Neonatal cranial ultrasound interpretation: a clinical audit reference
Arch Dis Child Fetal Neonatal Ed 2001;84:F92-5



  1. The coronal view demonstrates bilateral, posterior �flares�. The left parasagittal view confirms that the area of increased echodensity is in the region of the trigone.
  2. Serial ultrasound scans should be performed, and we would recommend scanning to at least 21 days after birth, a check scan at 34-35 weeks and a scan at term. Persistence of abnormality necessitates continued surveillance with neurodevelopmental follow-up.
  3. The causes of early ´flares´ are probably multiple and they are associated with a wide range of outcomes. Should the flares resolve within the next few days, they are not considered to be of major neurodevelopmental significance. Persistence of a flare without cystic change may be associated with increased clumsiness and mild diplegia.17 Flares may also undergo later cystic change, usually within 2-3 weeks with a high risk of cerebral palsy.18
  1. This parasagittal view shows a multi-loculated cystic lesion in the caudo-thalamic notch on the floor of the lateral ventricle.
  2. Whilst cysts in this region are common,19 and often due to resolving germinal layer haemorrhage (GLH), the multicystic and bulging appearances here are not typical of this aetiology.20 In addition, GLH would be unexpected at this gestation. The presence of prolonged jaundice should suggest other important causes, particularly cytomegalovirus (CMV) infection,21 22 which may be of postnatal acquisition in very preterm infants. Multicystic change in this region may also occur in very preterm infants after 4-8 weeks often in those with chronic lung disease,23 when it appears to be of benign significance. Other less common associations include dexamethasone, chromosomal abnormality and metabolic conditions, e.g. Zellwegers Syndrome.
  3. The prognosis is good,20 24 unless a specific cause e.g. congenital CMV infection or other metabolic problems, is found.



  1. The scans show bilateral lateral ventricular dilatation, greater on the right, and the ventricular margin on the left is slightly irregular. There is a large right-sided communicating porencephalic cyst in the parietal region. There is shift of the midline to the left. The third ventricle is also dilated. There is poor tissue definition posteriorly on the parasagittal view.
  2. Ventricular size and head circumference should be monitored regularly, and serial clinical neurological assessments are needed. A lumbar puncture would be recommended to check for CSF pressure and contents and for evidence of communication. If lumbar puncture does not indicate communication of CSF with the ventricles a ventricular tap on the side of the lesion to measure pressure, is warranted in view of the midline shift. If hydrocephalus develops, then insertion of a reservoir or shunt should be considered. However the ventriculomegaly will not necessarily worsen. Surveillance of head circumference and ventricular size should continue post-term for several months.
  3. Neurodevelopmental problems are probable, with a left-sided spastic hemiplegia being the most likely from these images. A MRI scan at term to assess the symmetry of myelination in the internal capsule allows accurate prognostication with regard to hemiplegia.25 A guarded to poor prognosis is appropriate, depending on the progress of the lesion and the neurology � however many of these children do surprisingly well despite their hemiplegia. There is a need for long term assessment of visual, visuoperceptual, language abilities and, behavioural and seizure development.
  1. There is bilateral periventricular cystic change in the fronto-parietal cortex, which is more pronounced on the right and confirmed by the right parasagittal view. The ventricles are moderately enlarged and the ventricular margins are slightly irregular.
  2. A scan at term is recommended to check that there has been no further ventricular dilatation, cyst formation (unlikely after 35 weeks) or evidence of global atrophy. Neurodevelopmental follow-up is needed
  3. A guarded prognosis is appropriate. Despite the presence of white matter damage, the cysts are located anteriorly in an area that should not lead to cerebral palsy.17 There are, however, other abnormalities on the scan i.e. the irregular ventricular margin and dilatation that may represent a more global insult.
  1. There are bright echodensities in the right subependymal zone, and the adjacent right parietal cortex, probably due to haemorrhagic parenchymal infarction. There is a blood clot in the right lateral ventricle and both lateral ventricles are enlarged, the right more than the left.
  2. Serial imaging and measurement of ventricular size and head circumference are indicated. Neurological examination with developmental follow-up will be necessary.
  3. A guarded prognosis is necessary. This lesion is likely to evolve to a right porencephalic cyst, and the prognostic comments for Question 3 would apply
  1. There is bilateral thalamic echogenicity, more easily seen in the 5MHz scans. There is also some compression of the normal gyral pattern and the lateral ventricles.
  2. The scan findings are compatible with severe, acute basal ganglia injury. Further assessment should be made. EEG and cerebral function monitoring in the first few days,26 27 and Doppler measurement of cerebral blood flow velocity between days 2 and 4,28 are good bedside prognostic tools. Whilst serial US scans should be done, prognostic information from them can be difficult and much more specific information obtained from a MRI scan done after a few days.29 30
  3. It is inappropriate to give a prognosis based on a cranial US scan only at this early stage, but if pushed to do so we would remain extremely guarded until the results of the other tests (above) were known, and a clearer clinical picture had formed. However, in our experience, thalamic brightness is important and carries a poor prognosis.
  4. The 5MHz setting is useful in term infants. It interrogates deeper structures such as the thalami and posterior fossa. Evolving thalamic damage from global hypoxia-ischaemia may not be well seen with a 7.5Mhz scan, as illustrated here.
(references 1-16 are in the main article)

17. De Vries LS, Regev R, Pennock JM, Wigglesworth JS, Dubowitz LM. Ultrasound evolution and later outcome of infants with periventricular densities. Early Hum Dev 1988;6(2-3):225-33.

18. Fawer CL, Diebold P, Calame A. Periventricular leucomalacia and neurodevelopmental outcome in preterm infants. Arch Dis Child 1987;62:30-6.

19. Shen EY, Huang FY. Subependymal cysts in normal neonates. Arch Dis Child 1985;60:1072-4.

20. Rademaker KJ, de Vries LS Barth PG. Subependymal pseudocysts:ultrasound diagnosis and findings at follow up. Acta Paediatr Scand 1993;82:394-9.

21. Butt W, Mackay RJ, de Crespigny LC, Murton LJ, Roy RN. Intracranial lesions of congenital cytomegalovirus infection detected by ultrasound scanning. Pediatrics 1984;73:611-14.

22. Sofer S, Maor E, Barki Y. Cytomegalic virus periventriculitis: a sonographic picture mimicking ventricular hemorrhage. J Clin Ultrasound 1985;13:574-6.

23. Smets K, De Kezel C, Govaert P. Subependymal caudothalamic groove hyperechogenicity and neonatal chronic lung disease. Acta Paediatr 1997;86:1370-3.

24. Ramenghi LA, Domizio S, Quartulli L, Sabatino G. Prenatal pseudocysts of the germinal matrix in preterm infants. J Clin Ultrasound 1997;25:169-73.

25. de Vries LS, Groenendaal F, van Haastert IC, Eken P, Rademaker KJ Meiners LC. Assymetrical myelination of the posterior limb of the internal capsule in infants with periventricular haemorrhagic infarction: an early predictor of hemiplegia. Neuropediatrics 1999;30:314-19.

26. Eken P, Toet MC, Groenendaal F, de Vries LS. Predictive value of early neuroimaging, pulsed Doppler and neurophysiology in full term infants with hypoxic-ischaemic encephalopathy. Arch Dis Child Fetal Neonatal Ed 1995;73:F75-F80.

27. al Naqueeb N, Edwards AD, Cowan FM, Azzopardi D. Assessment of neonatal encephalopathy by amplitude-integrated electroencephalography. Pediatrics 1999;103:1263-71.

28. Levene MI, Fenton AC, Evans DH, Archer LN, Shortland DB, Gibson NA. Severe birth asphyxia and abnormal cerebral blood-flow velocity. Dev Med Child Neurol 1989;31:427-34.

29. Rutherford M, Pennock J, Schweiso J, Cowan FM, Dubowitz L. Hypoxic-ischaemic encephalopathy: early and late magnetic resonance imaging findings in relation to outcome. Arch Dis Child Fetal Neonatal Ed 1996;75:F145-F151.

30. Rutherford MA, Pennock JM, Counsell SJ, Mercuri E, Cowan FM, Dubowitz LMS, Edwards AD. Abnormal magnetic resonance signal in the internal capsule predicts poor neurodevelopmental outcome in infants with hypoxic-ischemic encephalopathy. Pediatrics 1998;102(2 Pt 1):323-8.