Book contents
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface
- Section 1 Bilateral Predominantly Symmetric Abnormalities
- Section 2 Sellar, Perisellar and Midline Lesions
- Section 3 Parenchymal Defects or Abnormal Volume
- Section 4 Abnormalities Without Significant Mass Effect
- Section 5 Primarily Extra-Axial Focal Space-Occupying Lesions
- Section 6 Primarily Intra-Axial Masses
- 152 Acute Infarction
- 153 Glioblastoma Multiforme
- 154 Therapy-Induced Cerebral Necrosis (Radiation Necrosis)
- 155 Non-Hemorrhagic Metastases
- 156 Cerebral Abscess
- 157 Cerebral Toxoplasmosis
- 158 Primary CNS Lymphoma
- 159 Tumefactive Demyelinating Lesion
- 160 Tuberculoma
- 161 Oligodendroglioma
- 162 Low-Grade Diffuse Astrocytoma
- 163 Gliomatosis Cerebri
- 164 Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-Like Episodes (MELAS)
- 165 Pleomorphic Xanthoastrocytoma (PXA)
- 166 Ganglioglioma
- 167 Neurocysticercosis – Parenchymal
- 168 Dilated Perivascular Spaces
- 169 Neuroepithelial Cyst
- 170 Subependymal Giant Cell Astrocytoma (SEGA)
- 171 Subependymoma
- 172 Ependymoma
- 173 Pilocytic Astrocytoma
- 174 Medulloblastoma
- 175 Hemangioblastoma
- 176 Lhermitte–Duclos (Cowden Syndrome)
- 177 Hypertensive Hematoma
- 178 Amyloid Hemorrhage – Cerebral Amyloid Angiopathy
- 179 Cortical Contusion
- 180 Hemorrhagic Neoplasms
- 181 Hemorrhagic Venous Thrombosis
- 182 Arteriovenous Malformation
- 183 Cavernous Angioma (Cavernoma)
- Section 7 Intracranial Calcifications
- Index
- References
180 - Hemorrhagic Neoplasms
from Section 6 - Primarily Intra-Axial Masses
Published online by Cambridge University Press: 05 August 2013
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface
- Section 1 Bilateral Predominantly Symmetric Abnormalities
- Section 2 Sellar, Perisellar and Midline Lesions
- Section 3 Parenchymal Defects or Abnormal Volume
- Section 4 Abnormalities Without Significant Mass Effect
- Section 5 Primarily Extra-Axial Focal Space-Occupying Lesions
- Section 6 Primarily Intra-Axial Masses
- 152 Acute Infarction
- 153 Glioblastoma Multiforme
- 154 Therapy-Induced Cerebral Necrosis (Radiation Necrosis)
- 155 Non-Hemorrhagic Metastases
- 156 Cerebral Abscess
- 157 Cerebral Toxoplasmosis
- 158 Primary CNS Lymphoma
- 159 Tumefactive Demyelinating Lesion
- 160 Tuberculoma
- 161 Oligodendroglioma
- 162 Low-Grade Diffuse Astrocytoma
- 163 Gliomatosis Cerebri
- 164 Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, and Stroke-Like Episodes (MELAS)
- 165 Pleomorphic Xanthoastrocytoma (PXA)
- 166 Ganglioglioma
- 167 Neurocysticercosis – Parenchymal
- 168 Dilated Perivascular Spaces
- 169 Neuroepithelial Cyst
- 170 Subependymal Giant Cell Astrocytoma (SEGA)
- 171 Subependymoma
- 172 Ependymoma
- 173 Pilocytic Astrocytoma
- 174 Medulloblastoma
- 175 Hemangioblastoma
- 176 Lhermitte–Duclos (Cowden Syndrome)
- 177 Hypertensive Hematoma
- 178 Amyloid Hemorrhage – Cerebral Amyloid Angiopathy
- 179 Cortical Contusion
- 180 Hemorrhagic Neoplasms
- 181 Hemorrhagic Venous Thrombosis
- 182 Arteriovenous Malformation
- 183 Cavernous Angioma (Cavernoma)
- Section 7 Intracranial Calcifications
- Index
- References
Summary
Specific Imaging Findings
Tumoral intracranial hemorrhages can be difficult to distinguish from more common spontaneous hemorrhages, primarily due to hypertension, amyloid angiopathy, vascular malformations, or venous thrombosis. Features of an acute hemorrhage which favor the presence of an underlying tumor include a complex and heterogeneous appearance, the presence of a nonhemorrhagic mass within or adjacent to the hematoma, multiplicity (suggesting hemorrhagic metastases), and areas of nodular post-contrast enhancement. On CT neoplastic hemorrhages will be heterogeneously hyperdense acutely, and will occasionally demonstrate fluid levels if hemorrhage extends into a cystic portion of a tumor (fluid levels may notably be also seen with amyloid bleeds). The presence of enhancement within or adjacent to a hemorrhage on either CT or MRI is strongly suggestive of an underlying neoplasm, but contrast enhancement may be absent, particularly if the tumor is small and/or compressed or replaced by the hematoma. Evolution of blood products' signal characteristics on MRI tends to be delayed in neoplastic hemorrhages compared to the other etiologies. In the subacute stage, the T1 hyperintensity due to the presence of methemoglobin tends to be centrally located, just the opposite from nontumoral bleeds in which increased signal begins at the periphery and progresses inward. In addition, while edema surrounding other hemorrhages usually begins resolving within a week, edema will persist in the presence of a neoplasm. Lack of a complete hemosiderin ring around the periphery of a resolving hematoma after a few weeks is suggestive of tumor, but this is an inconsistent finding.
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- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 371 - 372Publisher: Cambridge University PressPrint publication year: 2012