Neuroimaging of Stroke: A Review

Andrew R. Xavier, MD; Adnan I. Qureshi, MD; Jawad F. Kirmani, MD; Abutaher M. Yahia, M; , Rohit Bakshi, MD

Disclosures

South Med J. 2003;96(4) 

In This Article

Computed Tomography

Computed tomographic (CT) images of the brain are produced by scanning a collimated beam of x-rays through the brain in thin, sequential slices. The x-ray output is counted, analyzed, and reconstructed for clinical interpretation. The newer generation scans use spiral technology, where the imaging is performed in a continuous helical fashion instead of the conventional slice-by-slice method. CT scanning is still the preferred method for imaging hyperacute stroke. It is widely available, can be performed on patients who have a pacemaker or are on a ventilator, and can be performed quickly on confused, delirious patients. In addition, interpretation in the hyperacute stroke setting is fairly straightforward without the need for special training.

In cases of hyperacute stroke (0-6 h), CT is usually not sensitive in the identification of cerebral infarction.[1] But, it is quite sensitive in identifying various forms of acute intracranial hemorrhage and other gross lesions that would preclude the use of thrombolytic therapy (Fig. 1).[2] In the first 24 hours, CT signs of infarction are sulcal effacement with loss of gray-white differentiation in superficial cortical infarction[3] and hypodensity of the basal ganglia[4,5] in cases of deep cerebral infarction (Fig. 2). The presence of these early changes spread over a large area (>1/3 of the parent arterial territory) is often associated with large infarctions and a relative contraindication to the use of thrombolytic therapy in a patient who would otherwise qualify for that therapy.[6,7,8,9] At a minimum, the presence of extensive CT abnormalities in a patient presenting in the first 3 hours for possible thrombolysis should necessitate a careful review of the time of stroke onset. A hyperdense large vessel, described in cases of middle cerebral artery (MCA) stroke[10] is often suggestive of a persistent large vessel occlusion with poor prognosis ("hyperdense MCA" or "dense MCA" sign) (Fig. 3).[11] The presence of this sign is not a contraindication for intravenous thrombolysis,[6] but is an indicator that a large clot burden may be present, and supplemental recanalization strategies might have to be considered. Recent advances in CT technology provide additional data that are helpful in the management of stroke patients. Two such promising techniques are CT angiography and perfusion CT. CT angiography (CTA) is a 3-dimensional reconstruction of the cerebral vasculature from source images showing contrast material in the cerebral vessels shortly after an intravenous contrast bolus. It is a fairly sensitive technique in identifying large vessel occlusions.[12,13,14,15,16] It can be also used to track patients with large vessel occlusions, who have undergone recanalization procedures. A normal CTA can potentially be used to exclude patients from further aggressive recanalization procedures. The contrast saturation in a slice of brain following a rapid intravenous injection of high volume contrast is used to construct perfusion CT images. The perfusion deficit gives a rough estimate of the extent of microvasculature hypoperfusion and hypometabolism and includes the cerebral infarction and the surrounding ischemic penumbra.[17,18,19,20]

A noncontrast CT scan (left, middle) and fast FLAIR MRI (right) was obtained 3 hours after the onset of a patient's severe headache. The CT shows hyperdensities (arrows) in the basal cisterns and left sylvian and frontal cortical sulci, consistent with acute subarachnoid hemorrhage. FLAIR-MRI shows bilateral hyperintense frontal and parietal sulci (arrow), consistent with acute subarachnoid hemorrhage. The MRI abnormalities are more conspicuous and more widespread than shown by CT.

An 89-year-old woman presented with slurred speech and confusion 12 hours before the performance of the initial noncontrast CT scan (left). Note the subtle asymmetry of findings. There is early hypodensity of the left posterior putamen (arrowhead) and peri-insular cortex (arrow) as compared with the contralateral side. Twenty-four hours after the initial scan, repeat CT (right) shows clear hypodensity involving the entire main stem middle cerebral artery territory with mild associated mass effect. The findings are diagnostic of an acute middle cerebral artery stroke.

Noncontrast CT scan is shown of a patient who presented 8 hours after onset of left-sided weakness and aphasia. Note the tubular hyperdensity (arrow) suggestive of acute clot in the left middle cerebral artery. This is accompanied by hypodensity of the ipsilateral temporal lobe in the middle cerebral artery territory (arrowhead). Compare these abnormalities to the contralateral (right) side of the brain. Taken together, these findings are highly suggestive of acute stroke.

In the acute period (6-24 h), the changes of ischemia become more apparent on the noncontrast CT scan. The loss of gray-white interface, sulcal effacement, hypodensity of basal ganglia, and hypodensity of the insular cortex become prominent (Fig. 3). The vascular distribution of the infarct becomes increasingly clear during this stage. In severe cases, edema and mass effect can appear at this stage.

During the subacute period (1-7 d), there is increasing edema and mass effect with lateral and vertical shift of infarcted tissue in cases of infarction involving large vessel territories. Edema and mass effect peak at 1 to 2 days and then decline. The edema surrounding the infarcts caused by occlusions of the deep, perforating branches are much more modest, with little, if any, associated mass effect. The first 1 to 2 days are also when hemorrhagic transformation peaks; this is noted in about 5 to 40% of all ischemic strokes.[21,22,23,24,25] When hemorrhagic transformation occurs, it is usually in the form of petechial hemorrhages and is clinically not significant but, in a minority, particularly in those who received thrombolytic or anticoagulant medication, it could take the form of a frank parenchymal hematoma with clinical deterioration (Fig. 4).[8,22,24] Contrast scans performed during this period have a characteristic "gyral enhancement" pattern.[26] Chronic infarctions are characterized by marked hypodensity and lack of mass effect on CT scans; the density is similar to cerebrospinal fluid (CSF) (Fig. 5).

Two patients with subacute hemorrhagic stroke. Patient 1 received intra-arterial urokinase treatment for a hyperacute stroke associated with internal carotid artery occlusion. After urokinase treatment, the patient developed increased function of the left side. Two days later, noncontrast CT was performed and is shown. Note the hematoma, seen as a round hyperdensity, in the right subcortical region (arrowhead). There is a completed subacute middle cerebral artery infarction. Patient 2 (right) obtained noncontrast CT scan 36 hours after stroke onset. Note the subtle linear and patchy hyperdensities (arrow) in the anterior and medial aspects of the operculofrontal infarction. The hyperdensities are consistent with petechial hemorrhagic transformation of infarction.

CT scans were obtained for two patients with chronic infarctions. Note the marked hypodensity of each lesion with similar density similar to cerebrospinal fluid and how each conforms to a known vascular distribution - central sulcal middle cerebral artery stroke and posterior cerebral artery occipital stroke.

Imaging of intracranial hemorrhage is fairly straightforward with CT,[27] where image contrast is determined by tissue density. Acute blood clots have a high density and appear hyperdense,[28] often strikingly so, when compared with the surrounding brain tissue. (Figure 1, Figure 4, Figure 6) Acute subarachnoid hemorrhage (SAH) appears as a high density in the subarachnoid spaces (Fig. 1).[29,30] The severity of SAH on CT is usually graded using the system described by Fisher,[31] and the CT findings are important predictors of clinical outcome.[32,33] The CT findings of SAH may be subtle (Fig. 1), particularly in the subacute stage.[34,35] Findings may only include a mild hydrocephalus, diffuse sulcal effacement, and subtle hyperdensities in the CSF spaces. Acute and subacute intraparenchymal hemorrhage is comparatively much easier to identify on CT as it has excellent contrast as compared with the surrounding brain tissue (Figure 4, Figure 6). The location of the hemorrhage often gives a clue to the underlying pathophysiology.[36] Hemorrhages due to chronic hypertension are commonly situated in the putamen,[37] thalamus, pons, cerebellum,[38] caudate,[39] and the subcortical white matter/gray-white junction.[40] It is controversial whether Charcot-Bouchard aneurysms are the primary underlying pathology in these cases. The location, size, and intraventricular extension correlate well with clinical severity and can predict clinical outcome.[32,41] In cases of amyloid angiopathy, the hemorrhages are usually large, superficial, lobar, and prone to recur (Fig. 6).[42,43,44] In the setting of anticoagulation, thrombolysis, or systemic coagulopathy, hemorrhages are often multiple, large, and associated with fluid-fluid levels due to impaired clotting ability.[35,45,46] Another common cause of nontraumatic intracranial hemorrhage is hemorrhagic transformation of cerebral infarction (described above) (Fig. 4). In patients who received intra-arterial thrombolysis treatment, extravasations (focal intraparenchymal extravasations) of the angiographic dye commonly occur during the procedure and may be confused with hemorrhagic transformation.[47,48]

Patient 1 is a 97-year-old woman who presented with acute onset coma. The noncontrast CT scan (left) shows a large acute intraparenchymal frontal lobar hemorrhage with severe mass effect. Patient 2 is a 75-year-old man who presented with lethargy. The noncontrast CT scan (right) shows an acute intraparenchymal occipital lobar hemorrhage (arrowhead) with mild to moderate mass effect. Autopsy of both patients showed widespread cerebral amyloid angiopathy.

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