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
178 - Amyloid Hemorrhage – Cerebral Amyloid Angiopathy
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
Cerebral amyloid angiopathy (CAA) typically presents in patients over 60 years of age with hemorrhages that are characteristically superficial, large, and lobar. They usually involve the cortex and subjacent white matter of the frontal and parietal lobes, with relatively minimal associated mass effect. The hemorrhage often extends to the subarachnoid and subdural spaces. Multiple hemorrhages of different ages and even multiple simultaneous bleeds may be seen. The blood products within the hematoma tend to sediment posteriorly, frequently giving the appearance of fluid levels. All these acute findings are well seen on CT images. The other characteristic feature of CAA are punctuate cortico-subcortical hypointensities on T2*-weighted images that correspond to chronic microhemorrhages. The sensitivity for microbleeds can be further increased with thin sections and susceptibility-weighted imaging (SWI). Superficial siderosis also occurs with high prevalence, and CAA is one of the most common causes of non-traumatic cortical subarachnoid hemorrhage. MRI is best suited for identification of small or chronic hemorrhages, exclusion of other causes, and assessment of disease progression.
Pertinent Clinical Information
CAA is probably the most common cause of spontaneous intracerebral hemorrhage after 70 years of age, and may be responsible for up to 10% of all nontraumatic intraparenchymal hemorrhages, with female predominance. There is a propensity for multiple and recurrent hemorrhages, and mortality is relatively low. However, many cases of CAA are asymptomatic. The diagnosis is established according to Boston criteria, with probable CAA defined as multiple T2*WI microbleeds restricted to lobar cortico-subcortical regions in patients≥ 55 years old.
- Type
- Chapter
- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 367 - 368Publisher: Cambridge University PressPrint publication year: 2012