Figure 1. 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.

Figure 2. 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.

Figure 3. 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.

Figure 4. 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.

Figure 5. 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.

Figure 6. 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.

Figure 7. MRI of hyperacute stroke at 2 hours postictus. The T2-weighted image is normal. The FLAIR image shows hyperintense vessels (HVS - see text) in the territory of the middle carotid artery (MCA) (arrow), consistent with slow arterial flow, but the FLAIR shows no tissue abnormality. Diffusion-weighted imaging (DWI) shows hyperintensity in the deep middle cerebral artery territory consistent with cytotoxic edema in an acute stroke (arrow), but there is no evidence of cortical ischemia. Perfusion-weighted imaging (PWI) (time-to-peak image) shows reduced perfusion in the full (cortical and subcortical) MCA territory. This suggests a much larger area of tissue at risk than shown by DWI or conventional images. This is known as a diffusion-perfusion mismatch (see text). Some areas of reduced perfusion show HVS on FLAIR whereas others do not. Three-dimensional time-of-flight magnetic resonance angiography (MRA) confirms a proximal MCA occlusion or severe stenosis.^[35]

Figure 8. MRI of acute middle carotid artery (MCA) stroke on MRI at 12 hours postictus. T2-weighted image shows mild hyperintensity of the middle carotid artery territory (arrows). Noncontrast T1-weighted image demonstrates early stroke changes with effacement of cortical sulci in the MCA territory associated with swelling and mild hypointensity of the cortical ribbon (arrows). After contrast (gadolinium) administration, intravascular enhancement is present, indicating sluggish flow in the ischemic zone (arrows).^[35]

Figure 9. Ten days postictus, MRI is consistent with subacute infarction. T2-weighted (proton density [PD]) MRI shows a markedly hyperintense well-demarcated lesion conforming to a lateral temporal branch territory of the middle cerebral artery. Postgadolinium contrast images show enhancement of the temporal cortex that conforms to a gyral pattern.

Figure 10. Two patients are shown. The left and middle images show a chronic occipital infarction. Note the marked hypointensity in core of the lesion (fluidity) on the FLAIR image surrounded by a rim of hyperintensity (chronic gliosis). There is no mass effect; instead, the adjacent CSF spaces are expanded in an ex vacuo manner. The diffusion-weighted image (DWI) shows hypointensity of the lesion, consistent with increased diffusion. A second patient (right image) had a stroke 3 years previously involving the left motor cortex (not shown). Ipsilaterally, the cerebral peduncle is shrunken (arrow), consistent with wallerian degeneration of the descending corticospinal tract.

Figure 11. The cerebral angiogram of an 87-year-old man with acute onset left hemiplegia. The right internal carotid artery (short arrow) injections are shown in the anteroposterior projection. The middle (long arrow) and anterior (arrowhead) cerebral arteries can be visualized. The image on the left (A) obtained preoperatively shows a middle cerebral artery (MCA) occlusion at the level of M1. The whole MCA distribution territory, including the lenticulostriate system, is affected with no collateral supply (Grade 3b). The image on the right (B) was obtained after intra-arterial thrombolysis. The M1 segment has recanalized with restoration of blood flow to the superior division. A persistent occlusion is noted in the inferior division (Grade 2).

Figure 12. The cerebral angiogram of a 67-year-old woman presenting with acute onset unresponsiveness and quadriparesis. The left vertebral artery (short arrow) injections are shown in the lateral view. The basilar artery (long arrow) and the posterior inferior cerebellar arteries (arrowhead) are visualized. The image on the left (A) shows an occlusion at the mid-basilar level with absent flow to the distal basilar artery as well as the distal branches of the basilar artery. Carotid injections (not shown) showed no collateral flow to the posterior circulation through the posterior communicating arteries (Grade 5 occlusion). Post-thrombolysis images (B) showed complete recanalization of the basilar artery. The superior cerebellar arteries (white arrowhead) and the posterior cerebral arteries (white arrow) can be visualized well (Grade 0 post-thrombolysis).

Figure 13. A 76-year-old man presented with an episode of blurred vision on the right side associated with headache. Color flow imaging of the right carotid system (shown here) identified a large, heterogeneous, calcified plaque (arrow) in the internal carotid artery (ICA) close to its origin at the carotid bifurcation, causing arterial narrowing. Calcified plaques appear bright and have a dark sonolucent zone (arrowhead) beneath the surface. The laminar blood flow in the common carotid artery (CCA) becomes turbulent beyond the site of arterial stenosis. The blood flow velocity was 354/112 cm/s, which correlates with a high-grade (80-99%) carotid stenosis. The patient underwent a right carotid endarterectomy.

Figure 14. A 75-year-old man presented with recurrent right-sided numbness, clumsiness, and speech difficulties. Duplex Doppler examination of the left carotid system (shown here) revealed a homogenous echogenic material filling up the common carotid artery (arrow) and the internal carotid artery (not shown). No Doppler signals could be identified (arrowhead). Cerebral angiogram (not shown) confirmed left common and internal carotid occlusion. The external carotid artery, middle cerebral artery, and anterior cerebral artery on the left side filled from collaterals.

Figure 15. A 58-year-old woman had an episode of near syncope followed by right-sided neck pain. Duplex Doppler imaging of the right common carotid (shown here) identified a false lumen and intimal flap (small arrows), which suggest an arterial dissection. The blood blow velocities were also elevated (202/37 cm/s).