Dr Praman Kushwah, profile picture
Uploaded byDr Praman Kushwah
PPTX, PDF1,415 views

Neonatal seizure by dr praman

This document provides an overview of neonatal seizures. Key points include: - Neonatal seizures have an incidence of 10.3 per 1000 live births and are more common in preterm infants. - They are defined as abnormal excessive neuronal activity causing alterations in motor, behavioral or autonomic functions. - Common causes include hypoxic-ischemic encephalopathy, structural brain lesions, infections, and metabolic disturbances. - Seizures are classified based on their clinical presentation and EEG findings as subtle, clonic, tonic, myoclonic or EEG-only. - Differentiating seizures from non-seizure events like apnea or jitteriness is important.

Embed presentation

Downloaded 82 times
NEONATAL SEIZURES DR PRAMAN DRNB NEONATOLOGY RESIDENT
OVERVIEW ▪ Epidemiology ▪ Definition ▪ Pathogphysiology ▪ Classification ▪ Non seizure events ▪ Etiology ▪ Approach to management ▪ Management ▪ Prognosis
1. INTRODUCTION ▪ RED ALERT ▪ SECONDARY BRAIN INJURY ▪ FOCAL OR MULTIFOCAL : SINGLE HEMISPHERE ▪ MAJORITY SUBCLINICAL OR SUBTLE ▪ LESS SEIZURE THRESHOLD BUT BETTER PROGNOSIS.
2. Epidemiology ▪ Incidence ▪ 10.3 per 1000 live- births (NNPD) ▪ 58 per 1000 live births in VLBWs ▪ 1 – 3.5 per 1000 live births in Terms
3. DEFINITION Abnormally excessive or synchronous neuronal activity in the brain causing paroxysmal disturbances in neurological function manifesting clinically as alteration in motor, behavioral and/or autonomic functions CAN ANYONE DEFINE EPILEPSY ?
4. Pathophysiology  Imbalance between neurotransmitters
Incresed Seizure Susceptibility • ↑excitatory neurotransmitters (glutamate) • ↓inhibitory neurotransmitters (GABA) • GABA acting as excitatory neurotransmitter ATP-dependent Na-K pump Failure NMDA AMPA
▪ Onset is focal /multifocal, spread within one hemisphere only ▪ Immature mylenation of cortical efferent systems & commissure. ▪ Advanced Cortical development in Limbic system - Subtle
Energy dependent ion pumping Decreased ATP & Phosphocreatine Stimulation of glycolysis and ↑ Lactate Vasodilation & ↑ blood supply SEIZURE EPISODE Incresed blood pressure Increased Cerebral blood flow This fall in brain glucose concentration and rise in brain lactate are directly reminiscent of a hypoxic- ischemic brain insult
Time Course of Epileptogenesis ▪ Seconds to minutes – gene induction and translation of receptor and ion-channel proteins ▪ hours to days - neuronal death, inflammation, and altered transcriptional regulation ▪ weeks to months - mossy fiber sprouting, gliosis, neurogenesis
5. Classification ▪ Types of Neonatal seizure ▪ Clinical Seizure ▪ Electro - clinical Seizure ▪ EEG - Only
Types of Clinical Seizures
Subtle ▪ Most common type ▪ Preterms > Terms ▪ Paroxysmal & Repetitive ▪ Oral-buccal-lingual movements ▪ Progression movements ▪ EEG+/- (Tonic eye deviation – a/w EEG)
Clonic ▪ Repetitive, rhythmic contractions of specific muscle groups ▪ Slow rate of repetition ▪ Close relationship to the EEG seizure pattern ▪ Mimics - jitteriness, tremulousness, and myoclonus FOCAL MULTIFOCAL Face , trunk, extremity on one side of body Several body parts, often migrating () usually focal neuropathology e.g. infarction Non jacksonian march
Tonic ▪ Hallmark of several neonatal epilepsy syndromes ▪ sustained flexion or extension of muscle groups ▪ Sustained, but transient, asymmetrical posturing ▪ Tonic deviation of the eyes (upward) ▪ Poor prognosis, a/w IVH & Kernicterus FOCAL GENERALIZED Sustained, asymmetrical Posturing Decerebrate/decorticate like posturing Mostly EEG discharges + 15% EEG +
Myoclonic ▪ Contractions of muscle groups of well-defined regions ▪ rapid, isolated jerk or may be repetitive ▪ Rate of recurrence may be slow, irregular, or erratic ▪ EEG discharges absent. ▪ Types : ▪ Focal – Typically upper extremity, flexor groups. ▪ Multifocal – involving several body parts , asynchronous twitching. ▪ Generalized - bilateral, symmetric jerking of all extremities and/or muscles of the trunk and neck. EEG +,
EEG Only Seizures ▪ High incidence ▪ Similar duration and encephalopathy degree to electroclinical ▪ electromechanical dissociation ▪ electroclinical EEG only ▪ caudal-to-rostral maturation of cl- transporters ▪ brainstem & spinal cord motor system chloride levels decreases before cortical neuronal levels.
Autonomic Seizuers ▪ Clinical changes related to the autonomic nervous system ▪ Apneas often associated with tachycardia ▪ Alterations ▪ Heart rate – Tachy/Brady ▪ Respiration – Tachy / Brady ▪ Blood pressure ▪ Flushing ▪ Salivation ▪ Pupil dilatation
6. Non-Seizure Events ▪ Absence of EEG change ▪ Provoked by stimulation ▪ Suppressed by restraining ▪ No autonomic disturbances ▪ No Head/ Eye deviation ▪ Temporal/Spatial summation - ↑ Intensity ▪ Few benign, but few needs evaluation ▪ Not All That Shakes Is A Seizure
▪Apnea - ▪ Pause in breathing for greater than 20 seconds ▪ Premature baby ▪ During active sleep ▪ Brainstem immaturity ▪ If (mostly term) accompanied with eye closure /opening, eye deviation, mouth movement, hypertension, tachycardia – Seizure
▪ Jitteriness ▪ Very Common ▪ Excessive response to stimulation ▪ Back-and-forth oscillation , Same amplitude & frequency ▪ Hypocalcemia, hypoglycemia, and hypoxic- ischemic encephalopathy ▪ Head or eye deviation during an episode → seizure
▪ Benign neonatal sleep myoclonus ▪ during sleep – NREM ▪ jerks are typically bilateral, symmetric ▪ can be stopped by rousing the infant ▪ does not involve the face ▪ Normal neurologically ▪ BZDs provokes / exacerbates ▪ Spontaneous resolution ~2 mo
▪ Hyperekplexia (startle disease) ▪ Congenital stiff-man syndrome ▪ Startle & sustained tonic spasms response to stimuli ▪ Nocturnal myoclonus. ▪ “minor”  excessive startle ▪ “major”  stiffness while awake, nocturnal myoclonus, risk of SIDS ▪ Glycine receptor gene mutations ▪ Clonazepam - effective treatment ▪ Resolution by 2 yr age
Normal Motor Activities ▪ Roving, sometimes dysconjugate eye movements, with occasional nonsustained nystagmoid jerks at the extremes of horizontal movement ▪ Sucking, puckering – NO ocular fixation or deviation ▪ While - Asleep ▪ Fragmentary myoclonic jerks (may be multiple) ▪ Isolated, generalized myoclonic jerk as infant wakes from sleep
7. Etiology Hypoxic-ischemic encephalopathy Structural brain lesions Central nervous system (CNS) or systemic infections Metabolic disturbances Neonatal onset epilepsies and ▪ (According to a recent multicentre study - EEG seizures were confirmed 35%. Most common cause was hypoxic- ischaemic encephalopathy 59%, followed by metabolic/genetic disorders 21% and stroke 13%)
a. Hypoxic Ischemic Encephalopathy Most common cause Presence of diagnostic cues With short, frequent and refractory episodes >50% - have subclinical seizures Treatment is urgent & complicated Can cause status in 15% term babies Therapeutic hypothermia - ↓ Burden of seizures
b. Ischemic Stroke ▪ 2ND Most common cause ▪ Usually a well appearing neonate ▪ Diagnosis missed if seizure missed ▪ Risk factors - trauma, congenital heart disease, coagulopathy and metabolic disturbances ▪ Cerebral sinus venous thrombosis ▪ diffuse and focal neurologic deficit ▪ Seizure in 1 in 8000 cases
c. Intracranial Hemorrhage ▪ 10 – 15% ▪ Instrumentation, Breech, Large for gestation ▪ Well appearing Neonates ▪ Subduaral – Falx tears
▪ Preterms Neonates– ▪ IVH/GM ▪ Persistent tonic ▪ b/w 3-7 days of life ▪ Poor outcome ▪ First 3 days in GM and Severe IVH • Term Neonates 1. Subarachnoid hemorrhage • infant delivered vaginally. • second day focal seizure • resolve rapidly • good prognosis. 2. Subdural hematomas • a/w trauma and cerebral contusion. • Focal seizures • First 2 days
d. INFECTIONS ▪ 4 % of total ▪ Term = Preterms ▪ Acquired Prenatally – ▪ Intra Uterine Infections – TORCH ▪ Microcephaly; poor intrauterine growth; prematurity; and skin, ophthalmic, and systemic findings ▪ Acquire postnatally – ▪ Meningitis – Bacterial / Viral / Fungal ▪ Associated clinical features
Acquired Prenatally ▪ TORCH Infections ▪ Toxoplasmosis, rubella and CMV – ▪ Seizures as sole manifestation ▪ Occur in first 3 days in the neonatal period ▪ Specific diagnostic clues ▪ HSV & Enterovirus causing encephalitis ▪ HSV – Seizure after 7 days
HSV ▪ CNS Involvement - 57%,Disseminated - 22%, SEM – Rare ▪ type 2 HSV – acquired during delivery ▪ Fetal scalp monitoring - a risk factor ▪ Neuroimaging - diffuse brain abnormalities ▪ In case of high suspicion - Empirical acyclovir therapy ASAP
Acquired Postnatally ▪ Bacterial meningitis - seizures later in the first post natal week ▪ Group B streptococci, listeria, Escherichia coli and other GM-
e. Structural malformation ▪ 4 - 5 % ▪ Most are seizure free in neonatal period ▪ Outcome – based on type & severity of malformation ▪ Seizures often refractory to medications ▪ Cerebral dysgenesis can cause seizures from the first day of life ▪ Examples - tuberous sclerosis, focal cortical dysplasia, hemimegalencephaly, lissencephaly, subcortical band heterotopia, periventricular nodular heterotopia, schizencephaly, and polymicrogyria
f. Transient Metabolic Disturbances ▪ 4 % - Transient disturbances ▪ Rapidly remediable conditions ▪ focus of the initial investigations 1. hypoglycemia 2. hypocalcemia 3. Hypomagnesemia (rare) ▪ 3% - Inborn error of metabolism
Hypoglycemia ▪ Most frequent in SGAs and IDMs ▪ Can be a part of other etiologies ▪ Symptoms of neuroglycopenia should prompt treatment ▪ Determinant for seizure probability – time elapsed ▪ Neurological symptoms commonly - jitteriness, stupor, hypotonia, apnea, and seizures. ▪ Treatment at <40 mg/dL <24 hours and <50 after 24 hours
Hypocalcemia ▪ Has two major peaks ▪ 1st Peak -DOL 2-3 LBWs, IDMs, IUGRs, Perinatal Asphyxia ▪ 2nd Peak- Late neonatal age in large, full-term ▪ Consumption of cow milk or wrong formula ▪ Hypomagnesemia is a frequent accompaniment ▪ a/w endocrinopathy (hypoparathyroidism) ▪ Jitteriness, muscle jerks, seizures, and rarely laryngospasm. ▪ Therapeutic response to IV calcium correlating with etiology
g. Inborn Errors of Metabolism ▪ 1-3% seizures, seizures may occur in virtually all IEM ▪ enzyme defect in the metabolic pathways and accumulation of toxic products ▪ initially appear well - placental clearance ▪ seizures > 2 to 3 days ▪ ↓Glucose, ↑pH,↑ ammonia are few of biochemical markers ▪ Diagnosis f/b counseling for later pregnancies ▪ Clues - family history of consanguinity, early sibling death along with organomegaly on examination
Cont. ▪ Presentation – ▪ Vomiting and anorexia or failure to feed ▪ Lethargy that can progress to coma ▪ Seizures ▪ Rapid, deep breathing that can progress to apnea ▪ Hypothermia ▪ Rhabdomyolysis ▪ Unexpected infant death
Amino acid or organic acid metabolism Defect ▪ Most common 1. Non-ketotic hyperglycinemia (Burst suppression) 2. Sulfite oxidase deficiency, 3. Multiple carboxylase deficiency, 4. Multiple acyl-coenzyme A dehydrogenase deficiency 5. Urea cycle defect ▪ Hyperammonemia or/and acidosis present ▪ glycine cleavage enzyme defect ▪ CSF glycine levels diagnostic. ▪ resolves spontaneously after ~6 weeks of age
Pyridoxine dependency ▪ Rare but treatable cause ▪ defect in the ALDH7A1/antiquitin gene ▪ Deficiency alpha amino-adipic semialdehyde (α-AASA) dehydrogenase ▪ Impact the metabolism of the neurotransmitters glutamate and GABA. ▪ Seizures present early, sometimes “in utero” ▪ seizure cessation and resolution of EEG abnormalities after IV Pyridoxine 100 mg is diagnostic.
Pyridoxamine phosphate oxidase deficiency (PNPO) ▪ Fetal seizures ▪ Encephalopathy as well as seizures in premature ▪ Treatment with pyridoxal-5 phosphate Folinic acid-responsive seizures ▪ Onset as early as the first hours of life ▪ Responsiveness to oral Folinic Acid 2-20 mg twice daily
h. Neonatal Epilepsy Syndromes ▪ Rare, accounting for about 1% of cases of seizures ▪ ILAE defines as “a complex of clinical features, signs, and symptoms that together define a distinctive, recognizable clinical disorder.” ▪ Major Epilepsy Syndromes With Onset in the Neonatal Period 1. Benign Familial Neonatal Epilepsy 2. Benign nonfamilial neonatal convulsions (fifth-day fits) 3. Early Myoclonic Epilepsy 4. Early Infantile Epileptic Encephalopathy (Ohtahara syndrome) 5. Malignant migrating partial seizures
Benign Familial Neonatal Epilepsy ▪ Otherwise well infants on DOL 2 or 3. ▪ Focal clonic or tonic (usually asymmetrical). ▪ Family history of seizures present ▪ Resolves usually within 6 months ▪ Abnormality of voltage-gated K channels, KCNQ2 & KCNQ3. ▪ Developmental outcome is normal ▪ 5% to 15% may have later non-febrile convulsions
Benign infantile neonatal seizures ▪ a/k/a “fifth day fits” ▪ suddenly on DOL 4 to 6. ▪ frequent seizures  status epilepticus. ▪ Seizures are focal clonic often with apnea ▪ Seizures resolves within 2 weeks. The etiology is unknown.
Early myoclonic epilepsy (EME) ▪ first few days of life ▪ focal motor seizures and myoclonus ▪ seizures are very refractory to medications. ▪ EEG - burst-suppression pattern - often exacerbated by sleep. ▪ Syndrome associated with underlying metabolic disorders ▪ Severely affected development
Early infantile epileptic encephalopathy ▪ a/k/a Ohtahara syndrome ▪ Early onset & refractory Seizures ▪ tonic spasms along with focal motor seizures. ▪ Burst-suppression pattern on EEG ▪ Brain structural lesions usually associated . ▪ Developmental prognosis poor ▪ Chaotic epileptiform pattern known as hypsarrhythmia on EEG
Malignant migrating partial seizures in infancy ▪ a/k/a Coppola syndrome ▪ Present from 1st to 10th month of age. ▪ Aggressively escalating Focal motor seizures ▪ Highly refractory to anticonvulsant medications. ▪ Developmental status is acutely affected ▪ Poor prognosis for normal outcome ▪ Etiology is unknown
Time Of Onset and Likely Etiology Age of Onset Likely Etiology <24 hrs HIE, Severe Birth Trauma, Congenital CNS Anomalies, Pyridoxine Dependency, Hypoglycaemia 24 – 48 hrs All the above + milder birth trauma, hypocalcaemia, hypomagnesaemia, infarcts, some IEMs <48 – 72 hrs All the above + dys-electrolytaemias, sepsis, other Encephalopathies >72 hsr – 1 week All the above + benign neonatal seizures <1 – 4 weeks Late hypocalcaemia, sepsis, progressive hydrocephalus, cerebral dysgenesis, epileptic syndromes, herpes encephalitis, some I EMs
8. Approach to management ▪ expedited evaluation for the etiology is warranted ▪ Most are symptomatic manifestations of acute brain injury ▪ many require urgent, specific treatment Diagnosis History Examination Investigations
History History Birth History Antenatal history Feeding history Seizure history Family history
History Attempted to identify risk factors for seizures and clues to the underlying etiology Gestational and birth history – Anoxic injury nuchal cord or cord thrombosis, fetal heart rate decelerations, meconium, low Apgar scores, and placental abnormalities. Nature of the delivery operative vaginal delivery  ICH birth injury  macrosomia, maternal obesity, abnormal fetal lie
Maternal history miscarriages  congenital anomalies gestational diabetes  neonatal hypoglycemia STD or other infections neonatal Sepsis Illness during pregnancy e.g. maternal rash and fever could suggest in utero viral infection clotting or bleeding tendencies (neonatal stroke or hemorrhage).
Family history Early sibling death from unknown causes Consanguinity  inborn errors of metabolism) Family history of epilepsy particularly neonatal(BFNC)
Perinatal history ▪ PERINATAL ASPHYXIA as the commonest cause ▪ History of ▪ fetal distress, ▪ decreased fetal movements, ▪ instrumental delivery, ▪ need for resuscitation in the labor room, ▪ Apgar scores, and ▪ abnormal cord pH (<7) & base deficit (>10 mEq/L)
Seizure History ▪ Description Of The Seizure ▪ History ▪ Associated Eye Movements, ▪ Change In Color Of Skin (Mottling Or Cyanosis) ▪ Conscious Or Sleeping ▪ Day Of Life ▪ Day 0-3 Perinatal Asphyxia, ICH, Metabolic Causes, ▪ Day 4-7 Sepsis, Meningitis, Metabolic Causes, Developmental Defects
Feeding history ▪ Inborn Errors Of Metabolism ▪ Lethargy, poor activity, drowsiness, and vomiting after initiation of breast-feeding ▪ Top Feeding With Cow’s Milk ▪ Late onset hypocalcemia considered
Examination Vital signs: Heart rate, respiration, blood pressure, capillary refill time and temperature General examination: Gestation, birth weight, and weight for age  seizures in a term ‘well baby’ or in large for date baby may be different presence of any obvious malformations or dysmorphic features.
Systemic examination CNS : ▪ Bulging fontanel  meningitis or intracranial haemorrhage ▪ Neurological examination  ▪ assessment of consciousness (alert/drowsy/comatose) ▪ tone (hypotonia or hypertonia), and ▪ Fundus examination for chorioretinitis. Other systems ▪ Organomegaly or an abnormal urine odor may be suggestive of IEM ▪ Skin neuro-cutaneous markers (e.g. hypopigmented macules or ash- leaf spot in Tuberous sclerosis.)
Investigations ▪ Essential Investigations 1. Blood sugar, 2. Serum sodium and calcium, 3. Cerebrospinal fluid (csf) examination, 4. Cranial ultrasound (us), and 5. Electroencephalography (eeg).
Additional Investigations ▪ Considered in neonates who do not responding to first line antiepileptics or neonates with specific features. ▪ Neuroimaging (ct, mri), ▪ Screen for congenital infections (TORCH) ▪ Screen for inborn errors of metabolism ▪ An ARTERIAL BLOOD GAS should be performed if IEM is strongly suspected
Neuroimaging 1. NEUROSONOGRAPHY ▪ Excellent bedside tool for detection of intraventricular and parenchymal hemorrhage. (But not SAH & SDH) ▪ done in all infants with seizures. 2. CT scan ▪ Should generally be avoided ▪ 2nd tier investigation ▪ subarachnoid hemorrhage and developmental malformations
▪ Magnetic resonance imaging (MRI) ▪ all neonates with seizures to evaluate ▪ Useful in hypoxic-ischemic injury, ICH , Stroke, brain malformations. ▪ MR angiography  ischemic stroke or vascular malformation ▪ MR venography  venous sinus thrombosis ▪ MR spectroscopy  evaluate metabolites like ▪ glycine (nonketotic hyperglycinemia), ▪ lactate (mitochondrial disorders), or ▪ loss of creatine (disorder of brain creatine metabolism)
EEG ▪ To determine the risk and presence of seizures ▪ Seizure is defined as abnormal EEG pattern which evolves, is of >2 microvolt amplitude, and has a duration of ≥10 seconds ▪ Video EEG monitoring — The gold standard for neonatal seizure diagnosis is multi-channel video EEG monitoring ▪ EEG should be performed for at least one hour. ▪ Background abnormality in both term and preterm high risk for neurological sequelae. ▪ emphasis on continuous EEG monitoring to aid in management of seizures in newborns.
▪ excess of sharp waves nonspecific indicator of encephalopathy. ▪ Bursts of repetitive or short, stereotyped evolving rhythmic bursts of sharp waves  increased seizure risk ▪ Evolving rhythmic discharges longer than 10 seconds seizures
Amplitude-integrated EEG (aEEG) ▪ widespread use at the bedside ▪ reduced number of electrodes single channel (2 electrodes) or dual-channel (4 electrodes) EEG tracing ▪ Final display showing several hours of aEEG data on a single screen generated. ▪ Electrographic seizures are characterized ▪ by upward arches
Management ▪ Who to treat ▪ Identify first  gold standard, conventional video EEG, or, limited channel aEEG ▪ potential adverse effects of seizures on ventilatory function, circulation, cerebral metabolism, and subsequent brain development, considered ▪ repeated seizures should be stopped ▪ World Health Organization recommended treatment of all clinical and electrographic seizures ▪ goal of therapy is the elimination of electrical seizure activity
Stabilization 1. Thermoneutral environment 2. ensure airway, breathing, and circulation (TABC). 3. Oxygen should be started, IV access should be secured, and blood should be collected for glucose and other investigations. 4. A brief relevant history should be obtained and quick clinical examination should be performed. 5. All this should not require more than 2-5 minutes
Easily correctable causes ▪ Correction of hypoglycemia hypocalcemia and hypomagnesemia : ▪ Hypoglycemia ▪ 2 mL/kg of 10% dextrose bolus injection followed by a continuous infusion ▪ hypoglycemia - treated / excluded ▪ Give 2 mL/kg of 10% calcium gluconate IV over 10 minutes under strict cardiac monitoring. ▪ If hypocalcemia ▪ Give additional calcium gluconate at 8 mL/kg/d for 3 days. ▪ If seizures continue despite hypocalcemia, 0.25 mL/kg of 50% magnesium sulfate should be given intramuscularly.
Ref.Uptodate 2021
Anti-epileptic drug therapy (AED) ▪ Even in a single clinical seizure and facilities for continuous EEG monitoring not available. ▪ Eliminating all electrical seizure activity should be the goal of AED therapy ▪ seizures persist even after metabolic correction
PHENOBARBITONE ▪ Drug of choice in neonatal seizures ▪ Loading -20 mg/kg/IV slowly over 20 minutes ▪ seizures persist additional doses of phenobarbitone 10 mg/kg every 20-30 minutes until a total dose of 40 mg/kg ▪ maintenance dose - 3-5 mg/kg/day in 1-2 divided doses, started 12 hours after the loading dose.
PHENYTOIN ▪ maximal dose of phenobarbitone failed ▪ or appearance of adverse effects like respiratory depression, hypotension, Bradycardia ▪ Loading Dose is 20 mg/kg IV ▪ Only NS dilution ▪ refractory seizures  repeat dose 10 mg/kg ▪ maintenance dose 3-5 mg/kg/d in 2-4 divided doses.
BENZODIAZEPINES ▪ may be required in up to 15-20% of neonatal seizures. ▪ lorazepam and midazolam. ▪ Diazepam - prolonged sedative effect, narrow therapeutic index, sodium benzoate as a preservative. ▪ Lorazepam - longer duration of action and less adverse effects ▪ Midazolam is faster acting than lorazepam and may be administered as an infusion. ▪ It causes less respiratory depression and sedation than lorazepam.
▪ The doses of these drugs are given below: ▪ 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 0.4mg/kg/hour.
LEVETIRACETAM ▪ Benign side effect profile, and limited interactions ▪ Loading doses vary from 10 to 20 mg/kg to as high as 40 to 50 mg/kg. ▪ Maintenance doses 10 to 80 mg/kg/day with most providers starting at 20 mg/kg/day, whereas others suggest 40 mg/kg/day. ▪ Although twice daily dosing is usual, three-times daily dosing has been suggested.
Antiepileptic drugs for refractory seizures LIDOCAINE: ▪ It is usually administered as a bolus dose of 4 mg/kg IV followed by an infusion rate of 2 mg/kg/hr. ▪ Adverse effects include arrhythmias, hypotension, and seizures. ▪ It should not be administered with phenytoin. PARALDEHYDE: ▪ A dose of 0.1-0.2 mL/kg/dose may be given IM ▪ 0.3 mL/kg/dose mixed with coconut oil in 3:1 may be used by per rectal route ▪ pulmonary hemorrhage, pulmonary edema, hypotension, and liver injury.
▪ SODIUM VALPROATE: ▪ Per rectal or IV route may be used in acute condition. ▪ The dose is 20-25 mg/kg/d followed by 5-10 mg/kg every 12 hours. ▪ Used with caution in newborns given the uncertain risk of hepatotoxicity following its use. ▪ VIGABATRIN: ▪ It has been used in neonates with infantile spasms. ▪ The dose is 50mg/kg/day.
▪ TOPIRAMATE: ▪ potential neuroprotective effect against injury caused by seizures. ▪ For refractory infantile spasms in infants. ▪ initial and maintenance doses of approximately 3 mg/kg
Other therapies ▪ PYRIDOXINE: ▪ A therapeutic trial of pyridoxine is reserved as a last resort in refractory seizures. ▪ Intravenous route is the preferred method ▪ intramuscular (IM) route be used ▪ hypotension and apnea can occur.
▪ EXCHANGE TRANSFUSION: ▪ Indicated in ▪ life-threatening metabolic disorders, ▪ accidental injection of local anesthetic, ▪ trans-placental transfer of maternal drugs (e.g. chlorpropamide) ▪ bilirubin encephalopathy.
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.
When to discontinue AED ▪ no specific guidelines ▪ Discontinue phenobarbitone as early as possible ▪ try to discontinue all medications 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 one 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, phenobarbitone is 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
Take home message ▪ Neonatal seizures are common in both the preterm and term born infant. ▪ • Electroencephalography is essential to diagnose and treat neonatal seizures because of the frequency with which clinical signs are misinterpreted as seizures OR seizures or status epilepticus can be clinically silent. ▪ • Seizures are a sign of neurologic dysfunction from a variety of etiologies, including hypoxic ischemia, such as stroke, and metabolic and infectious etiologies. Investigation to determine the etiology of neonatal seizures is necessary and often requires blood and cerebrospinal fluid sampling, electroencephalography, and magnetic resonance imaging. ▪ • Therapy for neonatal seizures is important to limit both the short-term physiologic impact of the seizures and the potential contribution to long-term outcomes. Phenobarbitol remains first-line anticonvulsant therapy. ▪ • Length of time with anticonvulsant therapy for neonatal seizures remains unknown, although more recent trends are to minimize exposure to anticonvulsants unless a protracted risk for seizures persists
REFERENCES 1. Cloherty and starks manual of neonatal care 8th edition. 2. Aiims protocols in neonatology 3. Avery’s diseases of the newborn. -- 9th ed. / [Edited by] christine A. Gleason, sherin U. Devask 4. Fanaroff and martin’s neonatal-perinatal medicine : diseases of the fetus and infant / [edited by] richard J. Martin, avroy A. Fanaroff, michele C. Walsh.—10th edition.
Thank You

More Related Content

PPT
Neonatal seizure
byhanaa adnan
 
PPTX
Neonatal seizures
byRanjithkumar Kondapaka
 
PPTX
Neonatal seizures
byKannan Chinnasamy
 
PPTX
Neonatal seizures
byAzad Haleem
 
PPTX
Neonatal seizures
byGurajala venkatesh
 
PPT
seminar on neonatal seizure
byDr. Habibur Rahim
 
PPTX
Neonatal seizure
byDrChandan Barnwal
 
PPTX
Neonatal seizures, dr amit vatkar, pediatric neurologist
byDr Amit Vatkar
 
Neonatal seizure
byhanaa adnan
 
Neonatal seizures
byRanjithkumar Kondapaka
 
Neonatal seizures
byKannan Chinnasamy
 
Neonatal seizures
byAzad Haleem
 
Neonatal seizures
byGurajala venkatesh
 
seminar on neonatal seizure
byDr. Habibur Rahim
 
Neonatal seizure
byDrChandan Barnwal
 
Neonatal seizures, dr amit vatkar, pediatric neurologist
byDr Amit Vatkar
 

What's hot

PPTX
Hypoxic Ischemic Encephalopathy
byYohaimi Cosme Ayala
 
PPTX
Neonatal seizures recent advances
bymandar haval
 
PPTX
Seizure Disorders in Children
byCSN Vittal
 
PPTX
Pediatric epilepsy syndromes
byNeurologyKota
 
PPT
Perinatal asphyxia
byTai Alakawy
 
PDF
Childhood seizure and its management
byTauhid Iqbali
 
PDF
Therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy
byMCH-org-ua
 
PPTX
NEONATAL SEIZURES
byDrhunny88
 
PPTX
Hypoxic ischemic encephalopathy
byDr.Mansoor Elahi
 
PPTX
Neonatal Hypoglycemia
byDavid Mendez
 
PPTX
Hie seminar
byDr Praman Kushwah
 
PPT
Pphn
byVarsha Shah
 
PPTX
Seizures in children
byAnusha kattula
 
PPTX
Birth asphyxia neurpathology
byChandan Gowda
 
PPS
pediatric Sleep disorders
byMarwa Elhady
 
PPTX
Neonatal seizures paeds
byfarranajwa
 
PPTX
Status epilepticus IN CHILDREN
byVirendra Hindustani
 
PPTX
Epilepsy in children by Dr.Shanti
byDr. Rubz
 
PPTX
Pediatric status epilepticus
byPramod Krishnan
 
PPT
hypoxic ischemic encephalopathy
byDr. Saad Saleh Al Ani
 
Hypoxic Ischemic Encephalopathy
byYohaimi Cosme Ayala
 
Neonatal seizures recent advances
bymandar haval
 
Seizure Disorders in Children
byCSN Vittal
 
Pediatric epilepsy syndromes
byNeurologyKota
 
Perinatal asphyxia
byTai Alakawy
 
Childhood seizure and its management
byTauhid Iqbali
 
Therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy
byMCH-org-ua
 
NEONATAL SEIZURES
byDrhunny88
 
Hypoxic ischemic encephalopathy
byDr.Mansoor Elahi
 
Neonatal Hypoglycemia
byDavid Mendez
 
Hie seminar
byDr Praman Kushwah
 
Pphn
byVarsha Shah
 
Seizures in children
byAnusha kattula
 
Birth asphyxia neurpathology
byChandan Gowda
 
pediatric Sleep disorders
byMarwa Elhady
 
Neonatal seizures paeds
byfarranajwa
 
Status epilepticus IN CHILDREN
byVirendra Hindustani
 
Epilepsy in children by Dr.Shanti
byDr. Rubz
 
Pediatric status epilepticus
byPramod Krishnan
 
hypoxic ischemic encephalopathy
byDr. Saad Saleh Al Ani
 

Similar to Neonatal seizure by dr praman

PPTX
PEDIA Neonatal seizures- Dr keerthana.pptx
bykmpadmavathiteacher
 
PPTX
Neonatal seizures NS in peadiatric population
byPooja Khose
 
PPTX
Presentation on Neontal seizures and its types , management and seizure mimics
byjoghikamal786
 
PPTX
Neonatal seziure
byasmaaabdelwakeel
 
PPTX
neonatal seizures IAP.pps.pptx presentation
bykrishnagrvpaed
 
PPTX
Neonatal seizures by Dr. David Maher
byShaju Edamana
 
PPTX
neontal_seizures.pptx
bysunilbaily1
 
PDF
Neonatal-Seizures diagnosis and management
byFelixBoamah3
 
PPTX
Neonatal seizures presentation
byNur Aisyah
 
PPTX
Neonatal seizures
byThe Medical Post
 
PPTX
Neonatal seizures
byCSN Vittal
 
PPTX
Convulsions in the neonate. Paediatricnursing.pptx
byJustinMutua
 
PPT
Neonatalseizure 150209133740-conversion-gate01
byBelal Elsais
 
PPTX
neonatal seizures and different modalities of treatment
byRakshaRao18
 
PPTX
Qavi ppt epileptic syndromes of neonate and infancy (2)
byqavi786
 
PPTX
neonatal seizures.presentation slides ptx
byyakemichael
 
PPT
1479279345-dr.m.mirzarahimi-neonatal-seizures.ppt
byCharutaKunjeer1
 
PPTX
PRESENTATION 5 CONVULSION.pptx1111111111
bysamuellamaryk
 
PDF
Neonatal convulsions , presentation about neunatal convulsions
byazozksa76
 
PPTX
Neonatal Seizures.pptx
byAmsaluSamuel1
 
PEDIA Neonatal seizures- Dr keerthana.pptx
bykmpadmavathiteacher
 
Neonatal seizures NS in peadiatric population
byPooja Khose
 
Presentation on Neontal seizures and its types , management and seizure mimics
byjoghikamal786
 
Neonatal seziure
byasmaaabdelwakeel
 
neonatal seizures IAP.pps.pptx presentation
bykrishnagrvpaed
 
Neonatal seizures by Dr. David Maher
byShaju Edamana
 
neontal_seizures.pptx
bysunilbaily1
 
Neonatal-Seizures diagnosis and management
byFelixBoamah3
 
Neonatal seizures presentation
byNur Aisyah
 
Neonatal seizures
byThe Medical Post
 
Neonatal seizures
byCSN Vittal
 
Convulsions in the neonate. Paediatricnursing.pptx
byJustinMutua
 
Neonatalseizure 150209133740-conversion-gate01
byBelal Elsais
 
neonatal seizures and different modalities of treatment
byRakshaRao18
 
Qavi ppt epileptic syndromes of neonate and infancy (2)
byqavi786
 
neonatal seizures.presentation slides ptx
byyakemichael
 
1479279345-dr.m.mirzarahimi-neonatal-seizures.ppt
byCharutaKunjeer1
 
PRESENTATION 5 CONVULSION.pptx1111111111
bysamuellamaryk
 
Neonatal convulsions , presentation about neunatal convulsions
byazozksa76
 
Neonatal Seizures.pptx
byAmsaluSamuel1
 

More from Dr Praman Kushwah

PPT
Antibiotic stewardship by dr praman
byDr Praman Kushwah
 
PPTX
Total parenteral nutrition in the nicu Total parenteral nutrition in the nicu
byDr Praman Kushwah
 
PPTX
Cytogenetics dr majaz Cytogenetics
byDr Praman Kushwah
 
PPTX
Infant of diabetic mother
byDr Praman Kushwah
 
PPTX
Steroids in neonatology Steroids in neonatology
byDr Praman Kushwah
 
PPTX
Intrauterine growth restriction Intrauterine growth restriction
byDr Praman Kushwah
 
PPTX
Intrapartum assessment of fetal well being (1)
byDr Praman Kushwah
 
PPTX
Aneuploidy screening Aneuploidy screening
byDr Praman Kushwah
 
PPTX
Thyroid disorders in neonate radha
byDr Praman Kushwah
 
PPTX
Pulmonary graphics radha
byDr Praman Kushwah
 
PPTX
Fluid homeostasis Fluid homeostasis
byDr Praman Kushwah
 
PPTX
Rop hearing
byDr Praman Kushwah
 
PPTX
Understanding mri in neonate
byDr Praman Kushwah
 
PPTX
Growh charts by praman
byDr Praman Kushwah
 
PPTX
Neurodevelopmental follow up
byDr Praman Kushwah
 
PPTX
Pain scales
byDr Praman Kushwah
 
PPTX
Pathophysiology of preterm labor
byDr Praman Kushwah
 
PPTX
Developmental supportive care in nicu
byDr Praman Kushwah
 
PPTX
approach to infant with Hydrops fetalis
byDr Praman Kushwah
 
PPTX
Rh isoimmunisation
byDr Praman Kushwah
 
Antibiotic stewardship by dr praman
byDr Praman Kushwah
 
Total parenteral nutrition in the nicu Total parenteral nutrition in the nicu
byDr Praman Kushwah
 
Cytogenetics dr majaz Cytogenetics
byDr Praman Kushwah
 
Infant of diabetic mother
byDr Praman Kushwah
 
Steroids in neonatology Steroids in neonatology
byDr Praman Kushwah
 
Intrauterine growth restriction Intrauterine growth restriction
byDr Praman Kushwah
 
Intrapartum assessment of fetal well being (1)
byDr Praman Kushwah
 
Aneuploidy screening Aneuploidy screening
byDr Praman Kushwah
 
Thyroid disorders in neonate radha
byDr Praman Kushwah
 
Pulmonary graphics radha
byDr Praman Kushwah
 
Fluid homeostasis Fluid homeostasis
byDr Praman Kushwah
 
Rop hearing
byDr Praman Kushwah
 
Understanding mri in neonate
byDr Praman Kushwah
 
Growh charts by praman
byDr Praman Kushwah
 
Neurodevelopmental follow up
byDr Praman Kushwah
 
Pain scales
byDr Praman Kushwah
 
Pathophysiology of preterm labor
byDr Praman Kushwah
 
Developmental supportive care in nicu
byDr Praman Kushwah
 
approach to infant with Hydrops fetalis
byDr Praman Kushwah
 
Rh isoimmunisation
byDr Praman Kushwah
 

Recently uploaded

PDF
Vaccinations in the First Year: Timing, Myths, and Why They Matter
byDr. Allen Cherer
 
PPTX
GS - Tamaka Shwasa Chikitsa -Dr Manasa M .pptx
byDr Manasa Manjunath
 
PPTX
Social pharmacy :Nutrition and Health programme
byRupali kote
 
PPTX
Foot and ankle examination for ortho residents
bysibasishBrahma1
 
PPTX
Basement membrane zone .pptx
bySaiDeshmukh23
 
PPTX
CASE_PRESENTATION_ON_subdural_hematoma(SDH)[1 FINAL PPT]-1.pptx
byAshokKumar365986
 
PPTX
Hormonal IUS (Mirena®) Common Myths.pptx
byWafaa Benjamin
 
PDF
The Basics of EHR - What Does EHR Stand For.pdf
byThinkitive Inc
 
PPTX
NDIS Accommodation in Redbank Plains.pptx
bysuperiorqualitycare
 
PPT
Anatomy of oesophagus physiology of the esophagus first attempt.ppt
byheadent
 
PPTX
Mental Status Examination | B.Sc Nursing 5th Semester | Mental Health Nursing I
bydhananjaydongare5
 
PPTX
opthalmology Red Eye - medicine and healthcare
byrenitanair2000
 
PPTX
Scoliosis ppt- Dr Chandresh Choudhary resident
byDr Chandresh Choudhary
 
PDF
Enhancing the Patient Journey in CIDP: Strategies for Improved Detection and ...
byi3 Health
 
PPTX
An Age Reversal Update -- Bill Faloon --
byChurch Of Perpetual Life
 
PPTX
1 Digestion of carbohydrates -digestion, absorption, clinical significance
byProf Viyatprajna Acharya
 
PPTX
chronic bronchitis.pptx By gokulakrishnan
byGOKULAKRISHNAN JANARTHANAN
 
PDF
appendix mucinous tumores.pdf jkljkljkljlkjkljlkjlk
byssuser947a1f
 
PPTX
A War on Heart Attacks -- Joel Kahn, MD, FACC
byChurch Of Perpetual Life
 
PPTX
PCOS ,PCOS MANAGEMENT, WEIGHT LOSS,INFERTILITY IN PCOS
bymukeshkumar559904
 
Vaccinations in the First Year: Timing, Myths, and Why They Matter
byDr. Allen Cherer
 
GS - Tamaka Shwasa Chikitsa -Dr Manasa M .pptx
byDr Manasa Manjunath
 
Social pharmacy :Nutrition and Health programme
byRupali kote
 
Foot and ankle examination for ortho residents
bysibasishBrahma1
 
Basement membrane zone .pptx
bySaiDeshmukh23
 
CASE_PRESENTATION_ON_subdural_hematoma(SDH)[1 FINAL PPT]-1.pptx
byAshokKumar365986
 
Hormonal IUS (Mirena®) Common Myths.pptx
byWafaa Benjamin
 
The Basics of EHR - What Does EHR Stand For.pdf
byThinkitive Inc
 
NDIS Accommodation in Redbank Plains.pptx
bysuperiorqualitycare
 
Anatomy of oesophagus physiology of the esophagus first attempt.ppt
byheadent
 
Mental Status Examination | B.Sc Nursing 5th Semester | Mental Health Nursing I
bydhananjaydongare5
 
opthalmology Red Eye - medicine and healthcare
byrenitanair2000
 
Scoliosis ppt- Dr Chandresh Choudhary resident
byDr Chandresh Choudhary
 
Enhancing the Patient Journey in CIDP: Strategies for Improved Detection and ...
byi3 Health
 
An Age Reversal Update -- Bill Faloon --
byChurch Of Perpetual Life
 
1 Digestion of carbohydrates -digestion, absorption, clinical significance
byProf Viyatprajna Acharya
 
chronic bronchitis.pptx By gokulakrishnan
byGOKULAKRISHNAN JANARTHANAN
 
appendix mucinous tumores.pdf jkljkljkljlkjkljlkjlk
byssuser947a1f
 
A War on Heart Attacks -- Joel Kahn, MD, FACC
byChurch Of Perpetual Life
 
PCOS ,PCOS MANAGEMENT, WEIGHT LOSS,INFERTILITY IN PCOS
bymukeshkumar559904
 

Neonatal seizure by dr praman

  • 1.
  • 2.
    OVERVIEW ▪ Epidemiology ▪ Definition ▪Pathogphysiology ▪ Classification ▪ Non seizure events ▪ Etiology ▪ Approach to management ▪ Management ▪ Prognosis
  • 3.
    1. INTRODUCTION ▪ REDALERT ▪ SECONDARY BRAIN INJURY ▪ FOCAL OR MULTIFOCAL : SINGLE HEMISPHERE ▪ MAJORITY SUBCLINICAL OR SUBTLE ▪ LESS SEIZURE THRESHOLD BUT BETTER PROGNOSIS.
  • 4.
    2. Epidemiology ▪ Incidence ▪10.3 per 1000 live- births (NNPD) ▪ 58 per 1000 live births in VLBWs ▪ 1 – 3.5 per 1000 live births in Terms
  • 5.
    3. DEFINITION Abnormally excessiveor synchronous neuronal activity in the brain causing paroxysmal disturbances in neurological function manifesting clinically as alteration in motor, behavioral and/or autonomic functions CAN ANYONE DEFINE EPILEPSY ?
  • 6.
    4. Pathophysiology  Imbalancebetween neurotransmitters
  • 7.
    Incresed Seizure Susceptibility •↑excitatory neurotransmitters (glutamate) • ↓inhibitory neurotransmitters (GABA) • GABA acting as excitatory neurotransmitter ATP-dependent Na-K pump Failure NMDA AMPA
  • 9.
    ▪ Onset isfocal /multifocal, spread within one hemisphere only ▪ Immature mylenation of cortical efferent systems & commissure. ▪ Advanced Cortical development in Limbic system - Subtle
  • 10.
    Energy dependent ion pumping DecreasedATP & Phosphocreatine Stimulation of glycolysis and ↑ Lactate Vasodilation & ↑ blood supply SEIZURE EPISODE Incresed blood pressure Increased Cerebral blood flow This fall in brain glucose concentration and rise in brain lactate are directly reminiscent of a hypoxic- ischemic brain insult
  • 12.
    Time Course ofEpileptogenesis ▪ Seconds to minutes – gene induction and translation of receptor and ion-channel proteins ▪ hours to days - neuronal death, inflammation, and altered transcriptional regulation ▪ weeks to months - mossy fiber sprouting, gliosis, neurogenesis
  • 13.
    5. Classification ▪ Typesof Neonatal seizure ▪ Clinical Seizure ▪ Electro - clinical Seizure ▪ EEG - Only
  • 14.
  • 15.
    Subtle ▪ Most commontype ▪ Preterms > Terms ▪ Paroxysmal & Repetitive ▪ Oral-buccal-lingual movements ▪ Progression movements ▪ EEG+/- (Tonic eye deviation – a/w EEG)
  • 17.
    Clonic ▪ Repetitive, rhythmiccontractions of specific muscle groups ▪ Slow rate of repetition ▪ Close relationship to the EEG seizure pattern ▪ Mimics - jitteriness, tremulousness, and myoclonus FOCAL MULTIFOCAL Face , trunk, extremity on one side of body Several body parts, often migrating () usually focal neuropathology e.g. infarction Non jacksonian march
  • 19.
    Tonic ▪ Hallmark ofseveral neonatal epilepsy syndromes ▪ sustained flexion or extension of muscle groups ▪ Sustained, but transient, asymmetrical posturing ▪ Tonic deviation of the eyes (upward) ▪ Poor prognosis, a/w IVH & Kernicterus FOCAL GENERALIZED Sustained, asymmetrical Posturing Decerebrate/decorticate like posturing Mostly EEG discharges + 15% EEG +
  • 20.
    Myoclonic ▪ Contractions ofmuscle groups of well-defined regions ▪ rapid, isolated jerk or may be repetitive ▪ Rate of recurrence may be slow, irregular, or erratic ▪ EEG discharges absent. ▪ Types : ▪ Focal – Typically upper extremity, flexor groups. ▪ Multifocal – involving several body parts , asynchronous twitching. ▪ Generalized - bilateral, symmetric jerking of all extremities and/or muscles of the trunk and neck. EEG +,
  • 22.
    EEG Only Seizures ▪High incidence ▪ Similar duration and encephalopathy degree to electroclinical ▪ electromechanical dissociation ▪ electroclinical EEG only ▪ caudal-to-rostral maturation of cl- transporters ▪ brainstem & spinal cord motor system chloride levels decreases before cortical neuronal levels.
  • 23.
    Autonomic Seizuers ▪ Clinicalchanges related to the autonomic nervous system ▪ Apneas often associated with tachycardia ▪ Alterations ▪ Heart rate – Tachy/Brady ▪ Respiration – Tachy / Brady ▪ Blood pressure ▪ Flushing ▪ Salivation ▪ Pupil dilatation
  • 24.
    6. Non-Seizure Events ▪Absence of EEG change ▪ Provoked by stimulation ▪ Suppressed by restraining ▪ No autonomic disturbances ▪ No Head/ Eye deviation ▪ Temporal/Spatial summation - ↑ Intensity ▪ Few benign, but few needs evaluation ▪ Not All That Shakes Is A Seizure
  • 25.
    ▪Apnea - ▪ Pausein breathing for greater than 20 seconds ▪ Premature baby ▪ During active sleep ▪ Brainstem immaturity ▪ If (mostly term) accompanied with eye closure /opening, eye deviation, mouth movement, hypertension, tachycardia – Seizure
  • 26.
    ▪ Jitteriness ▪ VeryCommon ▪ Excessive response to stimulation ▪ Back-and-forth oscillation , Same amplitude & frequency ▪ Hypocalcemia, hypoglycemia, and hypoxic- ischemic encephalopathy ▪ Head or eye deviation during an episode → seizure
  • 27.
    ▪ Benign neonatalsleep myoclonus ▪ during sleep – NREM ▪ jerks are typically bilateral, symmetric ▪ can be stopped by rousing the infant ▪ does not involve the face ▪ Normal neurologically ▪ BZDs provokes / exacerbates ▪ Spontaneous resolution ~2 mo
  • 28.
    ▪ Hyperekplexia (startledisease) ▪ Congenital stiff-man syndrome ▪ Startle & sustained tonic spasms response to stimuli ▪ Nocturnal myoclonus. ▪ “minor”  excessive startle ▪ “major”  stiffness while awake, nocturnal myoclonus, risk of SIDS ▪ Glycine receptor gene mutations ▪ Clonazepam - effective treatment ▪ Resolution by 2 yr age
  • 29.
    Normal Motor Activities ▪Roving, sometimes dysconjugate eye movements, with occasional nonsustained nystagmoid jerks at the extremes of horizontal movement ▪ Sucking, puckering – NO ocular fixation or deviation ▪ While - Asleep ▪ Fragmentary myoclonic jerks (may be multiple) ▪ Isolated, generalized myoclonic jerk as infant wakes from sleep
  • 30.
    7. Etiology Hypoxic-ischemic encephalopathy Structuralbrain lesions Central nervous system (CNS) or systemic infections Metabolic disturbances Neonatal onset epilepsies and ▪ (According to a recent multicentre study - EEG seizures were confirmed 35%. Most common cause was hypoxic- ischaemic encephalopathy 59%, followed by metabolic/genetic disorders 21% and stroke 13%)
  • 33.
    a. Hypoxic IschemicEncephalopathy Most common cause Presence of diagnostic cues With short, frequent and refractory episodes >50% - have subclinical seizures Treatment is urgent & complicated Can cause status in 15% term babies Therapeutic hypothermia - ↓ Burden of seizures
  • 34.
    b. Ischemic Stroke ▪2ND Most common cause ▪ Usually a well appearing neonate ▪ Diagnosis missed if seizure missed ▪ Risk factors - trauma, congenital heart disease, coagulopathy and metabolic disturbances ▪ Cerebral sinus venous thrombosis ▪ diffuse and focal neurologic deficit ▪ Seizure in 1 in 8000 cases
  • 36.
    c. Intracranial Hemorrhage ▪10 – 15% ▪ Instrumentation, Breech, Large for gestation ▪ Well appearing Neonates ▪ Subduaral – Falx tears
  • 39.
    ▪ Preterms Neonates– ▪IVH/GM ▪ Persistent tonic ▪ b/w 3-7 days of life ▪ Poor outcome ▪ First 3 days in GM and Severe IVH • Term Neonates 1. Subarachnoid hemorrhage • infant delivered vaginally. • second day focal seizure • resolve rapidly • good prognosis. 2. Subdural hematomas • a/w trauma and cerebral contusion. • Focal seizures • First 2 days
  • 40.
    d. INFECTIONS ▪ 4% of total ▪ Term = Preterms ▪ Acquired Prenatally – ▪ Intra Uterine Infections – TORCH ▪ Microcephaly; poor intrauterine growth; prematurity; and skin, ophthalmic, and systemic findings ▪ Acquire postnatally – ▪ Meningitis – Bacterial / Viral / Fungal ▪ Associated clinical features
  • 41.
    Acquired Prenatally ▪ TORCHInfections ▪ Toxoplasmosis, rubella and CMV – ▪ Seizures as sole manifestation ▪ Occur in first 3 days in the neonatal period ▪ Specific diagnostic clues ▪ HSV & Enterovirus causing encephalitis ▪ HSV – Seizure after 7 days
  • 42.
    HSV ▪ CNS Involvement- 57%,Disseminated - 22%, SEM – Rare ▪ type 2 HSV – acquired during delivery ▪ Fetal scalp monitoring - a risk factor ▪ Neuroimaging - diffuse brain abnormalities ▪ In case of high suspicion - Empirical acyclovir therapy ASAP
  • 43.
    Acquired Postnatally ▪ Bacterialmeningitis - seizures later in the first post natal week ▪ Group B streptococci, listeria, Escherichia coli and other GM-
  • 44.
    e. Structural malformation ▪4 - 5 % ▪ Most are seizure free in neonatal period ▪ Outcome – based on type & severity of malformation ▪ Seizures often refractory to medications ▪ Cerebral dysgenesis can cause seizures from the first day of life ▪ Examples - tuberous sclerosis, focal cortical dysplasia, hemimegalencephaly, lissencephaly, subcortical band heterotopia, periventricular nodular heterotopia, schizencephaly, and polymicrogyria
  • 45.
    f. Transient MetabolicDisturbances ▪ 4 % - Transient disturbances ▪ Rapidly remediable conditions ▪ focus of the initial investigations 1. hypoglycemia 2. hypocalcemia 3. Hypomagnesemia (rare) ▪ 3% - Inborn error of metabolism
  • 46.
    Hypoglycemia ▪ Most frequentin SGAs and IDMs ▪ Can be a part of other etiologies ▪ Symptoms of neuroglycopenia should prompt treatment ▪ Determinant for seizure probability – time elapsed ▪ Neurological symptoms commonly - jitteriness, stupor, hypotonia, apnea, and seizures. ▪ Treatment at <40 mg/dL <24 hours and <50 after 24 hours
  • 47.
    Hypocalcemia ▪ Has twomajor peaks ▪ 1st Peak -DOL 2-3 LBWs, IDMs, IUGRs, Perinatal Asphyxia ▪ 2nd Peak- Late neonatal age in large, full-term ▪ Consumption of cow milk or wrong formula ▪ Hypomagnesemia is a frequent accompaniment ▪ a/w endocrinopathy (hypoparathyroidism) ▪ Jitteriness, muscle jerks, seizures, and rarely laryngospasm. ▪ Therapeutic response to IV calcium correlating with etiology
  • 48.
    g. Inborn Errorsof Metabolism ▪ 1-3% seizures, seizures may occur in virtually all IEM ▪ enzyme defect in the metabolic pathways and accumulation of toxic products ▪ initially appear well - placental clearance ▪ seizures > 2 to 3 days ▪ ↓Glucose, ↑pH,↑ ammonia are few of biochemical markers ▪ Diagnosis f/b counseling for later pregnancies ▪ Clues - family history of consanguinity, early sibling death along with organomegaly on examination
  • 49.
    Cont. ▪ Presentation – ▪Vomiting and anorexia or failure to feed ▪ Lethargy that can progress to coma ▪ Seizures ▪ Rapid, deep breathing that can progress to apnea ▪ Hypothermia ▪ Rhabdomyolysis ▪ Unexpected infant death
  • 50.
    Amino acid ororganic acid metabolism Defect ▪ Most common 1. Non-ketotic hyperglycinemia (Burst suppression) 2. Sulfite oxidase deficiency, 3. Multiple carboxylase deficiency, 4. Multiple acyl-coenzyme A dehydrogenase deficiency 5. Urea cycle defect ▪ Hyperammonemia or/and acidosis present ▪ glycine cleavage enzyme defect ▪ CSF glycine levels diagnostic. ▪ resolves spontaneously after ~6 weeks of age
  • 51.
    Pyridoxine dependency ▪ Rarebut treatable cause ▪ defect in the ALDH7A1/antiquitin gene ▪ Deficiency alpha amino-adipic semialdehyde (α-AASA) dehydrogenase ▪ Impact the metabolism of the neurotransmitters glutamate and GABA. ▪ Seizures present early, sometimes “in utero” ▪ seizure cessation and resolution of EEG abnormalities after IV Pyridoxine 100 mg is diagnostic.
  • 52.
    Pyridoxamine phosphate oxidasedeficiency (PNPO) ▪ Fetal seizures ▪ Encephalopathy as well as seizures in premature ▪ Treatment with pyridoxal-5 phosphate Folinic acid-responsive seizures ▪ Onset as early as the first hours of life ▪ Responsiveness to oral Folinic Acid 2-20 mg twice daily
  • 53.
    h. Neonatal EpilepsySyndromes ▪ Rare, accounting for about 1% of cases of seizures ▪ ILAE defines as “a complex of clinical features, signs, and symptoms that together define a distinctive, recognizable clinical disorder.” ▪ Major Epilepsy Syndromes With Onset in the Neonatal Period 1. Benign Familial Neonatal Epilepsy 2. Benign nonfamilial neonatal convulsions (fifth-day fits) 3. Early Myoclonic Epilepsy 4. Early Infantile Epileptic Encephalopathy (Ohtahara syndrome) 5. Malignant migrating partial seizures
  • 54.
    Benign Familial NeonatalEpilepsy ▪ Otherwise well infants on DOL 2 or 3. ▪ Focal clonic or tonic (usually asymmetrical). ▪ Family history of seizures present ▪ Resolves usually within 6 months ▪ Abnormality of voltage-gated K channels, KCNQ2 & KCNQ3. ▪ Developmental outcome is normal ▪ 5% to 15% may have later non-febrile convulsions
  • 55.
    Benign infantile neonatalseizures ▪ a/k/a “fifth day fits” ▪ suddenly on DOL 4 to 6. ▪ frequent seizures  status epilepticus. ▪ Seizures are focal clonic often with apnea ▪ Seizures resolves within 2 weeks. The etiology is unknown.
  • 56.
    Early myoclonic epilepsy(EME) ▪ first few days of life ▪ focal motor seizures and myoclonus ▪ seizures are very refractory to medications. ▪ EEG - burst-suppression pattern - often exacerbated by sleep. ▪ Syndrome associated with underlying metabolic disorders ▪ Severely affected development
  • 57.
    Early infantile epilepticencephalopathy ▪ a/k/a Ohtahara syndrome ▪ Early onset & refractory Seizures ▪ tonic spasms along with focal motor seizures. ▪ Burst-suppression pattern on EEG ▪ Brain structural lesions usually associated . ▪ Developmental prognosis poor ▪ Chaotic epileptiform pattern known as hypsarrhythmia on EEG
  • 58.
    Malignant migrating partialseizures in infancy ▪ a/k/a Coppola syndrome ▪ Present from 1st to 10th month of age. ▪ Aggressively escalating Focal motor seizures ▪ Highly refractory to anticonvulsant medications. ▪ Developmental status is acutely affected ▪ Poor prognosis for normal outcome ▪ Etiology is unknown
  • 59.
    Time Of Onsetand Likely Etiology Age of Onset Likely Etiology <24 hrs HIE, Severe Birth Trauma, Congenital CNS Anomalies, Pyridoxine Dependency, Hypoglycaemia 24 – 48 hrs All the above + milder birth trauma, hypocalcaemia, hypomagnesaemia, infarcts, some IEMs <48 – 72 hrs All the above + dys-electrolytaemias, sepsis, other Encephalopathies >72 hsr – 1 week All the above + benign neonatal seizures <1 – 4 weeks Late hypocalcaemia, sepsis, progressive hydrocephalus, cerebral dysgenesis, epileptic syndromes, herpes encephalitis, some I EMs
  • 60.
    8. Approach tomanagement ▪ expedited evaluation for the etiology is warranted ▪ Most are symptomatic manifestations of acute brain injury ▪ many require urgent, specific treatment Diagnosis History Examination Investigations
  • 61.
  • 62.
    History Attempted to identifyrisk factors for seizures and clues to the underlying etiology Gestational and birth history – Anoxic injury nuchal cord or cord thrombosis, fetal heart rate decelerations, meconium, low Apgar scores, and placental abnormalities. Nature of the delivery operative vaginal delivery  ICH birth injury  macrosomia, maternal obesity, abnormal fetal lie
  • 63.
    Maternal history miscarriages congenital anomalies gestational diabetes  neonatal hypoglycemia STD or other infections neonatal Sepsis Illness during pregnancy e.g. maternal rash and fever could suggest in utero viral infection clotting or bleeding tendencies (neonatal stroke or hemorrhage).
  • 64.
    Family history Early siblingdeath from unknown causes Consanguinity  inborn errors of metabolism) Family history of epilepsy particularly neonatal(BFNC)
  • 65.
    Perinatal history ▪ PERINATALASPHYXIA as the commonest cause ▪ History of ▪ fetal distress, ▪ decreased fetal movements, ▪ instrumental delivery, ▪ need for resuscitation in the labor room, ▪ Apgar scores, and ▪ abnormal cord pH (<7) & base deficit (>10 mEq/L)
  • 66.
    Seizure History ▪ DescriptionOf The Seizure ▪ History ▪ Associated Eye Movements, ▪ Change In Color Of Skin (Mottling Or Cyanosis) ▪ Conscious Or Sleeping ▪ Day Of Life ▪ Day 0-3 Perinatal Asphyxia, ICH, Metabolic Causes, ▪ Day 4-7 Sepsis, Meningitis, Metabolic Causes, Developmental Defects
  • 67.
    Feeding history ▪ InbornErrors Of Metabolism ▪ Lethargy, poor activity, drowsiness, and vomiting after initiation of breast-feeding ▪ Top Feeding With Cow’s Milk ▪ Late onset hypocalcemia considered
  • 68.
    Examination Vital signs: Heart rate,respiration, blood pressure, capillary refill time and temperature General examination: Gestation, birth weight, and weight for age  seizures in a term ‘well baby’ or in large for date baby may be different presence of any obvious malformations or dysmorphic features.
  • 69.
    Systemic examination CNS : ▪Bulging fontanel  meningitis or intracranial haemorrhage ▪ Neurological examination  ▪ assessment of consciousness (alert/drowsy/comatose) ▪ tone (hypotonia or hypertonia), and ▪ Fundus examination for chorioretinitis. Other systems ▪ Organomegaly or an abnormal urine odor may be suggestive of IEM ▪ Skin neuro-cutaneous markers (e.g. hypopigmented macules or ash- leaf spot in Tuberous sclerosis.)
  • 71.
    Investigations ▪ Essential Investigations 1.Blood sugar, 2. Serum sodium and calcium, 3. Cerebrospinal fluid (csf) examination, 4. Cranial ultrasound (us), and 5. Electroencephalography (eeg).
  • 73.
    Additional Investigations ▪ Consideredin neonates who do not responding to first line antiepileptics or neonates with specific features. ▪ Neuroimaging (ct, mri), ▪ Screen for congenital infections (TORCH) ▪ Screen for inborn errors of metabolism ▪ An ARTERIAL BLOOD GAS should be performed if IEM is strongly suspected
  • 74.
    Neuroimaging 1. NEUROSONOGRAPHY ▪ Excellentbedside tool for detection of intraventricular and parenchymal hemorrhage. (But not SAH & SDH) ▪ done in all infants with seizures. 2. CT scan ▪ Should generally be avoided ▪ 2nd tier investigation ▪ subarachnoid hemorrhage and developmental malformations
  • 75.
    ▪ Magnetic resonanceimaging (MRI) ▪ all neonates with seizures to evaluate ▪ Useful in hypoxic-ischemic injury, ICH , Stroke, brain malformations. ▪ MR angiography  ischemic stroke or vascular malformation ▪ MR venography  venous sinus thrombosis ▪ MR spectroscopy  evaluate metabolites like ▪ glycine (nonketotic hyperglycinemia), ▪ lactate (mitochondrial disorders), or ▪ loss of creatine (disorder of brain creatine metabolism)
  • 76.
    EEG ▪ To determinethe risk and presence of seizures ▪ Seizure is defined as abnormal EEG pattern which evolves, is of >2 microvolt amplitude, and has a duration of ≥10 seconds ▪ Video EEG monitoring — The gold standard for neonatal seizure diagnosis is multi-channel video EEG monitoring ▪ EEG should be performed for at least one hour. ▪ Background abnormality in both term and preterm high risk for neurological sequelae. ▪ emphasis on continuous EEG monitoring to aid in management of seizures in newborns.
  • 77.
    ▪ excess ofsharp waves nonspecific indicator of encephalopathy. ▪ Bursts of repetitive or short, stereotyped evolving rhythmic bursts of sharp waves  increased seizure risk ▪ Evolving rhythmic discharges longer than 10 seconds seizures
  • 78.
    Amplitude-integrated EEG (aEEG) ▪widespread use at the bedside ▪ reduced number of electrodes single channel (2 electrodes) or dual-channel (4 electrodes) EEG tracing ▪ Final display showing several hours of aEEG data on a single screen generated. ▪ Electrographic seizures are characterized ▪ by upward arches
  • 79.
    Management ▪ Who totreat ▪ Identify first  gold standard, conventional video EEG, or, limited channel aEEG ▪ potential adverse effects of seizures on ventilatory function, circulation, cerebral metabolism, and subsequent brain development, considered ▪ repeated seizures should be stopped ▪ World Health Organization recommended treatment of all clinical and electrographic seizures ▪ goal of therapy is the elimination of electrical seizure activity
  • 80.
    Stabilization 1. Thermoneutral environment 2.ensure airway, breathing, and circulation (TABC). 3. Oxygen should be started, IV access should be secured, and blood should be collected for glucose and other investigations. 4. A brief relevant history should be obtained and quick clinical examination should be performed. 5. All this should not require more than 2-5 minutes
  • 81.
    Easily correctable causes ▪Correction of hypoglycemia hypocalcemia and hypomagnesemia : ▪ Hypoglycemia ▪ 2 mL/kg of 10% dextrose bolus injection followed by a continuous infusion ▪ hypoglycemia - treated / excluded ▪ Give 2 mL/kg of 10% calcium gluconate IV over 10 minutes under strict cardiac monitoring. ▪ If hypocalcemia ▪ Give additional calcium gluconate at 8 mL/kg/d for 3 days. ▪ If seizures continue despite hypocalcemia, 0.25 mL/kg of 50% magnesium sulfate should be given intramuscularly.
  • 82.
  • 83.
    Anti-epileptic drug therapy(AED) ▪ Even in a single clinical seizure and facilities for continuous EEG monitoring not available. ▪ Eliminating all electrical seizure activity should be the goal of AED therapy ▪ seizures persist even after metabolic correction
  • 84.
    PHENOBARBITONE ▪ Drug ofchoice in neonatal seizures ▪ Loading -20 mg/kg/IV slowly over 20 minutes ▪ seizures persist additional doses of phenobarbitone 10 mg/kg every 20-30 minutes until a total dose of 40 mg/kg ▪ maintenance dose - 3-5 mg/kg/day in 1-2 divided doses, started 12 hours after the loading dose.
  • 85.
    PHENYTOIN ▪ maximal doseof phenobarbitone failed ▪ or appearance of adverse effects like respiratory depression, hypotension, Bradycardia ▪ Loading Dose is 20 mg/kg IV ▪ Only NS dilution ▪ refractory seizures  repeat dose 10 mg/kg ▪ maintenance dose 3-5 mg/kg/d in 2-4 divided doses.
  • 86.
    BENZODIAZEPINES ▪ may berequired in up to 15-20% of neonatal seizures. ▪ lorazepam and midazolam. ▪ Diazepam - prolonged sedative effect, narrow therapeutic index, sodium benzoate as a preservative. ▪ Lorazepam - longer duration of action and less adverse effects ▪ Midazolam is faster acting than lorazepam and may be administered as an infusion. ▪ It causes less respiratory depression and sedation than lorazepam.
  • 87.
    ▪ The dosesof these drugs are given below: ▪ 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 0.4mg/kg/hour.
  • 88.
    LEVETIRACETAM ▪ Benign sideeffect profile, and limited interactions ▪ Loading doses vary from 10 to 20 mg/kg to as high as 40 to 50 mg/kg. ▪ Maintenance doses 10 to 80 mg/kg/day with most providers starting at 20 mg/kg/day, whereas others suggest 40 mg/kg/day. ▪ Although twice daily dosing is usual, three-times daily dosing has been suggested.
  • 89.
    Antiepileptic drugs forrefractory seizures LIDOCAINE: ▪ It is usually administered as a bolus dose of 4 mg/kg IV followed by an infusion rate of 2 mg/kg/hr. ▪ Adverse effects include arrhythmias, hypotension, and seizures. ▪ It should not be administered with phenytoin. PARALDEHYDE: ▪ A dose of 0.1-0.2 mL/kg/dose may be given IM ▪ 0.3 mL/kg/dose mixed with coconut oil in 3:1 may be used by per rectal route ▪ pulmonary hemorrhage, pulmonary edema, hypotension, and liver injury.
  • 90.
    ▪ SODIUM VALPROATE: ▪Per rectal or IV route may be used in acute condition. ▪ The dose is 20-25 mg/kg/d followed by 5-10 mg/kg every 12 hours. ▪ Used with caution in newborns given the uncertain risk of hepatotoxicity following its use. ▪ VIGABATRIN: ▪ It has been used in neonates with infantile spasms. ▪ The dose is 50mg/kg/day.
  • 91.
    ▪ TOPIRAMATE: ▪ potentialneuroprotective effect against injury caused by seizures. ▪ For refractory infantile spasms in infants. ▪ initial and maintenance doses of approximately 3 mg/kg
  • 92.
    Other therapies ▪ PYRIDOXINE: ▪A therapeutic trial of pyridoxine is reserved as a last resort in refractory seizures. ▪ Intravenous route is the preferred method ▪ intramuscular (IM) route be used ▪ hypotension and apnea can occur.
  • 94.
    ▪ EXCHANGE TRANSFUSION: ▪Indicated in ▪ life-threatening metabolic disorders, ▪ accidental injection of local anesthetic, ▪ trans-placental transfer of maternal drugs (e.g. chlorpropamide) ▪ bilirubin encephalopathy.
  • 95.
    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.
  • 96.
    When to discontinueAED ▪ no specific guidelines ▪ Discontinue phenobarbitone as early as possible ▪ try to discontinue all medications 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 one 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, phenobarbitone is 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
  • 97.
    Take home message ▪Neonatal seizures are common in both the preterm and term born infant. ▪ • Electroencephalography is essential to diagnose and treat neonatal seizures because of the frequency with which clinical signs are misinterpreted as seizures OR seizures or status epilepticus can be clinically silent. ▪ • Seizures are a sign of neurologic dysfunction from a variety of etiologies, including hypoxic ischemia, such as stroke, and metabolic and infectious etiologies. Investigation to determine the etiology of neonatal seizures is necessary and often requires blood and cerebrospinal fluid sampling, electroencephalography, and magnetic resonance imaging. ▪ • Therapy for neonatal seizures is important to limit both the short-term physiologic impact of the seizures and the potential contribution to long-term outcomes. Phenobarbitol remains first-line anticonvulsant therapy. ▪ • Length of time with anticonvulsant therapy for neonatal seizures remains unknown, although more recent trends are to minimize exposure to anticonvulsants unless a protracted risk for seizures persists
  • 98.
    REFERENCES 1. Cloherty andstarks manual of neonatal care 8th edition. 2. Aiims protocols in neonatology 3. Avery’s diseases of the newborn. -- 9th ed. / [Edited by] christine A. Gleason, sherin U. Devask 4. Fanaroff and martin’s neonatal-perinatal medicine : diseases of the fetus and infant / [edited by] richard J. Martin, avroy A. Fanaroff, michele C. Walsh.—10th edition.
  • 99.