Neonatal seizures or neonatal convulsions are epileptic fits occurring from birth to the end of the neonatal period. The neonatal period is the most vulnerable of. Neonatal Seizures. DEFINITION: A Neonatal seizures are the most common overt manifestation of neurological Benign Familial Neonatal Convulsions. Neonatal seizures can be difficult to diagnose because the seizure may be short and subtle. In addition, symptoms of neonatal seizures may mimic normal.
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Seizures, Syndromes and Management. Bladon Medical Publishing; Neonatal seizures or neonatal convulsions are convlusion fits occurring from birth to the end of the neonatal period. They may be short-lived events lasting for a few days only.
However, they often signify serious malfunction of or damage to the immature brain and constitute a neurological emergency demanding urgent diagnosis and management. The prevalence is approximately 1. The incidence in pre-term infants is very high 57— per live births.
Neonatal seizures, as with any other type of seizure, are nonattale, repetitive and stereotypical events. They are usually clinically subtle, inconspicuous and difficult to recognise from the normal behaviours of the inter-ictal periods or physiological phenomena. There is no recognisable post-ictal state. Generalised tonic clonic seizures GTCS are exceptional. The most widely used scheme is by Volpe 20 of five main types of neonatal seizure.
The neonatal period is defined as the first 28 days of life of a full-term infant. Neonatal seizures are those that occur from birth to the end of the neonatal period. Chronological age is the actual legal age of the infant from the time of birth.
Neonatal seizures differ from those of older children and adults. The most frequent neonatal seizures are described as subtle because the clinical manifestations are frequently overlooked.
These include tonic, horizontal deviation of the eyes with or without jerking, eyelid blinking or fluttering, sucking, smacking or other oral—buccal—lingual movements, swimming or pedalling movements and, occasionally, apnoeic spells. Other neonatal seizures occur as tonic extension of the limbs, mimicking decerebrate or decorticate posturing. These occur particularly in premature infants. Multifocal clonic seizures characterised by clonic movements of a limb, which may migrate to other body parts or other limbs or focal clonic seizures, which are much more localised, may occur.
In the latter, the infant is usually not unconscious.
Rarely, myoclonic seizures may occur and the EEG pattern is frequently that of suppression—burst activity. The tonic seizures have a poor prognosis because they frequently accompany intraventricular haemorrhage.
The myoclonic seizures also have a poor prognosis because they are frequently a part of the early myoclonic encephalopathy syndrome. In another scheme by Mizrahi 12 neonatal seizures are classified as follows: Nearly one-quarter of infants experience several seizure types and the same seizure may manifest with subtle, clonic, myoclonic, autonomic or other symptoms Figure 5.
Ictal EEG patterns in a 2-day-old boy with right middle cerebral artery thrombosis Top and middle: Apnoeic, myoclonic, clonic and subtle seizure of motor automatisms associated with various ictal EEG patterns and locations.
Subtle seizures are far more common than other types of neonatal seizures. They are described as subtle because the clinical manifestations are frequently overlooked. They imitate normal behaviours and reactions. These include the following. Clonic seizures are rhythmic jerks that may localise in a small part of the face or limbs, axial muscles and the diaphragm or be multifocal or hemiconvulsive.
Tonic seizures manifest with sustained contraction of facial, limb, axial and other muscles. They may be focal, multifocal or generalised, symmetrical or asymmetrical.
Neonatal seizure – Wikipedia
Truncal or nonztale tonic extension imitates decerebrate or decorticate posturing. Myoclonic seizures are rapid, single or arrhythmic repetitive jerks. They may affect a finger, a limb or the whole body. They may mimic the Moro reflex and startling responses. They are more frequent in pre-term than full-term infants indicating, if massive, major brain injury and poor prognosis.
Myoclonic seizures are associated with the most severe brain damage.
Neonates have cortical, reticular and segmental types of myoclonus, similar to adult forms. Spasms producing flexion or extension similar to those of West syndrome are rare. They are slower than myoclonic seizures and faster than tonic seizures. The duration of neonatal seizures is usually brief 10 s to 1—2 min and repetitive nonafale a median of 8 min in between each seizure.
Longer seizures and status epilepticus develop more readily at this age, but convulsive neonatal status epilepticus is not as severe as that of older infants and children.
By definition all neonatal seizures are epileptic in origin, generated by abnormal, paroxysmal and hypersynchronous neuronal discharges characteristic of epileptogenesis. The characterisation of neonatal seizures as epileptic and non-epileptic by Kellaway and Mizrahi 41027 is a topic of considerable debate.
Focal clonic, focal tonic and some types of myoclonic jerks are genuine epileptic seizures documented with ictal EEG changes and they have a high correlation with focal brain lesions and a favourable short-term outcome. Many of the subtle seizures, generalised tonic posturing and some myoclonic symptoms may be non-epileptic seizures.
These show clinical similarities to reflex behaviours of the neonates, they are not associated with ictal EEG discharges and are commonly correlated with diffuse abnormal brain processes such as hypoxic—ischaemic encephalopathy and a poor short-term outcome.
Hence, the term brain stem release phenomena: The argument to support the non-epileptic nature of these episodic clinical events is that they have the following characteristics.
Aetiology of neonatal seizures is extensive and diverse Table 5. The prevalence and significance of aetiological factors are continuously changing and differ between developed and developing countries depending on available improved neonatal and obstetric care.
By far the commonest cause is hypoxic—ischaemic encephalopathy.
Intracranial haemorrhage and infarction, stroke 29 and prenatal and neonatal infections are common. Most previously common acute metabolic disturbances such as electrolyte and glucose abnormalities have been minimised because of improved neonatal intensive care and awareness of nutritional hazards. Late hypocalcaemia is virtually eliminated, while electrolytic derangement and hypoglycaemia are now rare. Inborn errors of metabolism such as urea cycle disorders convulsiin rare.
Pyridoxine dependency, with seizures in the first days of life which are reversible with treatmentis exceptional. Exogenous causes of neonatal convulsions may be iatrogenic or due to drug withdrawal in babies born to mothers on drugs.
In most cases, the neonate may present with a combination of different neurological disturbances, each of which can cause seizures. The early postnatal development time is a period of increased susceptibility to seizures in relation to other convvulsion. This may be due to a combination of factors specific to the developing brain that enhance excitation and diminish inhibition.
There is an unequal distribution of anticonvulsant and proconvulsant neuro-transmitters and networks. Animal studies are contradictory regarding the effect of prolonged epileptic seizures on the developing immature brain.
Neonatal seizures represent one of the very few emergencies in the newborn.
Abnormal, repetitive and stereotypic behaviours of neonates convlsion be suspected and evaluated as possible seizures. Polygraphic video— EEG recording of suspected events is probably mandatory for an incontrovertible seizure diagnosis.
Etiology of convulsions in neonatal and infantile period.
Confirmation of neonatal seizures should initiate urgent and appropriate clinical and laboratory evaluation for the aetiological cause Table 5. Family and prenatal history is important. A thorough physical examination of the neonate should be coupled with urgent and comprehensive biochemical tests for correctable metabolic disturbances.
Although rare, more severe inborn errors of metabolism should be considered for diagnosis and treatment. Cranial ultrasonography, brain imaging with X-ray computed tomography CT scan and preferably magnetic resonance imaging MRI 37 should be used for the detection of structural abnormalities such as malformations of cortical development, intracranial haemorrhage, hydrocephalus and cerebral infarction.
Cranial ultrasonograghy is the main imaging modality of premature neonates and well suited for the study of neonates in general.
It is performed at convulslon bedside and provides effective assessment of ventricular size and other fluid-containing lesions as well as effective viewing of haemorrhagic and ischaemic lesions and their evolution. Cranial ultrasonography is limited in resolution and the type of lesions that it can identify. A CT brain scan is often of secondary or adjunctive importance to ultrasound. Last-generation CT brain scan images are of high resolution, nonatlae be generated within seconds and can accurately detect haemorrhage, infarction, gross malformations and ventricular and other pathological conditions.
A CT scan has low sensitivity in many other brain conditions such as abnormalities of cortical development where MRI is much superior. However, MRI interpretation should take into consideration the normal developmental and maturational states of neonates and infants. In infants younger than 6 months, cortical abnormalities are detected with T2-weighted images, whereas T1-weighted images are needed for the evaluation of brain maturation.
Polygraphic studies with simultaneous video—EEG recording are essential. Inter-ictal EEG epileptogenic spikes or sharp slow wave foci are not reliable markers at this age. Certain inter-ictal EEG patterns may have diagnostic significance Figure 5. Zip-like electrical discharges Top and middle: Continuous recording in a neonate with severe brain hypoxia. Zip-like electrical discharges consist of high frequency rapid spikes of accelerating and more Inter-ictal EEG in a neonate with benign neonatal non-familial seizures.
The theta pointu alternant pattern is usually associated with a good prognosis. The burst—suppression pattern in a neonate with severe hypoxic encephalopathy.
Etiology of convulsions in neonatal and infantile period.
Background EEG activity, mainly in serial EEGs, often provides objective evidence of the degree and severity of the underlying cause. The suppression—burst pattern is relatively comvulsion in the neonatal period. It is associated with heterogeneous seizures and can be induced by drugs.
Documentation of seizures with an ictal EEG is often mandatory in view of the subtle clinical seizure manifestations Figures 5. EEG ictal activity may be focal or multifocal appearing in a normal or abnormal background. The electrical ictal seizure EEG clnvulsion of neonatal seizures vary significantly even in the same neonate and in the same EEG recording Figure 5.