HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text Full Text (PDF) CME Test (opens in a new window) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chao, C. P. Articles by Patton, A. C. Search for Related Content PubMed PubMed Citation Articles by Chao, C. P. Articles by Patton, A. C. Related Collections Neuroradiology Pediatric Radiology

Neonatal Hypoxic-Ischemic Encephalopathy: Multimodality Imaging Findings¹

¹ From the Department of Radiology, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224 (C.P.C.); Department of Radiology, Nemours Children’s Clinic, Jacksonville, Fla (C.G.Z.); and Department of Radiology, Mayo Clinic, Rochester, Minn (A.C.P.). Presented as an education exhibit at the 2005 RSNA Annual Meeting. Received February 1, 2006; revision requested March 9 and received May 15; accepted May 24. All authors have no financial relationships to disclose.

View larger version (51K): [in this window] [in a new window] [Download PPT slide]   Figure 1.  Diagram summarizes the causes of HIE.

 

View larger version (87K): [in this window] [in a new window] [Download PPT slide]   Figure 2.  Patterns of brain injury in mild to moderate hypoperfusion. Schematic of the premature neonatal brain (left) and that of the term infant (right) illustrates how the vascular supply changes with maturation and affects the pattern of brain injury in HIE. The premature neonatal brain (left) has a ventriculopetal vascular pattern, and hypoperfusion results in a periventricular border zone (red shaded area) of white matter injury. In the term infant (right), a ventriculofugal vascular pattern develops as the brain matures, and the border zone during hypoperfusion is more peripheral (red shaded area) with subcortical white matter and parasagittal cortical injury.

 

View larger version (180K): [in this window] [in a new window] [Download PPT slide]   Figure 3a.  PVL in a preterm (30 weeks gestation) infant with a history of acute respiratory failure, mild to moderate hypotension, and necrotizing enterocolitis. (a, b) Initial coronal cranial US scans show symmetric, diffuse periventricular white matter echogenicity (arrows in a) and loss of regular parenchymal spacing. There are linear hyperechoic changes (arrows in b), findings suggestive of accompanying hemorrhage. (c) Follow-up axial T2-weighted MR image obtained at 36 weeks postconception shows hyperintense T2 signal in the periventricular white matter (*). Although this finding is often difficult to distinguish from inherent lack of myelination, when interpreted in conjunction with findings from the patient’s other neuroimaging studies, it was believed to be real and consistent with leukomalacia. (d, e) Axial (d) and sagittal (e) T1-weighted MR images show curvilinear T1 hyperintense signal (arrows) in the periventricular white matter, a finding consistent with hemorrhage.

 

View larger version (170K): [in this window] [in a new window] [Download PPT slide]   Figure 3b.  PVL in a preterm (30 weeks gestation) infant with a history of acute respiratory failure, mild to moderate hypotension, and necrotizing enterocolitis. (a, b) Initial coronal cranial US scans show symmetric, diffuse periventricular white matter echogenicity (arrows in a) and loss of regular parenchymal spacing. There are linear hyperechoic changes (arrows in b), findings suggestive of accompanying hemorrhage. (c) Follow-up axial T2-weighted MR image obtained at 36 weeks postconception shows hyperintense T2 signal in the periventricular white matter (*). Although this finding is often difficult to distinguish from inherent lack of myelination, when interpreted in conjunction with findings from the patient’s other neuroimaging studies, it was believed to be real and consistent with leukomalacia. (d, e) Axial (d) and sagittal (e) T1-weighted MR images show curvilinear T1 hyperintense signal (arrows) in the periventricular white matter, a finding consistent with hemorrhage.

 

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 3c.  PVL in a preterm (30 weeks gestation) infant with a history of acute respiratory failure, mild to moderate hypotension, and necrotizing enterocolitis. (a, b) Initial coronal cranial US scans show symmetric, diffuse periventricular white matter echogenicity (arrows in a) and loss of regular parenchymal spacing. There are linear hyperechoic changes (arrows in b), findings suggestive of accompanying hemorrhage. (c) Follow-up axial T2-weighted MR image obtained at 36 weeks postconception shows hyperintense T2 signal in the periventricular white matter (*). Although this finding is often difficult to distinguish from inherent lack of myelination, when interpreted in conjunction with findings from the patient’s other neuroimaging studies, it was believed to be real and consistent with leukomalacia. (d, e) Axial (d) and sagittal (e) T1-weighted MR images show curvilinear T1 hyperintense signal (arrows) in the periventricular white matter, a finding consistent with hemorrhage.

 

View larger version (110K): [in this window] [in a new window] [Download PPT slide]   Figure 3d.  PVL in a preterm (30 weeks gestation) infant with a history of acute respiratory failure, mild to moderate hypotension, and necrotizing enterocolitis. (a, b) Initial coronal cranial US scans show symmetric, diffuse periventricular white matter echogenicity (arrows in a) and loss of regular parenchymal spacing. There are linear hyperechoic changes (arrows in b), findings suggestive of accompanying hemorrhage. (c) Follow-up axial T2-weighted MR image obtained at 36 weeks postconception shows hyperintense T2 signal in the periventricular white matter (*). Although this finding is often difficult to distinguish from inherent lack of myelination, when interpreted in conjunction with findings from the patient’s other neuroimaging studies, it was believed to be real and consistent with leukomalacia. (d, e) Axial (d) and sagittal (e) T1-weighted MR images show curvilinear T1 hyperintense signal (arrows) in the periventricular white matter, a finding consistent with hemorrhage.

 

View larger version (108K): [in this window] [in a new window] [Download PPT slide]   Figure 3e.  PVL in a preterm (30 weeks gestation) infant with a history of acute respiratory failure, mild to moderate hypotension, and necrotizing enterocolitis. (a, b) Initial coronal cranial US scans show symmetric, diffuse periventricular white matter echogenicity (arrows in a) and loss of regular parenchymal spacing. There are linear hyperechoic changes (arrows in b), findings suggestive of accompanying hemorrhage. (c) Follow-up axial T2-weighted MR image obtained at 36 weeks postconception shows hyperintense T2 signal in the periventricular white matter (*). Although this finding is often difficult to distinguish from inherent lack of myelination, when interpreted in conjunction with findings from the patient’s other neuroimaging studies, it was believed to be real and consistent with leukomalacia. (d, e) Axial (d) and sagittal (e) T1-weighted MR images show curvilinear T1 hyperintense signal (arrows) in the periventricular white matter, a finding consistent with hemorrhage.

 

View larger version (112K): [in this window] [in a new window] [Download PPT slide]   Figure 4a.  Cystic PVL in a preterm (28 weeks gestation) infant with a history of central apnea and moderate hypotension. Coronal (a) and sagittal (b) cranial US scans show multiple anechoic cysts in the periventricular region (arrow).

 

View larger version (102K): [in this window] [in a new window] [Download PPT slide]   Figure 4b.  Cystic PVL in a preterm (28 weeks gestation) infant with a history of central apnea and moderate hypotension. Coronal (a) and sagittal (b) cranial US scans show multiple anechoic cysts in the periventricular region (arrow).

 

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   Figure 5a.  End-stage or chronic PVL in a preterm (28 weeks gestation) twin delivered prematurely because of maternal preeclampsia. (a) Sagittal cranial US scan of the 7-month-old infant shows enlarged lateral ventricles with irregular margins (arrows). (b) Follow-up axial CT scan obtained at 1 year of age shows the same findings (arrows), which are consistent with decreased myelination in the periventricular location and ex vacuo ventricular dilatation. (c) Axial fluid-attenuated inversion-recovery MR image obtained at 1 year of age shows a thin band of T2 hyperintensity along the ventricular surface (arrows), representing gliosis. Note that the deep, prominent sulci nearly abut the ventricular surface due to loss of white matter volume.

 

View larger version (121K): [in this window] [in a new window] [Download PPT slide]   Figure 5b.  End-stage or chronic PVL in a preterm (28 weeks gestation) twin delivered prematurely because of maternal preeclampsia. (a) Sagittal cranial US scan of the 7-month-old infant shows enlarged lateral ventricles with irregular margins (arrows). (b) Follow-up axial CT scan obtained at 1 year of age shows the same findings (arrows), which are consistent with decreased myelination in the periventricular location and ex vacuo ventricular dilatation. (c) Axial fluid-attenuated inversion-recovery MR image obtained at 1 year of age shows a thin band of T2 hyperintensity along the ventricular surface (arrows), representing gliosis. Note that the deep, prominent sulci nearly abut the ventricular surface due to loss of white matter volume.

 

View larger version (112K): [in this window] [in a new window] [Download PPT slide]   Figure 5c.  End-stage or chronic PVL in a preterm (28 weeks gestation) twin delivered prematurely because of maternal preeclampsia. (a) Sagittal cranial US scan of the 7-month-old infant shows enlarged lateral ventricles with irregular margins (arrows). (b) Follow-up axial CT scan obtained at 1 year of age shows the same findings (arrows), which are consistent with decreased myelination in the periventricular location and ex vacuo ventricular dilatation. (c) Axial fluid-attenuated inversion-recovery MR image obtained at 1 year of age shows a thin band of T2 hyperintensity along the ventricular surface (arrows), representing gliosis. Note that the deep, prominent sulci nearly abut the ventricular surface due to loss of white matter volume.

 

View larger version (131K): [in this window] [in a new window] [Download PPT slide]   Figure 6.  End-stage or chronic PVL in a 9-year-old boy, who was born prematurely and had a perinatal history of moderate hypotension. Midsagittal T1-weighted MR image shows thinning of the body of the corpus callosum (arrows), a finding indicative of chronic leukomalacia.

 

View larger version (180K): [in this window] [in a new window] [Download PPT slide]   Figure 7a.  Germinal matrix hemorrhage in a preterm (28 weeks gestation) infant with Apgar scores of 4 at 1 and 5 minutes, delivered to a mother with test results positive for the human immunodeficiency virus, hepatitis B virus, and syphilis. (a) Coronal US scan obtained on day 11 of life shows bilateral grade 3 germinal matrix hemorrhage (*). (b–d) Duplex Doppler images show that the RIs (*) of the right (b) and left (c) middle cerebral arteries and of the anterior cerebral artery (d) are moderately decreased for an infant of this age (expected RI for age = 0.90).

 

View larger version (88K): [in this window] [in a new window] [Download PPT slide]   Figure 7b.  Germinal matrix hemorrhage in a preterm (28 weeks gestation) infant with Apgar scores of 4 at 1 and 5 minutes, delivered to a mother with test results positive for the human immunodeficiency virus, hepatitis B virus, and syphilis. (a) Coronal US scan obtained on day 11 of life shows bilateral grade 3 germinal matrix hemorrhage (*). (b–d) Duplex Doppler images show that the RIs (*) of the right (b) and left (c) middle cerebral arteries and of the anterior cerebral artery (d) are moderately decreased for an infant of this age (expected RI for age = 0.90).

 

View larger version (52K): [in this window] [in a new window] [Download PPT slide]   Figure 7c.  Germinal matrix hemorrhage in a preterm (28 weeks gestation) infant with Apgar scores of 4 at 1 and 5 minutes, delivered to a mother with test results positive for the human immunodeficiency virus, hepatitis B virus, and syphilis. (a) Coronal US scan obtained on day 11 of life shows bilateral grade 3 germinal matrix hemorrhage (*). (b–d) Duplex Doppler images show that the RIs (*) of the right (b) and left (c) middle cerebral arteries and of the anterior cerebral artery (d) are moderately decreased for an infant of this age (expected RI for age = 0.90).

 

View larger version (82K): [in this window] [in a new window] [Download PPT slide]   Figure 7d.  Germinal matrix hemorrhage in a preterm (28 weeks gestation) infant with Apgar scores of 4 at 1 and 5 minutes, delivered to a mother with test results positive for the human immunodeficiency virus, hepatitis B virus, and syphilis. (a) Coronal US scan obtained on day 11 of life shows bilateral grade 3 germinal matrix hemorrhage (*). (b–d) Duplex Doppler images show that the RIs (*) of the right (b) and left (c) middle cerebral arteries and of the anterior cerebral artery (d) are moderately decreased for an infant of this age (expected RI for age = 0.90).

 

View larger version (146K): [in this window] [in a new window] [Download PPT slide]   Figure 8a.  Deep gray matter injury in a preterm (34 weeks gestation) infant who was delivered emergently because of fetal bradycardia and who developed severe hypotension. (a, b) Initial coronal (a) and sagittal (b) cranial US scans show diffuse hyperechogenicity, loss of deep gray matter definition (*), and left ventricular effacement. (c, d) Follow-up coronal cranial US scan (c) shows residual increased echogenicity (*) in the deep gray matter, with corresponding T2 hyperintensity (*) on the axial T2-weighted MR image (d), findings consistent with parenchymal hemorrhage.

 

View larger version (128K): [in this window] [in a new window] [Download PPT slide]   Figure 8b.  Deep gray matter injury in a preterm (34 weeks gestation) infant who was delivered emergently because of fetal bradycardia and who developed severe hypotension. (a, b) Initial coronal (a) and sagittal (b) cranial US scans show diffuse hyperechogenicity, loss of deep gray matter definition (*), and left ventricular effacement. (c, d) Follow-up coronal cranial US scan (c) shows residual increased echogenicity (*) in the deep gray matter, with corresponding T2 hyperintensity (*) on the axial T2-weighted MR image (d), findings consistent with parenchymal hemorrhage.

 

View larger version (144K): [in this window] [in a new window] [Download PPT slide]   Figure 8c.  Deep gray matter injury in a preterm (34 weeks gestation) infant who was delivered emergently because of fetal bradycardia and who developed severe hypotension. (a, b) Initial coronal (a) and sagittal (b) cranial US scans show diffuse hyperechogenicity, loss of deep gray matter definition (*), and left ventricular effacement. (c, d) Follow-up coronal cranial US scan (c) shows residual increased echogenicity (*) in the deep gray matter, with corresponding T2 hyperintensity (*) on the axial T2-weighted MR image (d), findings consistent with parenchymal hemorrhage.

 

View larger version (123K): [in this window] [in a new window] [Download PPT slide]   Figure 8d.  Deep gray matter injury in a preterm (34 weeks gestation) infant who was delivered emergently because of fetal bradycardia and who developed severe hypotension. (a, b) Initial coronal (a) and sagittal (b) cranial US scans show diffuse hyperechogenicity, loss of deep gray matter definition (*), and left ventricular effacement. (c, d) Follow-up coronal cranial US scan (c) shows residual increased echogenicity (*) in the deep gray matter, with corresponding T2 hyperintensity (*) on the axial T2-weighted MR image (d), findings consistent with parenchymal hemorrhage.

 

View larger version (109K): [in this window] [in a new window] [Download PPT slide]   Figure 9.  Definition of parasagittal distribution. Cerebral parenchyma between major vascular territories (ie, between the anterior cerebral arteries [ACA] and middle cerebral arteries [MCA] and between the middle and posterior cerebral arteries [PCA]) is called the watershed zone. In combination with the previously defined border zone (refer to Fig 2), the parasagittal parenchyma (areas shaded red on axial MR image) is at risk for ischemic injury from hypoperfusion.

 

View larger version (115K): [in this window] [in a new window] [Download PPT slide]   Figure 10a.  Parasagittal cortex and subcortical white matter brain injury in a term (38 weeks gestation) infant with a history of birth asphyxia, low Apgar scores, and moderate hypotension. Axial T2-weighted image (a) and diffusion-weighted MR image (b) obtained on day 10 of life show mild hyperintense T2 signal and restricted diffusion (*) in the parasagittal cortex and subcortical white matter in both occipital lobes.

 

View larger version (111K): [in this window] [in a new window] [Download PPT slide]   Figure 10b.  Parasagittal cortex and subcortical white matter brain injury in a term (38 weeks gestation) infant with a history of birth asphyxia, low Apgar scores, and moderate hypotension. Axial T2-weighted image (a) and diffusion-weighted MR image (b) obtained on day 10 of life show mild hyperintense T2 signal and restricted diffusion (*) in the parasagittal cortex and subcortical white matter in both occipital lobes.

 

View larger version (102K): [in this window] [in a new window] [Download PPT slide]   Figure 11a.  Changes in cellular metabolism at MR spectroscopy in a term neonate with a significant perinatal history of prolapsed cord, low Apgar scores, and moderate hypotension. (a) MR spectroscopy of a single voxel in the interarterial boundary zone was performed at echo times of 35 msec and 144 msec. (b) At an echo time of 35 msec, the spectrum demonstrates nonspecific accumulation of metabolite at 1.2–1.3 ppm (*), with a characteristic "doublet" configuration. Cho = choline, Cr = creatine, NAA = N-acetylaspartate. (c) Spectrum obtained at an echo time of 144 msec shows inversion of the same metabolite, which is characteristic for lactate.

 

View larger version (20K): [in this window] [in a new window] [Download PPT slide]   Figure 11b.  Changes in cellular metabolism at MR spectroscopy in a term neonate with a significant perinatal history of prolapsed cord, low Apgar scores, and moderate hypotension. (a) MR spectroscopy of a single voxel in the interarterial boundary zone was performed at echo times of 35 msec and 144 msec. (b) At an echo time of 35 msec, the spectrum demonstrates nonspecific accumulation of metabolite at 1.2–1.3 ppm (*), with a characteristic "doublet" configuration. Cho = choline, Cr = creatine, NAA = N-acetylaspartate. (c) Spectrum obtained at an echo time of 144 msec shows inversion of the same metabolite, which is characteristic for lactate.

 

View larger version (18K): [in this window] [in a new window] [Download PPT slide]   Figure 11c.  Changes in cellular metabolism at MR spectroscopy in a term neonate with a significant perinatal history of prolapsed cord, low Apgar scores, and moderate hypotension. (a) MR spectroscopy of a single voxel in the interarterial boundary zone was performed at echo times of 35 msec and 144 msec. (b) At an echo time of 35 msec, the spectrum demonstrates nonspecific accumulation of metabolite at 1.2–1.3 ppm (*), with a characteristic "doublet" configuration. Cho = choline, Cr = creatine, NAA = N-acetylaspartate. (c) Spectrum obtained at an echo time of 144 msec shows inversion of the same metabolite, which is characteristic for lactate.

 

View larger version (130K): [in this window] [in a new window] [Download PPT slide]   Figure 12a.  Central gray matter pattern of injury in a term (36 weeks gestation) infant with a history of low Apgar scores, abnormal cord pH of 6.8, and severe hypotension. (a, b) Coronal (a) and sagittal (b) cranial US scans obtained on day 1 of life show increased echogenicity of the brain parenchyma and small ventricles, findings consistent with cerebral edema. (c) Duplex Doppler US scan shows an RI that is abnormally low (expected RI for age = 0.83). (d, e) Axial T1-weighted (d) and T2-weighted (e) MR images obtained on day 10 of life show bilateral T1 hyperintensity and subtle T2 hypointensity of the posterior putamina and lateral thalami (*). (f, g) These same areas also demonstrate restricted diffusion, which appears bright on the diffusion-weighted MR image (f) and dark on the apparent diffusion coefficient map image (g).

 

View larger version (126K): [in this window] [in a new window] [Download PPT slide]   Figure 12b.  Central gray matter pattern of injury in a term (36 weeks gestation) infant with a history of low Apgar scores, abnormal cord pH of 6.8, and severe hypotension. (a, b) Coronal (a) and sagittal (b) cranial US scans obtained on day 1 of life show increased echogenicity of the brain parenchyma and small ventricles, findings consistent with cerebral edema. (c) Duplex Doppler US scan shows an RI that is abnormally low (expected RI for age = 0.83). (d, e) Axial T1-weighted (d) and T2-weighted (e) MR images obtained on day 10 of life show bilateral T1 hyperintensity and subtle T2 hypointensity of the posterior putamina and lateral thalami (*). (f, g) These same areas also demonstrate restricted diffusion, which appears bright on the diffusion-weighted MR image (f) and dark on the apparent diffusion coefficient map image (g).

 

View larger version (53K): [in this window] [in a new window] [Download PPT slide]   Figure 12c.  Central gray matter pattern of injury in a term (36 weeks gestation) infant with a history of low Apgar scores, abnormal cord pH of 6.8, and severe hypotension. (a, b) Coronal (a) and sagittal (b) cranial US scans obtained on day 1 of life show increased echogenicity of the brain parenchyma and small ventricles, findings consistent with cerebral edema. (c) Duplex Doppler US scan shows an RI that is abnormally low (expected RI for age = 0.83). (d, e) Axial T1-weighted (d) and T2-weighted (e) MR images obtained on day 10 of life show bilateral T1 hyperintensity and subtle T2 hypointensity of the posterior putamina and lateral thalami (*). (f, g) These same areas also demonstrate restricted diffusion, which appears bright on the diffusion-weighted MR image (f) and dark on the apparent diffusion coefficient map image (g).

 

View larger version (109K): [in this window] [in a new window] [Download PPT slide]   Figure 12d.  Central gray matter pattern of injury in a term (36 weeks gestation) infant with a history of low Apgar scores, abnormal cord pH of 6.8, and severe hypotension. (a, b) Coronal (a) and sagittal (b) cranial US scans obtained on day 1 of life show increased echogenicity of the brain parenchyma and small ventricles, findings consistent with cerebral edema. (c) Duplex Doppler US scan shows an RI that is abnormally low (expected RI for age = 0.83). (d, e) Axial T1-weighted (d) and T2-weighted (e) MR images obtained on day 10 of life show bilateral T1 hyperintensity and subtle T2 hypointensity of the posterior putamina and lateral thalami (*). (f, g) These same areas also demonstrate restricted diffusion, which appears bright on the diffusion-weighted MR image (f) and dark on the apparent diffusion coefficient map image (g).

 

View larger version (110K): [in this window] [in a new window] [Download PPT slide]   Figure 12e.  Central gray matter pattern of injury in a term (36 weeks gestation) infant with a history of low Apgar scores, abnormal cord pH of 6.8, and severe hypotension. (a, b) Coronal (a) and sagittal (b) cranial US scans obtained on day 1 of life show increased echogenicity of the brain parenchyma and small ventricles, findings consistent with cerebral edema. (c) Duplex Doppler US scan shows an RI that is abnormally low (expected RI for age = 0.83). (d, e) Axial T1-weighted (d) and T2-weighted (e) MR images obtained on day 10 of life show bilateral T1 hyperintensity and subtle T2 hypointensity of the posterior putamina and lateral thalami (*). (f, g) These same areas also demonstrate restricted diffusion, which appears bright on the diffusion-weighted MR image (f) and dark on the apparent diffusion coefficient map image (g).

 

View larger version (92K): [in this window] [in a new window] [Download PPT slide]   Figure 12f.  Central gray matter pattern of injury in a term (36 weeks gestation) infant with a history of low Apgar scores, abnormal cord pH of 6.8, and severe hypotension. (a, b) Coronal (a) and sagittal (b) cranial US scans obtained on day 1 of life show increased echogenicity of the brain parenchyma and small ventricles, findings consistent with cerebral edema. (c) Duplex Doppler US scan shows an RI that is abnormally low (expected RI for age = 0.83). (d, e) Axial T1-weighted (d) and T2-weighted (e) MR images obtained on day 10 of life show bilateral T1 hyperintensity and subtle T2 hypointensity of the posterior putamina and lateral thalami (*). (f, g) These same areas also demonstrate restricted diffusion, which appears bright on the diffusion-weighted MR image (f) and dark on the apparent diffusion coefficient map image (g).

 

View larger version (114K): [in this window] [in a new window] [Download PPT slide]   Figure 12g.  Central gray matter pattern of injury in a term (36 weeks gestation) infant with a history of low Apgar scores, abnormal cord pH of 6.8, and severe hypotension. (a, b) Coronal (a) and sagittal (b) cranial US scans obtained on day 1 of life show increased echogenicity of the brain parenchyma and small ventricles, findings consistent with cerebral edema. (c) Duplex Doppler US scan shows an RI that is abnormally low (expected RI for age = 0.83). (d, e) Axial T1-weighted (d) and T2-weighted (e) MR images obtained on day 10 of life show bilateral T1 hyperintensity and subtle T2 hypointensity of the posterior putamina and lateral thalami (*). (f, g) These same areas also demonstrate restricted diffusion, which appears bright on the diffusion-weighted MR image (f) and dark on the apparent diffusion coefficient map image (g).

 

View larger version (118K): [in this window] [in a new window] [Download PPT slide]   Figure 13a.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

View larger version (120K): [in this window] [in a new window] [Download PPT slide]   Figure 13b.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

View larger version (117K): [in this window] [in a new window] [Download PPT slide]   Figure 13c.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

View larger version (128K): [in this window] [in a new window] [Download PPT slide]   Figure 13d.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

View larger version (125K): [in this window] [in a new window] [Download PPT slide]   Figure 13e.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

View larger version (99K): [in this window] [in a new window] [Download PPT slide]   Figure 13f.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

View larger version (85K): [in this window] [in a new window] [Download PPT slide]   Figure 13g.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

View larger version (95K): [in this window] [in a new window] [Download PPT slide]   Figure 13h.  Mixed pattern of injury in a term (42 weeks gestation) infant delivered by emergency cesarean section due to late deceleration on fetal monitoring and who developed severe hypotension. (a) Axial CT scan obtained on day 1 of life shows subtle bilateral hypoattenuation of the basal ganglia and thalami, which are isoattenuated compared with surrounding white matter. (b–e) Axial T1-weighted MR images (b, c) obtained on day 5 of life show T1 hyperintensity and axial T2-weighted MR images (d, e) depict corresponding T2 hypointensity in the posterior putamina, lateral thalami, and the sensorimotor cortices bilaterally. (f–h) Diffusion-weighted MR images reveal hyper-intensity in the basal ganglia (f), hippocampi and occipital lobes (g), and the sensorimotor cortices (h), findings consistent with restricted diffusion and acute ischemic injury. These changes are not apparent on the conventional MR images.

 

---

HOME

HELP

FEEDBACK

SUBSCRIPTIONS

ARCHIVE

SEARCH

TABLE OF CONTENTS

RADIOGRAPHICS

RADIOLOGY

RSNA JOURNALS ONLINE

Copyright © 2006 by the Radiological Society of North America.