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
182 - Arteriovenous Malformation
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 arteriovenous malformations (AVMs) typically present with intracranial, primarily parenchymal, hemorrhage. In most cases a small iso- or slightly hyperdense nodular or tubular defect along the periphery of hemorrhage may be seen on non-enhanced CT, with enhancement on post-contrast images. AVMs without hemorrhage may show irregular hyperdense to calcified areas with contrast enhancement on CT. MRI is the modality of choice for AVM detection, showing the pathognomonic tangle of serpiginous flow-voids, also named “bag of worms”, which is best seen on T2-weighted images. The abnormal flow-voids are typically present adjacent to the hematoma in ruptured AVMs. AVM nidus commonly also enhances with contrast. CTA shows enlarged feeding arteries, the nidus, and draining veins. Routine 3D TOF MRA may demonstrate large feeders, while MR venograms better depict the nidus and draining veins. Findings associated with the risk of future hemorrhage include evidence of previous bleed, intranidal aneurysms, venous stenosis, deep venous drainage, and deep nidus location. Secondary effects of brain AVMs that lead to nonhemorrhagic neurologic deficits include edema from venous congestion (due to stenosis and thrombosis), gliosis, arterial steal (with large shunts), and hydrocephalus (from compression).
Pertinent Clinical Information
AVMs usually become evident through intracranial hemorrhage in young adults. Other typical presentations include seizures, progressive neurological deficits, and headaches. The risk of hemorrhage depends on localization and previous bleeding, estimated at 1–4% per year. Therapeutic options comprise microsurgery (primarily for superficially located lesions), radiosurgery, and endovascular embolisation, allowing effective multidisciplinary treatment.
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- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 375 - 376Publisher: Cambridge University PressPrint publication year: 2012