Presentation
Malaise and bilateral lower limb weakness, transient facial asymmetry at wake-up. Right upper limb ataxia and pronator drift on exam.
Patient Data
NECT shows no intracranial hemorrhage. No territorial hypodensity nor hyperdense artery (stroke window). Multiple lacunar infarctions (bilateral thalami, caudate nuclei). Moderate cortical atrophy. Dilated and elongated basilar artery. Calcified atheroma seen in cavernous segment internal carotid arteries and V4 segment of the right vertebral artery.
Perfusion study shows increased Tmax and MTT in the posterior circulation, with normal CBF and CBV.
CT angiogram reveals a dolichoectatic basilar artery occupying the left cerebellopontine angle, which bifurcates at the level of the third ventricle. Left internal carotid bifurcation appears dysplastic. At the cervical level, the right ICA has a retropharyngeal position, whereas the left is laterocervical.
No vascular occlusion, dissection or stenoses in either extra or intracranial segments.
MRI study the next day shows no acute stroke, lacunar or territorial.
Slow-flow artifact of the basilar artery visible on FLAIR and MRA sequences.
Chronic lacunar infarctions visible in the thalami, caudate nuclei. No associated micro-hemorrhages.
Case Discussion
Exact prevalence in the population is unknown. Aberrant vascular remodeling and arterial wall connective tissue abnormality is currently hypothesized as a primary pathophysiological process 1. It has been linked to posterior circulation strokes and their recurrence, which seems proportional to diameter increase 2,3. Associated atherosclerotic changes are an associated risk factor for ischemic event frequency and recurrence 3. A significant number of vertebrobasilar dolichoectasis progress on long-term follow up, resulting in increased morbidity and mortality 4.
This patient presented with multiple TIAs and ischemic strokes over the last couple of years, and suffers a longstanding, poorly controlled arterial hypertension. Cervical internal carotid artery elongation and left terminal ICA dysplasia might suggest a systemic vasculopathy 1.
The particularity of this case is the CTP study that demonstrates increased time sensitive perfusion parameter value (Tmax) in the setting of acute neurological deficit, without arterial occlusion. CTP parameters are often the first ones we look at in an acute setting, even before the non contrast study, even though they can be misleading (hope for an easy answer between the overflowing demands during our emergency CT shift). Tmax value in this case was likely influenced by delayed flow and temporal dispersion5.
Slow-flow artifact seen on FLAIR and MRA, with lowest flow near the vessel walls due to laminar flow (MRI key images). Loss of signal on TOF MRA in attributed to the same slow-flow 1, basilar artery permeability, without thrombosis, is documented on the CTA.
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