I. Neonatal Seizures

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I. Neonatal Seizures. II. Conditions That Mimic Seizures. Seizure. transient and reversible alteration of behavior caused by a paroxysmal, abnormal and excessive neuronal discharge attack of cerebral origin sudden and transitory abnormal phenomena motor, sensory, autonomic, or psychic - PowerPoint PPT Presentation

Transcript of I. Neonatal Seizures

  • I. Neonatal SeizuresII. Conditions That Mimic Seizures

  • Seizure transient and reversible alteration of behavior caused by a paroxysmal, abnormal and excessive neuronal discharge attack of cerebral origin sudden and transitory abnormal phenomena motor, sensory, autonomic, or psychic transient dysfunction of part or all of the brain

  • EpilepsyA paroxysmal brain disorder of various etiologies characterized by recurrent seizures due to excessive electrical discharge of cerebral neurons associated with a variety of clinical and laboratory manifestations

    two or more seizures not directly provoked by intracranial infection, drug withdrawal, acute metabolic changes or fever

  • Neonatal SeizuresTonic Seizuresfocal or generalized, may mimic decorticate or decerebrate posturing, primarily seen in preterms with intracranial hemorrhage & generally have poor prognosis

    Subtle seizuresConsist of chewing motion, excessive salivation and alteration in respiratory rate including apnea, blinking, nystagmus, bicycling and pedaling movements, changes in color

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

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

  • 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.

  • Neonatal SeizuresEEG ClassificationClinical seizure with consistent EEG eventClinical seizure occurs in relationship to seizure activityIncludes focal clonic, focal tonic and myoclonicResponds to antiepileptic drugsClinical seizure with inconsistent EEG eventClinical seizures with no EEG abnormalitySeen in all generalized tonic and subtle seizuresSeen in patients who are comatose, HIE

  • Neonatal SeizuresEEG ClassificationElectrical seizures with absent clinical seizuresElectrical seizures associated with markedly abnormal background EEGSeen in comatose patients

  • Epileptic vs Non-epileptic Neonatal Phenomena

    Clinical Characteristics EpilepticNon-epileptic

    Increases with Sensorystimulation RareCommonSuppresses with restraint -+Autonomic Accompaniments +-

  • Major Causes of Neonatal Seizures In Relation to Time of Seizure Onset and Relative Frequency TIME OF ONSET* RELATIVE FREQUENCYCause 0-3 Days >3 Days Premature Full TermHypoxic-Ischemic encephalopathy + +++ +++Intracranial hemorrhage + + ++ +Intracranial infection + + ++ ++Developmental defects + + ++ ++Hypoglycemia + + +Hypocalcemia + + + Other metabolic + + Epileptic syndromes + + +

  • Neonatal SeizuresEtiologic diagnosisHypoxic ischemic encephalopathyMetabolicInfectionsTraumaStructural abnormalitiesHemorrhagic and embolic strokesMaternal disturbances

  • Causes of neonatal seizuresAges 1 4 daysHIEDrug withdrawalDug toxicityLidocaine, penicillinIntraventricular hemorrhageAcute metabolic disorderHypocalcemiaHypoglycemiaInborn errors of metabolism

  • Causes of neonatal seizuresAges 4 14 daysInfectionMetabolic disordersHypocalcemiaDietHypoglycemiaInherited disorder of metabolism such as galactosemia,fructosemiaHyperinsulinemic hypoglycemiaBecwith syndromeAnterior pituitary hypoplasiaDrug withdrawalBenign neonatal convulsionKernicterus, hyperbilirubenemia

  • Causes of neonatal seizuresAges 2 8 weeksInfectionHead injurySubdural henatomaInherited disorder of metabolismAminoaciduriasUrea cycle defectsOrganic aciduriasNeonatal ALDMalformations of cortical developmentLissencephalyFocal cortical dysplasiaTuberous sclerosisSturge weber syndrome

  • Neonatal SeizuresEtiologic diagnosisBloodGlucose, calcium, magnesium, electrolytes, BUNIn hypomagnesemia MgSO4 0.2 ml/kgLumbar punctureIndicated in all neonates with seizures unless related to a metabolic disorderInborn errors of metabolismInherited as autosomal recessive or X-linked recessive

  • Neonatal SeizuresEtiologic diagnosisInborn errors of metabolismSerum ammonia urea cycle abnormalitiesAcidosis + anion gap + hyperammonemia urine organic acids should be determinedUnintentional injection of local anestheticSupportive measuresPromotion of urine output with IV fluids

  • Idiopathic Syndromes of Clinical Seizures in the NewbornEpileptic Syndromes Benign familial Neonatal SeizuresBenign idiopathic neonatal seizures (fifth-day fits)Early myoclonic encephalopathy Early infantile epileptic encephalopathy (Ohtahara syndrome)Malignant migrating partial seizuresNonepileptic SyndromesBenign neonatal sleep myoclonusHyperekplexia

  • Neonatal Seizures(Epileptic Syndromes)Benign familial neonatal seizuresBegins on the 2nd 3rd day of lifeSeizure frequency : 10 20 /dayPatients are normal between seizuresSeizure stops in 1 6 months

  • Neonatal Seizures

    Fifth-day fits 5th day of lifenormal appearing neonates with mulifocal seizuresPresent for less than 24 hoursGood prognosis

  • Neonatal SeizuresEtiologic diagnosisPyridoxine dependency resistant to conventional AEDsInherited as autosomal recessiveTx: Pyridoxine 100 200 mg IVMay not have a dramatic effect with IV pyridoxine thus maintain on oral pyridoxine 10 -20 mg/day x 6 weeksLifelong supplementation : 10 mg/day

  • Neonatal SeizuresEtiologic diagnosisDrug withdrawal seizuresBarbiturates, benzodiazepenes, heroin and methadoneJittery, irritable, lethargic, may show myoclonus or frank seizuresSerum or urine analysis may identify the responsible agent

  • Prognosis of Neonatal Seizures:Relation to Neurological DiseasesNeurological Disease* Normal DevelopmentHypoxic-ischemic encephalopathy 50%Intraventricular hemorrhage 10%Primary subarachnoid hemorrhage 90%Hypocalcemia Early-onset 50% Later-onset 100%Hypoglycemia 50%Bacterial meningitis 50%Developmental defect 0%

  • Why should the infant with epileptic seizures be treated with AEDPotential adverse effects of seizure on:Ventilatory function CirculationCerebral Metabolism Brain Development disturbance in cerebral blood flow energy metabolism homeostasis of excitotoxic amino acids neurogenesis and synaptic reorganization

  • Acute Therapy of Neonatal SeizuresWith Hypoglycemia --Glucose, 10% solution: 2 mL/kg, IVNo Hypoglycemia Phenobarbital: 20 mg/kg, IV (1-2 mg/kg/min)If necessary: Additional phenobarbital: 5 mg/kg IV to a max. of 40 mg/kg (consider omission of this additional phenobarbital if infant is severely asphyxiated) Phenytoin*: 20 mg/kg, IV (0.5-1.0 mg/kg/min) (Lorazepam: 0.05-0.10 mg/kg, IV) if available Midazolam: 0.2 mg/kg, IV;then,0.1-0.4 mg/kg/hr, IV

  • Acute Therapy of Neonatal SeizuresOther (as Indicated)Calcium gluconate, 5% solution: 4 mL/kg, IVMagnesium sulfate, 50% solution: 0.2 mL/kg, IMPyridoxine: 50-100 mg, IV; repeat to maximum of 500 mg if neededPyridoxal-5-phosphate,30 mg/kg/day, POFolinic Acid, 4 mg/kg/day, PO

  • Volpe, Neurology of the Newborn, 5th ed. 2008

    Maintenance Therapy of Neonatal SeizuresGlucose: < 8 mg/kg/, IVPhenobarbital: 3-4 mg/kg/24 hr, IV, IM, or POPhenytoin (as fosphenytoin): 3-4 mg/kg/24 hr, IVCalcium gluconate: 500 mg/kg/24 hr, PO Magnesium sulfate (50%): 0.2 mL/kg/24 hr, IM

  • Clinical Scenario 1F.M. a 36-37 month old baby boy is noted to have blinking of the eyelids with sucking movements of the mouth at 30 hours of life. The extremities are jittery when tactile stimuli is applied.

    Maternal history is unremarkable, NSD, G1P1 (1-0-0-1) no hypertension, no infection. Birth weight is 2.5kg. Apgar 8 and 10 at 1 and 5min.

    The blinking of the eyes and jittery movements of the extremities recur within the next hour.

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