Seizures in Neonates

3. Seizures in Neonates

4. Neonatal seizures are one of the few neonatal neurologic conditions that require immediatemedical attention.

5. Medical personnel vary significantly in their ability to recognize suspect behaviors, contributing to both overdiagnosisand underdiagnosis.

6. However, abnormal motor or autonomic behaviorsmay represent age- and state-specific behaviors in healthy infants, or nonepileptic paroxysmal conditions in symptomatic infants.

7. For these reasons, confirmation of suspect clinical eventswith coincident EEG recordings is now more widely recommended.

8. because in patients with few seizures, these may be missed as brief random events on routine EEG studies, synchronized video/EEG/polygraphic recordings potentially establish more reliable startpoints and endpoints for electrically confirmed seizures that require consideration for treatment intervention.

9. Clinical Categories • The clinical criteria for neonatal seizure diagnosis were historically subdivided into five clinical categories: • focal clonic • multifocal or migratory clonic • tonic • myoclonic • subtle seizures

10. SUBTLE SEIZURE • This is the most frequently observed category of neonatal seizures, which include repetitive buccolingual movements, orbital-ocular movements, unusual bicycling or peddling, and autonomic findings. • alterations in cardiorespiratory regularity, body movements, and other behaviorsduring active (rapid eye movement) sleep, quiet (non-rapid eye movement) sleep, or waking segments must be recognized before proceeding to a seizure evaluation. • Within the subtle category of neonatal seizures are stereotypical changes in heart rate, blood pressure, oxygenation, or other autonomic signs,particularly during pharmacologic paralysis for ventilatory care.

11. SUBTLE SEIZURE • Because subtle seizures are clinically difficult to detectand only variably coincident with EEG seizures, synchronized video/EEG/polygraphic recordings are recommended to document temporal relationships between clinical behaviors and coincident electrographic events.

13. CLONIC SEIZURES • Rhythmic movements of muscle groups in a focal distribution that consist of a rapid phase followed by a slow return movement are clonic seizures. • Clonic movements can involve any body part such as the face, arm, leg, and even diaphragmatic or pharyngeal muscles. • must be distinguishedfrom the symmetric “to-and-fro” movements of tremulousness or jitteriness. • Gentle flexion of the affected body part easily suppresses the tremor, whereas clonic seizures persist.

14. CLONIC SEIZURES • Generalized clonic activitiescan occur in the newborn but rarely consist of a classic tonic followed by clonic phase, characteristic of the generalized motor seizure noted in older children and adults. • Focal clonicand hemiclonic seizures have been described with localized brain injury, usually from cerebrovascularlesions,butcan also be seen with generalized brain abnormalities. • Clonic movements without EEG-confirmed seizures have been described in neonates with normal EEG backgrounds, and their neurodevelopmental outcome can be normal.

15. MULTIFOCAL CLONIC SEIZURES • Multifocal or migratoryclonic activities spread over body parts either in a random or anatomically appropriate fashion. Such seizure movements may alternate from side to side and appear asynchronously between the two halves of the child’s body. • Neonates with this seizure description suffer death or significant neurologic morbidity.

16. TONIC SEIZURES • Tonic seizures refer to a sustained flexion or extension of axial or appendicularmuscle groups. • Tonic movements of a limb or sustained head or eye turning may also be noted. • Tonic activity with coincident EEGneeds to be carefully documented because 30% of such movements lack a correlation with electrographic seizures.

17. TONIC SEIZURES • “Brainstem release”resulting from functional decorticationafter severe neocortical dysfunction or damage. • Extensive neocortical damage or dysfunction permits the emergence of uninhibited subcortical expressionsof extensor movements.

19. MYOCLONIC SEIZURES • Myoclonicmovements are rapid, isolated jerks that can be generalized, multifocal, or focalin an axial or appendicular distribution. • Myoclonuslacks the slow return phase of the clonic movement complex described. • Healthy preterm infants commonly exhibit myoclonic movementswithout seizures or a brain disorder. • EEG, therefore, is recommended to confirm the coincident appearance of electrographic discharges with these movements.

20. MYOCLONIC SEIZURES • Pathologic myoclonusin the absence of EEG seizures also can occur in severely ill pretermor full-term infants after severe brain dysfunction or damage. • myoclonusmay reflect injury at multiple levels of the neuraxis from the spine, brainstem, to cortical regions. • Rarely, healthy sleeping neonates exhibit abundant myoclonusthat subsides with arousal to the waking state,termed benign sleep myoclonus of the newborn.

21. Nonepileptic Behaviors of Neonates TREMORS Or JITTERINESS • Tremorsare frequentlymisidentified as clonic activity. • Unlike the unequal phases of clonic movements described earlier, the flexion and extension phases of tremor are equal in amplitude. • Children are usually alert or hyperalertbut may also appear somnolent. • Passive flexion and repositioning of the affected tremulous body part diminishes or eliminates the movement.

22. Nonepileptic Behaviors of Neonates TREMORS Or JITTERINESS • Such movements are usually spontaneousbut can be provoked by tactile stimulation. • Metabolic or toxin-induced encephalopathies, including mild asphyxia, drug withdrawal, hypoglycemia, hypocalcemia, intracranial hemorrhage, hypothermia, and growth restriction, are common clinical scenarios when such movements occur.

23. Nonepileptic Behaviors of Neonates TREMORS Or JITTERINESS • Neonatal tremors usually decrease with age; for example, in 38 full-term infants, excessive tremulousness resolved spontaneously over a 6week period, with 92% neurologically normal at 3 years of age. • Medications are rarely considered to treat this particular movement disorder.

24. NEONATAL MYOCLONUS WITHOUT ELECTROGRAPHIC SEIZURES • NEONATAL DYSTONIA/DYSKINESIA WITHOUT ELECTROGRAPHIC SEIZURES

26. ICTAL ELECTROENCEPHALOGRAPHIC PATTERNS • Neonatal EEG seizure patterns commonly consist of a repetitive sequence of waveforms that evolve in frequency, amplitude, electrical field, and morphology. • Four types of ictal patterns have been described: • focalictal patterns with normal background • focal patterns with abnormal background • multifocalictal patterns • focal monorhythmic periodic patterns of various frequencies

27. ICTAL ELECTROENCEPHALOGRAPHIC PATTERNS • It is generally suggested that a minimal duration of 10 seconds with the evolution of discharges is required to distinguish electrographic seizures from repetitive but nonictalepileptiform discharges. • The mean seizure duration was longer in the full-term infant (5 minutes) compared with the preterm infant (2.7 minutes).

28. ICTAL ELECTROENCEPHALOGRAPHIC PATTERNS • Uncoupling of the clinical and electrographic expressions of neonatal seizures after antiepileptic medication administration also contributes to an underestimation of the true seizure duration, including status epilepticus. • Estimated that 25% of neonates expressed persistent EEG seizures despite resolution of their clinical seizure behaviors after receiving antiepileptic medications, termed electroclinical uncoupling.

29. ICTAL ELECTROENCEPHALOGRAPHIC PATTERNS • Using clinical criteria, seizure incidences ranged from 0.5% in term to 22.2% in preterm neonates • Most neonatal electrographic seizures arise focally from one brain region. • Generalized synchronous and symmetric repetitive discharges can also occur.

30. ICTAL ELECTROENCEPHALOGRAPHIC PATTERNS • Neonates with brief discharges can suffer from hypoglycemia or PVL , which carries a higher risk for neurodevelopmental delay. • Extremity movements were more significantly associated with synchronized electro-clinical seizures.

31. InterictalElectroencephalographic Pattern Abnormalities • Interictal EEG abnormalities have important prognostic implications for both preterm and full-term infants. • Severely abnormal patterns include the • burst suppression pattern, • electrocerebral inactivity, • low-voltage invariant pattern, • persistently slow background pattern, • multifocal sharp waves, • and marked asynchrony.

32. InterictalElectroencephalographic Pattern Abnormalities • For infants with hypoxic-ischemic encephalopathy(HIE), subclassifications of specific EEG patterns such as burst suppression with or without reactivity may give a more accurate prediction of outcome. • Dysmaturity of the EEG sleep background for child’s corrected age has also been an important feature to recognize; discordance between cerebral and noncerebral components of sleep state, or immaturity of EEG patterns for the given postconceptional age of the infant predict a higher risk for neurologic sequelae.

34. InterictalElectroencephalographic Pattern Abnormalities • Focal or regional patterns have prognostic significance, such as with preterm infants who express repetitive positive sharp waves at the midline or central regionsoften noted with IVH & PVL • Screening infants at risk for neonatal seizures with a routine EEG soon after birth allows identification of more severe interictal EEG background abnormalities that more likely predict seizure occurrence on subsequent neonatal records.

35. InterictalElectroencephalographic Pattern Abnormalities • Serial EEG studies better assist the clinician in diagnostic and prognostic interpretations. • As with abnormal examination findings into the second week of life, the persistence of EEG abnormalitiesalso raises prognostic concerns. • normal EEG features during the first few days after birth, may experience comparatively fewer neurologic sequelae.

36. MAJOR ETIOLOGIES FOR SEIZURES Hypoxia -Asphyxia • Seizures may occur as part of an asphyxial brain disorder that is expressed after birth (termed HIE from intrapartum stress)

37. Hypoxia -Asphyxia • Hypoxia-ischemia (i.e., asphyxia) is traditionally considered the most common causal factor associated with neonatal seizures. • Neonate suffer asphyxiaeither before or during parturition, and only 10% of cases of asphyxia result from postnatal causes. • When asphyxia is suspected during the labor and delivery process, biochemical confirmation can be attempted.

38. Hypoxia -Asphyxia • Intrauterine factors in the hours to days before labor can result in antepartum fetal asphyxia without later documentation of acidosis at birth. • Some maternal illnesses such as thrombophilia or preeclampsia, or specific uteroplacental abnormalities such as abruptioplacentaeor cord compression may contribute to fetal asphyxialstress without providing the opportunity to document in utero acidosis at the end of parturition. • Antepartum maternal trauma and chorioamnionitis are additional acquired conditions that cause or contribute to intrauterine asphyxia secondary to uteroplacental insufficiency.

39. Hypoxia -Asphyxia • Placental weights < the 10th or > the 90th percentile suggest chronic perfusion abnormalities to the fetus. • Meconium passage into the amniotic fluid may also promote an inflammatory response in the placental membranes, causing vasoconstriction and additional asphyxia. • Therefore, asphyxia-induced brain injuries may result from in utero maternal-fetal-placental diseases that later are expressed in part as neonatal seizures, independent of the biochemical marker of acidosis at birth, as well as the evolving HIE syndrome in the days after birth.

40. Hypoxia -Asphyxia • Postnatal neonatal illnesses also cause or contribute to asphyxia-induced brain injury and seizures without HIE, and after an uneventful delivery without fetal distress during labor or neonatal depression at birth.

41. Hypoxia -Asphyxia • Post-asphyxial encephalopathy refers to an evolving clinical syndrome over days after birth depression during which neonatal seizures may occur, usually in children who also exhibit severe early metabolic acidosis, hypoglycemia or hypocalcemia, and multiorgan dysfunction. • Postasphyxial seizures usually occur within the first 3 days of life, depending on the length and degree of asphyxial stress during the intrapartum period.

42. Hypoxia -Asphyxia • An early occurrence of seizures, within several hours after delivery, sometimessuggests antepartum or peripartum occurrence of a fetal brain disorder when associated with specific fetal heart rate patterns. • Earlier seizure onset, within 4 hours of birth, in encephalopathic newbornsmaypredict a particularly adverse outcome independent of etiology for asphyxia.

43. Hypoxia -Asphyxia • The duration of asphyxia is difficult to assess based on either single or even multiple Po2values, but pH <7.2 are considered of greater clinical concern for predicting HIE, although the suggested guideline of a pH <7.0 is one criterion by which the clinical entity of HIE might be predicted. • A metabolic definition of asphyxiashould also include a base deficit of less than 12 mmol/L (BE > - 12) , although specific researchers suggest BE > - 16 mmol/L because of its higher predictive power for the emergence of the HIEsyndrome, including clinical seizures.

44. Hypoxia -Asphyxia • Low 1- and 5-minute Apgar scores indicate the continued need for resuscitation, but only low scores at 10, 15, and particulary 20 minutes more accurately predict sequelae. • Normal Apgar scores, however, do not eliminate the possibility of severe brain injury, either from asphyxia or other causes. • As many as 2/3 of neonates who exhibit CPat older ages had normal Apgar scores at birth without HIE.

45. Hypoxia -Asphyxia • Hypertonicity, often with cortical fisting, in a previously depressed childwho rapidly recovers after a resuscitative effort also commonly reflects longer-standing fetal neurologic dysfunction before labor or the mother’s admission to the hospital. • Sustained hypotonia and unresponsiveness for 3 to 7 days are the expected signs of HIE after asphyxial stress during labor, with or without brain injury.

46. MAJOR ETIOLOGIES FOR SEIZURES Hypoglycemia • Significant Hypoglycemia is usually defined as glucose levels less of 35 to 40 mg/dL (BS < 50). • No clear consensus exists concerning a direct cause-and-effect relationship of hypoglycemia with seizure occurrence. • Associated disturbances may coexist, such as hypocalcemia, craniocerebral trauma, cerebrovascular lesions, and asphyxia, which may also contribute to lowering the infant’s threshold for seizures.

47. MAJOR ETIOLOGIES FOR SEIZURES Hypocalcemia • Total serum calcium levels below 7 (7.5) to 8 mg/dLgenerally define hypocalcemia. • The ionized fraction is a more sensitive indicator of seizure vulnerability. • The exact level of hypocalcemia at which seizures occur is debatable. An ionized fraction of 0.6 mg/dL or less may have a more predictable association with the presence of seizures.

49. MAJOR ETIOLOGIES FOR SEIZURES Cerebrovascular Lesions • Hemorrhagicor ischemiccerebrovascular lesionsare associated with neonatal seizure. • IVH or periventricular hemorrhage (PVH) is the most common intracranial hemorrhage (ICH) of the preterm infant, and has been associated with seizures in as much as 45% of a preterm population with EEG-confirmed seizures.

50. Cerebrovascular Lesions • Intracranial hemorrhage is usually expected inthe first 72 hours of life of the preterm infant. • the most frequent presentation is asymptomatic; (25% to 50% of infants with GMH-IVH have no obvious clinical signs) , the neonate with a catastrophic deterioration of clinical status shows signs of apnea, bulging fontanelle, hypertonia, and seizures. • Term infants present less commonly with intraventricular hemorrhage.