PMC8326099_01
(a) An axial image of the computed tomography (CT) scan at admission shows diffuse subarachnoid hemorrhage. A CT angiography was performed subsequently (b) revealing a saccular basilar trunk aneurysms (arrow). Furthermore, the absence of contrast was noted in the distal extracranial segment of the left internal carotid artery (encircled), whereas the right internal carotid artery was clearly visible (arrow).
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F1
Scale (GCS) was 3 (E1M1V1) with anisocoria. Subsequent computed tomography (CT) scan of the head and neck showed diffuse SAH [Figure 1a]. On CT angiography, a saccular BTA [Figure 1b] and a dissection of the extracranial segment of the left internal carotid artery (ICA) with luminal stenosis [Figure 1c] were noted.
The digital subtraction angiography images from the coiling procedure are shown. The 3D reconstruction of the vertebrobasilar arterial system illustrates the saccular basilar trunk aneurysms (encircled) in (a). Complete obliteration of the aneurysm was accomplished by bare coiling (b). In the same session, the left internal carotid artery was assessed to evaluate the left-sided carotid artery dissection. As can be seen in (c), the dissection is no longer visible and there is no sign of obstruction or stenosis of the left internal carotid artery.
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F2
Following multidisciplinary consultation, it was decided to treat the BTA by endovascular coiling [Figure 2a and b]. During this procedure, that is, a digital subtraction angiography (DSA), the left ICA was reassessed as well, showing no signs of the dissection or stenosis [Figure 2c].
An axial slide of the noncontrast-enhanced computed tomography (CT) scan of the brain shows a cortical hypodensity within the left temporal lobe (a). The gray-white matter differentiation is difficult to assess due to the subarachnoid hemorrhage, but might be slightly reduced. Furthermore, the bilateral deep nuclei like basal ganglia and thalami seem to appear less distinctively. Both might suggest hypoperfusion or ischemia. The CT angiography (b) again revealed the mouse-tail appearance of the distal extracranial segment of the left internal carotid artery (oval), suggestive for recurrent severe stenosis of this segment due to a subintimal dissection.
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F3
This was probably due to the dissection of the left ICA [Figure 3a and b].
These digital subtraction angiography images show the left internal carotid artery pre- and post-stent placement, in image a and b, respectively. Clearly, contrast filling is increasingly reduced from around halfway the extracranial segment of the internal carotid artery until its entrance into the petrosal bone. Following placement of two stents, the stenosis is redressed and internal carotid artery is filling accordingly.
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F4
Following the placement of two stents (CASPER 5 x 30 mm and Solitaire 5 x 30m), the stenotic extracranial segment of the left ICA was reopened [Figure 4a and b].
(a-c) Axial FLAIR images of the magnetic resonance imaging depict hyperintensities within the mesencephalon, bilateral thalamic, and basal ganglia (left more pronounced than right). In addition, paramedian and lateral cortical hyperintensities within the frontal lobe (in particular on the left side) and in the left temporal lobe are visible. In combination with the findings on diffusion-weighted images and the apparent diffusion coefficient images (not shown), these hyperintensities were diagnosed as ischemia within these areas. The subintimal dissection of the left-sided internal carotid artery is probably the reason for the more pronounced left-sided location of the ischemic lesions.
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F5
The patient's GCS deteriorated to 3 (E1M1V1) and a magnetic resonance imaging of the head was performed showing extensive and diffuse ischemia in the mesencephalon, bilateral deep nuclei, thalamus, and watershed areas [Figure 5].