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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 22-day-old early term neonate with documented hypoglycemia and seizures. Coronal FLAIR (A) and T2WI (B) images at the level of parietooccipital lobes show cystic changes and edema (black arrows) involving white matter and increased gray-white differentiation. Axial FLAIR (C) at lateral ventricular level and T1WI (D) above lateral ventricles show white matter cystic changes and edema confined to parietooccipital lobes (black arrows)
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Figure 20: A 22-day-old early term neonate with documented hypoglycemia and seizures. Coronal FLAIR (A) and T2WI (B) images at the level of parietooccipital lobes show cystic changes and edema (black arrows) involving white matter and increased gray-white differentiation. Axial FLAIR (C) at lateral ventricular level and T1WI (D) above lateral ventricles show white matter cystic changes and edema confined to parietooccipital lobes (black arrows)

Mentions: Neonatal hypoglycaemia (<46 mg/dL) can occur in 5 to 15% of normal term neonates. The injury patterns described are white matter abnormalities (most common), cortical abnormalities, white matter hemorrhage, basal ganglia–thalamic lesions, and PLIC abnormalities. A predominant parietooccipital distribution of abnormalities is seen in approximately 30% of the patients [Figure 20].[22] Neonates with hypoxic ischemic encephalopathy (HIE) are at increased risk developing concurrent hypoglycemia [Figure 3]. These neonates show predominant pattern of HII as well as specific imaging features of hypoglycemia [Figure 21]. It is impossible to differentiate hypoglycemic brain injury from HII by imaging alone, unless it is of parietooccipital distribution.


Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury
A 22-day-old early term neonate with documented hypoglycemia and seizures. Coronal FLAIR (A) and T2WI (B) images at the level of parietooccipital lobes show cystic changes and edema (black arrows) involving white matter and increased gray-white differentiation. Axial FLAIR (C) at lateral ventricular level and T1WI (D) above lateral ventricles show white matter cystic changes and edema confined to parietooccipital lobes (black arrows)
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 20: A 22-day-old early term neonate with documented hypoglycemia and seizures. Coronal FLAIR (A) and T2WI (B) images at the level of parietooccipital lobes show cystic changes and edema (black arrows) involving white matter and increased gray-white differentiation. Axial FLAIR (C) at lateral ventricular level and T1WI (D) above lateral ventricles show white matter cystic changes and edema confined to parietooccipital lobes (black arrows)
Mentions: Neonatal hypoglycaemia (<46 mg/dL) can occur in 5 to 15% of normal term neonates. The injury patterns described are white matter abnormalities (most common), cortical abnormalities, white matter hemorrhage, basal ganglia–thalamic lesions, and PLIC abnormalities. A predominant parietooccipital distribution of abnormalities is seen in approximately 30% of the patients [Figure 20].[22] Neonates with hypoxic ischemic encephalopathy (HIE) are at increased risk developing concurrent hypoglycemia [Figure 3]. These neonates show predominant pattern of HII as well as specific imaging features of hypoglycemia [Figure 21]. It is impossible to differentiate hypoglycemic brain injury from HII by imaging alone, unless it is of parietooccipital distribution.

View Article: PubMed Central - PubMed

ABSTRACT

Perinatal hypoxic&ndash;ischemic brain injury results in neonatal hypoxic&ndash;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&ndash;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