MR Angiographic-Guided Percutaneous Sclerotherapy for Venous Vascular Malformations: A Radiation Dose-Reduction Strategy.

We present a new technique using MRA instead of the usual DSA to provide guidance in the treatment of venous vascular malformations. When one performs this embolization procedure, appropriate needle positioning within the malformation must be confirmed before injection of the sclerosing agent to prevent untoward complications. Time-resolved imaging of contrast kinetics-MRA can accurately depict the angioarchitecture of the lesion, which substantially reduces the total radiation dose in these patients who are commonly in the pediatric age group and usually require numerous treatment episodes.

Clinical pitfalls related to short and long echo times in cerebral MR spectroscopy.

MR-spectroscopy (MRS) is a multiparameter diagnostic tool and modification of each parameter results in spectrum morphology changes. In particular, changing the echo time (TE) represents a useful tool to highlight different diagnostic elements, but also has significant impact on the spectrum morphology. Diagnostic errors can result if the role of TE is not properly considered. This article reviews the four most common TE-related pitfalls of MRS interpretation. Clinical practical methods to avoid such pitfalls are also suggested.

Metabolite findings in tumefactive demyelinating lesions utilizing short echo time proton magnetic resonance spectroscopy.

BACKGROUND AND PURPOSE: To use MR spectroscopy to aid in the diagnosis of demyelinating disease and to help differentiate tumefactive demyelinating lesions from neoplastic processes. MATERIALS AND METHODS: MR imaging of the brain was obtained in 4 patients who presented clinically with focal neurologic deficits. MR imaging initially revealed parenchymal mass lesions. Single-voxel MR spectroscopy was then performed utilizing a point-resolved spectroscopy sequence protocol with a short echo time (30 msec). RESULTS: MR imaging revealed a focal ring-enhancing mass in one patient, multiple ring-enhancing lesions in the second patient, a large area of edema and mass effect without associated enhancement in the third patient, and multiple solid and peripherally enhancing lesions in the fourth patient. MR spectroscopic results in all 4 patients demonstrated marked elevation of the glutamate and glutamine peaks (2.1-2.5 ppm). Other nonspecific (and in a sense confounding) findings included elevation of the choline peak (3.2 ppm), elevation of the lactate peak (1.3 ppm), elevation of the lipid peak (0.5-1.5 ppm), and decrease in the N-acetylaspartate peak (2.0 ppm). All 4 patients were eventually given the diagnosis of multiple sclerosis based on CSF analysis, brain biopsy, and/or clinical follow-up. CONCLUSION: MR spectroscopic metabolite information may be useful in the diagnosis of demyelinating disease by demonstrating elevation of the glutamate/glutamine peaks because elevation of these peaks is typically not seen in aggressive intra-axial neoplastic processes. This is particularly beneficial in the rarer cases of tumefactive demyelinating lesions, which are very difficult to differentiate from neoplasms by imaging findings alone.

Analysis of complex framing coil stability in a wide-necked aneurysm model.

Appropriately sized 0.010- and 0.018-inch complex framing coils were placed in a wide-necked silicone aneurysm replica, and their stability was evaluated at variable physiologic flow rates using video recording. After detachment, the 0.010-inch coils demonstrated instability/prolapse that was proportional to flow rate. In contrast, 0.018-inch coils held their 3D configuration regardless of flow rate. The findings support the use of 0.018-inch coils (when possible) in aneurysms with unfavorable geometry, particularly in circulations with higher flow rates.

Artifact simulating subarachnoid and intraventricular hemorrhage on single-shot, fast spin-echo fluid-attenuated inversion recovery images caused by head movement: A trap for the unwary.

BACKGROUND AND PURPOSE: Single-shot, fast spin-echo, fluid attenuated inversion recovery (SS-FSE-FLAIR) images are frequently used to detect disease in the brain and subarachnoid space in confused or uncooperative patients who may move during the examination. In some of these patients, high signal intensity areas are seen on good-quality images in the subarachnoid space and ventricular system in locations not associated with high CSF flow. These artifacts may simulate hemorrhage or leptomeningeal disease. The purpose of this article was to determine the cause of these artifacts, describe ways to recognize them, and find methods to reduce or eliminate them. METHODS: Healthy volunteers were studied on 6 occasions with conventional multisection FSE-FLAIR images and SS-FSE-FLAIR images while at rest and while nodding and rotating their heads at different speeds. In addition, SS-FSE-FLAIR images with different section widths of the initial inverting pulse and a non-section-selective initial inversion pulse were performed with the subjects moving their heads in the same way. The scans of 30 successive patients with acute neurologic syndromes who had been studied with SS-FSE-FLAIR sequences were reviewed for evidence of high signal intensity in the CSF in regions not associated with high CSF flow. RESULTS: Each of the volunteers showed areas of increased signal intensity in CSF at sites apart from those associated with rapid pulsatile CSF flow on SS-FSE-FLAIR images acquired during head motion. The images were otherwise virtually free of motion artifact. The use of a wider initial inversion pulse section and a non-section-selected initial inversion pulse reduced the extent of these artifacts. Nineteen of the 30 patients showed areas of high signal intensity in the CSF in regions not associated with highly pulsatile CSF flow. Six of these patients had negative lumbar punctures for blood and xanthochromia and normal CSF protein levels. CONCLUSION: High signal intensity artifacts may be seen in CSF as a result of head movement on otherwise artifact-free images when imaging uncooperative patients with SS-FSE-FLAIR sequences. These artifacts have a different mechanism and distribution from those caused by CSF pulsation and may simulate subarachnoid and intraventricular hemorrhage. Artifact recognition is aided by signs of patient motion during the examination. The artifacts can be reduced by use of increased section width and non-section-selective initial inversion pulses. Recognition of these artifacts is important, because the circumstances in which the SS-FSE-FLAIR sequence is used and the particular properties of the sequence may conspire to produce a trap for the unwary.

Rapid prototyping to create vascular replicas from CT scan data: making tools to teach, rehearse, and choose treatment strategies.

Our goal was to develop and prove the accuracy of a system that would allow us to re-create live patient arterial pathology. Anatomically accurate replicas of blood vessels could allow physicians to teach and practice dangerous interventional techniques and might also be used to gather basic physiologic information. The preparation of replicas has, until now, depended on acquisition of fresh cadaver material. Using rapid prototyping, it should be able to replicate vascular pathology in a live patient. We obtained CT angiographic scan data from two patients with known arterial abnormalities. We took such data and, using proprietary software, created a 3D replica using a commercially available rapid prototyping machine. From the prototypes, using a lost wax technique, we created vessel replicas, placed those replicas in the CT scanner, then compared those images with the original scans. Comparison of the images made directly from the patient and from the replica showed that with each step, the relationships were maintained, remaining within 3% of the original, but some smoothing occurred in the final computer manipulation. From routinely obtainable CT angiographic data, it is possible to create accurate replicas of human vascular pathology with the aid of commercially available stereolithography equipment. Visual analysis of the images appeared to be as important as the measurements. With 64 and 128 slice detector scanners becoming available, acquisition times fall enough that we should be able to model rapidly moving structures such as the aortic root.

Manipulation of volume data to manufacture vascular replicas.

There are three reasons to create physical replicas of human anatomy: (1) to be able to better visualize the shape of a single organ, or a section of anatomy; (2) to be able to visualize the spatial relationships in three-dimensions; and (3) to use accurate replicas to practice or rehearse otherwise high-risk clinical procedures in the laboratory. This paper describes a project to fabricate a carotid artery. It discusses the gathering of data, the conversion to a volume, and the subsequent conversion to a manufacturable form.

Development of a posterior cerebral artery aneurysm subsequent to occlusion of the contralateral internal carotid artery for giant cavernous aneurysm.

We report a case of a patient who developed a left posterior cerebral artery aneurysm 5 years after balloon occlusion of the right internal carotid artery for a giant cavernous aneurysm. The location of the new aneurysm was outside of the primary collateral pathways to the contralateral, proximally occluded, anterior circulation, illustrating the complexity of hemodynamic factors contributing to the development of intracranial saccular aneurysms. The appearance of an aneurysm in this setting supports the hypothesis that degenerative factors and hemodynamic stresses are important in the etiology of intracranial aneurysms.

Analysis of slipstream flow in a wide-necked basilar artery aneurysm: evaluation of potential treatment regimens.

SUMMARY: A replica of a lethal wide-necked basilar artery aneurysm was created by casting a deceased patient's brain vessels and then placing the replica in a circuit of pulsating optically clear non-Newtonian fluid. Individual fluid slipstreams were opacified with isobaric dyes, and images were recorded on film. Studies were completed on the vascular replica, then were repeated, first after placement of a stent across the aneurysm neck and then after placement of Guglielmi detachable coils into the aneurysm sac through the stent. The slipstreams entered the untreated aneurysm via the distal aneurysm neck (the inflow zone), impacting against the distal lateral aneurysm wall. When the stent was placed across the aneurysm neck, the slipstreams lost coherence and did not strike the aneurysm sidewall. Placing the coils further disturbed and reduced aneurysmal flow, especially when the coils filled the inflow zone at the distal lateral aneurysm sac.

Spinal oligodendroglioma with gliomatosis in a child. Case report.

The authors present a rare case of oligodendrogliomatosis in a child, which they believe originated from a primary spinal cord tumor. At 2.5 years of age this boy developed poor balance, neck stiffness, and a regression in developmental milestones. A computerized tomography (CT) scan of the head initially revealed ventriculomegaly and multiple cystic cerebellar lesions. In addition, magnetic resonance (MR) imaging revealed a cystic intramedullary lesion involving the cervical spinal cord. A CT scan of the head and an MR image obtained 3 years later demonstrated diffuse small cysts on the surface of the brainstem, cerebellum, medial temporal and inferior frontal cortices, subcortical white matter, and corpus callosum suggestive of leptomeningeal tumor spread. Analysis of pathological specimens obtained at surgery showed neoplastic glial cells with small, uniform nuclei and perinuclear clear zones. The cells appeared to migrate along the subpial space but no tumor cells were present in the subarachnoid space. These findings were compatible with a diagnosis of oligodendrogliomatosis cerebri. Despite having a complicated course, chemotherapy with carboplatin has provided the patient with long-term palliation and a high quality of life. This case may represent the fifth report in the literature of oligodendrogliomatosis occurring in a child but only the third occurring with a spinal primary tumor.

Flow dynamics in a lethal anterior communicating artery aneurysm.

We describe and analyze the flow dynamics in replicas of a human anterior communicating artery aneurysm. The replicas were placed in a circuit of pulsating non-Newtonian fluid, and flows were adjusted to replicate human physiologic parameters. Individual slipstreams were opacified with isobaric dyes, and images were recorded on film and by CT/MR angiography. When flow in the afferent (internal carotid) and efferent (anterior and middle cerebral) arteries was bilaterally equal, slipstreams rarely entered the aneurysm. When flow in either the afferent or efferent vessels was not symmetrical, however, slipstreams entered the aneurysm neck, impinged upon the aneurysm dome, and swirled within the aneurysm. Unequal flow in carotid or cerebral systems may be necessary to direct pathologic, fluid slipstreams into an aneurysm.

Analysis of slipstream flow in two ruptured intracranial cerebral aneurysms.

Replicas of ruptured posterior communicating and basilar artery aneurysms were created from cadaveric specimens and then were placed in a circuit of pulsating non-Newtonian fluid. Individual fluid slipstreams were opacified with isobaric dyes, and images were recorded on film. The slipstreams entered the distal aneurysm neck with impact against the distal lateral wall of the aneurysm. They then swirled slowly in a reverse vortical pattern within the aneurysm sac. Fluid exited the aneurysm at the proximal neck. The flow pattern clearly shows the impact zone of entering slipstreams (the point of aneurysm rupture) and provides information pertaining to aneurysm growth and formation.

An experimental and angiographic explanation of why ulcerated carotid bulbs embolize.

SUMMARY: The flow dynamics and pressure relationships in an ulcerated atherosclerotic carotid bulb obtained at post-mortem were studied and correlated with angiographic findings in a similar live patient. Using the lost wax technique, we created replicas of an ulcerated atherosclerotic carotid bulb from a fresh cadaver, and placed those replicas in a circuit of pulsating non-Newtonian fluid. Flow profiles were adjusted to replicate human physiologic flows, and flow rates of 400, 600, and 800 milliliters per minute were evaluated. In the replicas, the slipstreams were opacified with isobaric dyes, and images were recorded both on 35 mm film and on SuperVHS high speed video. Data were collected from needles placed radially in the common carotid artery, in the region of the maximal atherosclerotic narrowing, and in the internal carotid artery. Though pressure relationships could not be obtained in the live human for ethical reasons, angiography in a similar stenosis was evaluated for slipstream dynamics. The post-mortem replica had a 55% diameter stenosis (88% area stenosis) of the carotid bulb with a shallow 3 mm ulcer. Flow in the common carotid artery showed undisturbed slipstreams, but as these slipstreams entered the narrow bulb, they crowded together, accelerating dramatically, with a jet continuing distally beyond the maximal narrowing for at least 2 vessel diameters, where flow again became normal. As fluid entered the narrowed bulb, radial pressures decreased and within the ulcer a vortex circulation was found. Similar findings were observed on the angiographic images of the live patient. This combination of events, the slowly swirling fluid in the ulcer, which would allow platelet aggregates to form, and the intermittent low pressure of the Bernoulli effect which could pull the aggregates into the adjacent rapidly flowing blood may help explain how ulcerated carotid plaques lead to embolic stroke.

Pressure Measurements across Vascular Stenoses. Practice and Pitfalls.

SUMMARY: We describe and analyze pressure measurements across vascular stenoses in an atherosclerotic human carotid bulb replica using catheters of different diameters. Replicas of an atherosclerotic human carotid bulb were created using the lost wax technique, and were placed in a circuit of pulsating nonnewtonian fluid. Flows were adjusted to replicate human physiologic flow profiles. Common carotid artery total flow volume of 600 milliliters/minute was studied. A pressure recording device was calibrated; data were received from catheters placed longitudinally in the common carotid artery and internal carotid artery. The internal carotid artery pressures were obtained both through the stenosis as is usually performed in the angiography suite and through the vessel side-wall beyond the stenosis as a control. Internal carotid artery flow volumes were also measured with and without the catheter through the stenosis. Multiple pressure recordings and volume measurements were obtained in the replica using 7 French, 5 French, and 2.5 French catheters. Measurements of the replica showed a 58% diameter stenosis and an 89% area stenosis of the carotid bulb. All longitudinal pressure measurements in the common carotid artery agreed with control values regardless of the diameter of the catheter used. Pressure measurements were also in agreement with control values in the internal carotid artery using the 2.5 French catheter. However, when larger diameter catheters were employed, pressures measured with the catheter through the stenosis fell when compared to control values. Additionally, internal carotid artery flow volumes were also decreased when the larger diameter catheters were placed across the stenosis. Large diameter catheters when placed across vascular stenoses may cause an occlusive or near-occlusive state and artifactually increase the measured transstenotic vascular pressure gradient as well as decrease forward vascular flow.

Why do ulcerated atherosclerotic carotid artery plaques embolize? A flow dynamics study.

PURPOSE: We describe and analyze flow dynamics and pressure relationships in an ulcerated atherosclerotic human carotid bulb. METHODS: Replicas of an ulcerated atherosclerotic human carotid bulb were created using the lost wax technique. The resulting replicas were placed in a circuit of pulsating non-Newtonian fluid and flows were adjusted to replicate human physiological flow profiles. Common carotid artery total flow volumes of 400, 600, and 800 mL/min were studied. Slipstreams were opacified with isobaric dyes. Images were recorded on 35 mm film and on super VHS video. A pressure recording device was calibrated; data were received from needles placed radially and longitudinally in the common carotid artery, narrowed bulb/ulcer, and internal carotid artery. Multiple pressure recordings were obtained in the replicas. RESULTS: Measurements of the replica showed a 59% diameter stenosis and an 88% area stenosis of the carotid bulb with a shallow 3.3-mm ulcer. Analysis of flow in the common carotid artery showed undisturbed slipstreams, but as these streams entered the narrowed carotid bulb they crowded together and accelerated significantly. This accelerated jet continued for at least two vessel diameters into the more normal portions of the internal carotid artery, where flow remained disturbed peripherally and often assumed a helical pattern but was nonturbulent. As fluid entered the narrowed bulb, radial pressures decreased. Most important, at peak systole, lower radial pressure with a vortex circulation was found at the ulceration. CONCLUSION: This combination of events (ie, slowly swirling fluid within the ulcer, allowing platelet aggregates to form, and the intermittent Bernoulli effect, pulling the aggregates into the rapidly flowing blood) may help explain how ulcerated carotid plaques lead to embolic stroke.