Type:
Educational Exhibit
Keywords:
Neuroradiology brain, MR, Imaging sequences, Haemorrhage, Ischaemia / Infarction
Authors:
Y. Gulseren1, M. Ayaz1, G. Durukan Günaydın1, I. Gülmez1, B. Atalay1, B. Baysal2; 1Istanbul/TR, 234437, AL/TR
DOI:
10.1594/ecr2018/C-1920
Findings and procedure details
Patterns of Brain Injury
1.
Preterm neonates
In preterm neonates with immature brain,
periventricular white matter (supplied by ventriculopetal penetrating arteries) is most vulnerable to the HI injury.
Mild to moderate HI injury results in PVL,
that may be focal (adjacent to frontal horns and trigones) or diffuse [Figure 1].
Progressive necrosis results in loss of periventricular white matter,
passive ventriculomegaly (irregular margins of the bodies and trigones of lateral ventricles) and thinning of corpus callosum .
Germinal matrix hemorrhage (GMH) is typically seen in preterm infants with HI injury.GMH can be graded into subependymal hemorrhage (Grade 1),
intraventicular hemorrhage without (Grade 2) and with (Grade 3) ventricular dilatation or parenchymal extension of the bleed with coexisting venous infarction (Grade 4).hypoxic-ischemic events in preterm neonates manifest predominantly as damage to the deep gray matter structures and brainstem.
2.
Term neonates
In term neonates,
mild to moderate HI injury produces parasagittal watershed zone infarcts between anterior/MCA and middle/posterior cerebral artery.
Both the cortex and underlying subcortical white matter are involved .
Severe HI injury results in injury to metabolically active tissues such as ventrolateral thalami,
posterior putamina,
hippocampi,
brainstem,
corticospinal tracts,
and sensorimotor cortex .
BG injury is more common than parasagittal pattern and carries the worst prognosis.
Severe global hypoxia may also lead to diffuse cerebral edema .
MR scan of term infants with chronic HIE may reveal cortical atrophy and thinning (ulegyria) and multicystic encephalomalacia.
The treatment is primarily supportive with correction of the underlying cause.
The supportive care includes maintenance of adequate ventilation,
metabolic status and vitals,
and control of brain edema and seizure.
The prognosis of HIE depends on the severity of injury and gestational age of the infant.
Cortex and BG involvement on conventional MRI,
diffusion restriction on DWI,
increased lactate on MRS within 24 h of life and severe EEG abnormalities predict poor outcome.
Term infants with mild encephalopathy generally have good prognosis and show complete recovery; however,
20% of infants may die in the neonatal period and another 25% may develop significant neurological deficit.
Preterm infants,
compared with term infants have poor prognosis.