Neonatal stroke

Intracranial haemorrhage

Subarachnoid haemorrhage

Subarachnoid haemorrhage (SAH) arises as a result of either rupture of veins bridging the subarachnoid space or rupture of vessels within the leptomeningeal plexus. SAH is a very common finding at autopsy and does not necessarily indicate the presence of underlying brain injury. Large SAH is particularly likely in babies with coagulopathy. A large collection of clotted subarachnoid blood can cause a convex space-occupying lesion (convexity haemorrhage), usually over the temporal or occipital region with an adjacent parenchymal venous infarction.
Convulsions are the most common sign associated with SAH in the term infant and usually present in the first 24 hours of life. Blood is always present in the subarachnoid fluid on lumbar puncture. The prognosis for SAH is good unless there is an extensive convexity bleed.
Cranial ultrasound is unreliable method for diagnosing this condition. Diagnosis is made by CT or MRI.


Subdural haemorrhage

Subdural haemorrhage (SDH) arises as a result of rupture of bridging veins, tearing of dural membranes or laceration of the dura from skull displacement. SDH is particularly associated with vacuum extraction.
Clinical signs include tense fontanelle, , hypotonia and lethargy; symptoms related to posterior fossa injury include apnoea, irregular sighing respiration, fixed bradycardia, opisthotonus and skewed deviation of the eyes. Seizures may not be prominent in subtentorial bleeds. SDH’s are also most reliably detected on CT or MRI scanning.



Most cases of SDH do not require active management of the haemotoma; neurosurgical intervention depends on the size and position of the lesion and whether the baby shows clinical signs of brainstem compression or obstruction to CSF outflow.


Cerebral artery infarction

This may be detected within the first few days of life and is an important cause of neonatal seizures. The most characteristic appearance is a large unilateral echodense region extending from the periventricular region to the cortex. It is localised to one of the cerebral artery distribution regions (most commonly the middle cerebral artery region). Over the next few weeks the echodensity becomes less obvious and multiple cysts may appear within the infarcted region. If multifocal infarction has occurred, several discrete areas of increased parenchymal echodensities may be observed.