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Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury

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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 12-day-old full-term neonate; HIE stage II—severe hypoxic ischemic injury involving deep grey matter structures. (A, B) Axial T1WI at the level of basal ganglia shows abnormal T1 hyperintensity of the ventrolateral thalamus and posterior putamen (black arrows). Note the absence of normal T1 hyperintensity of the posterior limb of internal capsule. (C, D) Axial T2WI at the level of basal ganglia shows abnormal T2 hyperintensity of the thalamus and putamen (black arrows). Note the absence of normal T2 hypointense signal of the posterior limb of internal capsule. (E, F) Axial DWI at the level of basal ganglia shows diffusion restriction involving the posterior putamina and internal capsules (black arrows). (G, H) Axial ADC maps at the level of basal ganglia show corresponding hypointensity in the posterior putamen and internal capsules, denoting diffusion restriction (black arrows)
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Figure 12: A 12-day-old full-term neonate; HIE stage II—severe hypoxic ischemic injury involving deep grey matter structures. (A, B) Axial T1WI at the level of basal ganglia shows abnormal T1 hyperintensity of the ventrolateral thalamus and posterior putamen (black arrows). Note the absence of normal T1 hyperintensity of the posterior limb of internal capsule. (C, D) Axial T2WI at the level of basal ganglia shows abnormal T2 hyperintensity of the thalamus and putamen (black arrows). Note the absence of normal T2 hypointense signal of the posterior limb of internal capsule. (E, F) Axial DWI at the level of basal ganglia shows diffusion restriction involving the posterior putamina and internal capsules (black arrows). (G, H) Axial ADC maps at the level of basal ganglia show corresponding hypointensity in the posterior putamen and internal capsules, denoting diffusion restriction (black arrows)

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 12-day-old full-term neonate; HIE stage II—severe hypoxic ischemic injury involving deep grey matter structures. (A, B) Axial T1WI at the level of basal ganglia shows abnormal T1 hyperintensity of the ventrolateral thalamus and posterior putamen (black arrows). Note the absence of normal T1 hyperintensity of the posterior limb of internal capsule. (C, D) Axial T2WI at the level of basal ganglia shows abnormal T2 hyperintensity of the thalamus and putamen (black arrows). Note the absence of normal T2 hypointense signal of the posterior limb of internal capsule. (E, F) Axial DWI at the level of basal ganglia shows diffusion restriction involving the posterior putamina and internal capsules (black arrows). (G, H) Axial ADC maps at the level of basal ganglia show corresponding hypointensity in the posterior putamen and internal capsules, denoting diffusion restriction (black arrows)
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Figure 12: A 12-day-old full-term neonate; HIE stage II—severe hypoxic ischemic injury involving deep grey matter structures. (A, B) Axial T1WI at the level of basal ganglia shows abnormal T1 hyperintensity of the ventrolateral thalamus and posterior putamen (black arrows). Note the absence of normal T1 hyperintensity of the posterior limb of internal capsule. (C, D) Axial T2WI at the level of basal ganglia shows abnormal T2 hyperintensity of the thalamus and putamen (black arrows). Note the absence of normal T2 hypointense signal of the posterior limb of internal capsule. (E, F) Axial DWI at the level of basal ganglia shows diffusion restriction involving the posterior putamina and internal capsules (black arrows). (G, H) Axial ADC maps at the level of basal ganglia show corresponding hypointensity in the posterior putamen and internal capsules, denoting diffusion restriction (black arrows)
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