Establishing The Diagnosis Of Ischemic Stroke

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Recent years have seen the emergence of successful treatment strategies for ischemic stroke, but these are most effective only when initiated within several hours after stroke onset. Therefore, extremely rapid diagnosis and initiation of treatment are critical in avoiding death or severe disability.

Unfortunately, there are a variety of other clinical conditions that may mimic the presentation of acute ischemic stroke. These include intracranial hemorrhage, seizure, sepsis, cardiogenic syncope, complicated migraine, dementia, nonischemic spinal cord lesion, peripheral neuropathy, transient global amnesia, and brain tumor, among others. One recent study found that, of patients presenting to a hospital with stroke-like symptoms, the diagnosis of stroke or transient ischemic attack was never established confidently in 31%, and alternative diagnoses were ultimately made in 19%.: Modern imaging techniques are capable of establishing the diagnosis with a high degree of certainty, and of doing so in the very rapid time frame required for emergent treatment.

Noncontrast CT

CT scanners are now nearly ubiquitous in or near the emergency departments of most North American hospitals. With multislice scanners, a noncontrast CT (NCCT) examination of the brain can be performed in well under 1 minute, with the newest scanners able to scan the head in 10 seconds or less. In most centers, the first (and sometimes only) imaging study undertaken for patients with suspected acute stroke is NCCT.

The primary purpose of NCCT in the acute stroke setting is not necessarily to diagnose ischemic stroke, but rather to exclude acute intracranial hemorrhage, whose presentation may mimic that of ischemic stroke. One large study found that, among patients with symptoms of acute stroke, NCCT achieved sensitivity and specificity of 90% and 99%, respectively, in detecting intracranial hemor-rhage.2 Detection of hemorrhage marks a critical decision point in the care of the acute stroke patient. Ischemic stroke therapies such as anticoagulation, thromboly-sis, and induced hypertension could have disastrous effects if mistakenly administered to a patient with acute hemorrhage.

In the absence of hemorrhage, ischemic brain tissue may become slightly hypo-dense in NCCT images within the first 3-6 hours after stroke onset, for perhaps a variety of pathophysiologic reasons.3 This early hypodensity is variably present. In one 1991 study, parenchymal hypodensity was detected in 44% of patients scanned within 5 hours after stroke onset.4 It is likely that early parenchymal hypodensity is appreciated somewhat more frequently in current NCCT scans, partly because modern CT scanners produce higher quality images and partly because CT images are now often viewed not on film but on computer monitors, which allow for manipulation of window and level settings to produce higher contrast images. In one study, sensitivity for detection of acute stroke (less than 6 hours after onset) increased from 57% to 71% when high-contrast settings were used.5

Subinsular White Matter

FIGURE 2.1 Early ischemic signs in NCCT images. The insular ribbon sign is shown in image (a). On the left, the relatively hyperdense ribbon of insular cortical gray matter can be distinguished from the adjacent subinsular white matter (long thin arrows). However, on the right, the insular ribbon cannot be distinguished from the underlying gray matter (short thick arrows), signifying the presence of a very early infarct. In image (b), the lateral margin of the left putamen cannot be seen (short arrows). This image also demonstrates hyperdense embolic material in a Sylvian branch of the middle cerebral artery (the ''MCA dot sign,'' long arrow). Image (c) shows hyperdense embolic material in the middle cerebral artery stem (the ''hyperdense MCA sign,'' arrows).

FIGURE 2.1 Early ischemic signs in NCCT images. The insular ribbon sign is shown in image (a). On the left, the relatively hyperdense ribbon of insular cortical gray matter can be distinguished from the adjacent subinsular white matter (long thin arrows). However, on the right, the insular ribbon cannot be distinguished from the underlying gray matter (short thick arrows), signifying the presence of a very early infarct. In image (b), the lateral margin of the left putamen cannot be seen (short arrows). This image also demonstrates hyperdense embolic material in a Sylvian branch of the middle cerebral artery (the ''MCA dot sign,'' long arrow). Image (c) shows hyperdense embolic material in the middle cerebral artery stem (the ''hyperdense MCA sign,'' arrows).

Early decreases in the CT density of ischemic tissue are often appreciated only indirectly. The process seems initially to affect gray matter more noticeably than white matter, decreasing the radiodensity of affected gray matter slightly, so that it approaches that of adjacent white matter. Therefore, loss of gray matter-white matter differentiation is a commonly described sign of acute infarction on NCCT. When infarction is in the territory of the middle cerebral artery (MCA), this is often manifested as obscuration of the basal ganglia (Fig. 2.1b) or as the "insular ribbon sign,'' in which the ribbon of gray matter in the insular cortex becomes indistinguishable from the subcortical white matter (Fig. 2.1a). Early edema is also sometimes visible because the increase in volume of slightly edematous brain tissue causes effacement of nearby cerebral sulci, cisterns, or ventricles.

Occasionally, the diagnosis of acute ischemia can be established by NCCT because embolic material can be visualized directly, usually in the MCA or its branches. Emboli are often more radiodense than normal brain tissue, and therefore an affected proximal MCA may appear as a linear hyperdensity ("hyperdense middle cerebral artery sign'' or HMCA sign, Fig. 2.1c). One study found that the HMCA sign was 100% specific for MCA occlusion, but only 27% sensitive, probably because the density of embolic material is often indistinguishable from that of the normal MCA.6

Hyperdense embolic material in a more distal MCA branch, within the Sylvian fissure and oriented perpendicular rather than parallel to the axial plane of imaging, may appear as a small, rounded hyperdensity ("MCA dot sign,'' Fig. 2.1b). One study found that the MCA dot sign was present in 16% of patients scanned within 3 hours of onset of stroke symptoms, whereas the HMCA sign was seen in only 5%.7 The HMCA sign portends a poor prognosis, ,9 probably because it signifies occlusion of the MCA stem and therefore ischemia affecting a large volume of tissue. The MCA dot sign has been associated with better post-thrombolytic outcome than the HMCA sign,7 perhaps because emboli in smaller arteries are more amenable to thrombolytic approaches, or because embolic occlusion of a more distal vessel results in ischemic damage affecting a smaller volume of tissue.

Despite the variety of ways in which acute infarction may be manifested in NCCT images, the overall sensitivity of NCCT is lower than that of other currently available imaging techniques that will be discussed below. The signs of acute stroke on NCCT are usually subtle and equivocal, such that inter- and even intraobserver agreements are low.10-12 In one study, radiologists' sensitivity for detecting these signs increased from 38% to 52% when the clinical history provided raised their suspicions by suggesting stroke.12

The Alberta Stroke Programme Early CT Score (ASPECTS) represents one effort to improve intra- and inter-rater reliability, even among "nonexpert" readers, by providing a framework for quantifying the extent of ischemic hypodensity in early NCCT scans.13 In ASPECTS, each of the 10 distinct regions in the territory of the MCA is assigned a score of 0 or 1 depending on the presence (1) or absence (0) of ischemic hypodensity, and the total number of ischemic regions is subtracted from 10. Thus, a score of 10 indicates no apparent hypodensity, whereas a score of 0 reflects hypodensity in the entire MCA territory. Measures like ASPECTS may be helpful not only in diagnosing acute stroke, but also in helping decide whether or not thrombolytic therapy should be initiated. Although one large study found that early ischemic signs in NCCT images were not independently associated with adverse outcomes after thrombolysis,14ASPECTS scores of 7 or less, indicating the presence of hypodensity in more than one third of the MCA territory, have been associated with a substantially increased risk of thrombolysis-related parenchymal hemorrhage.15

Because of the difficulty in detecting acute stroke using NCCT alone, in many centers the presence of a sufficiently suspicious clinical history, along with definite onset of symptoms within 3 hours and a negative NCCT exam, is considered strong enough evidence of acute stroke to warrant treatment with potentially dangerous intravenous thrombolysis. Indeed, such a treatment algorithm has been shown to result in an overall improvement in patient outcomes.16 However, more advanced CT- and MR-based techniques, which will be discussed ahead, can establish the diagnosis of acute stroke with greater sensitivity and specificity.

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