Brain Imaging

Brain Imaging (10)

The following section will be dedicated to brain imaging relevant to rehabilitation. Emphasis is placed on the imaging of ischemic and hemorrhagic strokes, head trauma, and common degenerative diseases. The imaging of brain neoplasms and infections will not be covered in this section, as it is beyond the scope of this text. 

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).

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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.

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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.

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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.

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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.

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Source: Physical Medicine and Rehabilitation - Principles and Practice

Subdural hematoma is most commonly caused by acceleration- deceleration shearing stresses that rupture the bridging veins that extend from the movable brain to the fixed dural venous sinuses. The blood accumulates in a pre-existing but essentially volumeless subdural space. Normally, the pressure of the CSF holds the arachnoid in contact with the dura, thereby creating a real interval that is without significant volume. Because the subdural space is a real space surrounding all external surfaces of the brain, subdural hemorrhage tends to spread extensively over many aspects of the brain surface.

On CT examination, the typical acute subdural hematoma appears as a diffuse crescent-shaped radiodensity that may extend onto many surfaces of the brain, including the cerebral convexity, skull base, interhemispheric fissure, upper or lower surface of the tentorium, and area around the brain stem (Fig. 6-89). One way to differentiate subdural from epidural hematomas is that subdural hematomas cross sutures lines yet do not cross midline, whereas epidural hematomas do not cross suture lines yet can cross midline. There are two ways of classifying subdural hematomas based on their changing radiographic appearance over time (83). One scheme divides them into acute (i.e., more radiodense than adjacent gray matter), subacute (i.e., isodense to gray matter), and chronic (i.e., hypodense to gray matter). Another scheme simply lumps the subacute and chronic into the chronic category. The subdural hematoma typically effaces the adjacent gyri, produces inward displacement of the gray-white matter junction, and may compress the ventricle or cause brain herniation under the falx or through the tentorium.

FIGURE 6-89. Bilateral panhemispheric chronic subdural hematomas with superimposed acute bleed and hematocrit levels (arrows).

As the subdural hematoma ages, the hemoglobin protein producing its radiodensity is broken down and removed, and a vascular granulation tissue develops along its inner surface. Over a few weeks, the subdural hematoma usually becomes isodense or hypodense to gray matter (84). Because of volume loss, the chronic subdural hematoma may lose its concave inner border and become more focal, even occasionally assuming a biconvex outline. Isodense subdural hematomas are more difficult to discriminate. Their presence can be implied indirectly by their mass effects on the underlying brain. An injection of contrast material will enhance both the vascular membrane and the displaced cortical vessels, allowing discrimination of the hematoma from the adjacent cortex.

Patients who present first with a chronic subdural hematoma may have no recollection of any antecedent trauma because the traumatic episode may have been so slight that it was forgotten. Chronic hematomas commonly involve the elderly, where loss of cerebral volume puts the bridging veins under increased stress and makes them more susceptible to rupture by minor trauma.

MRI has valuable unique imaging properties that make it very sensitive to the detection of some extracerebral hemorrhages. First, the high signal intensity that subacute hematomas display on T1- and T2-weighted images makes MRI more sensitive than CT for detecting hematomas that are isodense by CT (73). Even chronic subdural hematomas remain hyperintense to CSF and gray matter for several months, which is long after they have become isodense or hypodense on CT. Also, the ability of MRI to discern the displaced signal voids of cortical or dural vessels facilitates the identification of small extracerebral hemorrhages. In addition, when the hematoma collects around the obliquely placed tentorium, axial CT images may average it into adjacent tissues. In these cases, the multiplanar imaging properties of MRI can be very valuable. Also, small hematomas next to the calvarium can be better seen by MRI because they are contrasted against the osseous signal void.

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Source: Physical Medicine and Rehabilitation - Principles and Practice

Epidural hematoma is caused by tears of the middle meningeal artery or vein, or of a dural venous sinus. The blood accumulates in the interval between the inner table of the calvarium and the dura by gradually stripping the dura from its bony attachment. CT visualizes the epidural hematoma as a well-localized biconvex radiodense mass (83) (Fig. 6-88). It is commonly, though not invariably, associated with a skull fracture. It causes mass effect upon the adjacent brain parenchyma with effacement of the underlying sulci, compression of the brain and ventricles, and possible contralateral midline shift. It is important to note that midline shift is a secondary injury caused by subfalcine herniation, which is herniation of the cingulate gyrus under the falx cerebi, and can eventually lead to ipsilateral anterior cerebral artery infarction. When there is a question about whether the mass might be intraparenchymal, contrast injection enhances the dura, establishing the epidural position of the clot. As the clot lyses over the next few weeks, it shrinks and changes to isodense and then hypodense relative to the brain. The inner aspect of the clot vascularizes, and this may produce a thicker rim of enhancement on late contrast studies. The overlying dura may calcify. Epidural hematoma may be associated with subdural, subarachnoid, or intraparenchymal hemorrhages.

FIGURE 6-88. Epidural hematoma. Nonenhanced CT scan of the head shows a left parietal biconvex extra-axial hyperdensity (arrow).

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Source: Physical Medicine and Rehabilitation - Principles and Practice

Subarachnoid and intraventricular hemorrhage can be spontaneous, as in the case of a bleeding aneurysm or arteriovenous malformation, or secondary to trauma. CT is the imaging modality of choice for evaluating these types of hemorrhages because it detects the hemorrhage from its onset as a hyperdensity. However, subarachnoid hemorrhage is not as radiodense as epidural or subdural hemorrhage because the blood will be diluted by CSF. Unless blood replaces at least 70% of the CSF, the subarachnoid hemorrhage remains isodense to adjacent gray matter (82). When the volume of blood is sufficient to make the hemorrhage hyperdense, it accumulates in the extensions and expansions of the subarachnoid space. Subarachnoid hemorrhage appears as linear radiodensities within the sulci or fissures or as larger aggregations in the basal cisterns (Fig. 6-86). MRI will not visualize a very early hemorrhage when oxyhemoglobin, a nonparamagnetic substance, is the primary constituent, and thus CT is the study of choice in the very early stages. Subarachnoid and intraventricular hemorrhage can cause communicating hydrocephalus by virtue of red blood cells blocking the arachnoid granulations, the CSF resorption sites.

FIGURE 6-86. Subarachnoid hemorrhage secondary to a right middle cerebral artery aneurysm. CT shows this condition as hemorrhagic radiodensities within sulci and cisterns (arrow ).

Aneurysms and arteriovenous malformations can be detected directly by contrast-enhanced CT and MRI, or by their flow void characteristics on non–contrast-enhanced MR images (Fig. 6-87A,B).

FIGURE 6-87. A: CT of an anterior cerebral artery aneurysm (arrow ) that produced a subarachnoid hemorrhage with secondary hydrocephalus. B: Axial collapse image of a time of flight (TOF) MR angiogram in a different patient. The arrow points to a large aneurysm arising from the left anterior communicating artery.

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brain imagingSource: Physical Medicine and Rehabilitation - Principles and Practice

A stroke is considered truly hemorrhagic if blood is found within the first 24 hours after initial symptoms. When blood is noted after this time, it is usually hemorrhagic transformation of an ischemic stroke, which is due to reperfusion injury.

Hypertension is the most common cause of intraparenchymal hemorrhage, which can also be caused by ruptured aneurysm, arteriovenous malformation, and more rarely, by infarction, neoplasms, blood coagulation defects, and cerebral arteritis (81). Common hemorrhage sites include the putamen and the thalamus, which receive their major blood supply from the lenticulostriate and the thalamogeniculate arteries, respectively.

Because freshly extravasated blood is more radiodense than gray or white matter, an acute hemorrhagic stroke is well visualized by CT as a hyperdense region usually conforming to an arterial distribution (Fig. 6-84A,B). The radiodensity of the blood clot increases over 3 days because of clot retraction, serum extrusion, and hemoglobin concentration. The extruded serum may form a hypodense rim around the hyper- dense clot (Fig. 6-84C). As edema develops over 3 to 5 days, the hypodense rim may increase. Eventually, the hyperdensity of the clot gradually fades and usually disappears by 2 months, leaving only a narrow hypodense slit to mark the site where hemorrhage took place (Fig. 6-84D).

FIGURE 6-84. CT evaluation of early and evolving hemorrhagic strokes. A: Recent hemorrhagic stroke has occurred in the distribution of the right posterior cerebral artery, which appears hyperdense (arrows). B: A massive hypertensive hemorrhage involving most of the interior of the left cerebral hemisphere with intraventricular hemorrhage, midline shift to the right, and herniation of the left hemisphere under the falx cerebri. C: A 5-day-old hemorrhagic stroke involving the lenticular nucleus shows a hyperdense hemorrhagic center (arrow ) and a hypodense edematous rim (arrowhead). D: The same stroke patient displays replacement of the hyperdense hemorrhage with a narrow hypodense interval (arrows) several months later.

The appearance of hemorrhage by MRI depends on the state of the hemoglobin in the hemorrhage (81). The oxyhemoglobin present in a fresh hemorrhage is nonparamagnetic; therefore, very early hemorrhage is not detected by MRI. Within a few hours, the oxyhemoglobin will be converted to deoxyhemoglobin, which is a paramagnetic substance. Intracellular deoxyhemoglobin will cause acute hemorrhage to appear very hypointense on T2-weighted images and slightly hypointense or isointense on T1-weighted images (Fig. 6-85A). By 3 to 7 days, intracellular deoxyhemoglobin is oxidized to methemoglobin as the clot enters the subacute phase. Although a subacute hemorrhage has several subphases in which the signal intensity of methemoglobin varies, in general methemoglobin appears hyperintense on both T1- and T2-weighted images (Fig. 6-85B). Because the conversion to methemoglobin begins at the periphery of the clot, early in the subacute phase a hemorrhage can have a hyperintense margin and a central hypointense region still containing deoxyhemoglobin. Eventually the entire region of subacute hemorrhage becomes hyperintense. Over several months, the methemoglobin is gradually resorbed and the clot develops a rim of hemosiderin- containing macrophages. Hemosiderin is hypointense on both T1- and T2-weighted images. Therefore, a chronic hemorrhage of several months duration often has a hyperintense methemoglobin center and a hypointense hemosiderin rim. Because the hemosiderin deposits remain indefinitely, an old hemorrhage of several years duration shows up as a totally hypointense area. Gradient-echo sequences have recently been added to many brain MRI protocols, as they are very sensitive in the detection of degrading blood products, which appear as areas of hypointensity. As can be seen, CT provides the very earliest information about cerebral hemorrhage, whereas MRI is the better technique for determining hemorrhage age.

FIGURE 6-85. MRI evaluation of hemorrhagic stroke. A: An acute hemorrhagic stroke involving the occipital lobe appears hypointense (arrow ). B: In the subacute phase, the same area appears hyperintense (arrow ).

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brain imagingSource: Physical Medicine and Rehabilitation - Principles and Practice

Cerebral ischemia can be produced by thrombosis of large extracranial or small intracerebral vessels, emboli originating from atherosclerotic plaques or thrombi within more proximal vessels or the heart. In addition, decreased perfusion of systemic origin, such as shock, decreased cardiac output, or respiratory failure can also cause cerebral ischemia with or without infarction,

Cerebral ischemia can be completely or partially reversible, or irreversible leading to neuronal cell death, commonly known as infarction. Once blood flow to the brain is decreased or interrupted for a sufficient period of time, usually in a well- defined vascular territory, the chemical pumps within the neuronal cell membranes cease to function adequately disturbing the normal electrolyte homeostasis. Extracellular water subsequently rushes into the affected neuronal cells. This cascade of events initially causes neurons to halt cellular function in an attempt to survive. This “stunned” cell population is potentially salvageable with prompt reperfusion. If adequate reperfusion does not occur in a timely fashion, irreversible neuronal cell deaths will occur. Edema related to infarction involves both gray and white matter and has certain CT and MRI findings.

Nonenhanced CT is the initial study of choice in patients with suspected stroke, as it is readily available, can be performed quickly, and is highly sensitive in the detection of cerebral hemorrhage. On nonenhanced CT, edema related to a cerebral infarction appears as a hypodense or low attenuation area, which means that it appears darker than expected. Early nonenhanced CT signs of ischemic cerebral infarction in the MCA territory are as follows:

(1) Obscuration of the lentiform nucleus, sometimes referred to as the disappearing basal ganglia sign, which can be seen as early as 2 hours after symptom onset (77) (Fig. 6-70).

FIGURE 6-70. Obscuration of the lentiform nucleus. Nonenhanced CT shows effacement of the left lentiform nucleus (arrowhead). Compare with normal lentiform nucleus on the right (arrowhead).

(2) Insular ribbon sign, which refers to hypoattenuation of the insular cortex (Fig. 6-71).

FIGURE 6-71. Insular ribbon sign. CT changes of slight hypodensity, loss of normal gray-white matter differentiation, and effacement of overlying cortical sulci in the region of the right insula (arrow ).

(3) Hyperdense MCA sign, which refers to a fresh thrombus within the artery and can be seen as soon as 90 minutes after the event (Fig. 6-72). It is important to note that this sign implicates occlusion and not necessarily infarction. Nevertheless, nonenhanced CT is usually negative during the first few hours after an ischemic infarct, and it is only later that areas of hypoattenuation can be identified with associated effacement of the adjacent cortical sulci (Fig. 6-73).

FIGURE 6-72. MCA hyperdense sign. Tubular hyperdensity at location of the left middle cerebral artery, compatible with intraluminal thrombus.

FIGURE 6-73. Postinjury edema has peaked and the infarcted area is shown as a distinct hypodensity conforming to the territory of the right middle cerebral artery.

Edema reaches its peak at 3 to 5 days, and by this time non–contrast-enhanced CT typically demonstrates a well- defined hypodense area that usually corresponds to the vascular territory of one of the cerebral arteries or its branches. With large infarctions, brain swelling can eventually lead to brain herniation or obstructive hydrocephalus, which can be life threatening (Fig. 6-74A,B). With subsequent degeneration and phagocytosis of the infarcted brain tissue, there is volume loss that causes an increase in size of the overlying cortical sulci and underlying ventricles (78). When the infarction is caused by a systemically induced general reduction in brain perfusion, the infarcted areas correspond to the border zones between the territories of the major cerebral arteries because perfusion is most tenuous here (Fig. 6-75). Emboli can at times be directly visualized by noncontrast CT as hyperdensities within arteries. It is important to note that hemorrhage can not only occur de novo related to a hemorrhagic infarct, but that it can also occur within an ischemic infarct, as a consequence of reperfusion injury due to blood-brain barrier breakdown. When the latter occurs, it appears as a hyperdense mass within the hypodense edema of the infarct (Fig. 6-76).

FIGURE 6-74. A: Axial CT scan examination with large left subdural hematoma (arrowheads) and early subfalcine herniation (long arrow). B: Coronal multiplanar reformatted image (MPR) demonstrates to a better advantage the mass effect and the subfalcine herniaton (long arrow). The subdural hematoma has a lentiform shape (short arrow).

FIGURE 6-75. Axial diffusion weighted images (DWI) of an acute watershed infarct at the left superior frontal lobe. Increase signal intensity (arrow) represents restricted diffusion.

FIGURE 6-76. There is a hyperdense region at the left basal ganglia and thalamus surrounded by hypodense rim of edema, compatible with hemorrhagic transformation of an ischemic stroke. Patient had suffered an ischemic stroke 12 days earlier.

Injection of intravenous (IV) contrast provides no brain enhancement in the first day or two after a stroke. Contrast enhancement must await sufficient damage to the blood-brain barrier. It reaches its peak at 1 to 2 weeks and usually ceases to occur after 2 or 3 months (79). The greatest vascular damage to intact vessels is at the periphery of the infarct. Therefore, contrast-enhanced CT frequently visualizes a contrast-enhanced ring about the infarcted area or in the immediately adjacent cortical gyri, a phenomenon known as luxury perfusion (Fig. 6-77A,B).

FIGURE 6-77. Axial CT images of the brain of patient with small focal areas of low attenuation representing lacunar infarcts within the right inferior basal ganglia (A) and within the caudate nucleus (B).

Conventional MRI is more sensitive and specific than CT for the detection of acute ischemic brain infarcts, within the first few hours after the onset of symptoms. On MRI, the edema of an early infarct is of low signal intensity on T1-weighted images with corresponding high signal intensity on FLAIR (fluid-attenuated inversion recovery) and T2-weighted images (Fig. 6-78A,B). In addition, there is loss of gray-white matter differentiation, sulcal effacement, and mass effect analogous to CT imaging findings. With the administration of IV gadolinium-diethylenetriamine pentaacetic acid (DTPA), a damaged blood-brain barrier can often be visualized as a hyperintense area on T1-weighted images. MRI is more sensitive than CT at detecting lacunar infarcts, which are small infarcts of less than 1.5 cm (78) typically located in the basal ganglia, periventricular areas, and at the brain stem (Fig. 6-79A,B). Lacunar infarcts are most commonly caused by hypertension or diabetes-induced arteriolar occlusive disease of the deeply penetrating arteries, such as the lenticulostriate branches of the middle cerebral arteries. MRI is also superior to CT in detecting ischemic infarcts of the posterior cranial fossa, because MR images are not degraded by osseous structures. Another powerful tool in the imaging stroke arsenal is diffusion-weighted MR imaging (DWI). The concept here is that water molecules normally move within tissues in a random fashion known as Brownian motion. As was discussed earlier, acute stroke produces an electrolyte imbalance, which causes water molecules to rush into the intracellular compartment, where free random motion is no longer possible and therefore falling into a state of restricted diffusion. DW images reflect restricted diffusion as a signal increase, which corresponds with a signal drop in its accompanying sequence, the apparent diffusion coefficient (ADC) map. The combination of increased signal in the DW images and decreased signal in the ADC map is compatible with an infarct in the appropriate clinical setting, as other entities such as viscous abscesses and dense masses such as lymphomas can have a similar restricted diffusion pattern (Fig. 6-80A,B). One of the key features of DWI of acute cerebral ischemia is that it becomes positive as soon as 30 minutes after the insult and can remain positive for 5 days or more (80).

FIGURE 6-78. Subacute ischemic infarct. A: Axial CT image demonstrates an area of decreased attenuation (arrow) within the head of the caudate nucleus. B: Axial proton density (PD) sequence. There is increased signal intensity (arrow) due to restricted diffusion characteristic of an infarct.

FIGURE 6-79. Lacunar infarcts. A: CT shows multiple bilateral lacunar infarcts as small hypodense areas (arrows). B: By MRI, these infarcts are shown as multiple hyperintense areas (arrows).

FIGURE 6-80. Ischemic infarct. Restricted diffusion is shown as increased signal intensity in the diffusion-weighted image (A) with corresponding signal drop in the ADC map (B) (large arrows).

Nonenhanced CT is highly sensitive in detecting intracranial bleeds, which, in the setting of an ischemic stroke, represents hemorrhagic transformation. In MR imaging, T2*-weighted gradient-echo sequences depict areas of hemorrhage as focal regions of low signal intensity, secondary to a phenomenon known as blooming (Fig. 6-81).

FIGURE 6-81. Axial gradient echo T2* image shows an irregular area of signal drop with surrounding high–signal-intensity edema at the left superior parietal lobe, compatible with a hemorrhagic stroke.

As was stated before, cerebral ischemia can be reversible. Tissue that is potentially salvageable with prompt recanalization is referred to as penumbra. The goal of modern stroke imaging is not merely to document an infarct and exclude hemorrhage, but rather to differentiate infarcted from salvageable tissue (penumbra) in an effort to guide thrombolytic therapy and save as much brain tissue as possible. CT and MR imaging techniques that are currently being used with this purpose in mind will be briefly discussed. CT perfusion is a technique in which a bolus of contrast is injected into the patient with simultaneous imaging of a slice of tissue, usually chosen at the level of the basal ganglia, because it represents the three major vascular territories: Anterior, middle, and posterior cerebral arteries. The three main parameters obtained and compared throughout the slice are cerebral blood volume (CBV), cerebral blood flow (CBF), and mean transit time (MTT). In general terms, a mismatch between these parameters usually represents tissue suffering reversible ischemia or penumbra. MR perfusion is a contrast-dependent technique also utilized to determine the amount, if any, of salvageable brain tissue. In general terms, when a perfusion defect matches a diffusion defect, irreversible infarction has occurred. On the other hand, a perfusion- diffusion mismatch represents an area of reversible ischemia or penumbra, where infarction can possibly be avoided with timely thrombolytic treatment.

CTA is a technique that uses IV contrast to image extracranial and intracranial blood vessels. Different methods are utilized to reconstruct the arterial system, in an attempt to identify the cause of the patient’s symptoms, usually an obstructing thrombus or embolus, which is seen as a cut-off in one or various vessels. CTA information is commonly used to guide intra-arterial or mechanical thrombolysis in stroke centers. Just as in CTA, MRA can also be performed following injection of IV contrast. Nevertheless, MRI has the added bonus of being able to perform angiograms without having to inject contrast material based on the MR properties of flowing blood; a useful proposition in patients with renal insufficiency. Contrast-enhanced MRA findings are analogous to CTA findings, nevertheless in non–contrast-enhanced (time-of-flight) MRAs, normal vessels are depicted as a flow void and intra- arterial thrombus is seen as an area of increased signal intensity (Fig. 6-82).

FIGURE 6-82. Right middle cerebral artery thrombosis by MRA. Arrow points to vessel cut off.

Cerebral venous thrombosis is caused by aseptic or septic etiologies, and can lead to infarction in a nonarterial distribution. This rare cause of infarction has characteristic imaging features. Whether the thrombosis involves a deep cerebral vein or a dural venous sinus, the thrombus can be detected on a noncontrast CT as a hyperdensity within the vein (81). The hyperdensity may have a hypodense center, implying a residual lumen. In a contrast-enhanced CT, a thrombus appears as a filling defect, with tortuous dilated collateral venous channels occasionally demonstrated around the thrombosed vein. By MRI, while the thrombus is still in the oxyhemoglobin stage, which is isodense to brain tissue, it can be suspected

by the absence of the normal flow void in that vessel. In the deoxyhemoglobin stage the thrombus is hypointense on T1, and in the later methemoglobin stage it becomes hyperintense on T1-weighted images. The venous thrombus typically does not proceed to the hemosiderin phase because it usually lyses spontaneously and flow is reestablished. Contrast and non– contrast-enhanced MR venography techniques can also be utilized to diagnose venous thrombosis (Fig. 6-83).

FIGURE 6-83. Deep venous thrombosis. Sagittal noncontrast T1-weighted image. Arrow points to a thrombus-filled hyperintense superior sagittal sinus. Arrowhead points to a thrombus filled hyper- intense straight sinus.

A stroke-like clinical presentation frequently encountered in the ER is a transient ischemic attack (TIA). A TIA is a functional neurologic disturbance usually lasting a few minutes, which clears completely within 24 hours. TIAs typically produce no CT or MRI findings, yet one third of these patients eventually will suffer a cerebral infarction, 20% of them within the first month after the episode. Some stroke centers perform an MRI to all patients who suffered a TIA, as occasionally acute infarcts are actually found.

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Source: Physical Medicine and Rehabilitation - Principles and Practice
 

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