CT Head
Claim CME CreditPOINT OF CARE INFORMATION
This CME activity consists of the student reviewing the video of the professor reviewing the case as well as the associated DICOM image set related to the case in question.
Learning Objectives
As a result of participation in this activity, participants should be able to:
- Provide improved patient care.
- Greater knowledge of the imaging characteristics of the patient's disease.
- Understand a better approach to interpretation of studies.
Faculty Disclosure
Mehmet Albayram, MD, Ivan Davis, MD, Mariam Hanna, MD, Anthony Mancuso, MD, Ronald Quisling, MD, Dhanashree Rajderkar, MD, Priya Sharma, MD, Roberta Slater, MD and Joann Stamm, MBA have disclosed that they have no relevant financial relationships. No one else is a position to control content have any financial relationship to disclose.
CME Advisory Committee Disclosure:
Conflict of interest information for the CME Advisory Committee members can be found on the following website: https://cme.ufl.edu/disclosure/.
Continuing Medical Education Credit
Accreditation: The University of Florida College of Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.
Credit: The University of Florida College of Medicine designates this enduring material for a maximum of 0.5 AMA PRA Category 1 Credits. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
CA0361-CT Head
View Images
CA0361-CT Head
Case ReportHistory
Exam
Prior Study
Findings
CT head
There is no acute intracranial hemorrhage.
There is a hyperdense (acute thrombus) within the distal basilar artery extending into the Lt. P1 segment.
There is early cytogenic edema is evident within both mesial occipital lobes in the P4-PCA arterial distributions affecting mainly the mesial occipital parenchyma. Stroke age is likely in the 6-8 hour range on the right (more apparent) and 3-4 hour on the left (less conspicuity). No cytogenic edema is evident within the thalamus. The visual cortex is likely involved bilaterally.
There is a left PICA infarct in the mesial cerebellum with some volume loss consistent with an evolving (acute stage or older) infarct. There is less apparent edema (or chronic ischemic demyelination) in the left pons and the Lt. middle cerebellar peduncle. The distribution of the multiple infarcts and their apparent differing ages would suggest there has been an initial thrombus in the proximal left PICA/intradural vertebral artery junction with later secondary emboli to the other distal sites.
There is hypodensity (possibly stroke or chronic age-related ischemic demyelination) in the parenchyma of the superior cerebellar hemisphere extending toward the dentate nuclei (site for the cerebellar watershed zones. There is subtle mass effect affecting the left lateral part of the 4th ventricle consistent with either early cytogenic edema or physiologic hyperemia in the collateral zone around the other infarcts.
Impression
2. There are multiple strokes or potential strokes involving the Lt. PICA and both P4 segments of the PCA; cytogenic edema is already evident on noncontrast in the left PICA and right mesial occipital lobe. CT placing these ischemic events outside the hyperacute treatment timeline. Estimated stroke age is at least 10-12 hours. The other suspicious areas in the cerebellum watershed zones are either chronic ischemic demyelination or stroke. It is likely the original thrombus was located in the intradural vertebral artery initially occluding the left PICA. Later clot lysis resulted in the more recent bioccipital occipital strokes following secondary embolization to downstream arteries.
3. There is a background of age-related chronic vascular changes with scattered areas of ischemic demyelination throughout the cerebral hemispheres.
