MR T1-W Sequences
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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.
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.
CA0599-MR T1-W Sequences
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CA0599-MR T1-W Sequences
Case ReportExam
Prior Study
CT head
Acute thrombus has progressed and is now evident in most of the superior sagittal sinus (SSS), the straight sinus, the torcular herophile, the right transverse sinus and the initial segment of the left transverse sinus.
The hydrocephalus seen on initial imaging has resolved.
CT perfusion NO CT perfusion imaging is available
CTV of the neck NO neck CTV imaging was available
MRV of the head
There are progressive dural CVT changes (compared to the initial MRV) with widespread dural sinus thromboses (SSS, torcula, and both transverse sinuses). The lateral aspect of the left transverse sinus wall is opacified but drains not through its' lumen to the sigmoid sinus, but rather into dural emissary channels. There is no apparent cortical vein thrombosis. The major veins are all patent; the vertex veins interconnect across the midline through the vertex venous lacunae. The pial/dural anastomoses combine with expanded dural wall venous plexes, and opened emissary venous channels to provide the dominant means of cerebral venous egress in this case, where there is thrombosis of both sigmoid sinuses.
Findings
MR T1-W Sequence both with & without contrast
The noncontrast MR T1-w sequence demonstrates hyperintense thrombus within the posterior half of the SSS, the torcula, the straight sinus, the proximal segment of the left transverse sinus,the left sigmoid sinus, and all of the right transverse and sigmoid sinus. The lateral aspect of the left transverse sinus demonstrates marked expansion of the veins with the outer margin of the left tentorium; these represent pial/dural collaterals and provide evidence of left transverse sinus thrombosis even in the absence of obvious hyperintense thrombus.
The post contrast T1-w sequence demonstrates evidence of collateral venous egress through the expanded venous plexes within the dural sinus walls and through the dilated vertex venous lacunae. The left lateral venous confluence enters the left vein of Labbe', which fills retrograde into an expanded left superior sylvian vein complex, which drains outward through the cavernous sinus. There is prominence of the pharyngeal venous plexus indicating this is a pathway for venous egress from the cavernous sinus. The left superior sylvian vein also recieves collateral venous egress from the right hemisphere, which have passed throught the vertex venous lacunae. There is thickening of all the dural sinus walls including the tentoria bilaterally indicating the ability of the dural wall venous plexus to expand and shunt blood to egress vein which have remained patent. The patent deep central ICV veins drain into the superior vermic vein complex and through the lateral anastomotic (LAM) veins, since the straight sinus is thrombosed; there is only mild deep central vein congestion (no dilatation of the deep medullary veins); there are serpiginous pial collaterals along the cerebral surface and along the right cerebellar surface. The right cerebellar veins drain into mainly the right petrosal vein complex. This case exhibits many of the commonly used venous collateral routes activated in dural sinus thrombosis.
There is only slight ventriculomegaly (note the minimal expansion of the third ventricle), and, there does appear to be some residual optic hydrops. There is no evidence of downward central depression nor tonsillar displacement. These findings indicate that the venous re-routing is reasonably effect with only minimal secondary evidence of persistently raised intracranial pressure (ICP).
There was an incidental small left vertex arachnoid cyst evident on the initial exam, which is unchanged.
Impression
2. Reasonably functional collateral venous drainage is present utilizing expansion of the dural wall venous plexes, the left lateral tentorial venous confluence connected to the superior sylvian venous plexus egress route.
The major venous egress routes for the deep central and subependymal veins appear through supra to infratentoral connections through the superior vermic vein and LAM collaterals ultimately draining into the petrosal veins.
3. The minimal evidence of persistently raised CSF pressure.
4. There are expected post operative changes in the right mastoid area.
