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Magnetic resonance imaging of fetal acquired brain lesions
Abstracts / Clinical Imaging 30 (2006) 297–300 T2-weighted sequence was added to the routine protocol in 100 fetal MRIs obtained for various indications (19th to 37th gestational weeks) on a 1.5-T magnet using a five-element phased-array surface coil. Slice thickness adapted to fetal size and uterine geometry varied between 25 and 50 mm, as did the field of view (250 –350 mm). Acquisition of one image took less than 1 s. The pictorial essay shows that these images visualize fetal anatomy in a more comprehensive way than is possible with a series of 3- to 4-mm-thick slices. These thick-slab images facilitate the assessment of the whole fetus, fetal proportions, surface structures, and extremities. Fetal pathology may be captured in one image. Thick-slab T2-weighted images provide additional information that cannot be gathered from a series of images and are considered a valuable adjunct to conventional twodimensional MR images.
Magnetic resonance imaging of normal fetal brain development Prayer D, Kasprian G, Krampl E, Ulm B, Witzani L, Prayer L, Brugger PC (Department of Radiodiagnostics, Medical University of Vienna, Waerungergurtel 18-20, A-1090 Vienna, Austria). Eur J Radiol 2006;57:199 – 216. Normal fetal brain maturation can be studied by in vivo magnetic resonance imaging (MRI) from the 18th gestational week to term and relies primarily on T2-weighted and diffusion-weighted (DW) sequences. These maturational changes must be interpreted with a knowledge of the histological background and the temporal course of the respective developmental steps. In addition, magnetic resonance (MR) presentation of developing and transient structures must be considered. Signal changes associated with maturational processes can mainly be ascribed to the following changes in tissue composition and organization, which occur at the histological level: (1) a decrease in water content and increasing cell density can be recognized as a shortening of T1- and T2-relaxation times, leading to increased T1-weighted and decreased T2-weighted intensity, respectively; (2) the arrangement of microanatomical structures to create a symmetrical or asymmetrical environment, leading to structural differences that may be demonstrated by DW-anisotropy; (3) changes in nonstructural qualities, such as the onset of a membrane potential in premyelinating axons. The latter process also influences the appearance of a structure on DW sequences. Thus, we will review the in vivo MR appearance of different maturational states of the fetal brain and relate these maturational states to anatomical, histological, and in vitro MRI data. Then, the development of the cerebral cortex, white matter, temporal lobe, and cerebellum will be reviewed, and the MR appearance of transient structures of the fetal brain will be shown. Emphasis will be placed on the appearance of the different structures with the various sequences. In addition, the possible utility of dynamic fetal sequences in assessing spontaneous fetal movements is discussed.
Magnetic resonance imaging of fetal acquired brain lesions Prayer D, Brugger PC, Kasprian G, Witzani L, Helmer H, Dietrich W, Eppel W, Langer M (Department of Radiodiagnostics, Medical University of Vienna, Waerhringerguertel 18-20, A-1090 Vienna, Austria). Eur J Radiol 2006;57:233 – 249. Acquired fetal brain damage is suspected in cases of destruction of previously normally formed tissue, the primary cause of which is hypoxia. Fetal brain damage may occur as a consequence of acute or chronic maternal diseases, with acute diseases causing impairment of oxygen delivery to the fetal brain and chronic diseases interfering with normal placental development. Infections, metabolic diseases, fetofetal transfusion syndrome, toxic agents, mechanical traumatic events, iatrogenic accidents, and space-occupying lesions may also qualify as pathologic conditions that initiate intrauterine brain damage. Magnetic resonance (MR) manifestations of acute fetal brain injury (such as hemorrhage or acute ischemic lesions) can easily be recognized because they are hardly different from postnatal
299
lesions. The availability of diffusion-weighted sequences enhances the sensitivity in recognizing acute ischemic lesions. Recent hemorrhages are usually readily depicted on T2(*) sequences, where they display hypointense signals. Chronic fetal brain injury may be characterized by nonspecific changes that must be attributable to the presence of an acquired cerebral pathology. The workup in suspected acquired fetal brain injury also includes the assessment of extra-CNS organs that may be affected by an underlying pathology. Finally, the placenta, as the organ that mediates oxygen delivery from the maternal circulation to the fetus, must be examined on MR images.
Sonographic cerebral sulcal pattern in normal fetuses Ruiz A, Sembely-Taveau C, Paillet C, Sirinelli D (3 rue de la Varenne, F-37310, Courc¸ay, France). J Radiol 2006;87:49 – 65. Purpose: The objective of this study is to define normal sulcation patterns and their chronological order of appearance on transabdominal ultrasound by comparing them with brain maturation references available in fetopathological studies and MRI findings. Patients and methods: By means of a prospective study, 158 normal fetal brains aged 21 to 34 gestational weeks have been analyzed with standardized data by transabdominal ultrasound in 11 different views using axial, coronal, and sagittal orientation. Results: The sequential development of cerebral sulci has been described according to the gestational age. This chronology was consistent with anatomopathologic references presenting a mean late period of 1 week and with MRI but without any late period. This study is available on the following Web site: http://www.gyration-foetale.fr. Conclusion: This ultrasound study provides accurate landmarks and imaging features of normal fetal brain sulcation. The analysis and the knowledge of this sulcation provide better understanding of the brain cortex maturation and may be helpful in diagnosing brain diseases.
Magnetic resonance spectroscopy of normal and impaired fetal brain development Girard N, Fogliarini C, Viola A, Confort-Gouny S, Le Fur Y, Viout P, Chapon F, Levrier O, Cozzone P (Hoˆpital la Timone, Service de Neuroradiologie, Diagnostique et Interventionelle, 264 rue Saint-Pierre, F-13385 Marseille Cedex 05, France). Eur J Radiol 2006;57:217 – 225. Cerebral maturation in the human fetal brain was investigated by in utero localized proton magnetic resonance spectroscopy (MRS). Spectra were acquired on a clinical magnetic resonance (MR) system operating at 1.5 T. Body phased array coils (four coils) were used in combination with spinal coils (two coils). The size of the nominal volume of interest (VOI) was 4.5 cm3 (201515 mm). The MRS acquisitions were performed using a spin echo sequence at short and long echo times (TE=30 and 135 ms) with a VOI located within the cerebral hemisphere at the level of the centrum semiovale. A significant reduction in myo-inositol and choline and an increase in N-acetylaspartate were observed with progressive age. The normal MR spectroscopy data reported here will help to determine whether brain metabolism is altered, especially when subtle anatomic changes are observed on conventional images. Some examples of impaired fetal brain development studied by MRS are illustrated.
Fetal abdominal magnetic resonance imaging Brugger PC, Prayer D (Center of Anatomy and Cell Biology, Integrative Morphology Group, Medical University of Vienna, Wa¨ringerstrasse 13, 1090 Vienna, Austria). Eur J Radiol 2006;57:278 – 293. This review deals with the in vivo magnetic resonance imaging (MRI) appearance of the human fetal abdomen. Imaging findings are correlated
Magnetic resonance imaging of normal fetal brain development Prayer D, Kasprian G, Krampl E, Ulm B, Witzani L, Prayer L, Brugger PC (Department of Radiodiagnostics, Medical University of Vienna, Waerungergurtel 18-20, A-1090 Vienna, Austria). Eur J Radiol 2006;57:199 – 216. Normal fetal brain maturation can be studied by in vivo magnetic resonance imaging (MRI) from the 18th gestational week to term and relies primarily on T2-weighted and diffusion-weighted (DW) sequences. These maturational changes must be interpreted with a knowledge of the histological background and the temporal course of the respective developmental steps. In addition, magnetic resonance (MR) presentation of developing and transient structures must be considered. Signal changes associated with maturational processes can mainly be ascribed to the following changes in tissue composition and organization, which occur at the histological level: (1) a decrease in water content and increasing cell density can be recognized as a shortening of T1- and T2-relaxation times, leading to increased T1-weighted and decreased T2-weighted intensity, respectively; (2) the arrangement of microanatomical structures to create a symmetrical or asymmetrical environment, leading to structural differences that may be demonstrated by DW-anisotropy; (3) changes in nonstructural qualities, such as the onset of a membrane potential in premyelinating axons. The latter process also influences the appearance of a structure on DW sequences. Thus, we will review the in vivo MR appearance of different maturational states of the fetal brain and relate these maturational states to anatomical, histological, and in vitro MRI data. Then, the development of the cerebral cortex, white matter, temporal lobe, and cerebellum will be reviewed, and the MR appearance of transient structures of the fetal brain will be shown. Emphasis will be placed on the appearance of the different structures with the various sequences. In addition, the possible utility of dynamic fetal sequences in assessing spontaneous fetal movements is discussed.
Magnetic resonance imaging of fetal acquired brain lesions Prayer D, Brugger PC, Kasprian G, Witzani L, Helmer H, Dietrich W, Eppel W, Langer M (Department of Radiodiagnostics, Medical University of Vienna, Waerhringerguertel 18-20, A-1090 Vienna, Austria). Eur J Radiol 2006;57:233 – 249. Acquired fetal brain damage is suspected in cases of destruction of previously normally formed tissue, the primary cause of which is hypoxia. Fetal brain damage may occur as a consequence of acute or chronic maternal diseases, with acute diseases causing impairment of oxygen delivery to the fetal brain and chronic diseases interfering with normal placental development. Infections, metabolic diseases, fetofetal transfusion syndrome, toxic agents, mechanical traumatic events, iatrogenic accidents, and space-occupying lesions may also qualify as pathologic conditions that initiate intrauterine brain damage. Magnetic resonance (MR) manifestations of acute fetal brain injury (such as hemorrhage or acute ischemic lesions) can easily be recognized because they are hardly different from postnatal
299
lesions. The availability of diffusion-weighted sequences enhances the sensitivity in recognizing acute ischemic lesions. Recent hemorrhages are usually readily depicted on T2(*) sequences, where they display hypointense signals. Chronic fetal brain injury may be characterized by nonspecific changes that must be attributable to the presence of an acquired cerebral pathology. The workup in suspected acquired fetal brain injury also includes the assessment of extra-CNS organs that may be affected by an underlying pathology. Finally, the placenta, as the organ that mediates oxygen delivery from the maternal circulation to the fetus, must be examined on MR images.
Sonographic cerebral sulcal pattern in normal fetuses Ruiz A, Sembely-Taveau C, Paillet C, Sirinelli D (3 rue de la Varenne, F-37310, Courc¸ay, France). J Radiol 2006;87:49 – 65. Purpose: The objective of this study is to define normal sulcation patterns and their chronological order of appearance on transabdominal ultrasound by comparing them with brain maturation references available in fetopathological studies and MRI findings. Patients and methods: By means of a prospective study, 158 normal fetal brains aged 21 to 34 gestational weeks have been analyzed with standardized data by transabdominal ultrasound in 11 different views using axial, coronal, and sagittal orientation. Results: The sequential development of cerebral sulci has been described according to the gestational age. This chronology was consistent with anatomopathologic references presenting a mean late period of 1 week and with MRI but without any late period. This study is available on the following Web site: http://www.gyration-foetale.fr. Conclusion: This ultrasound study provides accurate landmarks and imaging features of normal fetal brain sulcation. The analysis and the knowledge of this sulcation provide better understanding of the brain cortex maturation and may be helpful in diagnosing brain diseases.
Magnetic resonance spectroscopy of normal and impaired fetal brain development Girard N, Fogliarini C, Viola A, Confort-Gouny S, Le Fur Y, Viout P, Chapon F, Levrier O, Cozzone P (Hoˆpital la Timone, Service de Neuroradiologie, Diagnostique et Interventionelle, 264 rue Saint-Pierre, F-13385 Marseille Cedex 05, France). Eur J Radiol 2006;57:217 – 225. Cerebral maturation in the human fetal brain was investigated by in utero localized proton magnetic resonance spectroscopy (MRS). Spectra were acquired on a clinical magnetic resonance (MR) system operating at 1.5 T. Body phased array coils (four coils) were used in combination with spinal coils (two coils). The size of the nominal volume of interest (VOI) was 4.5 cm3 (201515 mm). The MRS acquisitions were performed using a spin echo sequence at short and long echo times (TE=30 and 135 ms) with a VOI located within the cerebral hemisphere at the level of the centrum semiovale. A significant reduction in myo-inositol and choline and an increase in N-acetylaspartate were observed with progressive age. The normal MR spectroscopy data reported here will help to determine whether brain metabolism is altered, especially when subtle anatomic changes are observed on conventional images. Some examples of impaired fetal brain development studied by MRS are illustrated.
Fetal abdominal magnetic resonance imaging Brugger PC, Prayer D (Center of Anatomy and Cell Biology, Integrative Morphology Group, Medical University of Vienna, Wa¨ringerstrasse 13, 1090 Vienna, Austria). Eur J Radiol 2006;57:278 – 293. This review deals with the in vivo magnetic resonance imaging (MRI) appearance of the human fetal abdomen. Imaging findings are correlated