NEONATAL SEIZURES-PGPYREXIA REVIEW

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1 NEONATAL SEIZURES-PGPYREXIA REVIEW This is a very important Postgraduate topics will few Q asked in undergraduation also. Lets see them in detail. References: 1.Volpe s Neurology of newborn 2.Nelson s Pediatrics. Seizures:Definition: transient and reversible alteration of behavior (motor,sensory,autonomic or behavioural )caused by a paroxysmal, abnormal and excessive neuronal discharge,of cerebral origin due to dysnfunction of a part or all of the brain Epilepsy:Definition: A 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.it is clinically diagnosed by 2 or more seizures not directly provoked by intracranial infection, drug withdrawal, acute metabolic changes or fever Physiological reasons for Neonatal seizures: o The neonatal brain has incomplete glial proliferation, with continuing migration of neurons, establishing complex axonal & dendritic contacts and myelin deposition. o The electrical discharges therefore spread incompletely and may remain localized to one hemisphere. Classification of Neonatal Seizures: I.Clinical II.Electroencephalographic I. Clinical Seizure Subtle-Most common type, chewing motion, excessive salivation and alteration in respiratory rate including apnea, blinking, nystagmus, bicycling and pedaling movements, changes in color Tonic- focal or generalized,mostly in preterms,generally poor prognosis

2 Clonic-mostly in term babies Myoclonic- sudden flexor movements, if due to early myoclonic encephalopathy it carries a poor prognosis II.Electroencephalographic Epileptic - Consistently associated with electro-cortical seizure activity on the EEG, Related to hyper synchronous discharges of a critical mass of neuron Non-epileptic- No electro-cortical signature, Brainstem release phenomena (reflex) Major Causes of Neonatal Seizures In Relation to Time of Seizure Onset and Relative Frequency TIME OF ONSET* RELATIVE FREQUENCY Cause 0-3 Days >3 Days Premature Full Term Hypoxic-Ischemic encephalopathy Intracranial hemorrhage Intracranial infection Developmental defects Hypoglycemia Hypocalcemia Other metabolic + + Epileptic syndromes ***Etiology based on time of presentation: (very important) 1 4 days 4-14 days 2-8 weks o HIE Infection Infection o Drug withdrawal Metabolic disorders Head injury (benzodiazepine,ba Hypocalcemia Subdural

3 rbiturates,methado ne,heroin) o Dug toxicity: Lidocaine, penicillin o Intraventricular hemorrhage o Acute metabolic disorder o Hypocalcemia o Hypoglycemia o Inborn errors of metabolism Diet Hypoglycemia Inherited disorder of metabolism such as galactosemia,fructo semia Hyperinsulinemic hypoglycemia Beckwith syndrome Drug withdrawal Benign neonatal convulsion Kernicterus, hyperbilirubenemia hematoma 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 ***Another MCQ: Jitteriness Versus Seizure CLINICAL FEATURE JITTERINESS SEIZURE 1.Abnormality of gaze or eye O + movement 2.Movements exquisitely stimulus + O sensitive 3.Predominant movement Tremor Clonic jerking 4.Movements cease with passive + O flexion 5.Autonomic changes O + Laboratory Studies: Indicated

4 o Complete blood count, differential, platelet count; urinalysis o Blood glucose (Dextrostix), BUN, Ca, P, Mg, electrolytes o Blood oxygen and acid-base analysis o Blood, CSF and other bacterial cultures o CSF analysis o EEG On Clinical Suspicion of Specific Disease o Serum immunoglobulins, TORCH antibody titers, and viral cultures o Blood and urine metabolic studies (bilirubin,ammonia, lactate, FECl³, reducing substance.) o Blood and urine toxic screen o Blood and urine amino and organic acid screen o CT or ultrasound scan Idiopathic Syndromes of Clinical Seizures in the Newborn: Epileptic Syndromes Benign familial Neonatal Seizures Benign idiopathic neonatal seizures (fifth-day fits) Early myoclonic encephalopathy Early infantile epileptic encephalopathy (Ohtahara syndrome) Malignant migrating partial seizures Nonepileptic Syndromes Benign neonatal sleep myoclonus Hyperekplexia (The main three classical signs of hyperekplexia are generalized stiffness, excessive startle reflex beginning at birth and a short period of generalized stiffness following the startle reflex) ***Notes on few important conditions: Benign familial neonatal seizures Begins on the 2nd 3rd day of life Seizure frequency : /day Patients are normal between seizures Seizure stops in 1 6 months Fifth-day fits

5 5th day of life normal appearing neonates with mulifocal seizures Present for less than 24 hours Good prognosis Pyridoxine dependency resistant to conventional AED s Inherited as autosomal recessive Tx: Pyridoxine mg IV May not have a dramatic effect with IV pyridoxine thus maintain on oral pyridoxine mg/day x 6 weeks Lifelong supplementation : 10 mg/day ***This again is a very important table: Cause Hypoxic-ischemic encephalopathy Intraventricular hemorrhage Subarachnoid hemorrhage Hypocalcemia Early-onset Later-onset Hypoglycemia Bacterial meningitis Developmental malformations Benign familial neonatal convulsions Fifth-day fits % patients who have normal development ~100 ~100 Acute Therapy of Neonatal Seizures: With Hypoglycemia -- Glucose, 10% solution: 2 ml/kg, IV No Hypoglycemia -Phenobarbital: 20 mg/kg, IV (1-2 mg/kg/min) If necessary: -Additional phenobarbital: 5 mg/kg IV to a max. of 40 mg/kg (consider omission of this additional phenobarbital if infant is severely asphyxiated ) Phenytoin*: 20 mg/kg, IV ( mg/kg/min) (Lorazepam: mg/kg, IV) if available

6 Midazolam: 0.2 mg/kg, IV;then, mg/kg/hr, IV Other (as Indicated) Calcium gluconate, 5% solution: 4 ml/kg, IV Magnesium sulfate, % solution: 0.2 ml/kg, IM Pyridoxine: -100 mg, IV; repeat to maximum of 0 mg if needed Pyridoxal-5-phosphate,30 mg/kg/day, PO Folinic Acid, 4 mg/kg/day, PO Maintenance Therapy of Neonatal Seizures: Glucose: < 8 mg/kg/, IV Phenobarbital: 3-4 mg/kg/24 hr, IV, IM, or PO Phenytoin (as fosphenytoin): 3-4 mg/kg/24 hr, IV Calcium gluconate: 0 mg/kg/24 hr, PO Magnesium sulfate (%): 0.2 ml/kg/24 hr, IM Duration of Anticonvulsant Therapy Guidelines: Neonatal Period If neonatal neurological examination becomes normal, discontinue therapy If neonatal neurological examination is persistently abnormal, consider the cause and obtain an EEG. In most such cases: Continue phenobarbital Discontinue phenytoin Reevaluate in 1 month At 1 Month After Discharge If neurological examination has become normal, discontinue phenobarbital If neurological examination is persistently abnormal, obtain an EEG. If no seizure activity is noted on the EEG, discontinue Phenobarbital x that completes the topic x

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