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.
CA0391-CT Head
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CA0391-CT Head
Case ReportHistory
Exam
Prior Study
Findings
CT Head
There is no apparent hyperdense proximal stem artery thrombosis.
Punctate hyperdensity is evident in the Lt. mesial basal ganglia (BG). It has appearance of dystrophic basal ganglia calcifica. Another punctate calcification is evident in the right frontal vertex. Neither are likely to be acute micro-hemorrhages. Some areas of the left lateral cortex appear slightly hyperdense, but this findings is not definitive making confirmation of dense ischemic core difficult.
There is effacement of sulci, with minimal flattening of the Lt. lateral ventricle, and loss of GW differentiation, and reduced hyperdensity of centronuclear structures consistent with early cytogenic edema in the Lt. MCA-superior division and Lt. lateral orbitofrontal artery perfusion zones. Stroke-age is likely in the hyperacute phase.
Finding are consistent with a recent ischemic event affecting the Lt. lateral lenticulostriate, the Lt. MCA superior division and the Lt. orbitofrontal artery territories making the likely site of the occluding thrombus in the M1/2 segment with collateralization of the inferior MCA division.
Sulcal effacement is evident without reduced CT density in regions of brain above the stroke-zone consistent with compensatory hyperemia in the collateral zone.
There is encephalomalacia in the Rt. posterior sylvian region, consistent with chronic effects of a prior MCA branch stroke.
Impression
2. No intracranial hemorrhage nor hyperdense (acute) thrombotic arterial segments are evident.
