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
- 97 Dural Venous Sinus Thrombosis
- 98 Dural Arteriovenous Fistula
- 99 Subarachnoid Hemorrhage
- 100 Laminar Necrosis
- 101 Neurocutaneous Melanosis
- 102 Superficial Siderosis
- 103 Polymicrogyria
- 104 Seizure-Related Changes (Peri-Ictal MRI Abnormalities)
- 105 Embolic Infarcts
- 106 Focal Cortical Dysplasia
- 107 Tuberous Sclerosis Complex
- 108 Dysembroplastic Neuroepithelial Tumor (DNT, DNET)
- 109 Nonketotic Hyperglycemia With Hemichorea–Hemiballismus
- 110 Hyperdensity Following Endovascular Intervention
- 111 Early (Hyperacute) Infarct
- 112 Acute Disseminated Encephalomyelitis (ADEM)
- 113 Susac Syndrome
- 114 Diffuse Axonal Injury
- 115 Multiple Sclerosis
- 116 Progressive Multifocal Leukoencephalopathy (PML)
- 117 Nodular Heterotopia
- 118 Neurosarcoidosis
- 119 Meningeal Carcinomatosis
- 120 Meningitis (Infectious)
- 121 Perineural Tumor Spread
- 122 Moyamoya
- 123 Central Nervous System Vasculitis
- 124 Subacute Infarct
- 125 Active Multiple Sclerosis
- 126 Capillary Telangiectasia
- 127 Developmental Venous Anomaly
- 128 Immune Reconstitution Inflammatory Syndrome (IRIS)
- 129 Ventriculitis
- Section 5 Primarily Extra-Axial Focal Space-Occupying Lesions
- Section 6 Primarily Intra-Axial Masses
- Section 7 Intracranial Calcifications
- Index
- References
111 - Early (Hyperacute) Infarct
from Section 4 - Abnormalities Without Significant Mass Effect
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
- 97 Dural Venous Sinus Thrombosis
- 98 Dural Arteriovenous Fistula
- 99 Subarachnoid Hemorrhage
- 100 Laminar Necrosis
- 101 Neurocutaneous Melanosis
- 102 Superficial Siderosis
- 103 Polymicrogyria
- 104 Seizure-Related Changes (Peri-Ictal MRI Abnormalities)
- 105 Embolic Infarcts
- 106 Focal Cortical Dysplasia
- 107 Tuberous Sclerosis Complex
- 108 Dysembroplastic Neuroepithelial Tumor (DNT, DNET)
- 109 Nonketotic Hyperglycemia With Hemichorea–Hemiballismus
- 110 Hyperdensity Following Endovascular Intervention
- 111 Early (Hyperacute) Infarct
- 112 Acute Disseminated Encephalomyelitis (ADEM)
- 113 Susac Syndrome
- 114 Diffuse Axonal Injury
- 115 Multiple Sclerosis
- 116 Progressive Multifocal Leukoencephalopathy (PML)
- 117 Nodular Heterotopia
- 118 Neurosarcoidosis
- 119 Meningeal Carcinomatosis
- 120 Meningitis (Infectious)
- 121 Perineural Tumor Spread
- 122 Moyamoya
- 123 Central Nervous System Vasculitis
- 124 Subacute Infarct
- 125 Active Multiple Sclerosis
- 126 Capillary Telangiectasia
- 127 Developmental Venous Anomaly
- 128 Immune Reconstitution Inflammatory Syndrome (IRIS)
- 129 Ventriculitis
- Section 5 Primarily Extra-Axial Focal Space-Occupying Lesions
- Section 6 Primarily Intra-Axial Masses
- Section 7 Intracranial Calcifications
- Index
- References
Summary
Specific Imaging Findings
In the hyperacute stage (< 6 h), non-contrast CT is negative in anywhere from 20 to 70% of cases, the earlier obtained after ictus the more likely it is to appear normal. Early changes of cerebral infarction on CT include loss of the gray–white matter (GM–WM) differentiation (loss of the insular ribbon, deep gray matter definition, and focal cortico-subcortical differentiation), effacement of the cortical sulci, and a hyperdense vessel (usually middle cerebral artery) suggestive of acute thrombus. Viewing with stroke windows (such as W 30, L 30) often improves the conspicuity of the findings, especially the loss of the GM–WM differentiation. Diffusion MRI is by far the most sensitive technique for detection of hyperacute infarcts and becomes positive within 30 min after vessel occlusion. Infarcted tissue shows hyperintensity on DWI and low signal on ADC maps, consistent with reduced diffusion. Abnormalities on T2WI and FLAIR images usually become evident 3–6 h after onset, as increased signal intensity and mild swelling of the infarcted tissue. A hyperintense vessel may be seen on FLAIR, corresponding to CT hyperdensity. Contrast-enhanced T1WI may demonstrate arterial enhancement secondary to slow flow, collateral flow, or hyperperfusion following early recanalization. Parenchymal, frequently “gyriform” enhancement may occasionally appear early, suggesting higher hemorrhage risk. CTA and MRA demonstrate arterial occlusions and critical stenoses as well as the status of collateral vessels.
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- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 229 - 230Publisher: Cambridge University PressPrint publication year: 2012