Radiographic Indicators Of Progressing Stroke

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CT and MRI performed early during the evaluation of the stroke patient have become useful in the identification of risk factors for progressing stroke. In a series of 152 consecutive patients with acute ischemic stroke who were hospitalized within 5 hr of stroke onset, extended focal hypodensity on CT involving cortical or corticosubcortical areas increased the risk of neurologic worsening by a factor of 8.9 and predicted subsequent deterioration with a probability of 60% (7). The same relationship was found between early (<8 hr) CT findings of brain infarction, ischemic edema, and mass effect, which predicted the risk of progressing stroke in a prospective study of 128 subjects (9). In this study, early signs of infarction on CT were observed in 81% of progressing stroke, but in only 49% of nonprogressing stroke, correlating with the appearance of mass effect in 26% and 2.4%, respectively (p < 0.001). Analysis of the CT images obtained from patients enrolled in the first European Cooperative Acute Stroke Study (ECASS; see below) confirmed several radiographic features that are now accepted as hallmark indicators of early neurologic deterioration. Early CT focal hypodensity [odds ratio (OR): 1.9; 95% confidence interval (CI): 1.3-2.9] and hyperdensity of the middle cerebral artery (HMCA) sign (OR: 1.8; 95% CI: 1.1-3.1) were independent prognostic factors for early progressing stroke (within 24 hr of onset), whereas brain swelling at the initial CT, obtained within 6 hr of onset, predicted delayed progression (between 24 hr and 7 days) (11). Figure 1 shows representative

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Figure 1 Computed tomography (CT) of acute cerebral infarction. (A) and (B) were selected from a CT scan performed 90 min after the acute onset of left hemiplegia in a 52-year-old woman. The arrow in (A) identifies fresh thrombus lodged in the right middle cerebral artery [hyperdense middle cerebral artery (MCA) sign]. In (B), the arrow indicates subtle hypodensity affecting the right lenticular nuclei and blurring of the adjacent insular ribbon. (C) and (D) were selected from a CT scan performed 7 hr after the onset of left hemiplegia in a 48-year-old man. The arrow in (C) again indicates the hyperdense MCA sign. Note large hypodensity representing acute infarction within the vascular territory of the right MCA in (C) and (D); the sulcal indentations in the right frontotemporal region have been obliterated by gyral edema and the anatomical landmarks defining the right basal ganglia have been obscured.

Figure 1 Computed tomography (CT) of acute cerebral infarction. (A) and (B) were selected from a CT scan performed 90 min after the acute onset of left hemiplegia in a 52-year-old woman. The arrow in (A) identifies fresh thrombus lodged in the right middle cerebral artery [hyperdense middle cerebral artery (MCA) sign]. In (B), the arrow indicates subtle hypodensity affecting the right lenticular nuclei and blurring of the adjacent insular ribbon. (C) and (D) were selected from a CT scan performed 7 hr after the onset of left hemiplegia in a 48-year-old man. The arrow in (C) again indicates the hyperdense MCA sign. Note large hypodensity representing acute infarction within the vascular territory of the right MCA in (C) and (D); the sulcal indentations in the right frontotemporal region have been obliterated by gyral edema and the anatomical landmarks defining the right basal ganglia have been obscured.

examples of early focal hypodensity, HMCA, and brain swelling. The association between early hypodensity, HMCA sign, and progressing stroke is in agreement with angiographic and ultrasonographic studies that show that MCA occlusion with little or no collateral blood supply is responsible for the early development of intracellular edema and stroke progression (7,12).

MRI includes a variety of techniques that can be employed to predict outcome of progressing stroke and are described in detail in Chapter 18. Diffusion-weighted imaging (DWI) permits the in vivo measurement of the translational mobility of water in tissue and was first reported as a marker of acute ischemic brain injury in 1990 (13,14). The image intensity on DWI is dependent on the apparent diffusion coefficient (ADC), measuring the mobility of water molecules in tissue and the transverse relaxation time (T2) that might represent prior distortion of tissue architecture ("T2 shine-through"). In ischemic brain tissue, ADC values decline, leading to a region of hyperintensity on a gray-scale derived image. The ADC probably reflects the accumulation of intracellular water (cytotoxic edema) caused by disruption of energy metabolism and loss of ion homeostasis (15). These ADC changes do not occur uniformly throughout the ischemic lesion. Serial studies performed in experimental stroke models show that the most severe perfusion deficit has the earliest and correspondingly most severe drop in ADC value (16). Reversal of initial ADC changes after early reperfusion does not necessarily predict tissue salvage. In rats that were subjected to focal cerebral ischemia and reperfused up to 30 min afterward, ADC values completely reverted to normal within 90 min, but histopathology examination 3 days later demonstrated heterogeneous cell injury directly related to the severity of the initial decline in cerebral blood flow ( 17 ).

I n clinical imaging of ischemic stroke, DWI will indicate the volume of injured brain within as early as 1 hr after the onset of perfusion arrest (Fig. 2). Several studies are being conducted to assess the relationships between MR-derived lesion volumes and clinical measures of outcome at acute and chronic time points to determine the efficacy of establishing MRI as a surrogate marker of injury severity. In one of the first studies evaluating DWI and a companion technique, perfusion-weighted imaging (PWI), as predictors of stroke outcome, DWI or PWI lesion volumes obtained within 6.5 hr of ischemic stroke onset were correlated to performance on the NIHSS at 24 hr (18). A high correlation was noted between 24-hr NIHSS score and lesion volumes as determined by PWI (Pearson's r=0.96; p < 0.001) or DWI (r=0.67; p=0.03). Furthermore, a similar high correlation was noted between lesion size on routine T2-weighted (T2W) imaging and initial DWI and PWI size (r=0.99; p < 0.00001). Serial DWI and PWI were performed within 24 hr, subacutely within 5 days, and after a delay of 84 days in 18 patients with acute ischemic stroke (19). Acute PWI lesion volumes correlated with acute neurologic state, clinical outcome, and final infarct volume on T2W. Serial MRIs/DWIs were performed on 50 patients

Figure 2 Magnetic resonance (MR) imaging of acute cerebral infarction. (A) A selected view from a three-dimensional, time-of-flight MR angiogram performed 2 hr after the onset of acute left cerebral infarction. The arrow indicates the location of an embolus occluding the left middle cerebral artery. (B) A diffusion-weighted image obtained on the same subject and at the same time as the MR angiogram in (A). The arrow indicates a well-defined area of restricted diffusion representing the developing core of the infarct. (C) A mean transit-time map obtained after bolus administration of gadolinium contrast to define a perfusion-imaging deficit. The large, wedge-shaped area of lighter gray coloration represents hypoperfused brain tissue. Subtracting the smaller area of restricted diffusion in (A) from the much larger area of hypoperfusion shown in (B) will derive the perfusion-diffusion mismatch.

with ischemic stroke in the MCA territory, beginning within 24 hr after symptom onset and repeated at a median interval of 7.5 weeks (20 ). Acute DWI lesion volumes correlated with NIHSS (r=0.56), Barthel index (r=-0.60), and chronic lesion volumes (r = 0.80). Considered in aggregate, these studies support the conclusion that DWI lesion volumes predict the eventual severity of ischemic brain injury, thereby defining the potential for DWI as a surrogate marker of clinical efficacy in experimental studies that test new stroke treatments.

The combination of DWI and PWI is necessary for MRI to be fully predictive of injury progression after acute ischemic stroke. The need to assess perfusion-diffusion "mismatch" is driven by a dynamic balance between zones of ischemic tissue in brain that are at different levels of metabolic function, as affected by regional heterogeneity of blood flow (Fig. 2). Tissue within the developing infarct core that is subject to severe perfusion deficits (<15 mL/100 g brain/ min) that lead to failure of Na+/K+ -ATPase ion pumps in the neuronal plasma membrane are encompassed within early DWI lesion volumes. However, tissue within the peri-infarct zone, which includes the ischemic penumbra, has perfusion at intermediate levels (15-25 mL/100 g brain/min) that produces transient metabolic arrest in neurons, thereby causing a neurologic deficit that could be reversed with timely reperfusion. The resulting volume of hypoperfused, but potentially salvageable, tissue that surrounds the developing infarct core is described as the perfusion-diffusion mismatch, a functional definition of "tissue-at-risk" for conversion to infarct. Baird et al. (21) were among the first to suggest the potential value of the perfusion-diffusion mismatch as an indicator of stroke outcome in 13 patients who underwent DWI/PWI within the acute to subacute phase of cerebral infarction (2-53 hr after symptom onset) and after prolonged survival for up to 725 days later. These investigators found that eventual lesion volume increased by 230 ± 95% when the initial PWI volume was greater than the DWI volume but decreased by 47 ± 8% when the PWI volume was smaller than, or equivalent to, the DWI volume. Several confirmatory studies that show the perfusion-diffusion mismatch as a predictor of tissue at risk for stroke progression have been published (18,19,22-24). Recently, attempts have been made to define tissue viability thresholds, as quantified by cerebral blood volume or mean transit time of a blood flow tracer moving through the ischemic region, to predict rate of growth of the DWI lesion to fill the original "mismatch" volume (25,26), although this approach has yet to be confirmed in a prospective study that incorporates voxel-based, serial imaging. In another variant of multimodal prediction of stroke lesion progression, a "clinical-DWI mismatch" (CDM) has been described that incorporates quantification of neurologic deficit by standardized physical examination with DWI (NIHSS > 8 and ischemic volume < 25 mL on DWI) (27). These investigators found that patients with CDM were at greater risk for early neurological deterioration, defined as an increase in NIHSS > 4 points between acute (< 12 hr) and subacute (72 ± 12 hr) examination times, although again, this concept awaits validation in a prospective study that incorporates a large number of subjects.

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