Diagnosis and Treatment of Acute Stroke and Underlying Etiology Based on MRI

A stroke-MRI protocol consists at least of standard MR sequences such as T2-weighted imaging (T2-WI), FLAIR, and MR Angiography (MRA).

On T2-WI, ischemic infarction appears as a hyperintense lesion. Definite signal changes, however, are at the earliest seen 2 h after stroke onset in animal experiments and 6 to 8 h after stroke onset in human stroke [9]. Neither a diagnosis of parenchymal ischemia nor the differentiation of ischemic core from penumbral tissue is possible with T2-WI. On the other hand, T2-WI provides a good anatomical definition of the brain, and depicts microangiopathic changes, edema, old infarcts, or other pathologies [10] (Figure 9.1). FLAIR demonstrates hyperintense vessel sign [11] (Figure 9.2). MRA demonstrates vessel occlusion or patency [12] (Figure 9.3). T2-WI (e.g., source images from PWI) shows the presence or absence of acute and chronic intracranial hemorrhages.

The advent of perfusion-(PWI) and diffusion-(DWI) weighted imaging in the early 1990s has added another dimension to diagnostic imaging in stroke [13-15]. During the last years a growing body of evidence has accumulated, documenting the usefulness of this methodology in the clinical setting of acute ischemic stroke including the differentiation of infarct patterns in hyperacute stroke and the prediction of clinical outcome, which may allow a more rational selection of therapeutic strategies based on the presence or absence of a tissue at risk [16-21].

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FIGURE 9.1 Acute MCA infarction 2 h after symptom onset. T2-WI, axial, TR 3800 msec, TE 22 msec flip angle 180°, slice thickness 5 mm, FOV (mm) 240, acquisition matrix 128 X 256, acquisition time 1 min 42 sec.

Flip Angle Mri
FIGURE 9.2 Acute MCA infarction 2 h after symptom onset. FLAIR, axial, TR 4500 msec, TE 105 msec, TI 1870 msec, flip angle 90°, slice thickness 5 mm, FOV (mm) 230, acquisition matrix 224 X 256, acquisition time 3 min 22 sec.

Diffusion-weighted imaging (DWI) exploits the net movement of water in tissue due to random (Brownian) molecular motion as a contrast mechanism. It is based on a methodology described in 1965 [22] and was incorporated 20 years later into MRI sequences [23]. In tissue, the free movement of water is limited by physical and chemical interactions, thus leading to an apparent diffusion coefficient (ADC) (see also Chapter 8, Section 8.2 and Section 8.4). DWI, earlier than any other imaging modality, allows demonstratation of ischemic tissue changes within minutes after vessel occlusion with a reduction of the ADC [23]. A net shift of extracellular water into the intracellular compartment (cytotoxic edema) with a consecutive reduction of free water diffusion is the main underlying mechanism for ADC change [24]. First, it has to be stressed that decreases in the ADC and increased signal on DWI represent tissue bioenergetic compromise, and not necessarily irreversible ischemia. Secondly, in order to interpret changes on DWI correctly, a variety of artifacts must be known and identified, i.e., anisotropy (physical effects, like diffusion of molecules in the brain, depending on the direction in space are called anisotropic) and T2-shine through.


FIGURE 9.3 Acute MCA infarction 2 h after symptom onset. MRA (3D TOF), axial, TR 35 msec, TE 6.4 min flip angle 20°, slice thickness 319 mm, gap — 0.38 mm, FOV (mm) 240, acquisition matrix 160 X 512, acquisition time 6 min 14 sec.

In the clinical setting of a hyperacute stroke, a lesion on strongly isotropic DWI (indicating acute cellular edema) and a normal T2-WI (indicating that the hyperintense area on DWI is not older than 6 to 8 h) favor an acute lesion. The maximum information can be obtained when isotropic ADC maps are calculated, in addition to DWI and T2-WI. Whereas DWI provides only part of the information on cellular necrosis, ADC provides in addition dynamic information about cerebrovascular hemodynamics [25] (Figure 9.4).

A review of the current literature reveals that more than 1000 patients have been imaged with DWI for acute stroke within 12 h. In 93% of them was capable to demonstrate areas of acute ischemia. When individuals without stroke were included, DWI was negative (i.e., did not show ischemia) in all of them (100% specificity) [26], while in transient ischemic attacks (TIAs), where symptoms resolved within 24 h, DWI was positive in only 21% of the patients.

Perfusion-weighted MR imaging (PWI) allows the measurement of capillary perfusion with the dynamic susceptibility contrast-enhanced technique. Paramagnetic contrast agent is injected as an intravenous bolus and the signal change is tracked by ultrafast MR sequences in the area of interest (Figure 9.5). Cerebrovascular hemodynamic parameters, such as relative cerebral blood volume (CBV), mean transit time (MTT), time-to-peak (TTP), and cerebral blood flow (CBF) can be estimated from the MR-derived contrast-bolus over the time curve in a semiquantitative fashion. In ischemic brain tissue with reduced perfusion or zero perfusion less (or no) contrast agent is present and T2-WI thus do remain hyperintense, respectively, keep their high signal [27]. It is not yet clear, which PWI parameter gives the optimum approximation to critical hypoperfusion and allows to differentiate infarct core from penumbra and penumbra from oligemia. Most authors, however, agree that in clinical practice the MTT or the TTP give the best prognostic information [29]. Determination of the absolute CBF requires knowledge of the arterial input function, which in clinical practice is estimated from a major artery, such as the middle cerebral artery (MCA) or the internal carotid artery.

The attempt to differentiate potentially salvageable ischemic tissue, or tissue at risk, and nonsalvageable ischemia, that has reached a status in which recovery is no longer possible, by imaging techniques was made possible by introducing DWI and PWI into the clinical setting. In a simplified approach it has been hypothesized that DWI more or less reflects the irreversibly damaged infarct core and PWI the complete area of hypoperfusion [28]. The difference

FIGURE 9.4 Acute MCA infarction 2 h after symptom onset. DWI, axial, TR 6000 msec, TE 114 msec flip angle, slice thickness 5 mm, FOV (mm) 240, acquisition matrix 98 X 128, b = 0 and b = 1000 sec/mm2 (directions), acquisition time 23 sec.
FIGURE 9.5 Acute MCA infarction 2 h after symptom onset. PWI, axial, TR 0.8 msec, TE 47 msec flip angle 60°, slice thickness 7 mm, FOV (mm) 240, acquisition matrix 96 X 128, 40 phases, acquisition time 40 sec.

(or sometimes also the ratio) between the lesion volumes assessed by PWI and DWI, also termed PWI-DWI-mismatch, would therefore be a measure of the tissue at risk of infarction or the stroke-MRI correlate of the ischemic penumbra. On the other hand, if there is no difference in PWI and DWI volumes (PWI-DWI-match) or even a negative difference (negative PWI-DWI-mismatch), according to this model the patient is expected to have no penumbral tissue because of normalization of prior hypoperfusion or due to completion of infarction leading to total loss of the penumbra [15,29]. It may be criticized that this model does not take into account that the PWI lesion also encompasses areas of oligemia which are not in danger and that DWI abnormalities do not necessarily turn into infarction [30-33]. In other words, neither DWI nor PWI presently allows to completely and reliably differentiate ischemic core from critical hypoperfusion [30]. Also the assessment of mismatch as a percentage may be less reliable than previously thought [34]. Overall and besides these questions, however, the model of PWI-DWI-mismatch is attractive due to its simplicity; it seems to have a tolerable accuracy in most acute stroke patients and its findings seem to be consistent with our current pathophysiological understanding [15,29].

The hope prevails that by using the mismatch concept patients can be categorized into two groups: those that may profit from a specific therapy to salvage the penumbra and those where no ischemic tissue at risk is present any longer. Indeed, several smaller case series reported excellent correlations between findings on DWI and PWI with baseline and outcome clinical scores as well as with follow-up stroke volume [16,35]. Two large studies found that a combination of the baseline National Institute of Health Stroke Scale (NIHSS) score, the estimated time interval from stroke onset to the MRI examination, and the baseline stroke volume on DWI gave the best prediction of stroke recovery with a 77% sensitivity and 88% specificity. DWI volume was an independent predictor of outcome, together with age and NIHSS score [18,36]. Four other studies found significant positive correlations between the baseline lesion volumes assessed by PWI and DWI, and the outcome lesion volumes [5,37-39]. Yet, these studies were either retrospective, not blinded, or imaging was not performed within the relevant time window. There are only two studies that investigated the correlation of baseline DWI and PWI volumes with baseline stroke severity and clinical outcome in a blinded and independent fashion [17,40] and showed a good correlation with follow-up lesion volume acute and chronic NIHSS score. However, multiple linear regression analysis revealed a significantly lower acute NIHSS score on the right compared with the left side when adjusted for stroke volume on T2 imaging performed in the chronic phase. There are differences in NIHSS scores when the left hemisphere is affected, because usually the areas for speech are in the left hemisphere and patients with aphasia have a much higher NIHSS score [41]. In addition, it has also been reported that in the very early time window after symptom onset these correlations are substantially lower as DWI and PWI may reflect a best and worst case scenario at these time points [29]. Taken together, due to the heterogeneity of the present literature and the lack of truly randomized class I trials, it is still difficult to analyze the prognostic value of PWI-DWI-mismatch in MRI-based therapeutic trials.

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