A
Figure 1.
CT and CTA findings. Arterial dissection and subarachnoid hemorrhage were ruled out. A slight luminal narrowing in the basilar artery was depicted.
B
Figure 1.
CT and CTA findings. Arterial dissection and subarachnoid hemorrhage were ruled out. A slight luminal narrowing in the basilar artery was depicted.
C
Figure 1.
CT and CTA findings. Arterial dissection and subarachnoid hemorrhage were ruled out. A slight luminal narrowing in the basilar artery was depicted.
A
Figure 2.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Discrete parietal irregularities and focal narrowing of the basilar artery that promote slight reduction of the vascular lumen, associated with mild contrast enhancement evolving the vascular wall in the projection of the vertebrobasilar junction (yellow arrows).
B
Figure 2.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Discrete parietal irregularities and focal narrowing of the basilar artery that promote slight reduction of the vascular lumen, associated with mild contrast enhancement evolving the vascular wall in the projection of the vertebrobasilar junction (yellow arrows).
A
Figure 4.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Complete resolution of the slight smooth-looking gadolinium enhancement that previously involved the vascular wall near the vertebra-basilar transition, without new areas of paramagnetic contrast uptake in the time interval considered between studies. Important decrease of parietal irregularities and focal narrowing near the middle third of the basilar artery, with only a slight focal change remaining (yellow arrows).
B
Figure 4.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Complete resolution of the slight smooth-looking gadolinium enhancement that previously involved the vascular wall near the vertebra-basilar transition, without new areas of paramagnetic contrast uptake in the time interval considered between studies. Important decrease of parietal irregularities and focal narrowing near the middle third of the basilar artery, with only a slight focal change remaining (yellow arrows).
A
Figure 5.
VRT reconstruction, (A) pre-contrast and (B) post-contrast. Decrease of focal narrowing near the middle third of the basilar artery (yellow arrows).
B
Figure 5.
VRT reconstruction, (A) pre-contrast and (B) post-contrast. Decrease of focal narrowing near the middle third of the basilar artery (yellow arrows).
A
Figure 6.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Eccentric wall thickening with tenuous spontaneous hypersignal in T1 and contrast enhancement in the communicating segment of the internal carotid artery and M1 proximal to the right.
B
Figure 6.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Eccentric wall thickening with tenuous spontaneous hypersignal in T1 and contrast enhancement in the communicating segment of the internal carotid artery and M1 proximal to the right.
C
Figure 6.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Eccentric wall thickening with tenuous spontaneous hypersignal in T1 and contrast enhancement in the communicating segment of the internal carotid artery and M1 proximal to the right.
D
Figure 6.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Eccentric wall thickening with tenuous spontaneous hypersignal in T1 and contrast enhancement in the communicating segment of the internal carotid artery and M1 proximal to the right.
A
Figure 7.
VRT reconstruction.
A
Figure 8.
3D T1 Cube with HyperSense, (A, C) pre-contrast and (B, D) post-contrast. There was a significant reduction in the area of luminal stenosis involving the communicating segment of the right internal carotid artery and of the eccentric wall thickening, with a reduction in contrast enhancement of the vascular wall. Only tenuous parietal irregularities are noted in this topography in the follow-up study, with nearly complete resolution of the changes previously noted in segments A1 and M1, which suggest an important reduction of a likely inflammatory component in the projection of the previously evidenced atheromatous plaque. Convenient evolutionary control (yellow arrows).
B
Figure 8.
3D T1 Cube with HyperSense, (A, C) pre-contrast and (B, D) post-contrast. There was a significant reduction in the area of luminal stenosis involving the communicating segment of the right internal carotid artery and of the eccentric wall thickening, with a reduction in contrast enhancement of the vascular wall. Only tenuous parietal irregularities are noted in this topography in the follow-up study, with nearly complete resolution of the changes previously noted in segments A1 and M1, which suggest an important reduction of a likely inflammatory component in the projection of the previously evidenced atheromatous plaque. Convenient evolutionary control (yellow arrows).
C
Figure 8.
3D T1 Cube with HyperSense, (A, C) pre-contrast and (B, D) post-contrast. There was a significant reduction in the area of luminal stenosis involving the communicating segment of the right internal carotid artery and of the eccentric wall thickening, with a reduction in contrast enhancement of the vascular wall. Only tenuous parietal irregularities are noted in this topography in the follow-up study, with nearly complete resolution of the changes previously noted in segments A1 and M1, which suggest an important reduction of a likely inflammatory component in the projection of the previously evidenced atheromatous plaque. Convenient evolutionary control (yellow arrows).
D
Figure 8.
3D T1 Cube with HyperSense, (A, C) pre-contrast and (B, D) post-contrast. There was a significant reduction in the area of luminal stenosis involving the communicating segment of the right internal carotid artery and of the eccentric wall thickening, with a reduction in contrast enhancement of the vascular wall. Only tenuous parietal irregularities are noted in this topography in the follow-up study, with nearly complete resolution of the changes previously noted in segments A1 and M1, which suggest an important reduction of a likely inflammatory component in the projection of the previously evidenced atheromatous plaque. Convenient evolutionary control (yellow arrows).
A
Figure 9.
VRT reconstruction (yellow arrows).
A
Figure 3.
VRT reconstruction, (A) pre-contrast and (B) post-contrast, demonstrate focal narrowing of the basilar artery (yellow arrows).
B
Figure 3.
VRT reconstruction, (A) pre-contrast and (B) post-contrast, demonstrate focal narrowing of the basilar artery (yellow arrows).
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Bruno Augusto Telles, MD Radiologist
CETAC
Curitiba, Brazil
CASE STUDIES
3D T1 Cube with HyperSense optimized for high-resolution, black-blood intracranial vessel wall imaging
3D T1 Cube with HyperSense optimized for high-resolution, black-blood intracranial vessel wall imaging
by Bruno Augusto Telles, MD, Radiologist, CETAC, Curitiba, Brazil
Bruno Augusto Telles, MD Radiologist
CETAC Curitiba, Brazil
Introduction
High-resolution intracranial vessel wall MR imaging plays an increasing role in the diagnosis of intracranial vascular diseases. One of its main advantages compared with other methods, such as CT angiography and digital subtraction angiography (DSA), is the ability to visualize lesions in the vessel wall that do not necessarily show luminal narrowing. Plaque burden in intracranial atherosclerotic disease can be evaulated by a physician using vessel wall MR, while the ability to detect an aneurysm that tends to rupture, intracranial dissection and/or inflammatory/infectious diseases (i.e., vasculitis) is also supported. Reversible cerebral vasoconstriction syndrome (RCVS), a group of disorders, is characterized by severe headaches and a narrowing of the blood vessels in the brain.
In the case of RCVS, the visualization of vessel wall contrast enhancement in relation to surrounding vascular tissue is important and can be achieved by using high-resolution 3D T1 Cube with HyperSense. By adequately adjusting the sequence parameters, it becomes a "black-blood-like" technique that shows high contrast-to-noise ratio of the vessel wall to surrounding tissue, enabling the detection of even small changes in gadolinium contrast enhancement patterns, which is crucial for the correct diagnosis of RCVS. In this entity, it has been previously postulated that there was no enhancement after the gadolinium injection; however, using this sequence we can also depict a subtle and smooth pattern that generally resolves in a follow-up MR exam (typically three months after the previous MR exam), as well as the luminal narrowing.
Case 1
Patient history
A 32-year-old female with thunderclap headache onset during an exercise session after having performed a pre-workout 30 minutes before CT exam. First exam in the emergency was CT and CTA to exclude mainly arterial dissection and subarachnoid hemorrhage (Figure 1).
A
B
C
Figure 1.
CT and CTA findings. Arterial dissection and subarachnoid hemorrhage were ruled out. A slight luminal narrowing in the basilar artery was depicted.
Results
Patient was then referred for a brain MR with an MRA vessel wall protocol on a SIGNA™ Architect 3.0T. 3D T1 Cube with HyperSense demonstrated a narrowing of the basilar artery with slight reduction of the vascular lumen (Figures 2 and 3). Mild enhancement of the vascular wall in the vertebrobasilar junction was also depicted (Figure 2). Diagnosis was RCVS.
A
B
Figure 2.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Discrete parietal irregularities and focal narrowing of the basilar artery that promote slight reduction of the vascular lumen, associated with mild contrast enhancement evolving the vascular wall in the projection of the vertebrobasilar junction (yellow arrows).
A
B
Figure 3.
VRT reconstruction, (A) pre-contrast and (B) post-contrast, demonstrate focal narrowing of the basilar artery (yellow arrows).
Patient underwent a follow-up MR exam three months later, with complete resolution of the enhancement, as well as a decrease in the parietal irregularities and focal narrowing near the middle third of the basilar artery, with only a slight focal change remaining (Figures 4 and 5).
A
B
Figure 4.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Complete resolution of the slight smooth-looking gadolinium enhancement that previously involved the vascular wall near the vertebra-basilar transition, without new areas of paramagnetic contrast uptake in the time interval considered between studies. Important decrease of parietal irregularities and focal narrowing near the middle third of the basilar artery, with only a slight focal change remaining (yellow arrows).
A
B
Figure 5.
VRT reconstruction, (A) pre-contrast and (B) post-contrast. Decrease of focal narrowing near the middle third of the basilar artery (yellow arrows).
Case 2
Patient history
Diabetic, 64-year-old male complaining of vertigo was referred for an MR/MRA of the head and neck with the vessel wall protocol on a SIGNA™ Explorer 1.5T.
Results
Diagnosis of luminal stenosis involving the communicating segment of the right internal carotid artery and of the eccentric wall thickening.
Patient received a follow-up MR exam 11 months later.
A
B
C
D
Figure 6.
3D T1 Cube with HyperSense, (A) pre-contrast and (B) post-contrast. Eccentric wall thickening with tenuous spontaneous hypersignal in T1 and contrast enhancement in the communicating segment of the internal carotid artery and M1 proximal to the right.
A
Figure 7.
VRT reconstruction.
Discussion
3D T1 Cube with HyperSense is being used for vessel wall imaging due to inherent non sensitivity to flow, providing black-blood imaging capabilities. This sequence can help detect contrast enhancement patterns in the vessel wall, important for the diagnosis of RCVS. Early discrimination is important for patient management: in RCVS, CSF examination and brain biopsy have little utility other than to exclude mimics. Unlike RCVS, other arteriopathies require specific therapies, e.g., steroids for rheumatic or radiation-induced arteriopathy, synangiosis procedures for Moyamoya disease or dual antiplatelet therapy for atherosclerosis.
The protocol design is straightforward, with the goal to have bright cerebral parenchyma and dark vessels at the intended resolution for a confident diagnosis. CSF is recommended to be grey, not black, to differentiate from the vessel lumen. Improved grey/white matter contrast can be reduced for time savings. The use of FatSat further increases the dynamic scale of the overall image and makes the vessel wall brighter.
Non-invasive techniques such as MRA and black-blood 3D T1 Cube with HyperSense are increasingly being used in clinical practice, although cerebral angiography remains the criterion standard for the detection of cerebral vasoconstriction. HyperSense allows for an improvement in spatial resolution, which may not otherwise be viable in clinical exams due to long scan times. Typical image resolution is 0.8 mm isometric at 1.5T and 0.6 mm isometric at 3.0T, which provides improved resolution for small vessels. The lower the resolution, the faster the scan time for the same system. TR ranges from 550 ms-700 ms, and the longer the TR the brighter the parenchyma and CSF. HyperSense factor of 1.5 (and up to 2.0) helps reduce scan times.
A
B
C
D
Figure 8.
3D T1 Cube with HyperSense, (A, C) pre-contrast and (B, D) post-contrast. There was a significant reduction in the area of luminal stenosis involving the communicating segment of the right internal carotid artery and of the eccentric wall thickening, with a reduction in contrast enhancement of the vascular wall. Only tenuous parietal irregularities are noted in this topography in the follow-up study, with nearly complete resolution of the changes previously noted in segments A1 and M1, which suggest an important reduction of a likely inflammatory component in the projection of the previously evidenced atheromatous plaque. Convenient evolutionary control (yellow arrows).
A
Figure 9.
VRT reconstruction (yellow arrows).
References
1. Rocha EA1, Topcuoglu MA, Silva GS, Singhal A2. RCVS2 score and diagnostic approach for reversible cerebral vasoconstriction syndrome. Neurology. 2019 Feb 12;92(7):e639-e647.
2. Miller, T. R., Shivashankar, R., Mossa-Basha, M., & Gandhi, D. (2015). Reversible Cerebral Vasoconstriction Syndrome, Part 1: Epidemiology, Pathogenesis, and Clinical Course. American Journal of Neuroradiology, 36(8), 1392–1399.
3. Miller, T. R., Shivashankar, R., Mossa-Basha, M., & Gandhi, D. (2015). Reversible Cerebral Vasoconstriction Syndrome, Part 2: Diagnostic Work-Up, Imaging Evaluation, and Differential Diagnosis. American Journal of Neuroradiology, 36(9), 1580–1588. doi:10.3174/ajnr.a4215.
