What is Your Diagnosis

Transitory ischemic attack (TIA): This phenomenon cannot be imaged because the underlying blood clot is too small and vessel obstruction is transient, as is the change in the dependent parenchymal territory.

Stroke: Acute ischemic infarction (0-6 hours) causes dependent territorial edema and subtle fading of contrast of the cerebral parenchyma (Fig. 11.7a). However, early in-farcts more often than not are initially invisible on CT. Sometimes a dense thrombus is directly visible in the lumen of the medial cerebral artery (Fig. 11.7b). With modern CT angiography-perfusion imaging, defects can be detected more easily and early (Fig. 11.7c-i) Such an early nonhemorrhagic infarction can be treated with regional or systemic thrombolysis. The therapeutic success can be so dramatic that patients may be back on their feet the day after an initially paralyzing infarction. However, there is also a substantial risk of a lethal hemorrhage as a complication of thrombolysis, which must be weighed against the expected consequences of a conservatively treated infarction (Fig. 11.8).

Subacute brain infarction (6-32 hours) demarcates itself with more clarity against normal parenchyma (Fig. 11.9a) in comparison to the acute infarction. If, owing to the normal physiological thrombolytic processes, the previously obstructed vessels are reperfused, secondary intraparenchymal hemorrhage, so-called hemorrhagic transformation of the infarct, may be the consequence (Fig. 11.9b, c). Other underlying lesions and hemorrhage due to other etiologies must be considered and excluded (see p. 235). In most cases this differentiation is possible on the basis of the clinical history. In patients with a chronic ischemic infarct, the damaged, necrotic tissue is progressively cleared by microglial cells. During this process superperfusion or "luxury"-perfusion may occur (Fig. 11.10a, b). Eventually the infarcted area may become a CSF-filled parenchymal defect with the

I Acute Stroke

I Acute Stroke

Hemorrhagic Infarct Csf Shunt

Fig. 11.7 a In this patient with a one-hour history of left arm weakness, the right parietal sulci are swollen and the parenchymal density is decreased. b In another patient with right-sided hemiparesis, the noncontrast CTshows an obvious hyperdensity of the left medial cerebral artery—a phenomenon called "dense media sign." You are actually looking at the thrombus within the vessel! c In this patient there is a very subtle swelling of the left frontal lobe anterior to the sylvian fissure. d CT angiography of the circle of Willis shows vascular obstruction of a left middle cerebral branch (arrow). e The calculated perfusion image shows the perfusion defect where we suspected it on the

Fig. 11.7 a In this patient with a one-hour history of left arm weakness, the right parietal sulci are swollen and the parenchymal density is decreased. b In another patient with right-sided hemiparesis, the noncontrast CTshows an obvious hyperdensity of the left medial cerebral artery—a phenomenon called "dense media sign." You are actually looking at the thrombus within the vessel! c In this patient there is a very subtle swelling of the left frontal lobe anterior to the sylvian fissure. d CT angiography of the circle of Willis shows vascular obstruction of a left middle cerebral branch (arrow). e The calculated perfusion image shows the perfusion defect where we suspected it on the basis of the conventional imaging. Take a step back and look at c-e together. f This CT of a restless patient shows a dense media sign (arrow) on the right. No hemorrhage is seen here and elsewhere on the slices. g CT angiography confirms the obstruction of the right medial cerebral artery (arrow). h The flow map proves the perfusion defect in the vascular territory of the medial cerebral artery. i The mean transit time is visibly altered in the same area. The area does not exceed two-thirds of the vascular territory of the medial cerebral artery. This is a good case for immediate locoregional thrombolysis.

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