Meyers | Differential Diagnosis in Neuroimaging: Brain and Meninges | E-Book | sack.de
E-Book

E-Book, Englisch, 660 Seiten, PDF

Meyers Differential Diagnosis in Neuroimaging: Brain and Meninges


1. Auflage 2016
ISBN: 978-1-60406-702-6
Verlag: Thieme Medical Publishers
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 660 Seiten, PDF

ISBN: 978-1-60406-702-6
Verlag: Thieme Medical Publishers
Format: EPUB
Kopierschutz: 6 - ePub Watermark



Authored by renowned neuro-radiologist Steven P. Meyers, is a stellar guide for identifying and diagnosing brain pathologies based on location and neuroimaging results. The succinct text reflects more than 25 years of hands-on experience gleaned from advanced training and educating residents and fellows in radiology, neurosurgery, and neurology. The high-quality MRI, CT, PET, PET/CT, conventional angiography, and X-ray images have been collected over Dr. Meyers's lengthy career, presenting an unsurpassed visual learning tool.

The distinctive 'three-column table plus images' format is easy to incorporate into clinical practice, setting this book apart from larger, disease-oriented radiologic tomes. The layout enables readers to quickly recognize and compare abnormalities based on high-resolution images.

Key Highlights

  • Tabular columns organized by anatomical abnormality include brain imaging findings and a summary of key clinical data that correlates to the images
  • Comprehensive imaging of the brain, ventricles, meninges, and neurovascular system in both children and adults, including congenital/developmental anomalies and acquired disease
  • More than 1,900 figures illustrate the radiological appearance of intracranial lesions, masses, neurodegenerative disorders, ischemia and infarction, and more

This visually rich resource is a must-have diagnostic tool for radiologists, neurosurgeons, and neurologists, and residents and fellows. The highly practical format makes it ideal for daily rounds, as well as a robust study guide for physicians preparing for board exams.

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Autoren/Hrsg.


Weitere Infos & Material


1 Brain (Intra-Axial Lesions)
2 Ventricles and Cisterns
3 Extra-Axial Lesions
4 Meninges
5 Vascular Abnormalities


Prologue


Intracranial Abnormalities


Brain, Ventricles, Meninges, Skull, and Vascular Structures

Major advantages of magnetic resonance imaging (MRI) include excellent soft tissue contrast resolution, multiplanar imaging capabilities, dynamic rapid data acquisition, and the available contrast agents. MRI has proven to be a powerful imaging modality in the evaluation of congenital anomalies of the brain; disorders of histogenesis; neoplasms of the central nervous system, cranial nerves, pituitary gland, meninges, and skull base; traumatic lesions; intracranial hemorrhage; ischemia and infarction; infectious and noninfectious diseases; metabolic disorders; and dysmyelinating and demyelinating diseases.

Computed tomography (CT) has been used in the evaluation of neoplasms of the central nervous system, meninges, calvarium, and skull base; traumatic lesions; intracranial hemorrhage; ischemia and infarction (particularly using CT perfusion studies); infectious and noninfectious diseases; and metabolic disorders. Because of its widespread availability and rapid imaging capability, CT plays an important role in the evaluation of acutely injured patients in emergency departments. Multidetector CT is an excellent imaging modality for evaluation of the skull base, orbits, nasopharynx, oropharynx, and floor of the mouth. CT is a useful method for imaging the location and extent of osseous lesions at the skull base, such as metastastic tumors, myeloma, chordomas, and chondrosarcomas.

MRI and CT data can also be used to generate images of arteries and veins (MR angiography and CT angiography) in displays similar to conventional angiography. Other options with clinical MRI scanners include the acquisition of spectral data to characterize the biochemical properties of selected regions of interest in the brain (magnetic resonance spectroscopy), detection of water proton diffusion in brain and meninges (diffusion-weighted imaging and mapping of apparent diffusion coefficients), and evaluation of differing ratios of deoxyhemoglobin to oxyhemoglobin at sites of brain activation (functional MRI).

Appearance of Normal Brain Tissue on CT and MRI

The appearance of brain tissue depends on the CT technique and MRI pulse sequences used, as well as the age of the patient. Myelination of the brain begins in the fifth fetal month and progresses rapidly during the first 2 years of life. The degree of myelination affects the appearance of the brain parenchyma on MRI and CT. In adults, the cerebral cortex has an intermediate signal on T1-weighted images and is lower or hypointense relative to normal white matter. On T2-weighted images, gray matter has an intermediate signal that is higher in signal (hyperintense) relative to white matter. For infants less than 6 months old, the MRI pattern is reversed due to the immature myelination of their brain tissue. Maturation or myelination of the brain tissue, as seen on T1-weighted versus T2-weighted images, occurs at different rates. The myelination proceeds in a predictable and characteristic pattern with regard to location and timing. The changes on T1-weighted images become most evident during the first 6 months of postnatal life, whereas the changes on T2-weighted images are most apparent from 6 to 18 months. At around 6 months of age, the adult MRI signal pattern of the gray and white matter begins to progressively emerge. After 18 months, the brain has a mature MRI appearance with regard to the gray and white matter signal patterns.

On CT, the appearance of brain tissue depends on the mAs and kVp used. Immature myelin in neonates and infants has lower attenuation than myelin in older children. In adults, the cerebral cortex has an intermediate attenuation that is slightly higher relative to normal white matter. The imaging changes seen with myelin maturation are more optimally seen with MRI than with CT.

In addition to the commonly used standard fast spin echo sequences for evaluation of brain parenchyma, other MRI pulse sequences or imaging options are commonly used, such as inversion recovery (short TI inversion recovery [STIR] for fat suppression, T1-weighted or T2-weighted fluid attenuated inversion recovery [FLAIR], etc.), gradient recall echo T2* imaging, spoiled gradient recall echo T1-weighted imaging, steady-state free precession imaging, magnetic transfer, diffusion/perfusion MRI, and frequency selective chemical saturation. Detailed discussions of these sequences and options can be found elsewhere.

Appearance of Abnormal Brain Parenchyma on MRI and CT

Most pathologic processes decrease the CT attenuation values of the involved tissue and increase the MRI T1 and T2 relaxation coefficients, resulting in decreased signal on T1-weighted images and increased signal on T2-weighted images relative to adjacent normal tissue. Such processes include ischemia, infarction, inflammation, infection, demyelination, dysmyelination, metabolic or toxic encephalopathy, trauma, neoplasms, gliosis, radiation injury, and encephalomalacia-related changes. Other processes that can result in zones of low attenuation on CT include dermoids (intact or ruptured), teratomas, lipomas, and cystic structures with high protein concentration or cholesterol, as well as Pantopaque.

Areas where there is breakdown of the blood–brain barrier can be also evaluated with iodinated intravenous contrast on CT and with gadolinium-based intravenous contrast agents on MRI. Leakage of contrast agents through the blood–brain barrier results in increased attenuation on CT (contrast enhancement) and high signal on T1-weighted images. The high signal seen on MRI after contrast administration results from reduction of the T1 and T2 values of the hydrogen nuclei in brain tissue adjacent to the intraparenchymal contrast that leaked through the damaged blood–brain barrier. Contrast-enhanced CT and MR images are important portions of most imaging examinations of the head. In addition to the contrast enhancement in pathologically altered intracranial tissues, CT and MRI contrast enhancement can be seen normally in veins, the choroid plexus, the anterior pituitary gland, the pituitary infundibulum, the pineal gland, and the area postrema.

Intracranial Hemorrhage on MRI

on MRI can have varying appearances in the brain depending on the age of the hematoma, oxidation states of the iron in hemoglobin, hematocrit, protein concentration, clot formation and retraction, hemorrhage location, and hemorrhage size. Oxyhemoglobin in a hyperacute blood clot has ferrous iron and is diamagnetic. Oxyhemoglobin does not significantly alter the T1 and T2 values of the tissue environment, other than causing possible localized edema. After a few hours during the acute phase of the hematoma, the oxyhemoglobin loses its oxygen and forms deoxyhemoglobin. Deoxyhemoglobin also has ferrous iron, although it has unpaired electrons and becomes paramagnetic. As a result, deoxyhemoglobin shortens the T2 value of the acute clot but does not significantly change the T1 value. On MRI, deoxyhemoglobin in the clot will have an intermediate T1 signal and a low signal on T2-weighted spin echo or gradient echo images. Later, in the early subacute phase of the hematoma, deoyxhemoglobin becomes oxidized to the ferric state, methemoglobin, which is strongly paramagnetic. Methemoglobin shortens the T1 value of hydrogen nuclei, resulting in high signal on T1-weighted images. While the red blood cells in the clot are intact, with intracellular methemoglobin, the T2 values will also be decreased, resulting in a low signal on T2-weighted images. In the late subacute phase, breakdown of the membranes of the red blood cells results in extracellular methemoglobin, which causes high signal on both T1- and T2-weighted images. In the chronic phase, methemoglobin becomes further oxidized and broken down by macrophages into hemosiderin, which has a prominent low signal on T2-weighted images and a low-intermediate signal on T1-weighted images.

The MRI features of are variable, although the appearances can progress in patterns similar to those for intraparenchymal hematomas. Chronic subdural hematomas often have a low-intermediate signal on T1-weighted images and a high signal on T2-weighted images. is often difficult to see on T1- and T2-weighted images, although it can be sometimes identified on long TR/short TE (proton density-weighted images) or FLAIR images.

In the differential diagnosis of intracranial hemorrhage, other processes that can result in zones of high signal on T1-weighted images are fat, dermoids (intact or ruptured), teratomas, lipomas, and cystic structures with high protein concentration or cholesterol, as well as Pantopaque.

Intracranial Hemorrhage on CT

An on CT can have varying appearances in the brain depending on the age of the hematoma, hematocrit, protein concentration, clot formation and retraction, hemorrhage location, and hemorrhage size. In the first week, intraparenchymal hematomas typically have high attenuation.

In the late subacute phase (> 7 days to 6 weeks) decrease 1.5 Hounsfield units (HU) per day and become isodense to hypodense. Chronic hematomas have low attenuation with localized encephalomalacia. The CT features of are variable, although the appearances can progress in patterns similar to those for intraparenchymal hematomas. Acute subdural hematomas often have high attenuation. CT is the optimal exam in the diagnosis of acute and is...



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