Although presented elsewhere in this textbook (Chap,,220), determining the optimal approach to imaging cerebral infarction is becoming increasingly complex and is thus relevant to the discussion of modality selection in neuroimaging.

FDA guidelines require performance of a NECT prior to the institution of thrombolytic therapy. Intravenous contrast administration is of limited value in the CT evaluation of acute stroke. Contrast enhancement is generally not seen during the first three days. Experience from the European Cooperative Acute Stroke Trial (ECASS) has demonstrated that efficacy of treatment is contingent on accurate CT interpretation.4 Specifically, treated patients who had evidence of extensive infarction on CT had a worsened outcome. These patients should be excluded from treatment. However, this can be challenging because the signs of infarction initially are quite subtle. For example, trained readers did not detect 12 percent of areas of advanced infarction in the ECASS study. 4 Optimal treatment is most likely to occur when all members of the treatment team are familiar with the early signs of infarction (Iable,229-2). Briefly, the presence of hemorrhage or evidence of progressive infarct are contraindications to treatment (Fig..,229i5). The sensitivity of CT for the detection of hemorrhage has been previously discussed. An important sign of acute stroke is the hyperdense middle cerebral artery (HMCAS) sign. This corresponds to a thrombus (angiographically) and is demonstrable at the time of ictus. The early CT findings of infarction are due to cytotoxic edema—cellular injury with influx of fluid in the intracellular space. The four CT signs that can be seen in the acute period are: (1) blurring of the clarity of the internal capsule; (2) loss of distinctness of the insular ribbon cortex; (3) loss of differentiation between the cortical gray and the subjacent white matter; and (4) swelling of the cortical gray matter resulting in effacement of interposed sulci. In addition to the attenuation changes, morphologic changes occur due to the accumulation of intracellular fluid causing swelling of the cortical gyri. This results in effacement of the spaces demarcated by the gyral infoldings (sulci) and is referred to as "sulcal effacement." The extent of these changes determines whether treatment with thrombolysis is indicated.

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TABLE 229-2 CT Appearance Exclusion and Inclusion Criteria for the Administration of rt-PA in Patients Presenting Within 3 H of Ictus. Based on Recommendations by the American Heart Association and Experience from the NINDS and ECASS Trials

FIG. 229-5. Axial CT demonstrating clear evidence of decreased attenuation compatible with infarction ( straight arrow). Additional, there is a focal area of hemorrhage (curved arrow), which further obviates thrombolysis.

MR has a greater sensitivity and specificity than CT for the acute changes of stroke. In the first 24 h, over 80 percent of MR scans are positive as compared to 60 percent of CT scans. MR is particularly superior for the detection of stroke in the posterior fossa where CT is limited due to a beam-hardening artifact from the adjacent skull base (Fig 2.2.9.-1.). The earliest MR changes are morphologic swelling of the gray matter, increased signal intensity on the T2W and SDW (referred to as T2 hyperintensity), and loss of normal intravascular flow voids (see Chap, 297 for details on the physics of MR). More importantly, MRI can be combined with MRA

for the detection of large vessel occlusion.

Although superior to CT, conventional MRI remains incapable of demonstrating the parenchymal changes of infarction during the first three hours. A recently developed advanced MR technique known as MR diffusion imaging utilizes pulse sequences sensitive to small-scale water-molecule motion (i.e., diffusion). 5 Alterations in water motion indicative of infarction can be detected within four minutes of vascular occlusion. This sensitivity dramatically improves that ability to determine extent of infarction and thus should improve the safety profile of rt-PA administration.

Neither clinical examination, CT, nor conventional MR imaging techniques provides information on the ischemic penumbra. Two advanced MR imaging techniques, MR perfusion and MR spectroscopic imaging, appear capable of providing this information (see Chap.297). Perfusion imaging is performed following the bolus administration of intravascular contrast that result in changes in signal intensity proportional to regional cerebral blood volume and relative cerebral blood flow. 6 When ischemia is present, perfusion imaging shows a delay in peak signal loss in the affected distribution. MRS generates maps of hydrogen spectra containing major resonances from N-acetyl aspartate (NAA) and lactate.7 Signals from lactate are not normally detected, but are demonstrated in the presence of ischemia and acute infarction. NAA is thought to be a marker of neuronal viability with decreased NAA a marker for cell death. Clinical MRS has demonstrated central areas of infarction with decreased NAA that corresponded to areas of T2W signal increase. Peripheral areas with elevated lactate, but normal NAA is felt to correspond to the ischemic region at risk for infarction. Future studies are needed to validate these findings and to determine which, if any, interventions may improve outcome in the penumbral region and when intervention is indicated. As the logistic difficulties associated with MRI are resolved, the ability to detect regions of infarction and ischemia suggest that CT will eventually be replaced in the evaluation of acute ischemia.

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