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
114 - Diffuse Axonal Injury
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
Diffuse axonal injury (DAI, shear injury) on CT presents as small hypodense (nonhemorrhagic) or hyperdense (hemorrhagic) foci; however, the majority of DAI lesions are not detected on CT. Gray–white matter junction (especially paramedial), dorsolateral midbrain, and corpus callosum (especially the splenium) are the most typical DAI locations. Multiple oval lesions 1–15 mm in diameter are detected on T2WI and FLAIR images. T2 signal intensity depends on the presence of hemorrhage: hemorrhagic lesions show low signal, while the nonhemorrhagic ones are T2 hyperintense. On T1WI the lesions are usually hypointense and not well seen, hyperintensity is present in subacute hemorrhagic lesions. T2* sequences detect susceptibility effects of hemoglobin degradation products as areas of signal loss in hemorrhagic lesions. The detection of acute or chronic hemorrhagic DAI is improved by heavily T2*WI, such as with higher field strength and a longer echo time (TE), and even further with susceptibility-weighted imaging (SWI). Diffusion MR imaging is the most sensitive modality for DAI detection with bright signal on DWI in the acute phase. Some lesions may only be detected with DWI, some with T2* and a few with FLAIR. Presence of hemorrhage in the interpeduncular cistern on initial CT is a marker for possible brainstem DAI.
Pertinent Clinical Information
The main and classic DAI symptom is lack of consciousness; however, this is not always present. A conscious patient may show other signs of brain damage, depending on lesion location. Most patients (> 90%) with severe DAI remain in a persistent vegetative state. Milder forms of DAI in the chronic phase may cause residual neuropsychiatric problems and cognitive deficits, focal neurologic lesions, memory loss, concentration difficulties, intellectual decline, psychiatric disturbances, headaches, and seizures.
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- Information
- Brain Imaging with MRI and CTAn Image Pattern Approach, pp. 235 - 236Publisher: Cambridge University PressPrint publication year: 2012