Post contrast head CT
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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.
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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.
CA0395-Post contrast head CT
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CA0395-Post contrast head CT
Case ReportExam
Prior Study
Changes consistent with hyperacute stroke in the Lt. lateral lenticulostriate and the Lt. superior division MCA regions. This makes the likely level of occlusion in the Lt. M1/2 superior division MCA segment.
No intracranial hemorrhage nor hyperdense (acute) thrombotic arterial segments are evident.
CT Perfusion
Acute stroke with dense ischemic core evident in the Lt. lateral lentriculostriate, the Lt. orbitofrontal artery and the Lt. anterior insular M3 perfusion zones.
Minimally prolonged TTP is evident in the Rt. cerebellar hemisphere, but with normal CBV/CBF/MTT.
CTA of the Neck
Possibly flow-limiting (50-60%) proximal right vertebral artery stenosis with no other abnormality noted in the remaining cervical arteries or veins.
CTA of the Head
1. There is a short stenosis at the origin of the Lt. superior division MCA; there is minimal post stenotic dilatation placing the stenosis in the 50-60% range; there is, at this time, reasonable antegrade blood flow. Presumably, part of the original thrombus has lysed restoring antegrade flow, which now appears as a stenosis rather than an occlusion. The time interval of the occlusion likely produced the left MCA stroke, not the current stenosis.
2. There is subtle leak of contrast around the distal Lt. MCA arteries consistent with the minimal blood brain barrier associated with post ischemic arteriopathy.
Findings
Post contrast head CT for venocapillary pool analysis
There is a short stenosis at the origin of the Lt. superior division MCA with the current stenosis in the 50-60% range; there is now reasonable antegrade blood flow with no collateral gap on either the initial or delayed head CTA’s. Since the stroke-zone includes the lateral lenticulostriate perforator and the lateral orbitofrontal perfusion zones in addition to the superior division MCA zone, the initial thrombotic occlusion must have involved the M1/2 ICA segments and the current stenosis is actually a recanalized arterial segment and not a fixed atherosclerotic stenosis.
There is reduced anterior insular, left basal ganglia, and orbitofrontal cortical CT density within the venocapillary pool on the initial and delayed post contrast CTA head. However, these oligemic areas for the most part demonstrate a partial rise in the CT density on the delayed post contrast head CTA (i.e. they improve but not to normal). This indicates that these area have residual oligemia enough to put them in the ischemic penumbra and have the potential to proceed to completed infarction.
However, the CT density within the venocapillary pool on the delayed CTA head in the lateral orbitofrontal artery and anterior insular region remain more oligemic than other affected areas These two areas are more likely will proceed to completed infarction. This stroke-zone likely involves Broca’s area, which accounts for the aphasia symptoms.
There is minimal hyperemia with dilatation of the distal M4 pial arteries off the superior division Lt. MCA. In addition to the vasodilatation there is additional density in the sulci particularly in the most distal pial arteries. This extra density is likely leak of contrast into the sulcal CSF. This is consistent with post ischemic arterial wall changes altering the blood brain barrier (BBB). These findings are consistent post oligemic dysautoregulation. In part, there is likely some vasodilatation from compensatory expected physiologic response to stroke in the collateral zone.
The Rt. intradural carotid and posterior fossa arteries are NL.
There is no hemorrhagic conversion at this time.
Cerebral venous egress is within normal limits.
Impression
2. Persistently reduced CT density in the venocapillary pool within the Lt. lateral orbitofrontal and anterior insular cortex with enough oligemia to fall within the ischemic penumbra. The oligemia in the posterior insula and the Lt. lateral lenticulostriate perforator regions appear less extensive. Correlate with stroke protocol MR.
3. There subtle loss of BBB in the distal Lt. MCA (M4) pial branches consistent with post-ischemic arteriopathy.
4. Stroke-age, based on the findings on the noncontrast CT would fit the hypeacute timeframe.
Recommendations
Consider MR to evaluate for tissue ischemia that is not revealed on the CT perfusion or CT venocapillary pool and to evaluate status of intramedullary veins
