The aging brain is characterized on CT or MRI as demonstrating volume increases in both cortical sulci and ventricles (Fig. 6-96). T2-weighted MR images also frequently display small areas of hyperintense signal along the anterolateral margins of the anterior horns of the lateral ventricles. These changes may or may not be associated with neurologic findings.

FIGURE 6-96. A case of cortical atrophy of aging as seen by CT. Enlargement of cortical sulci and sylvian fissures (arrows) with ex vacuo ventricular dilatation (arrowheads).

Patients with Alzheimer’s disease (AD) and other dementing disorders consistently show these age changes, but because many normal elderly do also, these changes cannot be used to diagnose AD. However, the absence of these findings typically excludes AD. Findings more specifically related to AD are those involving the temporal lobe. The earliest findings in AD involve atrophy of the temporal lobe with dilation of the temporal horn of the lateral ventricle, as well as dilation of the choroidal and hippocampal fissures caused by atrophy of the hippocampus, subiculum, and parahippocampal gyrus (89).

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice

White matter diseases can be divided into demyelinating diseases, in which the white matter is normally formed and then pathologically destroyed, and dysmyelinating diseases, in which there is usually a genetically determined enzymatic disorder that interferes with the normal production or maintenance of myelin (86). The enzymatic disturbances are relatively rare; therefore, their imaging characteristics will not be described.

The most common of the demyelinating disorders is multiple sclerosis (MS). The demyelinating plaques of MS are better visualized by MRI than by CT. In fact, MRI has become the primary complementary test to confirm a clinical diagnosis of MS. It also provides a quantitative means of evaluating the present state of a patient’s disease and a mode of following its progress (87). Although the T1-weighted MR images are usually normal, the FLAIR and T2-weighted images demonstrate MS plaques as high–signal-intensity areas. These are most frequently seen in the periventricular white matter, especially around the atrium and the tips of the anterior and posterior horns of the lateral ventricles (Fig. 6-94A,B). The high–signal-intensity plaques also can be seen in other white matter areas of the cerebral hemispheres, the brain stem, and even the upper spinal cord. When these lesions are seen in patients younger than 40 years of age, they tend to be relatively specific for MS (86). In patients more than 50 years of age, the MRI findings of MS are similar to findings in some aging brains, and correlation with the clinical findings helps establish the diagnosis. Recent MS plaques that involve damage to the blood-brain barrier frequently enhance with the use of IV gadolinium-DTPA (Fig. 6-95).

FIGURE 6-94. T2-weighted (A) and FLAIR (B) MRI demonstrates the periventricular demyelinating plaques of MS as hyper- intense areas (arrows ) adjacent to the anterior horns and atria of the lateral ventricles.

FIGURE 6-95. Active MS. T1 gadolinium enhanced MR image shows periventricular enhancing MS plaques (arrows).

CT demonstrates MS plaques with less reliability than does MRI. On CT, these plaques appear as areas of hypodensity. Recent plaques in the acute phase of an exacerbation of the disease will have damage to the blood-brain barrier, and IV contrast will then enhance the periphery of the lesion. In the chronic plaque, no contrast enhancement occurs on CT or MRI. Other demyelinating diseases, although numerous, are of relatively low incidence and therefore are not described.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice

Diffuse brain injuries include diffuse axonal injury, diffuse cerebral swelling, and edema. Diffuse axonal injury is produced by high shearing stresses that occur at different parts of the brain, including at the gray matter-white matter interface. These shearing stresses cause axonal stretching commonly involving the corpus callosum, anterior commissure, and upper brain stem. Blood vessels may or may not be disrupted. When vessels are uninterrupted, the scattered small areas of edema are best demonstrated by T1-weighted MR images as slightly hypointense or isointense regions that become hyperintense on T2-weighted images. When vessel disruption produces hemorrhages, they appear early on CT as multiple sites of hyperdensity (Fig. 6-91).

FIGURE 6-91. Diffuse axonal injury. Nonenhanced CT scan shows hemorrhagic foci at the genu of the corpus callosum (arrows).

Diffuse cerebral swelling occurs with many types of head injury. It is thought to be produced by a rapidly increased volume of circulating blood. By MRI and CT, the general brain enlargement is visualized by an obliteration or encroachment of the normal CSF spaces: the cortical sulci, the perimesencephalic and basal cisterns, and the ventricles (85). By CT, the enlarged brain may show slightly increased density.

In generalized cerebral edema, the enlarged brain also encroaches on the CSF spaces, but by CT the edema produces a generalized hypodensity that usually takes longer to develop than diffuse cerebral swelling (Fig. 6-92). The edema may obscure gray matter-white matter boundaries.

Both diffuse brain swelling and generalized cerebral edema are emergencies, because if not treated promptly they may lead to brain herniation sometimes with fatal outcomes.

 

FIGURE 6-92. Diffuse brain edema. Nonenhanced CT scan shows diffuse hypodensity with sulci effacement and loss of gray/white matter differentiation. Mass effect is causing almost complete obliteration of the ventricular system. Compare low parenchymal attenuation with normal cerebellar density.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice

Brain injuries may be accompanied by a number of late or long-term complications. These secondary brain injuries include cerebral herniations, which may occur under the falx cerebri or through the tentorium. Herniations can cause compression of adjacent brain substance or vessels, with the production of secondary signs and symptoms (Fig. 6-93). Penetrating injuries or fractures can injure nearby large or small vessels, producing thrombosis, embolism, traumatic aneurysm formation, or internal carotid–cavernous sinus fistula. Basal skull fractures involving the dura and arachnoid can cause CSF leaks that show up as CSF rhinorrhea or otorrhea. Local or diffuse brain swelling can compress the cerebral aqueduct or fourth ventricle, producing obstructive hydrocephalus. Subarachnoid hemorrhage may obstruct CSF resorption and cause a late-developing communicating hydrocephalus. Focal cerebral atrophy can occur at sites of infarction, hemorrhage, or trauma. Generalized atrophy can follow diffuse injuries and can be demonstrated by an increased size of sulci, fissures, cisterns, and ventricles.

FIGURE 6-93. Nonenhanced CT scan shows a left MCA infarct with mass effect causing contralateral midline shift (arrow ) corresponding to subfalcine herniation.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice

Focal parenchymal injuries such as contusions and intraparenchymal hemorrhage usually develop as a result of contact of the brain with the osseous walls of the cranial cavity. The coup-type injuries occur at the point of contact, and the contrecoup injuries occur on the opposite side of the brain. Contusions often occur in areas where the walls of the cranial cavity are irregular, such as the anterior and middle cranial fossae. Therefore, frontal and temporal lobe contusions are common as the brain glides along these irregular surfaces (85) (Fig. 6-90A,B).

FIGURE 6-90. A: Nonenhanced CT scan shows a small left frontal hyperdense hemorrhagic foci (arrow ). Acute extra-axial bleed is also noted (arrowhead ). B: Left temporal post-traumatic hemorrhagic contusions (arrow ). Overlying acute extra-axial bleed is noted (arrowhead).

Cerebral contusions are heterogeneous lesions containing edema, hemorrhage, and necrosis, with any element predominating. When blood makes a major contribution, the contusion appears on CT as a poorly delimited irregular area of hyperdensity. A contusion with mostly edema or necrosis may not be detectable immediately, but after a few days it appears as a hypodense region. Where there is a general admixture of elements, contusions may have a heterogeneous density. Old contusions appear as hypodense areas. By MRI, the edematous and necrotic areas have low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, and thus MRI is more sensitive than CT in identifying these non- hemorrhagic contusions. The areas of hemorrhage in a contusion older than a few days will be hyperintense on both T1- and T2-weighted images.

Intraparenchymal hemorrhage differs from contusions by having better demarcated areas of more homogeneous hemorrhage. The CT and MRI characteristics of acute and evolving intraparenchymal hemorrhage are the same as for hemorrhagic stroke.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice

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