It is not possible to determine clinically whether a sudden neurological deficit is due to bleeding in the cerebral parenchyma or to a circulatory disturbance. Rapid imaging diagnosis is therefore key to decision-making.
If bleeding has been excluded using CT or MRI, it can be assumed that the cause of the acute neurological deficit is an ischemic cerebral infarction. In the second step, the imaging task is then to locate the vascular occlusion. Either CT angiography (CTA) or magnetic resonance angiography (MRA) methods can be used. Imaging of the cerebral vessels from the aortic arch to the peripheral branches of the cerebral arteries is obligatory, and with modern CT and MRI systems it takes less than a minute after contrast administration. Measurement of cerebral blood flow using perfusion CT or perfusion MR then follows, which also takes less than a minute.
When clinical and imaging diagnostic procedures have been completed, taking a maximum of 15–20 minutes, the following information must be available:
For the purposes of targeted treatment planning, an attempt is also made to use multimodal datasets from the initial imaging procedures to obtain information about the chemical composition and biomechanics of the thrombus, as well as its length.
Fig. 1.4–12a-c Multimodal MRI with penumbra. (a) The cytotoxic edema in the diffusion-weighted MRI in the anterior middle cerebral artery (MCA) territory is outlined in blue. (b) In the perfusion image, almost the entire MCA territory shows delayed perfusion (outlined in red). (c) The hypoperfused but still uninfarcted area corresponds to the penumbra (“tissue at risk”) and remains when area A is subtracted from area B.
Fig. 1.4–13 On multimodal perfusion CT, the penumbra is defined as an area of reduced cerebral blood flow (CBF) or a delayed mean transit time (MTT), but still with a normal cerebral blood volume (CBV). The CBV is also reduced in the cerebral tissue that has already undergone irreversible infarction.
1.4.4.1 Computed tomography
Although the cerebral cortex (gray matter) has a higher water content at around 82% than the medullary layer (white matter, water content approximately 70%), it has greater X-ray absorption and is therefore displayed with greater hyperdensity. The reason for this is that there is a lower lipid concentration in the cerebral cortex (33% in comparison with 55% of the dry weight) and higher concentrations of protein (55% vs. 39%) and oxygen. The difference is approximately 8 Hounsfield units (HU). Good, neuro-optimized CT devices, technically accurate examinations and well-windowed images make visual differentiation of as little as 4 HU possible. The infarct leads to a continuous increase in water content, which can be recognized on CT as a decline in density. The infarct’s hypodensity distinguishes it from the normal brain, but usually only after 2–4 hours.
At the same time, the density difference between the medulla and cortex declines. In the infarcted area, the basal ganglia are no longer distinguishable from the surrounding tracts (obscuration of the lentiform nucleus) (Fig. 1.4-14) and the contrast between the insula and the neighboring extreme capsule and external capsule disappears (insular ribbon sign; Fig. 1.4-15).
Slightly later, increasing water retention leads to local cerebral swelling, which becomes visible through compression of the adjacent sulci, with flattening of the relief of the cerebral gyri.
Large, compact thrombi are more dense and can be directly demonstrated on CT using the “hyperdense artery sign” in the absence of iodinated contrast (Fig. 1.4-16).
Fig. 1.4–14a-e (a) On the noncontrast CT, there is obscuration of the lentiform nucleus on the right side. (b) The hypodensity (ischemia) is better visualized with contrast enhancement. (c) Clear hypoperfusion, with the territory of the middle cerebral artery on the right. (d, e) Occlusion of the right internal carotid artery and middle and anterior cerebral artery (T occlusion) on the angio-CT.
Fig. 1.4–15a-c Early signs of middle cerebral artery (MCA) infarction on a noncontrast CT 2 hours after thromboembolic occlusion of the MCA. (a, b) There is hypodensity in the insula on the right, which is no longer distinguishable from the neighboring tracts of the external capsule and extreme capsule (insular ribbon sign). (c) The corresponding perfusion CT shows delayed perfusion in the entire circulation area of the middle cerebral artery on the right.
Fig. 1.4–16 Direct imaging of a large, hyperdense thrombus as the cause of acute middle cerebral artery infarction (dense artery sign).
1.4.4.2 Magnetic resonance imaging (MRI)
A diagnosis of cerebral infarction can be made within the first few minutes using multimodal MR techniques: