Bilateral cerebellar tonsil infarction

No intracranial hemorrhage. Ill-defined hypodensity, crossing grey-white matter junction, of bilateral cerebellar tonsils, suggesting subacute infarct. Ovoid shaped hypodensity within the left centrum semiovale is also likely a subacute/chronic lacunar type infarct. Differentiation at the grey-white matter interface is elsewhere preserved. CSF containing spaces are age appropriate in volume. Contents of the sella and posterior cranial fossa are unremarkable. Mild calcified atheroma of the terminal vertebral and internal carotid arteries.

IMPRESSION

Evidence of established bilateral cerebellar tonsillar infarcts (R>L), which could suggest variant PICA anatomy or an embolic source. Further assessment with CTA neck, and MRI brain is recommended.

Atherosclerosis along the right carotid bulb with greater than 50% narrowing of the origin of the right ICA. Normal opacification of the right ICA distal to the bulb.

Atherosclerosis of left carotid bulb with complete occlusion of the left ICA from its origin. The entire extracranial left ICA is unopacified. The intracranial portion is opacified from retrograde flow which is supplied from left foetal PCOM. The ACom is not convincingly demonstrated.

Normal opacification of bilateral vertebral arteries and the basilar artery. No large vessel occlusion of the proximal branches of the circle of Willis. No filling defect within the dural venous sinuses.

IMPRESSION

Atherosclerosis of bilateral carotid bulbs causing 50% stenosis of the proximal right ICA and complete thrombosis of the left ICA. The intracranial left ICA is supplied by retrograde flow from the left foetal PCOM. Appearances are of uncertain acuity, possibly chronic.

There are multiple foci of restricted diffusion in the cerebellar vermis and both medial cerebellar hemispheres, with associated hemorrhage within the vermis. This causes moderate mass effect at the foramen of Magendie although there is no obstructive hydrocephalus.

There is no supratentorial restricted diffusion. There are several gliotic foci in the left centrum semiovale, left precentral gyrus and superior parietal lobule.

Near complete loss of flow signal is returned from the intracranial left internal carotid artery with flow reconstituting at the level of the posterior communicating artery. The terminal ICA, A1 and M1 segments return normal flow signal. No flow signal returns from the left PICA, the right PICA has a normal appearance.

IMPRESSION

Multiple foci of acute infarct with hemorrhagic transformation in the cerebellar vermis and medial cerebellar hemispheres (PICA territory). No obstructive hydrocephalus. Occlusion of the left internal carotid artery is again noted, with distal ICA flow reconstituting via the posterior communicating artery.