Neurological disorders


Neonatal encephalopathy can be caused by hypoxia ischaemia due to birth asphyxia but also by other conditions including metabolic disorders and infections. These conditions should be excluded before a confident diagnosis of hypoxic ischaemic encephalopathy due to birth asphyxia can be accepted.

Table 11.5 Classification of severity of hypoxic ischaemic encephalopathy in the term newborn

Severity of encephalopathy

Table 11.5 Classification of severity of hypoxic ischaemic encephalopathy in the term newborn

Severity of encephalopathy

Clinical features




Level of consciousness



Stuporous, comatose

Muscle tone


Mild hypotonia






Intracranial pressure




Primitive reflexes



Weak or absent






Autonomic function


Generalized parasympathetic activity

Both systems depressed

sympathetic activity

EEG findings

Normal (awake)

Early: low-voltage delta and theta

Early: periodic pattern and suppression

Later: periodic pattern, seizures

Later: generalized suppression


<24 h

2-14 days


Data from Sarnat and Sarnat (1976), source from Roberton's Textbook of Neonatology 2005.

Data from Sarnat and Sarnat (1976), source from Roberton's Textbook of Neonatology 2005.

Hypoxia-ischaemia followed by resuscitation may lead to apparent recovery followed by inexorable deterioration beginning 6-8 h later and ending in severe cerebral injury. Consequently, it is frequently difficult to determine the prognosis soon after birth on clinical grounds alone. However, if asphyxia is severe or happened some time before delivery the infant will not develop spontaneous breathing; therefore, if despite advance life support there is no sign of spontaneous breathing 20 min after birth the outcome is extremely poor.

Hypoxic ischaemic encephalopathy is graded clinically using clinical signs. A frequently used grading system -that of Sarnat and Sarnat - is given in Table 11.5. Infants with grade 1 encephalopathy have a very good prognosis whereas infants with Grade 3 almost all die or are severely impaired. About half the infants with Grade 2 have severe neurodevelopmental impairment. Unfortunately a large number of infants at risk fall into Grade 2, limiting the utility of the system.

If asphyxia is suspected, further investigation is required, preferably by paediatricians specialized in neonatal neurology and with access to sophisticated equipment such as electrophysiology, magnetic resonance imaging or magnetic resonance spectroscopy. Diagnosis and an accurate guide to prognosis can then be obtained.


Cerebral palsy is a non-progressive brain syndrome which may not be apparent until after the first year of life and which cannot be confidently diagnosed at birth. Population based studies have shown that about 20% of all cases of cerebral palsy are due to birth asphyxia in the term infant, approximately one third are associated with preterm birth, and the remainder have no obvious fetal or perinatal antecedent.


Convulsions occurring just after delivery in term infants may be due to hypoxic ischaemic encephalopathy, metabolic disorders, infections, hypoglycaemia, hypocal-caemia, hypomagnesaemia or pyridoxine deficiency. Many otherwise idiopathic fits are caused by focal cerebral infarction, which have a much better prognosis than generalized hypoxic ischaemic injury but are difficult to diagnose without magnetic resonance imaging.


Preterm infants are at high risk of cerebral injury and approximately 10% of infantsborn preterm develop significant neurodevelopmental impairment and another 10% have minor neurological lesions: two classical lesions which occur in preterm infants.

First, intracerebral haemorrhage may affect only the germinal layers or ventricles in which case the prognosis is good; however, haemorrhage into the brain parenchyma is caused by haemorrhagic infarction and this is associated with neurodevelopmental impairment.

Second, in periventricular leucomalacia there is a general loss of white matter, sometimes with cavitation. Whereas haemorrhagic parenchymal infarctions can be usually seen by cerebral ultrasonography, periventricu-lar leucomalacia is difficult to see and is probably under diagnosed. Both these conditions seem to be becoming less common than a more subtle loss of cerebral matter; this may present as dilated cerebral ventricles on cerebral ultrasonography but is often only apparent with magnetic resonance imaging. The aetiology of this condition is poorly understood, the extremely preterm infant seems to be most at risk. The usefulness of cerebral ultrasonogra-phy alone to predict neurological prognosis in extremely preterm infants is therefore limited.

The more mature preterm infants with normal ultrasound scans at discharge from intensive care have a very low risk of neurodevelopmental impairment whereas those with definable loss of brain tissue from whatever cause have a greater than 50% chance of long-term impairment.


Brachial plexus injury occurs in 0.4-2.5 per 1000 live births. The commonest type, Erb's palsy, involves C5 and 6 nerve roots. The incidence has not declined over the past few decades; however, the prognosis for recovery, has improved with full recovery expected in the majority of babies with Erb's palsy. Injury to the brachial plexus results in the characteristic waiters tip position, a fracture to the clavical may also be present. Careful neurological examination is needed to determine the level of the lesion as this affects the prognosis for recovery of function; an associated Horner's syndrome is a bad prognostic sign.

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