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
99 - Subarachnoid Hemorrhage
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
On CT, subarachnoid hemorrhage (SAH) characteristically presents as hyperdense material filling the basal cisterns and/or fissures and cortical sulci. The density and extent depend on the volume of blood. If sufficiently diluted by the CSF, a small SAH may not be seen on CT. Dilution and redistribution may lead to intraventricular extension and the hyperdensity gradually fades away. Diluted SAH can appear as effacement of the cortical sulci. Traumatic SAH may be associated with other injuries such as parenchymal and extra-axial hematomas. The most common cause of nontraumatic SAH is aneurysmal rupture, usually presenting with diffuse SAH, while a filling defect within the hyper-dense clot may indicate the aneurysm location. An associated parenchymal hematoma may also be present. Nonaneurysmal SAH (NASAH) is most commonly perimesencephalic, located almost exclusively in the basal cisterns with possible minimal extension into the interhemispheric and sylvian fissures. Other types of NASAH tend to be located along the convexity - apart from trauma, vasculitis, cortical vein thrombosis, Moyamoya, and cerebral amyloid angiopathy may present this way. On MRI, SAH is best seen with FLAIR sequence, which is more sensitive than CT. T2*WI tend to show hypointensity, but this is variable. Hyperacute SAH (within the first few hours), similar to hyperacute hematoma, is extremely T2 hyperintense, brighter than the CSF; it becomes hypointense in the acute phase. T1 signal varies but is always hyperintense compared to the CSF. Leptomeningeal enhancement may be present. In patients with nontraumatic SAH and either the perimesencephalic pattern or no blood on CT, negative CTA is reliable in ruling out aneurysms. DSA is indicated for diffuse SAH with negative CTA.
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- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 205 - 206Publisher: Cambridge University PressPrint publication year: 2012