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Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury

View Article: PubMed Central - PubMed

ABSTRACT

Perinatal hypoxic–ischemic brain injury results in neonatal hypoxic–ischemic encephalopathy and serious long-term neurodevelopmental sequelae. Magnetic resonance imaging (MRI) of the brain is an ideal and safe imaging modality for suspected hypoxic–ischemic injury. The pattern of injury depends on brain maturity at the time of insult, severity of hypotension, and duration of insult. Time of imaging after the insult influences the imaging findings. Mild to moderate hypoperfusion results in germinal matrix hemorrhages and periventricular leukomalacia in preterm neonates and parasagittal watershed territory infarcts in full-term neonates. Severe insult preferentially damages the deep gray matter in both term and preterm infants. However, associated frequent perirolandic injury is seen in term neonates. MRI is useful in establishing the clinical diagnosis, assessing the severity of injury, and thereby prognosticating the outcome. Familiarity with imaging spectrum and insight into factors affecting the injury will enlighten the radiologist to provide an appropriate diagnosis.

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A 24-day-old term neonate with low birth weight, CSF proven meningitis, and meconium-stained amniotic fluid showing prolonged severe hypoxic ischemic injury; mixed pattern involving deep grey matter and white matter. Axial T1WI at the level of basal ganglia (A) and lateral ventricles (B). Note the abnormal T1 hyperintensity of the basal ganglia and thalami (compare with Figure 1) and T1 hypointensity of cystic changes in the periventricular and subcortical white matter. Also note the false positive T1 hyperintensity of the posterior limb of internal capsule. Axial T2WI at the level of basal ganglia (C) and lateral ventricles (D). Note the abnormal T2 hypointensity of the basal ganglia and thalami (compare with Figure 1) and T2 hyperintensity at the level of posterior limb of internal capsule. Also note the T2 hyperintensity of cystic changes in the periventricular and subcortical white matter. (E, F) Axial FLAIR images at the level of basal ganglia and lateral ventricles. Note the cystic changes in the periventricular and subcortical white matter
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Figure 13: A 24-day-old term neonate with low birth weight, CSF proven meningitis, and meconium-stained amniotic fluid showing prolonged severe hypoxic ischemic injury; mixed pattern involving deep grey matter and white matter. Axial T1WI at the level of basal ganglia (A) and lateral ventricles (B). Note the abnormal T1 hyperintensity of the basal ganglia and thalami (compare with Figure 1) and T1 hypointensity of cystic changes in the periventricular and subcortical white matter. Also note the false positive T1 hyperintensity of the posterior limb of internal capsule. Axial T2WI at the level of basal ganglia (C) and lateral ventricles (D). Note the abnormal T2 hypointensity of the basal ganglia and thalami (compare with Figure 1) and T2 hyperintensity at the level of posterior limb of internal capsule. Also note the T2 hyperintensity of cystic changes in the periventricular and subcortical white matter. (E, F) Axial FLAIR images at the level of basal ganglia and lateral ventricles. Note the cystic changes in the periventricular and subcortical white matter

Mentions: The injury primarily affects the deep gray matter–posterior putamina, ventrolateral thalami, hippocampi, and dorsal brainstem, and occasionally involves the perirolandic cortex. Usually minor cortical injuries may be seen, and more prolonged insults result in diffuse cortical involvement [Figure 12]. As described, DWI is the first sensitive modality beginning from the first day of life [Figure 13E and F]. The involved regions show T1 hyperintensity beginning from the 2nd day of life and persist for several months [Figure 11A and B, 12A and B, 13A and B]. These regions may show mildly increased T2 signal intensity (denoting edema), beginning from the 3rd day of life [Figure 13C and D]. By 7–10 days, basal ganglia and thalami show T2 hypointensity [Figure 12C and D). Chronic stage is marked by atrophy and T2 hyperintensity of the injured regions, particularly in the ventrolateral thalami and posterior putamina [Figure 11C and D]. Extensive injury involving gray and white matter finally results in cystic encephalomalacia [Figure 12].


Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury
A 24-day-old term neonate with low birth weight, CSF proven meningitis, and meconium-stained amniotic fluid showing prolonged severe hypoxic ischemic injury; mixed pattern involving deep grey matter and white matter. Axial T1WI at the level of basal ganglia (A) and lateral ventricles (B). Note the abnormal T1 hyperintensity of the basal ganglia and thalami (compare with Figure 1) and T1 hypointensity of cystic changes in the periventricular and subcortical white matter. Also note the false positive T1 hyperintensity of the posterior limb of internal capsule. Axial T2WI at the level of basal ganglia (C) and lateral ventricles (D). Note the abnormal T2 hypointensity of the basal ganglia and thalami (compare with Figure 1) and T2 hyperintensity at the level of posterior limb of internal capsule. Also note the T2 hyperintensity of cystic changes in the periventricular and subcortical white matter. (E, F) Axial FLAIR images at the level of basal ganglia and lateral ventricles. Note the cystic changes in the periventricular and subcortical white matter
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 13: A 24-day-old term neonate with low birth weight, CSF proven meningitis, and meconium-stained amniotic fluid showing prolonged severe hypoxic ischemic injury; mixed pattern involving deep grey matter and white matter. Axial T1WI at the level of basal ganglia (A) and lateral ventricles (B). Note the abnormal T1 hyperintensity of the basal ganglia and thalami (compare with Figure 1) and T1 hypointensity of cystic changes in the periventricular and subcortical white matter. Also note the false positive T1 hyperintensity of the posterior limb of internal capsule. Axial T2WI at the level of basal ganglia (C) and lateral ventricles (D). Note the abnormal T2 hypointensity of the basal ganglia and thalami (compare with Figure 1) and T2 hyperintensity at the level of posterior limb of internal capsule. Also note the T2 hyperintensity of cystic changes in the periventricular and subcortical white matter. (E, F) Axial FLAIR images at the level of basal ganglia and lateral ventricles. Note the cystic changes in the periventricular and subcortical white matter
Mentions: The injury primarily affects the deep gray matter–posterior putamina, ventrolateral thalami, hippocampi, and dorsal brainstem, and occasionally involves the perirolandic cortex. Usually minor cortical injuries may be seen, and more prolonged insults result in diffuse cortical involvement [Figure 12]. As described, DWI is the first sensitive modality beginning from the first day of life [Figure 13E and F]. The involved regions show T1 hyperintensity beginning from the 2nd day of life and persist for several months [Figure 11A and B, 12A and B, 13A and B]. These regions may show mildly increased T2 signal intensity (denoting edema), beginning from the 3rd day of life [Figure 13C and D]. By 7–10 days, basal ganglia and thalami show T2 hypointensity [Figure 12C and D). Chronic stage is marked by atrophy and T2 hyperintensity of the injured regions, particularly in the ventrolateral thalami and posterior putamina [Figure 11C and D]. Extensive injury involving gray and white matter finally results in cystic encephalomalacia [Figure 12].

View Article: PubMed Central - PubMed

ABSTRACT

Perinatal hypoxic–ischemic brain injury results in neonatal hypoxic–ischemic encephalopathy and serious long-term neurodevelopmental sequelae. Magnetic resonance imaging (MRI) of the brain is an ideal and safe imaging modality for suspected hypoxic–ischemic injury. The pattern of injury depends on brain maturity at the time of insult, severity of hypotension, and duration of insult. Time of imaging after the insult influences the imaging findings. Mild to moderate hypoperfusion results in germinal matrix hemorrhages and periventricular leukomalacia in preterm neonates and parasagittal watershed territory infarcts in full-term neonates. Severe insult preferentially damages the deep gray matter in both term and preterm infants. However, associated frequent perirolandic injury is seen in term neonates. MRI is useful in establishing the clinical diagnosis, assessing the severity of injury, and thereby prognosticating the outcome. Familiarity with imaging spectrum and insight into factors affecting the injury will enlighten the radiologist to provide an appropriate diagnosis.

No MeSH data available.


Related in: MedlinePlus