This document discusses the use of magnesium sulfate in treating neonatal seizures. It provides dosing and administration guidelines for magnesium sulfate via intravenous infusion to treat seizures refractory to other anticonvulsants, hypomagnesaemia, and severe persistent pulmonary hypertension. Possible adverse effects and special considerations are also outlined. The document also examines the use of magnesium sulfate in reducing mortality and neurological morbidity in neonates with moderate to severe perinatal asphyxia.

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) The 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 –
a) the tremor can be brought on with stimuli
and can be stopped with gentle passive
flexion and restraint of the affected limb
b) it is not associated with ocular phenomena,
such as forced eye deviation; and
c) 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.

27. THANK YOU
QUESTIONS?