouth and tongue movements
Apnea
Pedaling and tonic posturing of limbs
Tonic deviation of the eyes Repetitive fluttering of eyelids
Drooling, sucking, chewing Swimming movements of the
arms Pedaling movements of the legs Paroxysmal
laughing

Subtle seizures (ct)
Ocular - Tonic horizontal deviation of eyes or sustained
eye opening with ocular fixation or cycled flutering
Oralfaciallingual movements - Chewing, tongue-
thrusting, lip-smacking, etc.
Limb movements - Cycling, paddling, boxing-jabs, etc.
Autonomic phenomena - Tachycardia or bradycardia
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.
Bradycardia is thus not an early manifestation in
convulsive apnea but may occur later due to prolonged
hypoxemia.

Tonic seizures
Primarily in Preterm
May be focal or generalized
Sustained extension of the upper and
lower limbs (mimics decerebrate posturing)
Sustained flexion of upper with extension of
lower limbs (mimics decorticate posturing)
Signals severe ICH in preterm infants
This type refers to a sustained flexion (mainly in premature) or extension
(mainly in term) of axial or appendicular muscle groups.
Resemble decerebrate (tonic extension of all limbs) or decorticate
posturing (flexion of upper limbs and extension of lower limbs).
Usually there are no EEG changes in generalized tonic seizures.

Clonic
Primarily in term
Focal or multifocal
Clonic limb movements(synchronous or
asynchronous, localized or often with no anatomic order of progression)
Consciousness may be preserved
Signals focal cerebral injury
They are rhythmic movements of muscle groups.
They have both fast and slow components, occur with a frequency of 1-3 jerks per
second, and are commonly associated with EEG changes.
- Multifocal clonic seizures on the 5th day may be related to low zinc levels in the
CSF fluid (benign idiopathic neonatal convulsions).

Myoclonic
Rare
Focal, multifocal or generalized
Lightning-like jerks of extremities
(upper > lower)
These manifest as single or multiple lightning fast jerks of
the upper or lower limbs and are usually distinguished from
clonic movements because of more rapid speed of
myoclonic jerks, absence of slow return and predilection for
flexor muscle groups. Common changes seen on the EEG
include burst suppression pattern, focal sharp waves and
hypsarrhythmia

Benign familial neonatal seizures
Begins on the 2nd 3rd day of life

Seizure frequency : 10 20 /day
Patients are normal between seizures
Seizure stops in 1 6 months

5th day Seizures
5th day of life

normal appearing neonates with
mulifocal seizures
Present for less than 24 hours
Good prognosis

Jitteriness Versus Seizure
CLINICAL FEATURE JITTERINESS SEIZURE
Abnormality of gaze or eye O +

movement
Movements exquisitely stimulus + O
sensitive
Predominant movement Tremor Clonic jerking
Movements cease with passive + O

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

Weird Baby Movements
Jitteriness
Stimulus-sensitive
Tremor
Suppressable
Benign neonatal sleep myoclonus
Spinal myoclonus
Apnea of non-neurologic etiology
bradycardia

Non-epileptic movements
commonly confused with seizures
Jitteriness or tremors
Normal movements seen more commonly in preterm
infants
- Benign neonatal sleep myoclonus: Occurs during NREM
sleep in preterm infants in the first week of life. Restraint
and benzodiazepines may increase the frequency of
jerks, while on arousal they are usually abolished. EEG
will be normal in this condition.
- Fragmentary myoclonic jerks
- Eye movements: Roving or dys-conjugate eye
movements with occasional nonsustained nystagmoid
jerks.

Seizures
Clinical

seizure
I. Epileptic
Consistently associated with electro-
cortical seizure activity on the EEG
Cannot be provoked by tactile stimulation
Cannot be suppressed by restraint of
involved limb or repositioning of the infant
Related to hyper synchronous discharges
of a critical mass of neuron
seizures
II. Non-epileptic
No electro-cortical signature
Provoked by stimulation
Suppressed by restraint or repositioning
Brainstem release phenomena (reflex)
Neonatal Seizures
EEG Classification
Clinical seizure with consistent EEG event
Clinical seizure occurs in relationship to seizure
activity
Includes focal clonic, focal tonic and myoclonic
Responds to antiepileptic drugs
Clinical seizure with inconsistent EEG event
Clinical seizures with no EEG abnormality
Seen in all generalized tonic and subtle seizures
Seen in patients who are comatose, HIE

Neonatal Seizures
EEG Classification
Electrical seizures with absent clinical
seizures
Electrical seizures associated with markedly
abnormal background EEG
Seen in comatose patients

Epileptic vs Non-
epileptic Neonatal
Phenomena
Clinical Epileptic Non-epileptic
Characteristics
Increases with Rare Common

Sensory
stimulation
Suppresses with - +
restraint
Autonomic
Accompaniments
+ -
Does absence of EEG seizure
activity indicate that a clinical
seizure is nonepileptic?
Certain clinical seizures in the human
newborn originate from electrical seizures
in 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
Neonatal Seizures
EEG Classification
Clinical seizure with consistent EEG event
Clinical seizure occurs in relationship to seizure
activity
Includes focal clonic, focal tonic and myoclonic
Responds to antiepileptic drugs
Clinical seizure with inconsistent EEG event
Clinical seizures with no EEG abnormality
Seen in all generalized tonic and subtle seizures
Seen in patients who are comatose, HIE

EEG tracing

Exercices on movies

In addiction

Focal crisis

3. Etiology
of
neonatal convulsions
or seizures

Etiology
It is critical to recognize neonatal seizures,
to determine their etiology, and to treat
them for three major reasons:
1. Seizures are usually related to significant

illness, sometimes requiring specific
therapy

Etiology
2.Neonatal seizures may interfere with
important supportive measures, such as
alimentation and assisted respirations for
associated disorders.
3.Experimental data give some reason for

concern that under certain circumstances
the seizure per se may be a cause of brain
injury.

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 + + +

Comparison of prominent etiologic diagnoses of
seizures in the newborn period. (Data modified from
Mizrahi and Kellaway, 1987; Rose and Lombroso,
1970)
Fanaroff A, Martin R.Neonatal seizures. In:Neonatal and Perinatal Medicine, Diseases of the Fetus and Infant,6 th ed.
Etiology
Pregnancy history is important
Search for history that supports TORCH
infections
History of fetal distress, preeclampsia or
maternal infections

Major Causes of Neonatal Seizures In Relation to Time of Seizure Onset and
Relative Frequency
TIME OF ONSET*
RELATIVE FREQUENCY
Cause 0-3 Days >3 Days Premature
Full Term
Hypoxic-Ischemic encephalopathy + +++ +++

Intracranial hemorrhage + + ++ +
Intracranial infection + + ++ ++
Developmental defects + + ++ ++
Hypoglycemia + + +
Hypocalcemia + + +
Other metabolic + +
Epileptic syndromes + +
+

Neonatal Seizures
Etiologic diagnosis
Hypoxic ischemic encephalopathy
Metabolic
Infections
Trauma
Structural abnormalities
Hemorrhagic and embolic strokes
Maternal disturbances

Differential diagnosis of neonatal
seizures
24 hours
by peak time of onset
Bacterial meningitis and sepsis Direct drug effect
Hypoxic-ischemic encephalopathy Intrauterine infection
Intraventricular hemorrhage at term Laceration of tentorium or falx Pyridoxine dependency
Subarachnoid hemorrhage
24 to 72 hours
Bacterial meningitis and sepsis
Cerebral contusion with subdural hemorrhage
Cerebral dysgenesis
Cerebral infarction
Drug withdrawal
Glycine encephalopathy
Glycogen synthase deficiency
Hypoparathyroidismhypocalcemia
Idiopathic cerebral venous thrombosis
Incontinentia pigmenti
Intracerebral hemorrhage
Intraventricular hemorrhage in premature newborns
Pyridoxine dependency
Subarachnoid hemorrhage
Tuberous sclerosis
Urea cycle disturbances

Causes of neonatal seizures
Ages 1 4 days
HIE
Drug withdrawal
Dug toxicity
Lidocaine, penicillin
Intraventricular hemorrhage
Acute metabolic disorder
Hypocalcemia
Hypoglycemia
Inborn errors of metabolism

Ages 4 14 days
Infection Drug withdrawal
Metabolic disorders Benign neonatal
Hypocalcemia
convulsion
Diet
Hypoglycemia
Kernicterus,
Inherited disorder of hyperbilirubenemia
metabolism such as
galactosemia,fructosemia
Hyperinsulinemic
hypoglycemia
Becwith syndrome
Anterior pituitary hypoplasia

Ages 2 8 weeks
Infection Malformations of
Head injury cortical development
Subdural henatoma Lissencephaly
Focal cortical dysplasia
Inherited disorder of
Tuberous sclerosis
metabolism
Sturge weber syndrome
Aminoacidurias
Urea cycle defects
Organic acidurias
Neonatal ALD

Neonatal Seizures
Etiologic diagnosis
Blood
Glucose, calcium, magnesium, electrolytes,
BUN
In hypomagnesemia MgSO4 0.2 ml/kg
Lumbar puncture
Indicated in all neonates with seizures unless
related to a metabolic disorder
Inherited as autosomal recessive or X-linked
recessive

Neonatal Seizures
Etiologic diagnosis
Serum ammonia urea cycle abnormalities
Acidosis + anion gap + hyperammonemia
urine organic acids should be determined
Unintentional injection of local
anesthetic
Supportive measures
Promotion of urine output with IV fluids

Idiopathic Syndromes of Clinical
Seizures in the Newborn
Epileptic Syndromes
Benign familial Neonatal Seizures
Benign idiopathic neonatal seizures (fifth-day fits)
Early myoclonic encephalopathy
Early infantile epileptic encephalopathy (Ohtahara
syndrome)
Malignant migrating partial seizures
Nonepileptic Syndromes
Benign neonatal sleep myoclonus
Hyperekplexia
Neonatal Seizures
(Epileptic Syndromes)
Benign familial neonatal seizures

Begins on the 2nd 3rd day of life
Seizure frequency : 10 20 /day
Patients are normal between seizures
Seizure stops in 1 6 months

Neonatal Seizures
Fifth-day fits
5th day of life
normal appearing neonates with
mulifocal seizures
Present for less than 24 hours
Good prognosis

Neonatal Seizures
Etiologic diagnosis
resistant to conventional AEDs
Inherited as autosomal recessive
Tx: Pyridoxine 100 200 mg IV
May not have a dramatic effect with IV
pyridoxine thus maintain on oral pyridoxine
10 -20 mg/day x 6 weeks
Lifelong supplementation : 10 mg/day

Neonatal Seizures
Etiologic diagnosis
Drug withdrawal seizures
Barbiturates, benzodiazepenes, heroin and
methadone
Jittery, irritable, lethargic, may show
myoclonus or frank seizures
Serum or urine analysis may identify the
responsible agent

Causes of Neonatal Seizures
Within first 24 hours of life

Hypoxic ischemic encephalopathy
Meningitis/sepsis
Subdural/Subarachnoid/Interventricular
hemorrhage
Intrauterine infection
Trauma
Drug effect/withdrawal

Causes.
24-72 hours
Meningitis/sepsis
In premature infants: IVH
In full-term infants: infarction,
venous thrombosis
Cerebral dysgenesis

Causes.
72 hours to 1 week
Above causes
Hypocalcemia
Familial neonatal seizures
1 week to 4 weeks
Above causes
HSV

Causes of neonatal
seizures
Ages 1 4 days
HIE
Drug withdrawal
Dug toxicity
Lidocaine, penicillin
Intraventricular hemorrhage
Acute metabolic disorder
Hypocalcemia
Hypoglycemia

Other Syndromes
Benign idiopathic neonatal convulsions
(BINC or Fifth-day fits)
Benign familial neonatal convulsions
(BFNC)
Early myoclonic encephalopathy (EME)
Early infantile epileptic encephalopathy
(EIEE)
Glucose transporter type I

Inborn Errors of Metabolism Associated With
Neonatal Seizures
Conditions That Have a Specific Treatment

Pyridoxine (B6) dependency
Folinic acid-responsive seizures
Glucose transporter defect
Creatine deficiency
Other Conditions
Nonketotic hyperglycinemia
Sulfite oxidase deficiency
Molybdenum cofactor deficiency (combined deficiency)
Carbohydrate-deficient glycoprotein disorder
Lactic acid disorders
Mitochondrial disorders
Maple syrup urine disease
Isovaleric acidemia (sweaty feet, cheesy odor)

The patho physiology of
or seizures

Why are seizure patterns in
neonates more fragmentary than in
older children?
The cellular organization of the mature and
immature brain is different. The neonatal brain has
incomplete glial proliferation, w/ continuing
migration of neurons, establishing complex axonal
& dendritic contacts and myelin deposition.
The electrical discharges therefore spread incompletely

and may remain localized to one hemisphere. The
electrical discharges are slow to diffuse and bilateral
synchronous discharges are rare.

Perinatal Anatomical and Physiological
Features of Importance in Determining
Neonatal Seizure Phenomena
ANATOMICAL
Neurite outgrowthdendritic and axonal ramifications
in process
Synaptogenesis not complete
Deficient myelination in cortical efferent systems
Volpe JJ.Neonatal Seizures :Neurology of the Newborn.

Perinatal Anatomical and Physiological
Features of Importance in Determining
Neonatal Seizure Phenomena
PHYSIOLOGICAL
In limbic and neocortical regions,excitatory synapses develop
before inhibitory synapses ( N-methyl-D-aspartate receptor
activity, gamma-aminobutyric acid excitatory)
Immature hippocampal and cortical neurons more susceptible to
seizure activity than mature neurons
Deficient development of substantia nigra system for inhibition of
seizures
Impaired propagation of electrical seizures, and synchronous
discharges recorded from surface electroencephalogram may
not correlate with behavioral seizure phenomena
Volpe JJ.Neonatal Seizures.In:Neurology of the Newborn.4th ed.

Probable Mechanisms of Some Neonatal
Seizures
PROBABLE MECHANISM DISORDER
Failure of Na + -K + pump secondary to Hypoxemia, ischemia,

adenosine triphosphate and hypoglycemia
Excess of excitatory neurotransmitter
(eg.glutamic acidexcessive excitation) Hypoxemia, ischemia
and hypoglycemia
Deficit of inhibitory neurotransmitter Pyridoxine dependency
(i.e., relative excess of excitatory
neurotransmitter)
Membrane alteration Na + Hypocalcemia and
Permeability hypomagnesemia
______________________________________________________________
Volpe JJ.Neonatal Seizures:Neurology of the Newborn. ed.

Particularity of a Seizure
in a Neonate
Glutamate receptors predominate, and in addition, GABA, which later in life acts
as an inhibitory neurotransmitter, actually acts at at least one receptor in an
excitatory fashion.
some true seizures do not demonstrate a paroxysmal discharge on EEG.
Axons, dendrites, synapses are still in the process of forming and organizing, so
may not be capable of propagating widely enough for electrodes to see. .
The electrical activity is originating from deeper brain regions, such as the
midbrain.
in a few studies looking at human infants with subtle events and EEG
correlation, sometimes the events were associated with discharges and
sometimes not within the same child;
in those infants, the clinical onset was more likely to begin seconds before
discharge seen, suggesting that perhaps the discharges were originating from
deep and travelling up to the cortex.
Another possibility for not seeing discharges on EEG is that the event really is
not a seizure, but could be a brain stem release
brain stem and spinal motor patterns released from inhibition that normally is
imposed by a healthy forebrain and cortex.

Particularity of a Seizure
in a Neonate
Excitatory activity predominates: No
paroxysmal discharge on EEG?
True seizure
The cortex is undeveloped
Deeper origin
Brainstem release phenomena

Causes of neonatal
seizures
Ages
Infection
4 14 days
Drug withdrawal
Metabolic disorders Benign neonatal
Hypocalcemia
convulsion
Diet
Kernicterus,
Hypoglycemia
hyperbilirubenemia
metabolism such as
galactosemia,fructosemia
Hyperinsulinemic
hypoglycemia
Becwith syndrome
Anterior pituitary
hypoplasia

Causes of neonatal
seizures
Ages 2
Infection
8 weeks
Malformations of
Head injury cortical development
Subdural henatoma Lissencephaly
Focal cortical
dysplasia
metabolism Tuberous sclerosis
Aminoacidurias
Sturge weber
Urea cycle defects
syndrome
Organic acidurias
Neonatal ALD

Causes of neonatal
seizures
50-65% of all seizures < Hypoxic-ischemic encephalopathy (HIE)
Intracranial hemorrhage
Metabolic causes Common metabolic causes of seizures include
hypoglycemia, hypocalcemia, hypomagnesemia. Rare causes include
pyridoxine deficiency and inborn errors of metabolism (IEM).
Infections
Developmental defects Cerebral dysgenesis and neuronal migration disorders
are rare causes of seizures in the neonatal period.
Miscellaneous
- Polycythemia
- maternal narcotic withdrawal
- drug toxicity (e.g. theophylline, doxapram)
- local anesthetic injection into scalp (Accidental injection of local anesthetic into
scalp may be suspected in the presence of unilateral fixed and dilated pupils)
- phacomatosis (e.g. tuberous sclerosis, incontinentia pigmentii).
- Multifocal clonic seizures on the 5th day may be related to low zinc levels in the
CSF fluid (benign idiopathic neonatal convulsions).

Les entits cliniques et
lectrophysiologiques des
paroxysmes du nouveau-n
Syndrome post-hypoxique ou post-asphyxique : pointes-ondes en bouffes,
entrecoupes par des activits normales ;
Etat de mal convulsif focal ( occlusive vascular disorder ) : pointes lentes
rythmiques unilatrales ;
Etat de mal gnralis : pointes-ondes en bouffes ;
Convulsions nonatales bnignes ( j 4-5 ) : thta pointu alternant , avec
(myo)clonies ;
Convulsions nonatales bnignes familiales prcoces : souvent j 2-3, mais
parfois plus tard, avec prdominance chez le garon ( anamnse ! ) : pas de
trac spcifique ;
Encphalopathie myoclonique prcoce : pointes-ondes en bouffes, jamais
synschrones sur les deux hmisphres, spares par des tracs plats =
suppression bursts : penser une maladie mtabolique ( surtout une
hyperglycinmie ou une acidmie-D-glycrique ) ou annonce dune
encphalopathie pileptique infantile prcoce comme une hypsarythmie.
Convulsions gnralises relates un dysfonctionnement de la vitamine B6
( dosage de lacide pipcolique sanguin ) [ R/ 100 mg IV pyridoxine ] ;
ou de lacide folinique ( dosage acide pipcolique, AA sanguins , HVA et 5 HIAA
dans les urines ; [ R/ 100 mg vit B6 et 2.5 mg acide folique ];
anomalie du transporteur 1 du glucose vers le SNC ( GLUT1 deficiency ) :
anomalie distance des repas.

AG ou APC Faits marquants
24-27 semaines Ondes polymorphes, discontinues, amples
Possibilits de courtes priodes (1-2 min) dactivits continues
Eveil/sommeil indissociable
28-32 semaines Bouffes theta (donc trac discontinu)

NB 28-29 semaines : ces bouffes sont synchrones (dans les 2
hmisphres)
Aprs 30 semaines, il y a des bouffes delta
Eveil / sommeil indissociables
32 36 semaines Disparition des bouffes theta

Pointes multifocales
Eveil / sommeil dissociables
> 36 semaines Eveil / sommeil structur

Eveil : bas voltage, diffus
REM :ondes lentes avec pisodes dondes rapides, activit continue
NREM : activit discontinue
> 44 semaines Trac continu en sommeil calme
> 46 semaines Fuseau de sommeil dans les rgions centrales
> 48 semaines Activit rythmique occipitale qui disparat louverture des yeux
4 5 mois Bouffes dondes pointes frontales ( encoches )

6 8 mois Rythme theta pendant lendormissement

The evaluation
or seizures

Maladies mtaboliques
et pH
Une acidose mtabolique avec ctonurie et avec acidose lactique : penser une maladie
mitochondriale ;
Une acidose mtabolique avec ctonurie et sans acidose lactique : penser une acidurie
organique ;
Une acidose mtabolique avec ctonurie, avec ou sans acidose lactique : penser une
leucinose ;
Une acidose mtabolique sans ctonurie, avec acidose lactique et avec hypoglycmie :
penser une glycognose ou dfaut de la gluconogense ou dfaut doxydation des
acides gras ;
Une acidose mtabolique avec ctonurie, sans hypoglycmie et sans acidose lactique :
penser un dfaut de la chane respiratoire ;
Une acidose mtabolique avec ctonurie sans acidose lactique et sans hypoglycmie :
penser aussi une acidurie organique et une acidurie pyroglutamique ;
Pas dacidose mtabolique sans actonurie avec hyperammonimie et hypoglycmie :
penser un dfaut doxydation des acides gras, un dfaut en glutamate
dshydrognase ;
Pas dacidose mtabolique sans actonurie avec hyperammonimie et sans
hypoglycmie : penser un dfaut du cycle de lure.
Pas dacidose mtabolique sans actonurie sans hyperammonimie et sans
hypoglycmie : penser hyprglycinmie ( sans ctose ), ou un dficit en sulfite oxydase.
Pas dacidose mtabolique avec actonurie :penser une leucinose.

Mandatory
investigations
- blood sugar
- Hematocrit
- bilirubin (if jaundice is present clinically)
- serum electrolytes (Na, Ca, Mg)
- arterial blood gas, anion gap
- cerebrospinal fluid (CSF) examination: CSF examination should
be done in all cases as seizures may be the first sign of
meningitis. It should not be omitted even if another etiology such
as hypoglycemia is present, because meningitis can often
coexist. CSF study may be withheld temporarily if severe cardio-
respiratory compromise is present or in cases with severe birth
asphyxia (documented poor cord pH, seizure onset within 12-24
hrs). An arterial blood gas (ABG) may have to be performed if
IEM is strongly suspected.
- cranial ultrasound (US)
- electroencephalography (EEG).

Specific
investigations
Imaging
- Neurosonography
- CT scan should be done in all infants where an etiology is not available after the first line of
investigations. It can be diagnostic in sub-arachnoid hemorrhage and developmental
malformations.
- MRI scan is indicated only if investigations do not reveal any etiology and seizures are
resistant to usual anti-epileptic therapy. It can be diagnostic in cerebral dysgenesis,
lissencephaly and other neuronal migration disorders.
Screen for congenital infections A TORCH screen and VDRL should be considered in the
presence of hepato-splenomegaly, thrombocytopenia, growth retardation, small for gestational
age and presence of chorioretinitis.
Metabolic screen A metabolic screen includes blood and urine ketones, urine reducing
substances, blood ammonia, anion gap, urine and plasma aminoacidogram, serum and CSF
lactate/ pyruvate ratio
Electro-encephalogram (EEG) EEG
- Ictal EEG may be useful for the diagnosis of suspected seizures and also for diagnosis of
seizures in muscle-relaxed infants. It should be done as soon as the neonate is stable enough
to be transported for EEG, preferably within first week.
- EEG should be performed for at least 1 hour
- Inter-ictal EEG is useful for long-term prognosis of neonates with seizures.
- A background abnormality in both term and preterm neonates indicates a high risk for
neurological sequelae. These changes include burstsuppression pattern, low voltage invariant
pattern and electro-cerebral inactivity

Evaluation of Neonatal Seizures
Serum lytes (gluc, Ca, Mg, Na)
CSF
Head ultrasound
EEG (B6?)
Tox screen
CT or MRI of brain
?metabolic w/u, congenital infection w/u

Grading IVH

1. Where is the hemorrhage?
2. Name the Anatomy
3. Grade the Hemorrhage
Grade II Hemorrhage
Extension into lateral ventricle without dilation
Normal Anatomy
Germinal Matrix Extension into

Lateral Ventricle
(no dilation) Choroid Plexus

seizure
I. Epileptic
Consistently associated with electro-
cortical seizure activity on the EEG
Cannot be provoked by tactile stimulation
Cannot be suppressed by restraint of
involved limb or repositioning of the infant
Related to hyper synchronous discharges
of a critical mass of neuron

seizures
II. Non-epileptic
No electro-cortical signature
Provoked by stimulation
Suppressed by restraint or repositioning
Brainstem release phenomena (reflex)

Does absence of EEG seizure
activity indicate that a clinical
seizure is nonepileptic?
Certain clinical seizures in the human

newborn originate from electrical seizures
in 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

Surface EEG-Silent Seizure
Can surface EEG-silent seizure in the
newborn result to brain injury?
Can this be eliminated by conventional
anticonvulsant therapy?
Further investigation needed

Laboratory Studies to Evaluate
Neonatal Seizures
Indicated
Complete blood count, differential, platelet count;

urinalysis
Blood glucose (Dextrostix), BUN, Ca, P, Mg,
electrolytes
Blood oxygen and acid-base analysis
Blood, CSF and other bacterial cultures
CSF analysis
EEG
Laboratory Studies to Evaluate
Neonatal Seizures
Clinical Suspicion of Specific Disease
Serum immunoglobulins, TORCH antibody titers, and

viral cultures
Blood and urine metabolic studies (bilirubin,ammonia,
lactate, FECl, reducing substance.)
Blood and urine toxic screen
Blood and urine amino and organic acid screen
CT or ultrasound scan

Metabolic Evaluation for Refractory
Neonatal Seizures
Consider individually by case specifics
Serum
Glucose
Electrolytes (sodium, potassium, chloride, carbon dioxide), blood urea nitrogen, chromium,
calcium, phosphorus, magnesium
Uric acid
Creative kinase
Serum ammonia
Lactic and pyruvic acids
Biotinidase
Amino acids
Serum carnitine, acylcarnitines
Serum transferrin
Copper and ceruloplasmin
Cholesterol
Fatty acids (short-chain, medium-chain, long-chain)
Pipecolic acid
NeoReviews vol.5 no.6 June 2004

Metabolic Evaluation for Refractory
Neonatal Seizures
Urine
Organic acids
Acylglycines
Uric acid
Sulfites
Xanthine, hypoxanthine
Guanidinoacetate
Pipecolic acid
Cerebrospinal Fluid
Cell count, glucose,protein
Lactic and pyruvic acids
Amino acids
Organic acids
Neurotransmitters
Other Studies
Skin biopsy
Muscle biopsy
Magnetic resonance imaging with magnetic resonance spectroscopy (especially for
creatine)

The treatment of
or seizures

Treatment
Identify the underlying cause:
hypoglycemia - D10 solution
hypocalcemia - Calcium gluconate
hypomagnesemia- Magnesium sulfate
pyridoxine deficiency- Pyridoxine
meningitis- initiation of antibiotics

Treatment
To minimize brain damage
Some controversy when to start
anticonvulsants
If seizure is prolonged (longer than 3
minutes), frequent or associated
with cardiorespiratory disturbance

Acute therapy of neonatal
seizures
If with hypoglycemia- Glucose 10%: 2ml/k IV
If no hypoglycemia- Phenobarbital:20mg/k IV
loading dose
If necessary : additional phenobarbital:
5 mg/kg IV to a max of 20 mg/kg
(consider omission of this additional
Phenobarbital
if with baby is asphyxiated)
Phenytoin: 20 mg/kg, IV (1 mg/kg/min)
Lorazepam:0.05-0.10 mg/kg, IV

Treatment of neonatal
convulsions
Within 5 minutes:
- baby in thermoneutral environment and ensure airway, breathing and
circulation. O2 should be started, IV access should be secured, and
blood should be collected for sugar and other investigations. A brief
relevant history should be obtained and quick clinical examination
should be performed. All this should not require more than 2-5 minutes.
- If hypoglycemia or if there is no facility to test blood sugar immediately,
2 ml/kg of 10% dextrose should be given as a bolus injection followed
by a continuous infusion of 6-8 mg/kg/min.
If hypoglycemia has been treated or excluded as a cause of
convulsions, the neonate should receive 2ml/kg of 10% calcium
gluconate IV over 10 minutes under strict cardiac monitoring. If ionized
calcium levels are suggestive of hypocalcemia, the newborn should
receive calcium gluconate at 8 ml/kg/d for 3 days. If seizures continue
despite correction of hypocalcemia, 0.25 ml/kg of 50% magnesium
sulfate should be given intramuscularly (IM).
- Anti-epileptic drug therapy (AED)

Acute Therapy of Neonatal Seizures
With Hypoglycemia --
Glucose, 10% solution: 2 mL/kg, IV
No Hypoglycemia
Phenobarbital: 20 mg/kg, IV (1-2 mg/kg/min)
If necessary:
Additional phenobarbital: 5 mg/kg IV to a max. of 40 mg/kg
(consider omission of this additional phenobarbital

if infant is severely asphyxiated)
Phenytoin*: 20 mg/kg, IV (0.5-1.0 mg/kg/min)
(Lorazepam: 0.05-0.10 mg/kg, IV) if available
Midazolam: 0.2 mg/kg, IV;then,0.1-0.4 mg/kg/hr, IV
Acute Therapy of Neonatal Seizures
Other (as Indicated)

Calcium gluconate, 5% solution: 4 mL/kg, IV
Magnesium sulfate, 50% solution: 0.2 mL/kg, IM
Pyridoxine: 50-100 mg, IV; repeat to maximum of 500 mg if
needed
Pyridoxal-5-phosphate,30 mg/kg/day, PO
Folinic Acid, 4 mg/kg/day, PO

Drug Therapy For Neonatal Seizures
Standard Therapy
AED Initial Dose Maintenance Dose Route
Phenobarbital 20mg/kg 3 to 4 mg/kg per day lV, lM, PO
Phenytoin 20 mg/kg 3 to 4 mg/kg per day lV, PO
Fosphenytoin 20 mg/kg phenytoin 3 to 4 mg/kg per day lV, lM
equivalents
Lorazepam 0.05 to 0.1 mg/kg Every 8 to 12 hours lV
Diazepam 0.25 mg/kg Every 6 to 8 hours lV
AED= andtiepileptic drug; lV= intravenous; lM= intramuscular; PO= oral

Oral phenytoin is not well absorbed.
Benzodiazepines typically not used for maintenance therapy.
Lorazepam preferred over diazepam.

Pharmacological properties of
Phenobarbital
Enters the CSF/brain rapidly with high efficiency
The blood level is largely predictable from the
dose administered
It can be given IM or IV(more preferred)
Maintenance therapy accomplished easily with
oral therapy
Protein binding lower in newbornfree levels of
drug are higher
Entrance to the brain increased by local acidosis
associated with seizures

Anti-epileptic drug therapy (AED)
Equipment for resuscitation and assisted ventilation
should be available at the bedside of all neonates given
multiple doses
Phenobarbitone
- It is the drug of choice in neonatal seizures.
- The dose is 20 mg/kg/IV slowly over 20 minutes (not faster than 1 mg/kg/min). If seizures persist after completion
of this loading dose, repeat dose of phenobarbitone 10 mg/kg may be used every 20-30 minutes till a total dose of
40 mg/kg has been given.
- The maintenance dose is 3-5 mg/kg/day in 1-2 divided doses, started 12 hours afterthe loading dose.
- Recommendation for use of prophylactic phenobarbitone still awaits further studies.
Phenytoin and Fosphenytoin
- Phenytoin is indicated if the maximal dose of phenobarbitone (40 mg/kg) fails to resolve seizures or earlier, if
adverse effects like respiratory depression, hypotension or bradycardia ensue with phenobarbitone.
- The dose is 20 mg/kg IV at a rate of not more than 1 mg/kg/min under cardiac monitoring. Phenytoin should be
diluted in normal saline as it is incompatible with dextrose solution. A repeat dose of 10 mg/kg may be tried in
refractory seizures. The maintenance dose is 3-5 mg/kg/d (maximum of 8 mg/kg/d) in 2-4 divided doses. Oral
suspension has very erratic absorption from gut in neonates, so it should be avoided. Thus only IV route is
preferred in neonates and it should preferably be discontinued before discharge.
- Fosphenytoin, the prodrug of phenytoin, does not cause the same degree of hypotension or cardiac
abnormalities, has high water solubility (therefore can be given IM), and is less likely to lead to soft-tissue injury
compared with phenytoin. It is dosed in phenytoin equivalents (1.5 mg/kg of fosphenytoin is equivalent to 1 mg/kg
of phenytoin).
Benzodiazepines
Lorazepam is preferred over diazepam as it has a longer duration of action and results in less adverse effects (sedation and cardiovascular
effects). Midazolam is faster acting than lorazepam and may be administered as an infusion.
Diazepam: 0.25 mg/kg IV bolus (0.5 mg/kg rectal); may be repeated 1-2 times.
Lorazepam: 0.05 mg/kg IV bolus over 2-5 minutes; may be repeated
Midazolam: 0.15 mg/kg IV bolus followed by infusion of 0.1 to 0.4 mg/kg/hour.
Clonazepam: 0.10.2 mg/kg IV bolus followed by infusion 10-30 g/kg/hr.

Antiepileptic drugs for refractory seizures
The expected response to anticonvulsants is 40% to the initial 20- mg/kg loading dose of
phenobarbitone, 70% to a total of 40 mg/kg of PB, 85% to a 20- mg/kg LD of PHT, and
95% to 100% to 0.05 to 0.10 mg/kg lorazepam4. In exceptional circumstances when the
seizures are refractory to these first-line drugs, the following second-line drugs might
be tried.
Lidocaine: Start with 4mg/kg/hr IV on first day, reduce by 1mg/kg/hr on each
subsequent day or load with 2mg/kg IV and maintain on 6 mg/kg/hr. Adverse effects
include arrythmias, hypotension and seizures. It should not be administered with
phenytoin.
Paraldehyde: It may be used in seizures refractory to the first line drugs. A dose of 0.1-
0.2 ml/kg/dose may be given IM or 0.3 ml/kg/dose mixed with coconut oil in 3:1 may be
used by per rectal route. Additional doses may be used after 30 minutes and q 4-6
hourly. Adverse effects include pulmonary hemorrhage, pulmonary edema,
hypotension, and liver injury.
Pyridoxine: Therapeutic trial of pyridoxine is reserved as a last resort. IV administration
is the preferred method; however, suitable IV preparations are not available at present
in India. Hence intramuscular (IM) route may have to be used instead (1 ml of neurobion
has 50-mg pyridoxine and 1 ml each may be administered in either the gluteal region or
anterolateral aspect of thigh).
Sodium valproate: It can be used for maintenance therapy in neonates. Per rectal route
may be used in acute condition. IV preparation is now available. Dose is 20-25 mg/kg/d
followed by 5-10 mg/kg every 12 hours.
Vigabatrin: It has been used in neonates for refractory seizures, primarily for infantile
spasms. The dose is 50 mg/kg/day.
Topiramate: It shows promise in neonatal seizures because of its potential
neuroprotective but has also secondary effects

Alternative Antiepileptic Drugs (AED)
for Neonatal Seizures
Intravenous AEDs
High-dose phenobarbital: >30 mg/kg
Pentobarbital: 10 mg/kg, then 1 mg/kg per hour
Thiopental: 10 mg/kg, then 2 to 4 mg/kg per hour
Midazolam: 0.2 mg/kg, then 0.1 to 0.4 mg/kg per hour
Clonazepam: 0.1 mg/kg
Lidocaine: 2 mg/kg, then 6 mg/kg per hour
Valproic acid: 10 to 25 mg/kg, then 20 mg/kg per day in 3 doses
Paraldehyde: 200 mg/kg, then 16 mg/kg per hour
Chlormethiazole: Initial infusion rate of 0.08 mg/kg per minute
Dexamethasone: 0.6 to 2.8 mg/kg
Pyridoxine (B6): 50 to 100 mg, then 100 mg every 10 minutes
(up to 500mg)
Alternative AEDs for Neonatal
Seizures
Oral AEDs
Primidone: 15 to 25 mg/kg per day in 3 doses
Clonazepam: 0.1 mg/kg in 2 to 3 doses
Carbamazepine: 10 mg/kg, then 15 to 20 mg/kg per day in 2 doses
Oxcarbamazepine: no data on neonates, young infants
Valproic acid: 10 to 25 mg/kg, then 20 mg/kg per day in 3 doses
Vigabatrin: 50 mg/kg per day in 2 doses, up to 200 mg/kg per day
Lamotrigine: 12.5 mg in 2 doses
Topiramate: 3 mg/kg per day
Zonisamide: 2.5 mg/kg per day
Levetiracetam: 10 mg/kg per day in 2 doses
Folinic acid: 2.5 mg BID, up to 4 mg/kg per day

Maintenance Therapy of Neonatal Seizures
Glucose: < 8 mg/kg/, IV
Phenobarbital: 3-4 mg/kg/24 hr, IV, IM, or PO
Phenytoin (as fosphenytoin): 3-4 mg/kg/24 hr, IV
Calcium gluconate: 500 mg/kg/24 hr, PO
Magnesium sulfate (50%): 0.2 mL/kg/24 hr, IM
Volpe, Neurology of the Newborn, 5th

ed. 2008

Treatment of Electroclinical
Seizures
Phenobarbital 20 mg/kg
10 mg/kg boluses until 40-50 microgm/ml
Phenytoin 20 mg/kg
Lorazepam 0.1 mg/kg
Pyridoxine 50-100 mg IV with EEG

Maintenance
anti-epileptic therapy
Monotherapy is the most appropriate
strategy to control seizures. Attempts
should be made to stop all anti-epileptic
drugs and wean the baby to only
phenobarbitone at 3-5 mg/kg/day.
If seizures are uncontrolled or if clinical
toxicity appears, a second AED may be
added. The choice may vary from
phenytoin, carbamezepine, and valproic
acid.

Why should the infant with
epileptic seizures be treated
with AED
Potential adverse effects of seizure on:
Ventilatory function
Circulation
Cerebral Metabolism
Brain Development
disturbance in cerebral blood flow

energy metabolism
homeostasis of excitotoxic amino acids
neurogenesis and synaptic reorganization

Determinants of Duration of
anticonvulsant therapy for neonatal
seizures
Neonatal neurological examination
Cause of neonatal seizure
Electroencephalogram

Duration of anticonvulsant
therapy-Guidelines
Neonatal period
If neonatal neurological examination
becomes normal discontinue therapy
If neonatal neurological examination is
persistently abnormal,consider etiology and
obtain EEG
In most such cases- Continue
phenobarbital
- Discontinue phenytoin
- Reevaluate in 1 month

Duration of anticonvulsant
therapy-Guidelines
One month after discharge
If neurological examination has become
normal, discontinue phenobarbital
If neurological examination is persistently
abnormal,obtain EEG
If no seizure activity on EEG, discontinue
phenobarbital

When to discontinue
AED
This is highly individualized
Volpe:
- try to discontinue all medication at discharge if clinical
examination is normal, irrespective of etiology and EEG. If
neurological examination is persistently abnormal at discharge,
AED is continued and the baby is reassessed at 1 month.
- If the baby is normal on examination and seizure free at 1
month, phenobarbitone is discontinued over 2 weeks. If
neurological assessment is not normal, an EEG is obtained. If
EEG is not overtly paroxysmal, AED are tapered and stopped. If
EEG is overtly abnormal, the infant is reassessed in the same
manner at 3 months and then 3 monthly till 1 year of age.
Ellison

Score de Patricia Ellison:
Stopper le traitement si < 5 terme ou < 6 3 mois du terme
Poids de naissance :
< 1500g 2
> 1500 g 1
type de paroxysme :
subtil ou atypique 0
clonique 1
tonique ou myoclonique 2
facteur dclenchant :
inconnu 0
hypocalcmie, hypoglycmie 1
hmorragie sous arachnodienne ou stades 1 1
Sarnat stade 2 2
Mningite 2
Hmorragie stade 3,4 2
Malformation crbrale 2
Sarnat stade 3 2
EEG :
Normal 0
Anomalies mineures 1
Anomalies marques 2
Examen neurologique :
Normal 0
hypotonie modre, hyperexcitabilit 1
Hmi syndrome, hyper- hypo tonie majeure 2

Duration of Anticonvulsant Therapy Guidelines
Neonatal Period
If neonatal neurological examination becomes normal, discontinue
therapy
If neonatal neurological examination is persistently abnormal, consider
the cause and obtain an EEG.
In most such cases:
Continue phenobarbital
Discontinue phenytoin
Reevaluate in 1 month
At 1 Month After Discharge
If neurological examination has become normal, discontinue
phenobarbital
If neurological examination is persistently abnormal, obtain an EEG.
If no seizure activity is noted on the EEG, discontinue phenobarbita
Volpe, Neurology of the Newborn, 5th ed. 2008

The following and prognosis
of
or seizures

Outcome
45 % controlled after either phenobarb
or phosphenytoin
60 % controlled with both
30% of survivors develop epilepsy
WORSE: HIE, meningitis, dysplasia
WORSE: electrographic seizures
BETTER: hypoCa, BINC, BIFC, stroke

Prognosis
Two most useful approaches in utilizing outcome
EEG
Recognition of the underlying neurological

disease

Prognosis of Neonatal seizures in
relation to EEG
EEG BACKGROUND NEUROLOGICAL SEQUELAE(%)
Normal 10
Severe abnormalities 90
Moderate abnormalities ~50
Based primarily on data reported by Rowe JC, Holmes GL, Hafford J, et al:
Electroencephalogr Clin Neurophysiol 60:183-196, 1985; Lombroso CT: In
Wasterlain CG, Treeman DM, Porter R, editors: Advances in neurology, New
York, 1983, Raven Press; and includes both full-term and premature infants.
Burst-suppression pattern, marked voltage suppression, and
electrocerebral
Silence.
Voltage asymmetries and immaturity.

Complications
Cerebral palsy
Hydrocephalus
Epilepsy
Spasticity
Feeding difficulties

Consultations
Neurology consult needed for
- evaluation of seizures
- evaluation of EEG and video EEG
monitoring
- management of anticonvulsant
medications

Further Outpatient Care
Neurology outpatient evaluation
Developmental evaluation for early
identification of physical or cognitive
deficits
Orthopedic evaluations if with joint
deformities
Consider physical medicine/physical
therapy referral if indicated

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Professeur Oreste Battisti

Battisti: Convulsions nonatales 1

Battisti: Convulsions nonatales 2

Battisti: Convulsions nonatales 3

prvalence:80-120 /100,000 naissances

Battisti: Convulsions nonatales 4

Battisti: Convulsions nonatales 5

Hypoxic-ischemic encephalopathy 50%

Battisti: Convulsions nonatales 6

Battisti: Convulsions nonatales 7

Battisti: Convulsions nonatales 8

paroxysmal discharge of cerebral

Battisti: Convulsions nonatales 9

Apnea with tonic stiffening of body

Battisti: Convulsions nonatales 10

Immature CNS cannot sustain a

Battisti: Convulsions nonatales 12

Battisti: Convulsions nonatales 13

CLINICAL SEIZURE COMMON UNCOMMON

Volpe JJ.Neonatal Seizures:Neurology of the Newborn.4th ed.

Battisti: Convulsions nonatales 16

Subtle Preterm and Term Eye deviation (Term) Usually No

Tonic Primarily preterm May be focal or generalized Usually No

Clonic Primarily term May be focal or multifocal Yes

Myoclonic Rare Focal, multifocal, or generalized Lightning-like jerks +

Battisti: Convulsions nonatales 17

Battisti: Convulsions nonatales 18

Battisti: Convulsions nonatales 19

Myoclonic- sudden flexor movements (lightning-like

Battisti: Convulsions nonatales 20

Battisti: Convulsions nonatales 21

Battisti: Convulsions nonatales 22

Battisti: Convulsions nonatales 23

Battisti: Convulsions nonatales 24

Battisti: Convulsions nonatales 25

Battisti: Convulsions nonatales 26

Battisti: Convulsions nonatales 27

Battisti: Convulsions nonatales 28

Begins on the 2nd 3rd day of life

Battisti: Convulsions nonatales 29

5th day of life

Battisti: Convulsions nonatales 30

Abnormality of gaze or eye O +

Movements cease with passive + O

Battisti: Convulsions nonatales 31

Battisti: Convulsions nonatales 32

Battisti: Convulsions nonatales 33

Battisti: Convulsions nonatales 34

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Increases with Rare Common

Battisti: Convulsions nonatales 41

Battisti: Convulsions nonatales 42

Battisti: Convulsions nonatales 44

Battisti: Convulsions nonatales 45

Battisti: Convulsions nonatales 46

Battisti: Convulsions nonatales 47

1. Seizures are usually related to significant

Battisti: Convulsions nonatales 48

3.Experimental data give some reason for

Battisti: Convulsions nonatales 49

TIME OF ONSET* RELATIVE

Battisti: Convulsions nonatales 50