Download Free Medical Les Convulsions Neonatales PowerPoint Presentation

Les Convulsions Neonatales PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Neurology, which is titled "Les convulsions néonatales", to know about the seizures in the newborn period.

Tags : Neurology, Les convulsions néonatales, seizures, newborn period

Published on : Aug 23, 2021 | Views : 1576 | Downloads : 5

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Battisti: Convulsions néonatales 1 Les convulsions néonatales Professeur Oreste Battisti Faculté de Médecine Université de Liège
Slide 2-

Battisti: Convulsions néonatales 2 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.
Slide 3-

Battisti: Convulsions néonatales 3 Structure of presentation Introduction and epidemiology Definitions and patterns of convulsions or neonatal seizures Classification: clinical and EEG Etiology Physiopathology Treatment and follow-up
Slide 4-

Battisti: Convulsions néonatales 4 Epidémiologie prévalence:80-120 /100,000 naissances Incidence:1-5/1000 La période néonatale est particulièrement ciblée
Slide 5-

Battisti: Convulsions néonatales 5 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
Slide 6-

Battisti: Convulsions néonatales 6
Slide 7-

Battisti: Convulsions néonatales 7 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
Slide 8-

Battisti: Convulsions néonatales 8 Definition, classification and patterns of neonatal: seizures convulsions epilepsy
Slide 9-

Battisti: Convulsions néonatales 9 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”
Slide 10-

Battisti: Convulsions néonatales 10 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
Slide 11-

Why do neonatal seizures have such unusual presentations? Immature CNS cannot sustain a synchronized, well orchestrated generalized seizure
Slide 12-

Battisti: Convulsions néonatales 12 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 jerks—may be multiple Isolated, generalized myoclonic jerk as infant wakes from sleep Volpe Neurology of the Newborn..
Slide 13-

Battisti: Convulsions néonatales 13 Classification of Neonatal Seizures Clinical Electroencephalographic
Slide 14-

Classification I. Clinical Seizure Subtle Tonic Clonic Myoclonic
Slide 15-

Classification II. Electroencephalographic seizure Epileptic Non-epileptic
Slide 16-

Battisti: Convulsions néonatales 16 Classification of Neonatal 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.
Slide 17-

Battisti: Convulsions néonatales 17 Classification of neonatal seizures
Slide 18-

Battisti: Convulsions néonatales 18 Classification of Neonatal Seizures Clinical Electroencephalographic
Slide 19-

Battisti: Convulsions néonatales 19 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
Slide 20-

Battisti: Convulsions néonatales 20 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
Slide 21-

Battisti: Convulsions néonatales 21 Clinical Classification Focal/Multifocal Clonic Not generalized Migratory Focal Tonic Generalized Myoclonic
Slide 22-

Battisti: Convulsions néonatales 22 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, there’s this funny classification that’s 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 sz’s in term. The most common subtle manifestation is tonic horizontal eye deviation.
Slide 23-

Battisti: Convulsions néonatales 23 Clinical Classification Subtile (“Hypomotor”) Motor activity arrest Apnea Eye deviation Autonomic changes Motor automatisms Oral-buccal-lingual movements Swimming Bicycling
Slide 24-

Battisti: Convulsions néonatales 24 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 »
Slide 25-

Battisti: Convulsions néonatales 25 Subtle seizures (ct) Ocular - Tonic horizontal deviation of eyes or sustained eye opening with ocular fixation or cycled flutering Oral–facial–lingual 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.
Slide 26-

Battisti: Convulsions néonatales 26 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.
Slide 27-

Battisti: Convulsions néonatales 27 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).
Slide 28-

Battisti: Convulsions néonatales 28 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
Slide 29-

Battisti: Convulsions néonatales 29 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
Slide 30-

Battisti: Convulsions néonatales 30 5th day Seizures 5th day of life normal appearing neonates with mulifocal seizures Present for less than 24 hours Good prognosis
Slide 31-

Battisti: Convulsions néonatales 31 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 + ------------------------------------------------------------------------------------------------------------------
Slide 32-

Battisti: Convulsions néonatales 32 Weird Baby Movements Jitteriness Stimulus-sensitive “Tremor” Suppressable Benign neonatal sleep myoclonus Spinal myoclonus Apnea of non-neurologic etiology bradycardia
Slide 33-

Battisti: Convulsions néonatales 33 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 non- sustained nystagmoid jerks.
Slide 34-

Battisti: Convulsions néonatales 34 Classification of Neonatal Seizures Clinical Electroencephalographic
Slide 35-

Electroencephalographic 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
Slide 36-

Electroencephalographic seizures II. Non-epileptic No electro-cortical signature Provoked by stimulation Suppressed by restraint or repositioning Brainstem release phenomena (reflex)
Slide 37-

Battisti: Convulsions néonatales 37 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
Slide 38-

Battisti: Convulsions néonatales 38 Neonatal Seizures EEG Classification Electrical seizures with absent clinical seizures Electrical seizures associated with markedly abnormal background EEG Seen in comatose patients
Slide 39-

Battisti: Convulsions néonatales 39 Epileptic vs Non-epileptic Neonatal Phenomena
Slide 40-

Does absence of EEG seizure activity indicate that a clinical seizure is non- epileptic? 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
Slide 41-

Battisti: Convulsions néonatales 41 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
Slide 42-

Battisti: Convulsions néonatales 42 EEG tracing
Slide 43-

Battisti: Convulsions néonatales 43
Slide 44-

Exercices on movies Battisti: Convulsions néonatales 44
Slide 45-

In addiction Battisti: Convulsions néonatales 45
Slide 46-

Focal crisis Battisti: Convulsions néonatales 46
Slide 47-

Battisti: Convulsions néonatales 47 3. Etiology of neonatal convulsions or seizures
Slide 48-

Battisti: Convulsions néonatales 48 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
Slide 49-

Battisti: Convulsions néonatales 49 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.
Slide 50-

Battisti: Convulsions néonatales 50 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 + + +
Slide 51-

Battisti: Convulsions néonatales 51 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,6th ed.
Slide 52-

Battisti: Convulsions néonatales 52 Etiology Pregnancy history is important Search for history that supports TORCH infections History of fetal distress, preeclampsia or maternal infections
Slide 53-

Battisti: Convulsions néonatales 53
Slide 54-

Battisti: Convulsions néonatales 54 Neonatal Seizures Etiologic diagnosis Hypoxic –ischemic encephalopathy Metabolic Infections Trauma Structural abnormalities Hemorrhagic and embolic strokes Maternal disturbances
Slide 55-

Battisti: Convulsions néonatales 55 Differential diagnosis of neonatal seizures by peak time of onset 24 hours 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 Hypoparathyroidism–hypocalcemia Idiopathic cerebral venous thrombosis Incontinentia pigmenti Intracerebral hemorrhage Intraventricular hemorrhage in premature newborns Pyridoxine dependency Subarachnoid hemorrhage Tuberous sclerosis Urea cycle disturbances
Slide 56-

Battisti: Convulsions néonatales 56 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
Slide 57-

Battisti: Convulsions néonatales 57 Causes of neonatal seizures Ages 4 – 14 days Infection Metabolic disorders Hypocalcemia Diet Hypoglycemia Inherited disorder of metabolism such as galactosemia,fructosemia Hyperinsulinemic hypoglycemia Becwith syndrome Anterior pituitary hypoplasia Drug withdrawal Benign neonatal convulsion Kernicterus, hyperbilirubenemia
Slide 58-

Battisti: Convulsions néonatales 58 Causes of neonatal seizures Ages 2 – 8 weeks Infection Head injury Subdural henatoma Inherited disorder of metabolism Aminoacidurias Urea cycle defects Organic acidurias Neonatal ALD Malformations of cortical development Lissencephaly Focal cortical dysplasia Tuberous sclerosis Sturge weber syndrome
Slide 59-

Battisti: Convulsions néonatales 59 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 Inborn errors of metabolism Inherited as autosomal recessive or X-linked recessive
Slide 60-

Battisti: Convulsions néonatales 60 Neonatal Seizures Etiologic diagnosis Inborn errors of metabolism 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
Slide 61-

Battisti: Convulsions néonatales 61
Slide 62-

Battisti: Convulsions néonatales 62 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
Slide 63-

Battisti: Convulsions néonatales 63 Neonatal Seizures Fifth-day fits – 5th day of life normal appearing neonates with mulifocal seizures Present for less than 24 hours Good prognosis
Slide 64-

Battisti: Convulsions néonatales 64 Neonatal Seizures Etiologic diagnosis Pyridoxine dependency resistant to conventional AED’s 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
Slide 65-

Battisti: Convulsions néonatales 65 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
Slide 66-

Battisti: Convulsions néonatales 66 Causes of Neonatal Seizures Within first 24 hours of life Hypoxic ischemic encephalopathy Meningitis/sepsis Subdural/Subarachnoid/Interventricular hemorrhage Intrauterine infection Trauma Pyridoxine dependency Drug effect/withdrawal
Slide 67-

Battisti: Convulsions néonatales 67 Causes…. 24-72 hours Meningitis/sepsis In premature infants: IVH In full-term infants: infarction, venous thrombosis Cerebral dysgenesis
Slide 68-

Battisti: Convulsions néonatales 68 Causes…. 72 hours to 1 week Above causes Inborn errors of metabolism Hypocalcemia Familial neonatal seizures 1 week to 4 weeks Above causes HSV
Slide 69-

Battisti: Convulsions néonatales 69 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
Slide 70-

Battisti: Convulsions néonatales 70 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
Slide 71-

Battisti: Convulsions néonatales 71 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)
Slide 72-

Battisti: Convulsions néonatales 72 The patho physiology of neonatal convulsions or seizures
Slide 73-

Battisti: Convulsions néonatales 73 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.
Slide 74-

Battisti: Convulsions néonatales 74 Perinatal Anatomical and Physiological Features of Importance in Determining Neonatal Seizure Phenomena ANATOMICAL Neurite outgrowth—dendritic and axonal ramifications—in process Synaptogenesis not complete Deficient myelination in cortical efferent systems Volpe JJ.Neonatal Seizures :Neurology of the Newborn.
Slide 75-

Battisti: Convulsions néonatales 75 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.
Slide 76-

Battisti: Convulsions néonatales 76 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 acid—excessive 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.
Slide 77-

Battisti: Convulsions néonatales 77 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.
Slide 78-

Battisti: Convulsions néonatales 78 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”
Slide 79-

Battisti: Convulsions néonatales 79 Causes of neonatal seizures Ages 4 – 14 days Infection Metabolic disorders Hypocalcemia Diet Hypoglycemia Inherited disorder of metabolism such as galactosemia,fructosemia Hyperinsulinemic hypoglycemia Becwith syndrome Anterior pituitary hypoplasia Drug withdrawal Benign neonatal convulsion Kernicterus, hyperbilirubenemia
Slide 80-

Battisti: Convulsions néonatales 80 Causes of neonatal seizures Ages 2 – 8 weeks Infection Head injury Subdural henatoma Inherited disorder of metabolism Aminoacidurias Urea cycle defects Organic acidurias Neonatal ALD Malformations of cortical development Lissencephaly Focal cortical dysplasia Tuberous sclerosis Sturge weber syndrome
Slide 81-

Battisti: Convulsions néonatales 81 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).
Slide 82-

Battisti: Convulsions néonatales 82 Les entités cliniques et électrophysiologiques des paroxysmes du nouveau-né Syndrome post-hypoxique ou post-asphyxique : « pointes-ondes en bouffées, entrecoupées par des activités normales » ; Etat de mal convulsif focal (  occlusive vascular disorder ) : « pointes lentes rythmiques unilatérales » ; Etat de mal généralisé : « pointes-ondes en bouffées » ; Convulsions néonatales bénignes ( à j 4-5 ) : « théta pointu alternant », avec (myo)clonies ; Convulsions néonatales bénignes familiales précoces : souvent j 2-3, mais parfois plus tard, avec prédominance chez le garçon ( anamnèse ! ) : « pas de tracé spécifique » ; Encéphalopathie myoclonique précoce : « pointes-ondes en bouffées, jamais synschrones sur les deux hémisphères, séparées par des tracés plats = suppression bursts » : penser à une maladie métabolique ( surtout une hyperglycinémie ou une acidémie-D-glycérique ) ou annonce d’une encéphalopathie épileptique infantile précoce comme une hypsarythmie. Convulsions généralisées relatées à un dysfonctionnement de la vitamine B6 ( dosage de l’acide pipécolique sanguin ) [ R/ 100 mg IV pyridoxine ] ; ou de l’acide folinique ( dosage acide pipécolique, 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 à distance des repas.
Slide 83-

Battisti: Convulsions néonatales 83
Slide 84-

Battisti: Convulsions néonatales 84 The evaluation neonatal convulsions or seizures
Slide 85-

Battisti: Convulsions néonatales 85 Maladies métaboliques et pH Une acidose métabolique avec cétonurie et avec acidose lactique : penser à une maladie mitochondriale ; Une acidose métabolique avec cétonurie et sans acidose lactique : penser à une acidurie organique ; Une acidose métabolique avec cétonurie, avec ou sans acidose lactique : penser à une leucinose ; Une acidose métabolique sans cétonurie, avec acidose lactique et avec hypoglycémie : penser à une glycogénose ou défaut de la gluconéogenèse ou défaut d’oxydation des acides gras ; Une acidose métabolique avec cétonurie, sans hypoglycémie et sans acidose lactique : penser à un défaut de la chaîne respiratoire ; Une acidose métabolique avec cétonurie sans acidose lactique et sans hypoglycémie : penser aussi à une acidurie organique et à une acidurie pyroglutamique ; Pas d’acidose métabolique sans acétonurie avec hyperammoniémie et hypoglycémie : penser à un défaut d’oxydation des acides gras, à un défaut en glutamate déshydrogénase ; Pas d’acidose métabolique sans acétonurie avec hyperammoniémie et sans hypoglycémie : penser à un défaut du cycle de l’urée. Pas d’acidose métabolique sans acétonurie sans hyperammoniémie et sans hypoglycémie : penser à hyprglycinémie ( sans cétose ), ou un déficit en sulfite oxydase. Pas d’acidose métabolique avec acétonurie :penser à une leucinose.
Slide 86-

Battisti: Convulsions néonatales 86 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).
Slide 87-

Battisti: Convulsions néonatales 87 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
Slide 88-

Battisti: Convulsions néonatales 88 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
Slide 89-

Battisti: Convulsions néonatales 89 Grading IVH
Slide 90-

Battisti: Convulsions néonatales 90 Germinal Matrix Extension into Lateral Ventricle (no dilation) Where is the hemorrhage? Name the Anatomy Grade the Hemorrhage Normal Anatomy Choroid Plexus Grade II Hemorrhage Extension into lateral ventricle without dilation
Slide 91-

Battisti: Convulsions néonatales 91 Electroencephalographic 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
Slide 92-

Battisti: Convulsions néonatales 92 Electroencephalographic seizures II. Non-epileptic No electro-cortical signature Provoked by stimulation Suppressed by restraint or repositioning Brainstem release phenomena (reflex)
Slide 93-

Battisti: Convulsions néonatales 93 Does absence of EEG seizure activity indicate that a clinical seizure is non- epileptic? 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
Slide 94-

Battisti: Convulsions néonatales 94 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
Slide 95-

Battisti: Convulsions néonatales 95 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
Slide 96-

Battisti: Convulsions néonatales 96 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, FECl³, reducing substance.) Blood and urine toxic screen Blood and urine amino and organic acid screen CT or ultrasound scan
Slide 97-

Battisti: Convulsions néonatales 97 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
Slide 98-

Battisti: Convulsions néonatales 98 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) NeoReviews vol.5 no.6 June 2004
Slide 99-

Battisti: Convulsions néonatales 99 The treatment of neonatal convulsions or seizures
Slide 100-

Battisti: Convulsions néonatales 100 Treatment Identify the underlying cause: hypoglycemia - D10 solution hypocalcemia - Calcium gluconate hypomagnesemia- Magnesium sulfate pyridoxine deficiency- Pyridoxine meningitis- initiation of antibiotics
Slide 101-

Battisti: Convulsions néonatales 101 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
Slide 102-

Battisti: Convulsions néonatales 102 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
Slide 103-

Battisti: Convulsions néonatales 103 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)
Slide 104-

Battisti: Convulsions néonatales 104
Slide 105-

Battisti: Convulsions néonatales 105
Slide 106-

Battisti: Convulsions néonatales 106 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, POª Fosphenytoin 20 mg/kg phenytoin 3 to 4 mg/kg per day lV, lM equivalents Lorazepam² 0.05 to 0.1 mg/kg Every 8 to 12 hours lV Diazepam²´ 0.25 mg/kg Every 6 to 8 hours lV AED= andtiepileptic drug; lV= intravenous; lM= intramuscular; PO= oral ªOral phenytoin is not well absorbed. ²Benzodiazepines typically not used for maintenance therapy. ³Lorazepam preferred over diazepam.
Slide 107-

Battisti: Convulsions néonatales 107
Slide 108-

Battisti: Convulsions néonatales 108 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 newborn—free levels of drug are higher Entrance to the brain increased by local acidosis associated with seizures
Slide 109-

Battisti: Convulsions néonatales 109 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: 0.1–0.2 mg/kg IV bolus followed by infusion 10-30 ìg/kg/hr.
Slide 110-

Battisti: Convulsions néonatales 110 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
Slide 111-

Battisti: Convulsions néonatales 111 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)
Slide 112-

Battisti: Convulsions néonatales 112 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 NeoReviews vol.5 no.6 June 2004
Slide 113-

Battisti: Convulsions néonatales 113 Volpe, Neurology of the Newborn, 5th ed. 2008
Slide 114-

Battisti: Convulsions néonatales 114 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
Slide 115-

Battisti: Convulsions néonatales 115 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.
Slide 116-

Battisti: Convulsions néonatales 116 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
Slide 117-

Battisti: Convulsions néonatales 117 Determinants of Duration of anticonvulsant therapy for neonatal seizures Neonatal neurological examination Cause of neonatal seizure Electroencephalogram
Slide 118-

Battisti: Convulsions néonatales 118 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
Slide 119-

Battisti: Convulsions néonatales 119 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
Slide 120-

Battisti: Convulsions néonatales 120 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
Slide 121-

Battisti: Convulsions néonatales 121
Slide 122-

Battisti: Convulsions néonatales 122 Score de Patricia Ellison: Stopper le traitement si ∑ < 5 « à terme » ou < 6 à 3 mois du terme
Slide 123-

Battisti: Convulsions néonatales 123
Slide 124-

Battisti: Convulsions néonatales 124 The following and prognosis of neonatal convulsions or seizures
Slide 125-

Battisti: Convulsions néonatales 125 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
Slide 126-

Battisti: Convulsions néonatales 126 Prognosis Two most useful approaches in utilizing outcome EEG Recognition of the underlying neurological disease
Slide 127-

Battisti: Convulsions néonatales 127 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.”
Slide 128-

Battisti: Convulsions néonatales 128 Complications Cerebral palsy Hydrocephalus Epilepsy Spasticity Feeding difficulties
Slide 129-

Battisti: Convulsions néonatales 129 Consultations Neurology consult needed for - evaluation of seizures - evaluation of EEG and video EEG monitoring - management of anticonvulsant medications
Slide 130-

Battisti: Convulsions néonatales 130 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