Case 26 A 58-year-old man was admitted to a district general hospital with right-sided sensorimotor hemisyndrome and dysarthria. Several weeks earlier he had complained of transient vertigo and a gait disorder. The patient had known vascular risk factors of arterial hypertension, hypercholesterolemia, and diabetes mellitus. On admission he presented fluctuating symptoms with a moderate proportional hemiparesis, hemihypesthesia on the right side, and dysarthria (National Institute of Health Stroke Scale [NIHSS] score: 7). The initial cerebral CT scan showed hypodensities in both cerebellar hemispheres and a small hypodense area in the right pons consistent with subacute infarction (Fig. B26.1). Diffusion-weighted MRI revealed acute left paramedian pontine ischemia (Fig. B26.2) MR angiography (MRA) was not performed. Recurrent ischemia in the vertebrobasilar artery territory suspicious of basilar artery (BA) pathology (plaque, stenosis, or thrombosis). Digital subtraction angiography (DSA) demonstrated a high-grade stenosis in the middle segment of the BA. The vertebral and carotid arteries were normal (Fig. B26.3). In view of the remitting clinical symptoms, and the lesions on MRI, interventional percutaneous transluminal angioplasty of the BA followed by stent implantation was performed via the left vertebral artery (VA). This was technically and clinically successful and a follow-up CT scan showed a patent BA without evidence of bleeding or new ischemic lesions (Fig. B26.4). Secondary stroke prevention was commenced with aspirin and clopidogrel and the patient was referred to a rehabilitation center. By this stage there had still not been any neurosonologic examination. Two weeks after the stenting, the patient had a transient ischemic attack (TIA) with double vision and a left-sided hemiparesis that lasted a few hours. Furthermore, the residual right-sided hemiparesis and the dysarthria mildly worsened. The patient was then admitted to our department for the first time. B-mode imaging of the carotid arteries showed moderate atherosclerotic vascular changes, more pronounced in the carotid bifurcation. Doppler spectrum analysis demonstrated normal findings. The left VA showed a marked increase in caliber in the V2-VA segment at the vertebral level between C5 and C6 with a maximal diameter of 10.5 mm in B-mode and color-mode imaging. The diameter of the V1-VA segment was 5.5 mm. A constant diameter ranging from 4.3 mm to 4.5 mm was seen in all segments of the right VA. The Doppler spectrum analysis demonstrated normal flow signals in the left middle and distal V2-VA segment as well as in the right V2-VA segment (Figs. B26.5–B26.10, see also Video Transtemporal insonation yielded normal findings in the anterior (ACA), middle (MCA), and posterior (PCA) cerebral arteries on both sides. Transforaminal insonation demonstrated normal flow signals in the BA and the intracranial segment of both VA (not shown). Suspected left VA dissection with formation of a dissecting aneurysm in the proximal V2-VA segment at the C5/C6 level. There were no signs of detectable restenosis in the stented BA. Cranial CT confirmed the known cerebellar and pontine infarctions. In addition, a new paramedian pontine infarct of moderate size was seen on the right side adjoining the BA stent (Fig. B26.11). CT angiography (CTA) confirmed the widening of the left V2-VA segment between C5 and C6 which was diagnosed as a VA dissecting aneurysm (Fig. B26.12). The VA dissection was thought to be of iatrogenic origin, generated during the initial DSA with BA stent implantation. The recent pontine infarction was attributed to a stent-related secondary occlusion of a perforating artery. An embolic event, potentially originating from the aneurysm, could not be excluded but seemed unlikely because of the infarct location. Nonetheless, oral anticoagulation with phenprocoumon was started and the patient was again referred to a rehabilitation center. He was then lost to follow-up. Primary left-sided pontine infarction and old right-sided pontine and cerebellar infarctions caused by BA stenosis of assumed atherosclerotic origin. Secondary right-sided pontine infarction after successful BA stenting, probably induced by secondary occlusion of a pontine perforator artery within the stented region or by artery-to-artery embolism from left V2-VA dissecting aneurysm. Fig. B26.1 Unenhanced cranial CT, axial plane. Hypodensities in the right cerebellar hemisphere and a small right-sided hypodense area within the pons suggestive of non-acute stroke (arrows). Note the enlarged BA (arrowhead).
Extracranial Left Vertebral Artery Dissecting Aneurysm Following Basilar Artery Stenting
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Conventional Angiography
Clinical Course (1)
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B26.1).
Transcranial Duplex Sonography
Conclusion
Cranial CT and CT Angiography (Day 1)
Clinical Course (2)
Final Diagnosis
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