Please note that all guidance is currently under review and some may be out of date. We recommend that you also refer to more contemporaneous evidence in the interim.
Newborn babies have a central nervous system that is vulnerable to epileptogenic activity, and as a result they have a relatively high incidence of seizures (12 per 1,000 term infants).
Neonatal seizures are paroxysmal alterations in neurological function.
This definition allows the inclusion of clinical seizures associated with EEG abnormalities as well as paroxysmal clinical activities (such as lip smacking and cycling) that are not associated with EEG alteration.
Seizures represent the brain’s response to a wide variety of pathological insults. As such, they are often a manifestation of significant neurological disease. They are rarely idiopathic and are a major predictor of adverse outcome in the newborn.
The most common identifiable causes are:
- hypoxic-ischaemic encephalopathy-HIE (49 per cent)
- cerebral infarction (12 per cent)
- cerebral trauma (7 per cent)
- central nervous system infection (5 per cent)
- metabolic abnormalities including hypoglycaemia (3 per cent)
- narcotic drug withdrawal (4 per cent).
Differential diagnosis for seizures include the following:
- During the neonatal period any unusual repetitive or stereotypic movement may represent a seizure.
- Alterations in autonomic functions such as blood pressure or heart rate may represent seizure activity.
- The relationship between a clinical seizure and abnormal electrical activity on an EEG is inconsistent.
- The four different types of clinical seizures are summarised in the following table.
Clinical classification of neonatal seizures
|Subtle||Eye: staring, deviation, blinking etc.
Oral: chewing, sucking, lip smacking
Limbs: cycling, swimming rowing
Systemic: apnoea, tachycardia, blood pressure alterations
|It may be difficult to differentiate subtle seizures from extremes of normal behaviour. Many subtle seizures are thought to arise from the basal ganglia as a result of diminished cortical inhibition. Further depression of the cortex with anticonvulsants may not alter these seizures|
|Clonic||Usually involve one limb or one side of the body jerking rhythmically at 1-4 times per second.
Consciousness usually preserved.
|May be a clue to an underlying focal neuropathology such as haemorrhage or cerebral infarction.|
|Myoclonic||Rapid isolated jerking of muscles.
May be focal or multifocal.
|Seen in drug withdrawal (especially opiates). If it occurs during sleep then it is probably ‘benign neonatal sleep myoclonus’. Can also occur in a very severe form of encephalopathy.|
|Tonic||Sustained posturing of the limbs or trunk or deviation of the head. It may mimic decerebrate or decorticate posturing. Only 30% have EEG correlates.||Often difficult to treat with anticonvulsants|
It is important to distinguish seizures from jitteriness and benign neonatal sleep myoclonus.
There are three videos available on the Stanford Medical website which demonstrate seizure activity (available at image 11/15). The videos demonstrate:
- the appearance of seizure activity in a newborn. In contrast to jitteriness, seizure activity cannot be stopped by holding the involved area. Any newborn with seizures requires monitoring and evaluation -- it is a pathologic physical finding.
- along with the arm movement, activity in the legs is also seen in the second video. This is frequently referred to as "bicycling" motion. It is one manifestation of seizure.
- sucking movements in the first portion of the last video are a third manifestation of seizure activity. Seizures may be caused by a wide variety of problems in the newborn period, including ischaemic injury, metabolic disorders, anatomical CNS abnormalities, or neonatal abstinence syndrome.
The following clinical features will help separate jitteriness and benign neonatal sleep myoclonus from seizures.
|Benign neonatal sleep myoclonus||
Assessment of seizures involves:
- Review family history of seizures, maternal diabetes, maternal drug use, infections, evidence of fetal distress in labour and history of birth trauma to provide vital clues to the aetiology of the seizures.
- Perform physical and neurological examination.
Pathology tests include:
- blood glucose level (BGL)
- serum electrolytes, calcium and magnesium
- full blood examination (FBE)
- blood cultures
- arterial blood gas (ABG)
- lumbar puncture: if there is any suggestion of infection, then meningitis should be suspected and CSF examination performed
- If it is not possible to obtain a sample of CSF then treatment with ampicillin (100 mg/kg 12-hourly) and cefotaxime (50 mg/kg 12-hourly) should be commenced. These drug doses apply to term babies only.
Appropriate neuroimaging includes the following:
- Cranial ultrasound to exclude intracranial haemorrhage.
- MRI (or CT if MRI unavailable) is required if there are seizures following traumatic delivery, particularly if there is significant head trauma or if the seizures are clonic .
If the seizures are difficult to control, and/or require the use of multiple anticonvulsants then an EEG may assist to determine the cause of the seizures as well as guiding treatment.
- First identify and treat the underlying cause such as hypoglycaemia.
- Seizure control will be very difficult unless the underlying cause is addressed.
- There is some controversy over when to commence anticonvulsants. An anticonvulsant should be commenced if the seizure is prolonged (longer than 3 minutes), frequent (> 2-3 per hour), or associated with cardiorespiratory disturbance.
Medications that are generally effective
|Anticonvulsant||Loading dose||Maintenance||% infants controlled|
|Phenobarbitone||20 mg/kg IV or IM over 30 minutes *||2.5-5 mg/kg 12-hourly, 24 hours after the loading dose||70%|
|Phenytoin||15 to 20 mg/kg IVI over at least 30 minutes||4-5 mg/kg/dose 12-hourly in term infants starting 12 hours after the loading dose||85%|
|Midazolam||0.15 mg/kg over 5 minutes||Infusion:
|Clonazepam||0.1 to 0.25 mg IV (not per kg)||0.01 mg/kg/dose 8 hourly, 8 hours after the loading dose||90-100%|
|Pyridoxine **||100 mg IV or IM||50 mg daily|
- *Some recommend additional loading doses of 5 mg/kg up to a total of 40 mg/kg. However, such high doses cause CNS depression, which may complicate the assessment of infants with hypoxic ischaemic encephalopathy.
- They may also cause respiratory depression, which may necessitate endotracheal intubation.
- Some of the above drugs can also be a negative inotrope, which underlines the importance of monitoring and supporting blood pressure and circulation to maintain adequate cerebral perfusion. (Negative inotropes weaken the force of the heartbeat)
- **Pyridoxine may be tried if the aetiology is obscure and the seizures are not responding to the usual medications.
Areas of uncertainty in clinical practice
Areas of uncertainty include the following:
- Routine anticonvulsant therapy following perinatal asphyxia should be restricted to those babies who are having prolonged or frequent clinical seizures.
- It remains unclear whether the goal of anticonvulsant therapy should be the complete elimination of abnormal EEG activity or the abolition of clinical seizures. The elimination of abnormal EEG activity may require very large doses of anticonvulsants. These may have adverse effects upon the developing brain. Similarly, it is not clear how long therapy should be continued following the initial seizures.
- There is no indication that prolonged treatment of anticonvulsant therapy reduces the risk for the later development of epilepsy.
- The only recommendation for continuing anticonvulsant therapy (phenobarbitone 3-4 mg/kg/day) is in the setting of profound neonatal encephalopathy or severe brain injury and then only for six to eight weeks.
- Queensland Health (2011) Clinical guidelines neonatal seizures (PDF)
- Photo Gallery Index: Newborn Nursery at LPCH - Stanford University, School of Medicine
- Evans D, Levene M. Cochrane Database Syst Rev 2000;(2):CD001240
- Hill A. Neonatal Seizures. Pediatr. Rev. 2000 21: 117-121.
- Rennie J. 1999 Seizures in the newborn. In, Rennie JM and Roberton NRC (eds) Textbook of Neonatology, 3rd edn. Edinburgh, Churchill Livingstone, pp 1213-1223
- Menkes JH. 1991 Paroxysmal disorders. In Taeusch HW, Ballard RA and Avery ME (eds) Schaeffer and Avery's Diseases of the newborn, 6th edn, Philadelphia, W.B. Saunders Company, pp 445-449.
- Volpe JJ. 2001 Neonatal seizures. In Volpe JJ, ed. Neurology of the newborn. 4th edn. Philadelphia, W.B. Saunders Company
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First published: May 2015
Last web update: October 2018
Review by: August 2019
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Page last updated: 17 Feb 2021