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
167 - Neurocysticercosis – Parenchymal
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
Brain parenchymal cysticercosis (CC) usually manifests with multiple lesions. The lesions are commonly located at the junction of gray and white matter, reflecting hematogenous disease spread. The early (vesicular) infection stage is seen as CSF density/intensity cysts with a tiny eccentric calcification representing the scolex, usually without surrounding edema and with possible minimal peripheral enhancement. The scolex is best seen as a bright dot on FLAIR images. The colloidal stage is usually a cyst with ring contrast enhancement and surrounding edema. The cyst density/intensity may be slightly different from CSF. The granular stage shows a contracted nodular or ring enhancement without a cystic component. There may be a thin rim of surrounding edema. The final nodular stage is seen as a calcified lesion which may show a rim of high T1 signal, contrast enhancement, and surrounding edema. Most patients harbor parasites in all phases of their evolution, leading to frequent heterogenous imaging appearance. Delayed post-contrast T1WI identifies the highest number of CC lesions.
Pertinent Clinical Information
Neurocysticercosis is a major cause of acquired epilepsy in most low-income countries and it is becoming more common in high-income countries because of increased migration and travel. The most common clinical presentation is seizures (over 70%) and headache. Calcified CC lesions may be incidentally seen in patients investigated for other disease processes.
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- Chapter
- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 345 - 346Publisher: Cambridge University PressPrint publication year: 2012