Presentation
Two weeks of intermittent nausea, vomiting and headache, with gait unsteadiness and multiple falls. Nil past medical history, extensive smoker.
Patient Data
Hypoattenuation with loss of grey-white matter differentiation through the right inferior cerebellar hemisphere. Ill-defined cortically based hyperattenuation posteriorly. With contrast there is no definite enhancement in this region, and no other enhancing intracranial foci.
Significant local mass effect with deviation of the falx cerebelli 8mm to the left. Descent of the right cerebellar tonsil down to the level of the foramen magnum.
Lateral ventricles remain patent with hydrocephalus or midline shift.
- Probable large subacute infarct of the right inferior cerebellar hemisphere, corresponding to a right PICA vascular territory.
- Right posterior cerebellar cortical hyperattenuation could relate to early hemorrhagic transformation or cortical laminar necrosis.
Typical aortic arch branching pattern with patent origin of common carotid and vertebral arteries. No mural irregularity, aneurysm or stenosis of anterior or posterior circlulation from aortic arch to circle of Willis.
Abrupt loss of opacification of the right PICA approximately 10mm from its origin. Circle of Willis is complete without aneurysm, stenosis, or filling defect.
There is a possibility of the right cerebellar lesion being a mass rather than infarct. There is occlusion of the right PICA secondary to extrinsic compression by mass effect within the right cerebellum.
Large area of abnormal signal in the right cerebellar hemisphere, involving the inferior and medial aspects as well as the cerebellar vermis.
The abnormality is predominantly T2 hyperintense with areas of corresponding abnormal increased diffusion restriction (with some pseudo-normalization of ADC). There are large areas of susceptibility related signal loss in keeping with hemorrhage.
Patchy enhancement within the abnormality, predominantly at the margins of the cerebellar folia. Marked mass effect results in almost complete effacement of the fourth ventricle, distortion of the medulla, and herniation of the medial portion of the right cerebellar hemisphere across the midline.
Ventricular size remains stable compared to previous CT scans. Patchy periventricular white matter T2 hyperintensity is felt to represent chronic small vessel disease, as opposed to trans ependymal fluid shift.
No intra-axial lesion elsewhere. No extra axial mass or collection.
On time-of-flight MRA, no flow-related signal is demonstrated in the right posterior inferior cerebellar artery. The left PICA is patent but does not appear to contribute significantly to the right side of the cerebellum. No intracranial occlusive disease or aneurysm was identified otherwise.
- Findings consistent with subacute PICA territory infarct, with areas of petechial hemorrhage.
- No convincing evidence of underlying mass
Case Discussion
Given the patient's subacute presentation yet significant findings on imaging, he was transferred to the nearest tertiary center for monitoring in the event surgical intervention was imminently required
During a short admission for observation, he did not require intervention and continued medical management by his treating team.
He was then transferred to rehabilitation where he made a good functional recovery.