Thứ bảy, 15 Tháng 3 2014 08:32

Ischemic Stroke Imaging Featured

Written by Edgar Colón, Jorge Vidal, Eduardo Labat, Gory Ballester and Angel Gomez
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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.


Source: Physical Medicine and Rehabilitation - Principles and Practice
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