Case 21 A 33-year-old woman acutely developed left-sided weakness and drowsiness. In the days preceding presentation she had had an occipital headache of moderate severity. She had no relevant medical history and no known vascular risk factors. In particular, she had no history of migraine. Neurologic examination revealed an impaired level of consciousness, a left-sided hemiparesis, and gaze deviation to the left (National Institute of Health Stroke Scale [NIHSS] score: 17). Initial CT 6 hours after onset of symptoms showed normal findings, in particular no signs of subarachnoid hemorrhage (SAH). Assuming a diagnosis of basilar artery (BA) disease, emergency digital subtraction angiography (DSA) was performed, which revealed a severe narrowing of the middle segment of the BA including an “intimal flap” suggestive of BA dissection. Perfusion of the posterior cerebral artery (PCA) territory was maintained by the BA (not shown). No interventional treatment was performed. Brainstem ischemia in the vertebrobasilar territory caused by BA dissection. Heparinization was commenced with the aim of achieving a partial thromboplastin time (PTT) that was double the normal value. Her mental status improved. Clinical follow-up 2 days later demonstrated left hemiataxia and mild left hemihypesthesia. In addition the patient had right-sided hemianopia and severe dysarthria, both of which had initially been masked by her impaired consciousness. An MRI scan taken 2 days after admission revealed multiple ischemic lesions in the vertebrobasilar territory, particularly in the left occipital lobe, left thalamus, bilateral pontine regions, and cerebellar hemispheres, the latter being considered to present infarctions in the territories of the anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA) (Fig. B21.1). 3D time-of-flight MR angiography (TOF-MRA) demonstrated absence of flow signals in the middle segment of the BA (Fig. B21.2). Examination of the carotid arteries revealed normal results. The diameter of both V2-VA segments was within the normal range (left 3.6 mm, right 4.4 mm). Doppler spectrum analysis showed reduced flow velocity and a mildly increased pulsatility in both VAs (Fig. B21.3 and Fig. B21.4). Normal flow signals were found in both middle (MCA) and anterior (ACA) cerebral arteries. Increased velocities and turbulent flow were detected in the right posterior communicating artery (PCoA). The right P1-PCA segment and the top of the BA demonstrated a reversed flow signal while the P2-PCA segment was normal. The left P1-PCA segment revealed a stenotic flow signal (flow velocity 124/83 cm/s). Turbulence, mildly increased flow velocities (systolic flow velocity ~90 cm/s), and reduced pulsatility were seen throughout the left P2- and P3-PCA segments, suggestive of postischemic hyperemia caused by the large PCA infarction. Digital tapping of the right internal carotid artery (ICA) yielded positive oscillation effects in both PCAs and in the retrograde BA confirming collateral blood flow from the right ICA via the right PCoA toward the posterior circulation (Figs. B21.5–B21.11). Transforaminal insonation revealed reduced flow velocities in both V4-VA segments, comparable with the extracranial findings. There was a distinctly reduced flow signal in the proximal BA but there was no signal more distally, despite the presence of excellent insonation conditions. Intravenous echo contrast administration (5 mL Levovist, 300 mg/dL) confirmed the absence of distal basilar flow. A prominent signal was seen in the both AICAs and in the right posterior inferior cerebellar artery (PICA) (Fig. B21.12, Fig. B21.13, Fig. B21.14, Fig. B21.15). Fig. B21.2 3D TOF-MRA. Circle of Willis, sagittal maximal intensity projection (MIP). Absent flow signal in the mid-segment of the BA (arrowhead). Note that no prominent PCoA is visible. Fig. B21.3 Extracranial duplex, longitudinal plane. Reduced flow velocity and mild increased pulsatility in the left V2-VA with a diameter of 3.6 mm (flow velocity 37/13 cm/s, PI = 1.1). Fig. B21.4 Extracranial duplex, longitudinal plane. Identical flow signal in the right V2-VA revealing a diameter of 4.4 mm (flow velocity 37/13 cm/s). Mid-BA occlusion distal to the AICA origin. Collateral blood flow toward both PCAs and the upper BA segment from the right ICA via the right PCoA. In addition, suspected left-sided P1-PCA stenosis, probably caused by a partially resolved embolus. DSA on the next day confirmed mid-BA occlusion distal to the AICA origin, with collaterals via the right PCoA as well as retrograde filling of the distal BA with supply of both SCAs. A left P1-PCA stenosis was not visible (Fig. B21.16, Fig. B21.17, Fig. B21.18, Fig. B21.19). A schematic of the patient’s extra- and intracranial brain-supplying arteries is shown in Fig. B21.20. Because of the long time delay and the large areas of infarcted brain parenchyma, no interventional treatment was considered. The etiology of the BA dissection with secondary occlusion remained unclear. There was no history of trauma and no findings suggestive of vasculitis or inflammatory vessel disease. Fibromuscular dysplasia (FMD) had been excluded by DSA, and laboratory data had ruled out coagulopathy. On extensive cardiologic examination, no source of embolism was found. Because of the intracranial location, treatment was changed from heparin to aspirin. Three weeks after admission the patient was transferred to a rehabilitation clinic, awake and with moderate left-sided hemiataxia, right-sided hemianopia, and cerebellar dysarthria. After 6 months the patient had remained stable with regression of the ataxia and dysarthria. Ultrasound examination showed unchanged signs of BA occlusion but complete regression of the left P1-PCA stenosis (not shown). Fig. B21.6 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Doppler spectrum analysis in the right PCoA. Functional stenosis with increased velocity and turbulent flow (flow velocity 173/100 cm/s). Fig. B21.7 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Positive oscillation effect in the right P2-PCA caused by slight tapping of the right extracranial ICA (arrows; flow velocity 30/20 cm/s). Fig. B21.8 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Increased flow velocity in the left P1-PCA (flow velocity 124/83 cm/s). Note the positive oscillation effect in the left P1-PCA caused by slight tapping of the right extracranial ICA (arrows). Note also the retrograde red-coded flow signal in the right P1-PCA (arrow). Spontaneous BA dissection with secondary persistent mid-BA occlusion distal to the AICA origin and consecutive multiple embolic infarcts within the vertebrobasilar artery territory. Here we describe a 33-year-old woman who sustained multiple infarcts within the posterior circulation. A spontaneous BA dissection was diagnosed, leading to secondary BA occlusion and causing in-situ thrombotic and artery-to-artery embolic infarctions. There are no detailed epidemiological data on the incidence and prevalence of intracranial dissections. An intracranial dissection is a rare cause of stroke, and rare in comparison to extracranial dissections. In a recent Chinese study 1.5% of all ischemic strokes were related to intracranial dissections. A perforator-related stroke was the most often assumed cause in one-third of patients. As main radiologic signs, MRI and MRA revealed an intima flap or double lumen in 44% and a dissecting aneurysm in 13% of cases (H. Chen et al 2015). Smaller case series and single case reports suggest that predominantly younger patients between 30 and 50 years of age and more males than females are affected, at least in vertebral dissection (Basseti et al 1994, Caplan et al 1988). In the posterior circulation, dissections most frequently occur in the V4-VA segment, close to the PICA origin, but may also affect primarily the PICA itself (Matsumoto et al 2014). An extension into the BA might also be seen, but isolated BA dissections are extremely rare (Alexander et al 1979).
Mid-basilar Artery Occlusion Due to Intracranial Dissection
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Clinical Course (1)
Follow-up Neuroradiologic Findings (Day 3)
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings (Day 3)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Conventional Angiography (Day 4)
Clinical Course (2)
Final Diagnosis
Discussion
Clinical Aspects
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