Seizures in neonates

Seizure-like events in neonates

1. 1. USE OF MAGNESIUM SULPHATE IN NEONATAL SEIZURES 2.ABNORMAL MOVEMENTS IN CHILDREN BY ANNE E. ODARO MCM/2017/69852

2. MGSO4 Dose and Administration Initial Dose 200mg/kg dose. Dilute to 8% concentrate in D5W. Infuse IV for 30 minutes. DO NOT exceed 150 mg/minute. Continuous IV infusion 20 - 50mg/kg/hour. Dilute to 8% concentration in D5W. Usual dilution 4 grams magnesium sulphate to make 50ml with D5W = 80mg/ml 0.25ml x weight = 20mg/kg/hour

3. Indications Seizures refractory to other anticonvulsant therapy. Hypomagnesaemia. Severe persistent pulmonary hypertension of the newborn  unresponsive to other vasodilation management. Contraindications and Precautions Patients with heart block or myocardial damage. CAUTION in patients with impaired renal function and/or electrolyte imbalance.

4. Possible Adverse Effects ECG changes (prolongation of the atrio -ventricular conduction time, sinoatrial block and atrio -ventricular block). Circulatory collapse, hypotension. Gastrointestinal disturbances ( diarrhoea , abdominal distension, absence of bowel sounds). Urinary retention. CNS depression (central sedation, muscle relaxation, hyporeflexia and decreased excitability). Calcium and potassium disturbances. Respiratory depression. Special Considerations Anticipate change in calcium and phosphorus balance. Drug interaction has been reported between magnesium sulphate and  gentamicin  (respiratory arrest). Monitor serum magnesium and calcium levels. Antidote for hypermagnesaemia is calcium gluconate .

5. In a study done Neonatal Intensive Care Unit (NICU) of a teaching hospital situated in a rural area of Bihar to ascertain the impact of postnatal magnesium sulfate (MgSO4) infusion on moderately to severely asphyxiated neonates, the outcome was as follows: a) The incidence of moderate (stage II) and severe (stage III) encephalopathy at NICU admission was the same in both the groups, that is, 18 (72.0%) and 7 (28.0%), respectively.

6. b) The MgSO4-treated group had an eventual mortality rate of 5.6% (1 out of 18) for neonates with stage II (moderate) encephalopathy and 42.8% (3 out of 7) for those with stage III (severe) encephalopathy. c) T he group that was not given MgSO4 suffered a mortality of 22.2% (4 out of 18) among newborns with HIE stage II (moderate encephalopathy) and 85.7% (6 out of 7) for stage III (severe) encephalopathy.

7. d) Seizures were present on day 1 in all the 18 patients (100%) with stage II (moderate) encephalopathy in both the control and the treatment groups, but while only 2 (11.1%) of them in the treatment arm still had seizures at 24 hours of admission, 6 (33.3%) of neonates with moderate encephalopathy (HIE stage II) in the control arm had electroencephalographic (EEG) evidence of active seizures at 24 hours, even though all the patients with seizures were treated according to the same standard protocol for neonatal seizures due to perinatal asphyxia.

8. e) The control group had abnormal neurological findingsin 60.0% of surviving neonates (9 out of 15 surviving) and 36.0% (9 out of 25) of the total number of babies in the control group. No significant adverse effects of MgSO4 were observed at the used dosage on hemodynamic parameters and respiration. Conclusion : Intravenous MgSO4 therapy decreases mortality and neurological morbidity in neonates with moderate (stage II) to severe (stage III) perinatal asphyxia and improves short-term outcomes.

9. A post hoc subgroup analysis was done to determine the effect of magnesium on neonatal seizures in infants with moderate-severe hypoxic ischemic encephalopathy (HIE) who received postnatal magnesium therapy for perinatal asphyxia.

10. Sixty infants were included in magnesium and 60 in placebo group. Both groups were similar in baseline characteristics. Of 36 infants in magnesium group with moderate to severe HIE, 25 (69%) had neonatal seizures vs 27 (82%) of 33 infants in placebo group (p value 0.23). Among those with seizures, seizure control was achieved with single anticonvulsant in 24 infants (96%) in magnesium group vs 20 (74%) in placebo (p value 0.02).

11. Seizures got controlled early in magnesium group compared to placebo, 36.5 hours vs 55 hours (p value 0.02). At discharge, anticonvulsant was required for 2 infants in magnesium group and 3 in placebo group. Conclusions: Postnatal magnesium therapy as a neuroprotective agent in moderate-severe HIE may decrease the duration of clinical seizures and need for multiple anticonvulsants during the critical period of neuronal damage.

12. ABNORMAL MOVEMENTS IN NEONATES Also known as non-epileptic motor phenomena in the neonate. The newborn infant is prone to clinical motor phenomena that are not epileptic in nature. These include tremors, jitteriness, various forms of myoclonus and brainstem release phenomena. They are frequently misdiagnosed as seizures, resulting in unnecessary investigations and treatment with anticonvulsants, which have potentially harmful side effects.

13. Tremor, jitteriness and benign neonatal sleep myoclonus are frequently encountered, while other abnormal movements including neonatal hyperekplexia are less commonly seen. Many of these phenomena are benign and have no bearing on the neonate’s eventual neurodevelopmental outcome.

14. Differentiating nonepileptic phenomena from epileptic seizures is important to avoid unnecessary parental anxiety, investigations and treatment with potentially harmful medications. While this can often be done clinically, in some circumstances, electroencephalogram (EEG) and other neuroinvestigations are required.

15. Tremor can be defined as an involuntary, rhythmical oscillatory movement of equal amplitude around a fixed axis. It can be either fine with a high frequency (greater than 6 Hz) and low amplitude (lower than 3 cm) or coarse with a low frequency and higher amplitude.   Although tremor in older children and adults usually denotes a lesion within the cerebellum, basal ganglia, red nucleus or thalamus, this does not appear to be the case in the neonate.

16. Tremor is the most common abnormal movement encountered in the neonate. Up to two-thirds of healthy newborns will have some fine tremor in the first three days of life. One theory is that neonatal tremor is due to immaturity of spinal inhibitory interneurons causing an excessive muscle stretch reflex. As the neonate gets older and the interneurons mature, the tremor resolves . Another theory is that elevated levels of circulating catecholamines account for the tremor .

17. Jitteriness refers to recurrent tremor. In the present review, the terms tremor and jitter are used interchangeably . Parker et al reported that up to 44% of newborns were jittery. Tremor and jitteriness may be benign or pathological. Pathological conditions that may be associated with tremor include hypoglycemia, hypocalcemia , sepsis, hypoxic ischemic encephalopathy, intracranial hemorrhage, hypothermia, hyperthyroid state and drug withdrawal

18. In general, fine tremor is usually benign or secondary to metabolic disturbance such as hypoglycemia. Coarse tremor should raise suspicion of intracranial pathology, such as hypoxic ischemic encephalopathy and intracranial hemorrhage. Coarse tremor is frequently associated with the ‘neonatal hyperexcitability syndrome’ in mildly asphyxiated neonates with increased tendon reflexes and excessive Moro response.

19. Two follow-up studies, showed that jittery infants without a history of perinatal complications had normal neurodevelopmental outcome, regardless of whether the tremor was fine or coarse. Jittery neonates with a history of perinatal complications were at a 30% risk of adverse neurodevelopmental outcome, in particular, those with coarse tremor as part of the ‘neonatal hyperexcitability syndrome ’.  

20. Tremor can be differentiated from seizure if the following characteristics are observed – the tremor can be brought on with stimuli and can be stopped with gentle passive flexion and restraint of the affected limb it is not associated with ocular phenomena, such as forced eye deviation; and is not associated with significant autonomic changes such as hypertension or apnea 

21. Myoclonus is a brief shock-like movement of a limb caused by muscle contraction. It can be either localized to one body part or generalized. It can be a single event, but is often repetitive. Unlike tremor, it is irregular and arrhythmic. Myoclonus also tends to have a higher amplitude than tremor.

22. Myoclonus can originate from any level of the central nervous system, in particular, the cortex, brainstem and spinal cord. In the neonate, epileptic myoclonus is uncommon and is infrequently associated with synchronous discharges on the EEG. Epileptic myoclonus should not be provoked by stimulus, and cannot be suppressed by restraining the affected body part.

23. Benign neonatal sleep myoclonus is characterized by rhythmical myoclonic jerks seen only during sleep. It is common and frequently misdiagnosed as seizures. Benign neonatal sleep myoclonus can be distinguished from epileptic myoclonus by the fact that it only occurs in sleep and stops abruptly and consistently when the child is aroused. During myoclonus , the EEG is normal. It tends to occur in healthy, full-term newborns. It can be seen in any stage of sleep

24. NEONATAL HYPEREKPLEXIA Hyperekplexia is a rare disorder characterized by generalized muscle rigidity in the neonate, nocturnal myoclonus and an exaggerated startle reaction to auditory, tactile and visual stimuli. The startle reaction is a normal response to stimuli that consists of facial grimace and blinking followed by flexion of the trunk. The startle response is exaggerated when it interferes with normal activities, and causes apnea and frequent falls.

25. OTHER TRANSIENT MOVEMENT DISORDERS A movement disorder results from dysfunction within the basal ganglia circuitry. While many are transient and benign, some may result from permanent basal ganglia injury. Up to 1/3 of the transient benign movement disorders of childhood can be seen in the first three months of life. Benign paroxysmal torticollis is characterized by episodes of painless lateral neck flexion or torticollis often associated with pallor, emesis and abnormal eye movements. The attacks may last up to several days.

26. REFERENCES Futagi Y, Suzuki Y, Toribe Y, Kato T. Neurologic outcomes of infants with tremor within the first year of life.   Pediatr Neurol. 1999;21:557–61. [ PubMed ]   Shuper A, Zalzberg J, Weitz R, Mimouni M. Jitteriness beyond the neonatal period: A benign pattern of movement in infancy . J Child Neurol. 1991;6:243–5. [ PubMed ]  Sims M, Artal R, Quach H, Wu PYK. Neonatal jitteriness of unknown origin and circulating catecholamines .  J Perinatal Med.  1986;14:123–6  [ PubMed ] Berger A, Sharf B, Winter ST. Pronounced tremors in newborn infants: Their meaning and prognostic significance.   Clin Pediatr . 1975;14:834–5. [ PubMed ] Prechtl HFR.  The neurological Examination of the Full Term Infant . 2nd edn . London: William Heimemann ; 1991. The observation period; pp. 12–6 .

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