Knowledge of the nature and time course of ischemic changes on CT and conventional MRI is necessary as an aid to diagnosis, infarct localization and selection of patients for acute stroke therapy. While hemorrhage is visible almost immediately on CT, ischemia takes longer to manifest, although changes have been reported as early as 22 minutes in one study (von Kummer et al.2001). Consistent with its end-artery vascular system, the striatocap- sular area exhibits irreversible damage very early in patients with middle cerebral artery stem occlusion whereas the cortical areas usually fall within the penumbra. The earliest signs of ischemia are of brain tissue swelling, as shown by effacement of cortical sulci, asymmetry of the sylvian fissures and ventricular distortion (Fig. 11.2) (Kucinskiet al.2002). Occasionally the segment of the artery occluded by the thrombus, particularly in the case of the main trunk of the middle cerebral artery, may appear hyperdense, although inter- observer agreement on such signs is only moderate (von Kummeret al.1996; Grottaet al.
1999). Early brain swelling is followed by the development of parenchymal hypodensity, corresponding to cytotoxic edema, and is seen on CT as loss of the normal gray/white matter differentiation in the cortex, insular ribbon or basal ganglia.
The early ischemic changes on CT are subtle and the CT may appear normal if performed in the first few hours. The sensitivity of CT within five hours of ischemic stroke was reported as 58% in one early study (Horowitzet al.1991) although a higher rate of 68% has been reported within two hours (von Kummer et al. 1994) and even higher of 75% within three hours with middle cerebral artery infarction (Barber et al.2000). The inter- observer reliability and reproducibility of CT in the estimation of the degree of ischemic
Fig. 11.2. Early ischemic change on CT (a) showing very subtle loss of white/gray matter differentiation in the internal capsule/ basal ganglia (arrow) in a patient with a massive infarction in the right territory middle cerebral artery. This is seen clearly on CT scan three days after stroke onset (b). Chapter 11: Brain imaging in major acute stroke
change is modest (von Kummeret al. 1996; von Kummer et al.1997; Grotta et al.1999; Schrigeret al. 1998) although use of a systematic CT review system, the Alberta Stroke Program Early CT Score (ASPECTS) by trained observers has better inter-rater reliability (Couttset al.2004). Sensitivity is less for small infarcts and infarcts in the posterior fossa, and a significant minority of clinically definite strokes are not associated with an appropriate lesion on CT even after two or three days.
One to two days after stroke onset, the infarcted area appears as an ill-defined hypodense area as vasogenic edema becomes predominant. Within two or three days, the attenuation values become lower, the ischemic area is better demarcated and there may be evidence of mass effect (Figs. 5.1and11.3). Later, there may be ipsilateral ventricular dilatation owing to loss of brain substance. Hemorrhagic transformation usually occurs a few days after stroke onset in large infarcts, but it may develop within hours and result in appearances very similar to primary intracerebral hemorrhage (Fig. 16.1) (Bogousslavsky1991).
The site of any hypodensity relates to the underlying arterial distribution, allowing for differences between individuals in arterial anatomy. A small proportion of patients with first-ever strokes have focal hypodensities on CT in areas inconsistent with the presenting symptoms. Others have widespread diffuse periventricular hypodensity, making any new infarcts difficult to delineate (Chodoshet al.1988). Further, despite the temporal sequence of ischemic changes on CT, it is often difficult to determine the age of an infarct from the CT appearance. Diffusion-weighted MR imaging overcomes these limitations (Figs. 10.3–10.9).
In summary, the main role of CT in acute stroke is to exclude hemorrhage. Owing to the limitations in visualization of ischemia, especially in the early stages, CT cannot be used to stratify participants reliably according to infarct location or size in trials of acute stroke therapy, although it is currently used to exclude major completed infarction prior to early thrombolysis.
The earliest ischemic change on conventional MRI, immediately detectable, is loss of the normal flow void in the affected artery, the MRI equivalent of the hyperdense artery sign on Fig. 11.3. Later ischemic change with hypodensity indicating a cerebellar stroke.
CT, and arterial enhancement if contrast has been used (Mohr et al. 1995). Subsequent changes are swelling on T1-weighted images caused by cytotoxic edema, which is present in
up to half of patients within six hours, hyperintensity on T2-weighted images from
vasogenic edema, present within eight hours, and T1-weighted signal change, within
16 hours (Yuh et al. 1991). Consequently, the sensitivity of conventional MRI is low in the first few hours following the onset of stroke symptoms, with values similar to CT (Mohr et al.1995; Mullinset al.2002). In subacute ischemic stroke, conventional MRI has higher sensitivity than CT owing to its better spatial resolution and lack of posterior fossa artefact (Simmons et al. 1986; Bryan et al. 1991) but conventional MRI may still be normal in clinically definite stroke.
Conventional MRI is poor at distinguishing acute from chronic infarction. This is a particular problem in patients with multiple infarcts and in the elderly, in whom multiple T2-weighted abnormalities in the corona radiata, basal ganglia and brainstem are common
and in whom neurological symptoms may develop with intercurrent illness on a back- ground of previous stroke. This, together with the poor sensitivity in the acute stroke period, means that, as for CT, conventional MRI is often unable to stratify patients according to infarct presence, ischemic stroke subtype, size or location prior to therapy or randomization in acute stroke trials. Both MRI and MR venography will help where there is a possibility of venous rather than arterial infarction.