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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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An 8-day-old term neonate with history of perinatal depression and prolonged mild-to-moderate hypoxic ischemic injury. Axial DW (A) and ADC (B) images show restricted diffusion in the corpus callosum (arrow) and faint restriction in frontal and parietal deep white matter. (C, D) Axial T1WI show cortical highlighting (arrow) in the frontoparietal lobes involving perirolandic region
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Figure 15: An 8-day-old term neonate with history of perinatal depression and prolonged mild-to-moderate hypoxic ischemic injury. Axial DW (A) and ADC (B) images show restricted diffusion in the corpus callosum (arrow) and faint restriction in frontal and parietal deep white matter. (C, D) Axial T1WI show cortical highlighting (arrow) in the frontoparietal lobes involving perirolandic region

Mentions: Prolonged partial asphyxia results in injury to the watershed zones of cerebrum, i.e., parasagittal white matter, and whenever severe, extending to the overlying cortex [Figures 14–17]. This is due to the relative hypoperfusion of these areas as the result of autoregulation. The major etiologies for this type of injury are prolonged difficult delivery and long standing antenatal risk factors. Again, DWI is the earliest to change and show cortical and subcortical white matter restriction [Figure 14A]. By the 2nd day, T2WI may often show cortical swelling, loss of gray-white differentiation, and hyperintensity in the cortex and subcortical white matter. T1WI show abnormal cortical high signal intensity beginning from the 3rd day of life, reaches the maximum during the 2nd week, and lasts for several weeks. This is referred to as cortical highlighting [Figure 14C and 15C and D). On T2WI, the abnormal cortex may show subtle low signal intensity [Figure 14E].


Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury
An 8-day-old term neonate with history of perinatal depression and prolonged mild-to-moderate hypoxic ischemic injury. Axial DW (A) and ADC (B) images show restricted diffusion in the corpus callosum (arrow) and faint restriction in frontal and parietal deep white matter. (C, D) Axial T1WI show cortical highlighting (arrow) in the frontoparietal lobes involving perirolandic region
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC5036328&req=5

Figure 15: An 8-day-old term neonate with history of perinatal depression and prolonged mild-to-moderate hypoxic ischemic injury. Axial DW (A) and ADC (B) images show restricted diffusion in the corpus callosum (arrow) and faint restriction in frontal and parietal deep white matter. (C, D) Axial T1WI show cortical highlighting (arrow) in the frontoparietal lobes involving perirolandic region
Mentions: Prolonged partial asphyxia results in injury to the watershed zones of cerebrum, i.e., parasagittal white matter, and whenever severe, extending to the overlying cortex [Figures 14–17]. This is due to the relative hypoperfusion of these areas as the result of autoregulation. The major etiologies for this type of injury are prolonged difficult delivery and long standing antenatal risk factors. Again, DWI is the earliest to change and show cortical and subcortical white matter restriction [Figure 14A]. By the 2nd day, T2WI may often show cortical swelling, loss of gray-white differentiation, and hyperintensity in the cortex and subcortical white matter. T1WI show abnormal cortical high signal intensity beginning from the 3rd day of life, reaches the maximum during the 2nd week, and lasts for several weeks. This is referred to as cortical highlighting [Figure 14C and 15C and D). On T2WI, the abnormal cortex may show subtle low signal intensity [Figure 14E].

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