Neonatal Seizures DR. MAHMOUD MOHAMED OSMAN MBBCh, MSc (Pedia), MRCPCH (UK), FRCP (Edinburgh) Consultant Pediatrician & Neonatologist Al Yammamah Hospital,

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Neonatal Seizures DR. MAHMOUD MOHAMED OSMAN MBBCh, MSc (Pedia), MRCPCH (UK), FRCP (Edinburgh) Consultant Pediatrician & Neonatologist Al Yammamah Hospital, MOH 1

2 Learning Objectives:  Introduction  Major causes of neonatal seizures  Diagnosis  Investigations  Managements  Prognosis

1. INTRODUCTION:  A seizure is a paroxysmal behavior caused by hyper- synchronous discharge of a group of neurons.  Seizures may be symptomatic of an underlying disorder or due to a primary epileptic condition.  In neonates, the majority of seizures are symptomatic of underlying disorders.  The occurrence of seizure may be the first clinical indication of neurologic disorder.  Seizures may interfere with cardiorespiratory function and with nutrition and may have detrimental long-term effects on cerebral development.

2. MAJOR CAUSES OF N. SEIZURES:  Hypoxic-Ischemic Encephalopathy.  Acute Metabolic Disorders.  Hypoglycemia  Hypocalcemia  Hypomagnesemia  Hyper/Hyponatremia  Congenital CNS Abnormalities.  Inherited Metabolic Disorders.  Amino Acid, Organic Acid  Urea Cycle Disorders  Drug Withdrawal  Pyridoxine Dependency (Vitamin B6)

 Intracranial infection  Bacterial meningitis (E. coli, Group B Strep, Listeria)  Viral Encephalitis (Herpes Simplex, Enterovirus)  Intrauterine Infection (CMV, Toxoplasm., HIV, Rubella, Syphilis)  Cerebral Vascular Accidents  Hemorrhages (Intraventricular, Subarachnoid, Subdural, Epidural)  Focal Ischemic Necrosis (Stroke)  Developmental defects  Neurocutaneous Disorders (Tuberous Sclerosis).  Epilepsy Syndromes  Epileptic Encephalopathies (Early Myoclonic Encephalopathy)  Benign Familial Neonatal Convulsions

3. DIAGNOSIS: 3. DIAGNOSIS: Diagnosis of seizures in the neonate requires: 1. Knowledge of the clinical patterns associated with electrographic seizures at this age. 2. Confirmation of the abnormal electrical discharge this may be recorded by electroencephalography (EEG).

1. 1. COMMON CLINICAL SEIZURES PATTERNS: 1.Subtle seizure Eye deviation - Blinking, fixed stare Repetitive mouth & tongue movements Pedaling, tonic posturing of limbs Apnea 2. Tonic seizure (focal or generalized) Tonic extension or flexion of limbs (severe ICH in preterm) 3. Clonic seizure (focal or multifocal) Clonic limb movements (synchronous or asynchronous) Consciousness may be preserved 4. Myoclonic seizure (focal, multifocal, or generalized) Lightning-like jerks of extremities (upper>lower)

2. EEG diagnosis 2. EEG diagnosis 1. Routine neonatal EEG recording: Typically of 1 hour duration, allows assessment of background activity, developmental maturity, and epileptic potential. 2. Video telemetry: Is very helpful in neonates to clarify the nature of non-epileptic behaviors and also to avoid misinterpretation of artifactual EEG patterns.

Electrographic seizure begins in the left parasagittal area (open arrow), and 12 seconds later, focal clonus of the right foot is noted.

3. Amplitude-integrated EEG (aEEG):  It is a bedside technique increasingly being used by neonatologists for neuromonitoring.  This technique allows the neonatologist to continually assess:  The background EEG characteristics, and thereby judge the severity of encephalopathy,  The improvement or deterioration over time,  The response to therapies.

Amplitude integrated EEG

4. INVESTIGATIONS. Investigations should be modified by the individual case history, with an emphasis on early identification of correctable disorders.  Sepsis work up (include lumbar puncture ) should be considered.  General metabolic screening  Screening for inborn errors of metabolism.  Cranial ultrasound: may identify intracranial hemorrhage.  Head CT, and brain MRI, are more helpful to confirm these disorders. However, usually require transportation, with the risk of destabilization of ill infants.

5. MANAGEMENT: 1. Ensure adequate ventilation and perfusion. 2. Correct metabolic disturbances.  Hypoglycemia: (10% glucose in water) 2 mL/kg IV as bolus. Follow with continuous infusion at up to 8 mg/kg/min IV.  Hypocalcemia: (calcium gluconate 10%) 100 mg/kg IV over 1 to 3 minutes (Monitor cardiac rhythm for baradycardia) Follow with maintenance of 500 mg/kg/24 hrs IV or PO.  Hypomagnesemia: (magnesium sulfate 10%) mg/kg/dose IV. 3. Begin anticonvulsant therapy. NB: Giving anticonvulsant medications only after adequate ventilation and perfusion have been established and the blood glucose concentration has been measured.

Anticonvulsant Drug Doses for Initial Management of Neonatal Seizures

4. Pyridoxine deficiency: It is a rare cause of neonatal seizures and should be considered in any newborn with intractable seizures. The diagnosis is made by pyridoxine IV with concurrent EEG.

6. PROGNOSIS.  Advances in obstetric management and in neonatal intensive care have yielded a reduction in mortality in infants with neonatal seizures from about 40% to <20%.  Morbidity rates have changed less, partly due to increased numbers of survivors among ill, premature newborns, who have a greater risk of neurologic sequelae.  Long-term sequelae, including cerebral palsy and intellectual disabilities, still occur at a high rate.  The most important factor affecting outcome for infants with neonatal seizures is the underlying etiology.

 Normal development can be expected in infants with benign idiopathic neonatal seizures. Whereas only 50% of those with HIE.  Gestational age is also an important factor with increasing mortality and morbidity with increasing immaturity.  Useful clinical indicators for a good outcome include a normal neonatal neurologic exam, normal or mildly abnormal neonatal EEG background activity, and normal neuro-imaging.