Wk 2, Case 5 - Review

Patient History

Patient presents with new dysarthria and ataxia.

Findings

Non-contrast CT Head:

There are scattered hypodensities involving the left cerebral peduncle as well as the cerebellar hemispheres.

Additional nonspecific white matter hypodensities are present and consistent with sequela of chronic microvascular ischemia. There is no hemorrhagic conversion. There is no mass effect or midline shift.

The ventricles are normal in caliber. The orbital contents are normal. The paranasal sinuses and mastoid air cells are clear. There is no suspicious osseous lesion.

CT Perfusion Head:

There is elevated Tmax and MTT involving the bilateral cerebellar hemispheres, entirety of the brain stem, left medial occipital lobe, and left thalamus without corresponding defects of cerebral blood volume or severe decrease of cerebral blood flow.

Automated analysis demonstrates an ischemic at-risk parenchyma of 120 mL and infarct core of 0 mL.

CTA Head and Neck:

There is thrombus within the V4 segment of the right vertebral artery distally extending to the insertion on the basilar artery. The distal basilar artery and the left vertebral artery are patent while the right vertebral artery is seen but not contrast opacified. The right vertebral artery is otherwise diminutive in the more proximal portions,which demonstrate poor contrast opacification compared to the left.

No narrowing at the origin of the left vertebral artery. The left vertebral artery is patent throughout. A focus of atheromatous carotid calcification is present in the left V4 segment without substantial narrowing.

There is abrupt occlusion of the proximal portion of the basilar artery with minimal distal reconstitution of the basilar artery terminus and the proximal P1 segments.

Only a diminutive left posterior communicating artery is present resulting in diminutive opacification of the left PCA and its branches. On the right, however, a robust right posterior communicating artery is present resulting in opacification of the right PCA and its branches. There are, however, multifocal areas of stenosis including an area of moderate stenosis spanning the 4 mm length of the right P2 segment.

The aortic arch is normal. Both subclavian arteries are normal. The common carotid arteries are without stenosis. The carotid bifurcations are without stenosis. The cervical internal carotid arteries are without substantial narrowing.

There are multifocal areas of atherosclerosis with mild to moderate narrowing involving the anterior circulation including both supraclinoid ICAs, MCAs and their branches, and ACA and their branches. Most notably, there is a focal area of moderate to severe stenosis involving the right A2 segment with a similar area of moderate stenosis involving the left A2 segment.

There is no incidental soft tissue abnormality in the neck. There is tree-in-bud nodularity within the left upper lobe possibly due to aspiration or other infectious/inflammatory process. There is no suspicious osseous lesion.

There is multifocal degenerative change in the cervical spine without substantial spinal canal or neural foraminal narrowing. Patient is status post instrumented posterior fixation in the thoracic spine.

MRI brain:

There are numerous foci of restricted diffusion in the bilateral cerebellar hemispheres, with the largest foci demonstrating increased signal intensity on T2/FLAIR imaging.

There are additional foci of restricted diffusion within the central pons, left midbrain/cerebral peduncle, medial left thalamus. and left occipital lobe with associated subtle T2/FLAIR hyperintensity in these regions.

There is an additional linear focus of elevated DWI signal in the periatrial white matter of the right parietal lobe without associated low ADC signal.

There are chronic lacunar infarcts in the bilateral corona radiata, left striatocapsular region, and right thalamus.

Focus of susceptibility artifact in the periventricular white matter adjacent to the body of the right lateral ventricle likely represents sequelae of prior microhemorrhage. There is no acute intracranial hemorrhage or extra axial fluid collection.

There are no abnormal areas of brain parenchymal or meningeal enhancement.

There is expected loss of flow void in the mid and distal basal artery on T2/FLAIR imaging, as well as within the more superior basal artery and proximal posterior cerebral arteries.

There are degenerative changes of the visualized cervical spine.

Small right mastoid effusion is present. The paranasal sinuses are clear. The orbits are normal.

Perfusion Weighted Imaging:

Adequate contrast bolus. There is elevated time to peak perfusion in the bilateral superior cerebellar hemispheres, pons, midbrain, and left PCA territory involving the posterior medial left temporal lobe and left occipital lobe as well as the left thalamus. Findings are compatible with a moderately-sized ischemic penumbra relative to infarcts identified on DWI images.

MRA Head and Neck:

Examination is degraded by motion.

The vertebral artery origins are grossly patent. The left vertebral artery is dominant. V1 and V2 segments of the vertebral arteries are patent bilaterally. V3 and V4 segments of the left vertebral artery are patent.

The V3 and V4 segments of the right vertebral artery are diminutive with luminal irregularity and multifocal moderate to severe narrowing of the distal V4 segment of the right vertebral artery. There is mild focal narrowing of the proximal right V3 vertebral artery.

The inferior basal artery is patent. There is abrupt cut off of the mid basilar artery on time-of-flight MRA. There is nonvisualization of the mid basilar artery on postcontrast angiographic imaging. There is minimal postcontrast signal hyperintensity/flow within the more superior basal artery distal to the nonvisualized segment, which may be related to retrograde flow. No flow related enhancement within the more superior basal artery on time-of-flight imaging.

No flow related enhancement in the P1, P2 and P3 segments of the left posterior cerebral artery on time-of-flight imaging. Minimal flow noted in the left posterior communicating artery as it courses to the expected position of the left P2 segment.

Some flow is noted within the P1 and proximal P2 segment of the left posterior cerebral artery on postcontrast imaging. There is marked narrowing or occlusion of the P2 segment of the left posterior cerebral artery with distal reconstitution.

Fetal origin of the right posterior cerebral artery noted. Time of flight images demonstrate short segment marked luminal narrowing of the proximal right P3 segment, which is only moderately narrowed on post contrast MRA neck images.

There is tortuosity of the partially visualized thoracic aorta.

The common carotid arteries, carotid bifurcations, and cervical internal carotid arteries are patent bilaterally. No measurable stenosis according to NASCET criteria.

The petrous, cavernous, paraclinoid, and supraclinoid internal carotid arteries are grossly patent bilaterally. There is luminal irregularity of the paraclinoid and supraclinoid internal carotid arteries bilaterally, likely secondary to calcified plaque demonstrated on prior CT. There is mild narrowing of the left carotid terminus.

The M1 and M2 segments of the middle cerebral arteries, and A1 and A2 segments of the anterior cerebral arteries are grossly patent bilaterally. There is luminal irregularity of the proximal A1 of the left anterior cerebral artery as well as the M1 and M2 segments of the middle cerebral arteries bilaterally with multifocal mild luminal narrowing, likely secondary to atherosclerosis.

Conclusion

CT head, CT Perfusion, CTA head and neck:

1. No acute intracranial hemorrhage.

2. CT perfusion demonstrates a large area of ischemic at-risk parenchyma involving nearly the entirety of the brain stem, near-entirety of the cerebellum, as well as large portions of the left occipital lobe and left thalamus.

3. Abrupt occlusion of the proximal basilar artery. The V4 segment of the right vertebral artery also appears thrombosed at least distally as it does not opacify when it inserts on the basilar artery despite the distal basilar artery being patent and opacified at that location.

4. Right PCA predominantly supplied by a patent and robust right posterior communicating artery with a moderate focus of stenosis in the P2 segment. Diminutive opacification of the left PCA.

5. Multifocal intracranial atherosclerosis, including areas of moderate to severe stenosis involving the A2 segments.

MRI brain, MRA head and neck:

1. Multifocal acute infarcts in the bilateral cerebellar hemispheres, left occipital lobe, central pons, left midbrain/cerebral peduncle, and left thalamus. Moderately sized region of decreased time to peak perfusion in the pons, midbrain, left thalamus, and left PCA territory and bilateral superior cerebellar hemispheres, suggesting penumbra.

2. Abrupt occlusion of the mid basilar artery on time-of-flight and postcontrast angiographic imaging. Nonvisualization of the more superior basal artery and left posterior cerebral artery on time-of-flight imaging, with trace flow noted in the in these regions on postcontrast imaging, possibly due to retrograde flow supplied by right posterior communicating artery. Suspected severe narrowing or occlusion of the P2 segment of the left posterior cerebral artery on postcontrast imaging with distal reconstitution.

3. Left dominant vertebral artery. Multifocal marked narrowing of the V3 and V4 segments of the right vertebral artery.

4. Focal moderate narrowing of the right P3 segment of the posterior cerebral artery.

5. Intracranial atherosclerosis as above, with multifocal areas of mild luminal narrowing involving the middle cerebral arteries, left supraclinoid ICA and left A1 versus decreased flow secondary to inflow stenosis.