A narrative review of endoscopic optical coherence tomography imaging in neurointervention: practical applications for intracranial aneurysms

Introduction

Background

Intracranial aneurysms are acquired lesions with an overall reported prevalence of 3.2% (1) ranging in the literature between ~1.8 and 8.8% (2). Although only a small number of aneurysms will ultimately rupture, aneurysm-related subarachnoid hemorrhage (SAH) is a feared life-threatening complication. SAH carries a mortality rate exceeding 30% within the first days (3), reaching 44% within 30 days (4), and a morbidity rate with permanent neurologic deficit up to 66% (5). Multiple studies have evaluated the rupture risk of unruptured intracranial aneurysms (UIA) based on their natural history and use of variables such as size, shape, and location (6-11). However, the long-term natural history of UIAs in unselected populations remains poorly understood (12). Despite rigorous attempts to stratify risk and categorize aneurysms with increased vulnerability, it remains unclear which of the aneurysmatic lesions will eventually rupture, and when. It has been repeatedly shown that the risk of rupture increases with aneurysm size and this variable has been widely used in decision-making on which lesion to treat; however, many ruptured aneurysms are small, the well-known aneurysm size paradox (7,13,14). This paradigm leads us to believe that important pieces of the theories around aneurysm rupture are still missing. The primary tool guiding our management plan relies on information received from available imaging modalities, mainly computed tomography angiography (CTA), magnetic resonance angiography (MRA) and digital subtraction angiography (DSA). Such imaging provides detail on luminal changes but is less accurate in depicting the microstructure of the vessel wall (15-17) and the perivascular environment (18) due to their insufficient spatial and/or contrast resolution. Additionally, successful treatment of aneurysms using endovascular techniques requires accurate imaging of the interaction between the vessel and the device intraprocedurally, to avoid complications and enhance outcomes. While advances in device engineering led to the development of smaller and thinner endoprostheses capable of navigating the cerebrovascular tortuosity, they reduced device visibility on commonly used medical imaging modalities, further emphasizing the need for detailed high-resolution imaging (19). High-resolution intravascular imaging using optical coherence tomography (OCT) has addressed similar limitations in coronary and peripheral artery procedures (20). OCT provides cross-sectional, high-resolution imaging of the vessel wall microstructure, intraluminal objects, and therapeutic devices, offering information that complements X-ray-based imaging and MRA (21). However, existing OCT imaging catheters are unsuitable for reliable use in the tortuous anatomy of the intracranial vasculature (22,23). To address this, neuro OCT (nOCT^TM, Spryte Medical, Bedford, MA, USA) technology has recently been proposed.

Rationale and knowledge gap

This narrative review discusses the development of nOCT, a high-resolution intravascular imaging technology specifically designed for use in cerebral circulation. Unlike other articles on this topic, we specifically focus on the potential applications of OCT in the context of intracranial aneurysms. We begin by summarizing recent literature on the development of nOCT, its role in enabling preclinical neurovascular research, and the initial clinical experience. We then present and analyze existing preclinical and clinical evidence on the role of OCT for evaluation and treatment of intracranial aneurysms. Furthermore, the authors share their own initial experience using the nOCT imaging platform.

Objective

The objective of this review is to present the current state of OCT technology and to explore its potential applications in the imaging and management of intracranial aneurysms.

Methods

Ad hoc PubMed searches were conducted to identify studies published between January 2010 and August 2025 that report on the development of nOCT technology, as well as studies on preclinical research involving OCT and its initial clinical applications for intracranial aneurysms (Table 1). Separate ad hoc PubMed searches were also performed to identify clinical literature on hemorrhagic stroke without time frame constraints. This article is a narrative review that discusses recent developments in OCT technology for neurovascular applications and is not a systematic review.

Development of nOCT technology and applications for intracranial aneurysms

OCT technology

OCT is an advanced interferometric imaging technique that originated from optical low-coherence reflectometry, which utilizes a broadband light source and a Michelson interferometer to measure “echoes of light”. The term “OCT” was first introduced in 1991, when transverse scanning enabled two-dimensional (2D) imaging of the human retina (24). Since its inception, OCT has expanded into a wide range of applications across ophthalmology, cardiovascular medicine, dermatology, and digital pathology (25). Endoscopic OCT has become a standard tool for intravascular imaging (26,27), and it recently earned a Class 1A recommendation in the guidelines for optimizing complex coronary interventions (28-30). State-of-the-art intracoronary OCT systems operate in the near-infrared spectrum, using laser light sources with a central wavelength of ~1,300 nm and a bandwidth of around 70 to 100 nm. OCT imaging works by detecting and analyzing backscattered light from tissue. Infrared light is delivered to the coronary artery through an optical fiber housed within an imaging catheter. A miniaturized lens near the catheter tip focuses the light on the vessel wall and therapeutic devices and collects the backscattered signal. The received light is transmitted back to the console through the same optical fiber. The axial profile of optical reflectivity, known as the A-scan line (or A-line) is obtained by measuring the interference between light returning from the tissue and light from a reference arm within the interferometer, effectively measuring both the amplitude and the time-of-flight of the backscattered signal. Due to the high speed of light, direct time-delay measurements are impractical; therefore, OCT relies on interferometric techniques to extract depth-resolved reflectivity. To create a two-dimensional cross-sectional image, multiple A-lines are collected by rotating and retracting the catheter’s internal optics, performing a helical scan of the vessel. Modern intracoronary OCT systems utilize Fourier-domain OCT technology, which employs a rapidly tunable swept-source laser. This technology enables high-speed imaging, with acquisition rates exceeding 100,000 A-lines per second and hundreds of cross-sectional images per second, while maintaining high sensitivity (e.g., >100 dB) (31-33). Intracoronary OCT cross-sectional images depict in high resolution the coronary lumen anatomy, the vessel wall microstructure, and the interaction between tissue and therapeutic devices not seen with other intraprocedural imaging modalities (34,35).

Limitations of conventional intravascular OCT imaging technology and requirements for neurovascular applications

Intracoronary OCT catheters are routinely used to guide and optimize percutaneous coronary interventions (36,37). Coronary imaging catheters feature a monorail tip and use rapid exchange techniques, coupled with 0.014-inch wires. Imaging the cerebral vasculature, however, poses distinct challenges and requirements. Intracranial arteries exhibit significantly higher vascular tortuosity and a broader range of diameters. Unlike cardiovascular devices, neurovascular devices have a high degree of flexibility and are commonly delivered using microcatheters. Therefore, for neurointerventional use, an intravascular imaging device must be capable of safely and reliably navigating tortuous pathways while being compatible with standard neurovascular tools and microcatheters. In addition, when placed in tortuosity, the imaging catheter must produce artifact-free images (without rotational distortions) (38) and with uniform image brightness. Furthermore, ideally, both the tissue and devices used to treat pathology should be depicted with high image quality and spatial resolution, free of artifact, enabling simultaneous visualization of the arterial wall microstructure and device features. The method should be reliable, capable of imaging a wide range of vascular anatomies, with varying vessel sizes and locations, including segments of the distal intracranial circulation. It should also support high imaging speed and frame rates for rapid and comprehensive data acquisition.

The design and characteristics of existing coronary imaging catheters, however, are not well-suited for imaging tortuous, intracranial arteries (39). Intracoronary OCT imaging catheters typically have diameters ranging from ~2.5-F to 2.7-F, and are incompatible with commonly used neurovascular microcatheters (20,27,40-42). Moreover, these catheters utilize a rapid exchange tip for navigation and use a torque cable to rotate the catheter’s optical fiber and lens. This design leads to a stiffness profile that hinders navigation through tortuous arteries and, furthermore, prevents a reliable and uniform rotation of the catheter optics (43). Recently, miniaturized coronary catheters (e.g., diameters <2.0-F) have been introduced (44,45). While they present a significantly smaller profile, they are still designed for coronary applications, and thus they are still unsuitable for navigating and imaging in the high tortuosity found in neurovascular systems. Furthermore, coronary OCT technology has a limited field-of-view, optimized for imaging coronary arteries with diameters under 5.0 mm, which further limits its use in neurovascular imaging.

Development and characteristics of recently proposed neurovascular OCT technology

Taking these requirements into account, a dedicated nOCT imaging probe has been developed (46). nOCT utilizes Fourier-Domain OCT technology with a central wavelength of approximately 1,300 nm, optimized for vascular imaging (47). The nOCT imaging probe is a flexible, ~1.3-F, wire-like device compatible with 0.021-inch microcatheters. It features a fiber-optic design and presents a high degree of flexibility specifically optimized for navigating the tortuous anatomy of the neurovascular circulation. Miniaturized optics near the tip of the probe focus near-infrared light onto the arterial wall and collect the backscattered light. nOCT images have an axial resolution approaching 10 µm in tissue, a lateral resolution of approximately 35 µm at the focal point, and a field of view of about 14.4 mm in diameter in contrast media (n=1.44). nOCT is optimized for imaging both small and large neurovascular arteries, up to ~6 mm in diameter. In conjunction with the imaging console, the probe can acquire up to 250 images per second and can be rapidly retracted through the vessel in <3 seconds, capturing up to 100 mm of vessel length (46). Cross-sectional nOCT images are generated and displayed in real time, with the entire data set available for review immediately after acquisition. In an early first-in-human experience, nOCT has been successfully used in 32 human cases, demonstrating safety (i.e., no device-related adverse events were reported in this initial series) and excellent imaging performance, even in the presence of challenging vessel tortuosity (48). In all cases, nOCT successfully obtained high-quality imaging requiring only modest volumes of contrast agent (~16–18 mL).

OCT imaging of intracranial aneurysms, technical considerations

To acquire OCT images, blood needs to be briefly displaced from the arterial lumen during data acquisition. Standard protocols used for 3D-rotational angiography (3D-RA) have been shown to adequately clear the blood from the field of view, allowing for high-quality OCT imaging in clinical settings. In the first-in-human experience with the nOCT probe, a very high procedural success rate was reported across a wide range of different intracranial arteries in both distal and proximal anterior and posterior intracranial circulations (48). Contrast media is injected using a power injector, and prior to initiating the acquisition, the live nOCT preview image can be used to determine the optimal timing to begin the pullback (49-51). Contrast is injected in the same way it is injected for obtaining angiography images. Specifically, for nOCT acquisitions, contrast is injected through a distal access catheter and care should be taken to ensure that the rotational hemostatic valve is tightly sealed around the microcatheter to avoid contrast leakage. Once the live preview image shows a clear vessel lumen, the acquisition can be initiated.

The nOCT probe is delivered to the target artery via a 0.021-inch microcatheter. The microcatheter is positioned distal to the segment to be imaged with the help of a microwire. Once in position, the microwire is removed and the nOCT probe inserted. The microcatheter is then unsheathed, exposing the nOCT probe. Prior to initiating an acquisition, users need to ensure removal of excessive slack from the nOCT probe, particularly in cases of elevated tortuosity and imaging at distal locations, to avoid repeated imaging frames at the beginning of the data set. Contrast is then injected, and the pullback is initiated once a blood-free image can be observed. The pullback can be performed by the operator manually retracting the probe, or with the assistance of an automated pullback device, which is a small, disposable, sterile motorized module that attaches to the proximal end of the imaging probe withdrawing it at a constant rate.

The use of OCT for aneurysm imaging offers valuable complementary information with respect to traditional imaging techniques. In pre-operative settings (i.e., prior to intervention and therapeutic device implantation), among others, OCT imaging can be used for:

• The assessment of the thickness of the aneurysmatic sac, allowing identification of thinner areas that may indicate a risk of impending rupture (48).
• Visualization of the presence of intra-aneurysmal thrombus, which is particularly important in cases of suspected aneurysm-related thromboembolic events and downstream ischemia (48,52).
• Visualization of the thickness of the arterial layers and the transition between normal vessel layered architecture and the thinner aneurysm sac; i.e., thinning of the media and disruption of the internal elastic lamina can be visualized, allowing for accurate identification of the aneurysm neck and beginning of the sac (48,52).
• Visualization of the role of the perianeurysmal environment in aneurysm morphology (53).
• Assessment and characterization of the vessel wall. OCT can inform on presence of vascular pathologies, such as atherosclerosis and vasculitis, thus enabling better characterization of the aneurysm type. As an example, OCT can visualize and differentiate atherosclerotic plaque composition, allowing for assessment of lipid-rich plaques, calcifications, and fibrotic tissue (46).
• Visualization of markers indicating vessel wall inflammatory processes, such as macrophage accumulations (48,54).
• OCT can image through cerebrospinal fluid (CSF) (an optically transparent medium) and visualize the subarachnoid space (SAS) and structures surrounding the artery. In cases of SAH or sentinel bleeds, OCT can detect presence of blood mixed with CSF. Blood causes haziness and, depending on its concentration, a rapid attenuation of the OCT signal obscuring the perianeurysmal environment. Both of these characteristics can be used to detect presence of SAH (55).
• Accurate depiction of small perforating vessels in high resolution as well as small-caliber important branches, such as the anterior choroidal artery or the subcallosal artery (43). Mapping of the exact anatomy is valuable for treatment planning and avoidance of ischemic complications, especially when stents or flow-diverters (FDs) are to be used.
• Accurate sizing of devices is crucial for successful intervention. The micrometer resolution of OCT is superior to other imaging modalities. Quantification of vessel lumen diameter can aid in proper device selection, while multiple diameters of the aneurysm sac could be beneficial in selection of coils and intrasaccular devices, especially in small aneurysms.

In post-operative settings (i.e., following interventions and implantation of therapeutic devices), OCT can be used to assess:

• Acute thrombus formation on device-struts or at origin of branches and perforators, informing need for administration of thrombolytics to avoid thromboembolic complications (48,56).
• Expansion and apposition of endoluminal and intrasaccular devices at the neck and in the parent artery (e.g., FD fish mouthing), informing need for further intervention (57,58).
• Presence of vessel dissections.
• Neointima formation, both thickness and composition, informs lesion healing and need for continuation of antiplatelet therapy during follow-up (59-63).
• Luminal stenosis due to neointimal hyperplasia, with quantitative characterization and occlusion of side branches (examples in Figures 1,256).

Figure 1 Clinical assessment of flow diverting stent apposition using nOCT. (A) The image shows an ophthalmic aneurysm treated with a FD stent. (B) After implant, CBCT imaging shows complete FD apposition. (C) nOCT imaging immediately post-implant, however, reveals malapposition (arrow). (D) After FD manipulation using a microwire, nOCT imaging shows improved wall apposition. (E-G) Images present the use of nOCT for the assessment of a PCom aneurysm. (E) nOCT shows malapposition (arrows) of the FD over the neck (dashed line). (F) nOCT also shows malapposition at the distal end of the FD (arrow). Following balloon angioplasty, a Neuroform Atlas stent was deployed. (G) Following this additional procedure, nOCT shows good expansion of the underlying FD. Scale bars are equal to 1 mm. CBCT, cone beam computed tomography; FD, flow diverter; nOCT, neuro optical coherence tomography; PCom, posterior communicating.

Figure 2 Examples of clinical imaging of the vessel wall using nOCT. (A) nOCT shows eccentric intimal hyperplasia (arrow) at 1-year follow-up of a PCom aneurysm treated with an FD. (B) In a small MCA-bifurcation aneurysm, nOCT shows disruption of the normal three-layered appearance of the vessel wall where the aneurysm sac originates (arrow). (C) The image shows 3D angiography of a small PCom aneurysm remnant post-treatment and (D) the nOCT image reveals a small coverage gap at aneurysm neck, responsible for the incomplete occlusion (arrows). Scale bars are equal to 1 mm. 3D, three-dimensional; FD, flow-diverter; MCA, middle cerebral artery; nOCT, neuro optical coherence tomography; PCom, posterior communicating.

Like other imaging modalities, intravascular OCT has limitations. The following aspects need to be considered when interpreting OCT images:

• The dedicated nOCT system offers an increased field of view compared to other intravascular systems (20). However, in very large aneurysms, the available field of view may still be insufficient to visualize the entire sac.
• OCT image quality can be affected by luminal blood residuals and care should be used when interpreting such images (e.g., to accurately distinguish between uncleared blood and thrombus).
• OCT images are generated perpendicular to the long axis of the probe and in relation to its position inside the vessel lumen. As such, on its own, OCT cannot provide complete information about the true vessel geometry. Similarly, the location of the imaging probe relative to the arterial wall needs to be considered when interpreting cross-sectional OCT images. For example, in the case of a narrow neck and the probe in an eccentric position, the entire aneurysm might not be visible due to shadowing artifacts (i.e., neck tissue hiding the tissue behind).
• Without the use of accurate, software-based, co-registration techniques (64), depending on the complexity of the anatomy, identification of the location of a given OCT cross-sectional image with respect to DSA images or cone beam computed tomography (CBCT) images can only be approximately obtained.

Imaging applications for the clinical diagnosis and treatment of aneurysmatic lesions with OCT

It is widely accepted that the risk of cerebral aneurysm rupture increases with size; however, many patients develop SAHs due to rupture of small cerebral aneurysms (65,66). One potential explanation for that is the aneurysm wall thickness, as thin-walled, hypocellular aneurysms are more prone to rupture. Histologic observations have shown that saccular cerebral aneurysms undergo morphologic changes before rupture and aneurysms with thin, thrombosis-lined, hypocellular walls are associated with 100% risk of rupture (15). However, the exact thickness of the wall remains inaccessible with available imaging modalities. In contrast, OCT allows for accurate wall thickness assessment being able to depict not only thickness as low as 10 µm, but also to assess the aneurysm wall in its entirety showing with exquisite detail the microstructure of the wall and areas of thrombus formation (Figure 3).

Figure 3 nOCT clinical imaging of perforating arteries and native intracranial aneurysms. (A) nOCT image of a human basilar artery showing a posteriorly oriented small perforating vessel (arrow). Multiple subarachnoid fibers attached to the vessel wall and brain parenchyma can be seen (stars). (B) nOCT image showing a small MCA, M1-segment aneurysm, where differences in aneurysm dome thickness can be appreciated (arrowheads). The arrow indicates the position of a small branch originating next to the aneurysm neck. (C) The nOCT image shows a small MCA-bifurcation aneurysm (white arrow) and its relationship with the M2 branch (yellow arrow). Scale bars are equal to 1 mm. MCA, middle cerebral artery; nOCT, neuro optical coherence tomography.

DSA alone has a limited value in diagnosing partially thrombosed aneurysms because it only allows for visualization of the patent lumen. Intra-aneurysmal thrombus increases the risk of stroke in treatments involving aneurysm manipulations such as coiling or use of intrasaccular flow disruptors (67). OCT imaging is able to visualize presence of thrombus with high sensitivity which could be useful for preoperative imaging (46). DSA provides the most accurate information on aneurysm geometry, including percentage of the circumference of parent vessel involved and side branches arising from the aneurysm neck (68), but high-resolution axial OCT imaging with multiple frames at a given location could serve as an adjunctive, complementary method of better understanding the anatomical relationships. Importantly, OCT shows the disruption of the internal elastic lamina and therefore enables a more precise identification of the true neck of the aneurysm.

Non-invasive imaging such as computed tomography (CT)/CTA and magnetic resonance imaging (MRI)/MRA can greatly aid in the non-invasive evaluation of aneurysmatic lesions, but false positives due to reduced spatial resolution, imaging artefacts, anatomy, and overlapping of venous structures can occur (68). Although MRI is able to depict thrombus formation inside the aneurysmatic sac, thrombus will have varying appearances depending on its age and distinguishing thrombus from atheroma or slow flow can be challenging (69,70). Much interest has evolved in high-resolution, vessel wall imaging MRI, either with the administration of contrast to study aneurysm enhancement (71) or permeability (72) or using quantitative susceptibility maps (73). Being noninvasive, these are practical techniques for aneurysm rupture risk assessment during surveillance imaging. Preliminary pathological studies have shown that vessel wall enhancement is related to the extent of aneurysm inflammation (74), commonly associated with rupture risk (17). However, the specificity of vessel wall enhancement has been questioned with causation identified by a multitude of factors including complex hemodynamics resulting in contrast stagnation, intra-aneurysmal thrombus permeability, or neurovasculature of thickened aneurysm walls (75). A recent review analyzing pathological underpinnings of vessel wall enhancement concluded that it is difficult to draw conclusive diagnosis from this imaging (76). Fundamentally, both MR-, even at high field strength, and CT-based techniques fundamentally lack the spatial resolution to ascertain histological features of the aneurysm wall.

Endovascular procedures have increasingly become the preferred treatment approach for aneurysmatic lesions (77,78). To ensure successful treatment, however, certain factors need to be taken into consideration. Accurate lesion, vessel lumen, and device sizing are of paramount importance to ensure adequate sealing of the aneurysm without unnecessary protrusion or vessel or aneurysm overexpansion. Currently, aneurysm dimensions and device sizing are selected upon measurements performed from DSA, 3D-RA with use of multiple projection reformats, and CBCT, with accuracy typically within ~0.5 mm. For DSA, accuracy depends on calibration which often is not properly performed (79), and is influenced by both magnification and projection (80). For 3D-RA, accurate measurements rely on optimal adjustment of threshold and window levels and improper settings might lead to overestimation or underestimation of the vessel size, although once that is overcome measurements seem more accurate compared to DSA (81). On the other hand literature suggests that when measuring neck and aneurysm size, 3D-RA underestimates the dome-to-neck ratio (82). Both imaging techniques ultimately provide the operator with only an estimation of the neck location and size based on lumen morphology. OCT provides more accurate and detailed measurements due to its high resolution and ability to visualize the vessel wall microstructure as well as the lumen (83).

Healing of aneurysm neck and complete occlusion of aneurysmatic lesion are other important factors influencing the need for continuation of dual antiplatelet therapy and the need for re-treatment. Intravascular OCT has been shown to strongly correlate with histology in measuring neointima formation (84). Characterization of intrasaccular device neck coverage with OCT is able to prognosticate exclusion of aneurysms from the circulation by showing small gaps in the construct at the level of the aneurysm neck, able to possibly predict treatment failure (85). It is also able to provide longitudinal healing information of intrasaccular devices and flow diverters (Figure 4) (56,59,86). Device vessel interaction for FDs and device aneurysm neck interaction for endosaccular devices are crucial in treatment prognosis. While histological evidence suggests that FD malapposition is predictive of delayed healing (58), malapposition cannot be accurately assessed on DSA. Identifying communicating malapposition at the neck of the aneurysm has been used to predict aneurysm healing (87) and OCT-based measurements have successfully predicted aneurysm occlusion based on quantitative thresholds (Figure 5) (88). Features of adequate intrasaccular device deployment can be clearly visualized by OCT and can be used to monitor healing progression and prognosticate aneurysm occlusion (61). Acute postoperative thrombus formation on stents and FDs is a feared complication which if left untreated can lead to thromboembolic complications (89), where ischemic stroke due to thromboembolism is the most frequent perioperative and postoperative complication associated with FD deployment (90). Acute thrombus formation on stent struts is difficult to detect with DSA or CBCT unless larger amount of clot accumulates. Compared to CBCT, OCT provides an order of magnitude improved spatial resolution (91), making it much more sensitive and with higher inter-observer agreement for detection and quantification of intraluminal clots and interaction of neurovascular devices with arterial wall (Figure 6) (46,92).

Figure 4 Examples of nOCT in vivo pre-clinical imaging of flow-diverting stents and intracranial devices. (A) The image shows nOCT imaging of an intrasaccular device (arrow) in a rabbit aneurysm at baseline and (B) at 12 weeks follow-up. Complete neointima formation over the aneurysm neck is seen (white bracket). (C) nOCT imaging assessment of a flow-diverting stent in a rabbit carotid at baseline and (D) at 30-day follow-up. Thin but complete (i.e., 360°) neointima formation over the stent struts is seen. (E) Longitudinal healing (i.e., left to right time progression) of a canine bifurcation aneurysm with OCT (top row) and DSA (bottom row). Scale bars are equal to 1 mm. DSA, digital subtraction angiography; nOCT, neuro optical coherence tomography; OCT, optical coherence tomography.

Figure 5 nOCT in vivo evaluation of flow diverting stent apposition. (A) DSA imaging shows a well-apposed flow diverter over the aneurysm neck in a rabbit model, which often results in complete aneurysm occlusion at 30-day follow-up. (B) On the contrary, this image shows an example of communicating malapposition at the aneurysm neck (arrow), which in this rabbit aneurysm model typically results in persistent aneurysm filling, and hence failed treatment, at 30 days follow-up. (C,D) The images show an example of malapposition of a flow diverter detected by nOCT but not seen on CBCT. Scale bars are equal to 1 mm. CBCT, cone beam computed tomography; DSA, digital subtraction angiography; nOCT, neuro optical coherence tomography.

Figure 6 Example of nOCT in vivo pre-clinical imaging showing acute thrombus formation of flow diverting stents. (A) CBCT image and (B) co-registered nOCT image from a swine IMAX showing multiple clots (arrows) attached to the FD surface but not readily visible on the CBCT image. (C) DSA imaging in a canine model implanted with overlapping flow diverters in the basilar artery. (D) nOCT imaging shows a clot formation (arrow) at the orifice of a basilar branch causing thromboembolic events as shown in (E) SWI (circles and arrows). Scale bars are equal to 1 mm unless otherwise indicated. CBCT, cone beam computed tomography; DSA, digital subtraction angiography; FD, flow-diverter; IMAX, internal maxillary artery; nOCT, neuro optical coherence tomography; SWI, susceptibility weighted imaging.

OCT imaging of SAH

Sentinel headaches with warning leaks can occur in 15–60% of patients with spontaneous SAH (93). Available imaging modalities, such as CT and MRI allow imaging of SAH, with CT being the modality of choice, when a substantial amount of blood is present in the SAS, or when a certain threshold is reached. Occult or sentinel subarachnoid bleeds are often missed because of the reduced sensitivity of these modalities to detect small or trace amounts of blood. In cases where a minor blood leakage from the aneurysm can precede aneurysm rupture, it can be difficult to confirm the presence of blood with CT imaging and even lumbar puncture results can come back negative or inconclusive. MR imaging with the use of susceptibility weighted imaging (SWI) (94,95), T1-weighted imaging and FLAIR mismatch have shown promise in identifying hemosiderin deposits or presence of bright hyperintense subarachnoid blood (96,97). However, skull-base bone artifacts, the heterogeneity of subarachnoid blood producing diverse signal intensities, and decreased sensitivity in cases of small bleeds, all present important limitations. Although presence of blood products precludes imaging by obscuring imaging of adjacent tissue due to increased attenuation, in the case of small subarachnoid bleeds, the sensitivity of OCT to blood can be used to advantage. Red blood cells diffusely scatter OCT light, causing significant light attenuation and shadowing. OCT signal attenuation increases exponentially with the number of erythrocytes present, causing either complete lack of penetration in cases of massive SAHs or partial lack of penetration in cases of smaller bleeds. This property makes OCT highly sensitive to detect even the smallest amount of blood. Additionally, the clear CSF allows light penetration and imaging through the vessel wall into the SAS (53). In cases of minor hemorrhages OCT signal attenuation can be used to our advantage in detecting minute amounts of blood in the vicinity of aneurysmatic lesions (Figure 7, unpublished data).

Figure 7 Example of nOCT in vivo pre-clinical imaging of subarachnoid hemorrhage. (A) DSA imaging of a flow diverter deployment in the basilar artery in a canine model. (B) The image shows multiple nOCT cross-sections acquired post-FD deployment with the subarachnoid space showing a hazy appearance (asterisks) suggesting that occult SAH occurred perioperatively. The nOCT image appearance (i.e., moderate optical attenuation and scattering in the subarachnoid space) indicates presence of blood in the CSF at a low concentration. (C) On the contrary, SWI and (D) FLAIR do not show signs of bleeding, likely due to the small amount of blood. Scale bars are equal to 1 mm. CSF, cerebrospinal fluid; DSA, digital subtraction angiography; FD, flow-diverter; FLAIR, fluid-attenuated inversion recovery; nOCT, neuro optical coherence tomography; SAH, subarachnoid hemorrhage; SWI, susceptibility weighted imaging.

Perianeurysmal environment considerations

Intracranial vessels travel inside the SAS which is filled with CSF. As discussed above, the optical transparency of CSF, similar to water, allows for near-infrared light transmission, giving the opportunity of imaging the SAS and the perianeurysmal environment through the vessel wall. Intracranial aneurysms are considered luminal outpouchings or widenings of the arterial lumen and most available imaging modalities depict the luminal changes of intracranial segments harboring aneurysmatic lesions without true consideration of aneurysm wall characteristics and most importantly without consideration of the perianeurysmal environment. The perianeurysmal environment is the immediate area surrounding the aneurysmatic lesion inside a sub-compartmentalized cistern of the SAS. Characteristic trabecular fibers and subarachnoid membranes form a variety of configurations, from loose to dense trabecular networks and honeycomb appearing membranous structures as well as thicker continuous membranes that embrace and stabilize the arterial segments and consecutively their respective aneurysms (98) (Figure 8).

Figure 8 Example of transvascular subarachnoid space pre-clinical in vivo imaging with nOCT in a canine model and ex vivo imaging in a human cadaveric model. The nOCT images show thick multiperforated membranes at the (A) distal basilar artery location and (B) at the basilar tip in the canine model in vivo (arrows). (C,D) Same color rendered nOCT images; the membrane is seen in green, the vessel wall shown in red, and the brain parenchyma is depicted in yellow. (E,F) The images show multiple trabeculae at the proximal basilar location (in vivo canine model) with attachments to the vessel wall, pia, and dural layers. The image in (E) shows a small perforating artery entering the brain parenchyma (arrow). (G) The image shows subarachnoid trabeculae along the MCA of a human cadaver (ex vivo) surrounding multiple perforating vessels (arrow) and (H) attached to the M2 segment (arrows). Atherosclerosis is also seen in image (G), with thickening of the vessel wall intimal layer (arrowheads). Scale bars are equal to 1 mm. MCA, middle cerebral artery; nOCT, neuro optical coherence tomography.

“The fact that we do not see abluminal factors with our currently available imaging modalities does not justify ignoring them in our diagnostic and therapeutic considerations. We need to learn more about them and develop imaging modalities which will allow us to visualize them directly. This will allow us to accomplish the conceptual and technical paradigm shift in targeting of aneurysm treatment, from the lumen to the wall and its environment and therefore the transformation of the endovascular aneurysm treatment from a currently mostly symptomatic, to a hopefully, truly curative one.” (Anton Valavanis, 2012, NeuroNews).

Numerous cadaveric anatomical studies have shown the diverse trabecular fibers traversing the subarachnoid cisterns (99-103). Similar in vivo findings were shown in animal studies with the help of intravascular OCT imaging (53,104). Finally, modern neuroradiology with the advent of high-field MRI scanners has come to appreciate the importance of imaging of the SAS’s arachnoid membranes, recognizing their significance (105). The presence of daughter sacs is a morphologic feature that has been significantly associated with increase in aneurysm rupture risk (7). The ELAPSS study showed that presence of blebs, wall protrusions and multiple lobules was a feature associated with increased rupture risk (7,106). Although such morphological changes are shown to increase the risk of rupture it is unclear whether they are attributed to intrinsic aneurysm parameters such as flow dynamics and wall shear stress forces, weakening of the aneurysm’s wall due to exacerbation of inflammatory factors and further breakdown of the tunica media, or are the effect of the aneurysm’s conformability to its perianeurysmal environment, as it grows adjacent to arachnoid fibers and membranes. If that were the case, then not all lobulations should be considered to have the same severity and the same risk of rupture. A characteristic example of such an effect is different configurations of basilar tip aneurysms due to the presence of the Liliequist’s membrane, located in the vicinity of the interpeduncular cistern (107). Unfortunately, routine imaging used for evaluation of aneurysm morphology disregards the perianeurysmal environment, since only what can be seen can also be assessed and most arachnoid fibers are not detected with current imaging modalities, except for a few thicker membranes that are within the spatial resolution of high-field MRI. Intravascular OCT, on the other hand, offers the potential for detailed evaluation of the immediate perianeurysmal surroundings due to its micrometer-scale resolution and optical transparency of the CSF. The ability to simultaneously evaluate wall thickness and perianeurysmal architectonics could give us useful insight and enhance our understanding of certain aneurysm morphologies and their concomitant risk profile.

Limitations

This review describes the development of a dedicated OCT technology for use in neurovascular arteries. It focuses specifically on the need for this technology in the assessment of intracranial aneurysms, the use of OCT in preclinical neurovascular research, and early clinical experience. While the article describes how OCT imaging can provide a wealth of additional information not available with other clinical imaging modalities, further studies are needed to collect additional data and evidence to support improved clinical decision-making using OCT in patients.

Conclusions

Intravascular imaging with high-resolution OCT is now possible in the intracranial circulation. Extensive experience in preclinical research along with initial clinical experience in patients undergoing various neurointerventional diagnostic and therapeutic procedures has shown the promise of this technology to more accurately diagnose, guide treatment, and surveil procedural response in vivo, at a level of detail that was previously only observable in post-mortem pathology studies. Drawing parallels from decades of experience in interventional cardiology using intravascular imaging to diagnose and treat coronary atherosclerosis, OCT holds the promise to improve patient outcomes in the endovascular treatment of brain aneurysms. “To see is to know, not to see is to guess” (unattributed)—and for the first time, we are now able to see cerebrovascular disease in situ.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was commissioned by the Guest Editors (Tufail Patankar, Ricardo Hanel and Jeremy Lynch) for the series “Intracranial Aneurysms Current Status and Future Prospects” published in Journal of Neurointervention. The article has undergone external peer review.

Peer Review File: Available at https://jni.amegroups.com/article/view/10.21037/jni-25-18/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jni.amegroups.com/article/view/10.21037/jni-25-18/coif). The series “Intracranial Aneurysms Current Status and Future Prospects” was commissioned by the editorial office without any funding or sponsorship. V.A. has received consulting fees from the following entities: Stryker Neurovascular, Medtronic, Neurovascular, Imperative Care, Scientia, Spryte Medical, Q’Apel, Jacobs Institute, Maduro Medical. G.J.U. is an employee of Spryte Medical. P.L. received consulting fees in the past by Gentuity LLC. T.A. reports consulting fees for Anaconda, J&J Medical-Cerenovus/Neuravi, Cortirio, Optimize Neurovascular, Rapid Medical, Spryte Medical, and expert testimonies for University of Turku, Finland, University of Lund, Sweden, University of Kuopio, Finland, and University of Galway, Ireland (PhD opponent twice, expert testimonies for appointments of professor and associate professor). T.A. has one patent in conjunction with Ceroflo Inc., reports DSMB-member for ATHENA-study-Anaconda, Ceretrieve Device Safety & Performance Study-Ceretrieve. T.A. holds stock or stock options of Ceroflo. MJG received grants from NIH, US-Israel, Binational Science Foundation, Department of Defense, Gilbert Foundation, Cerebrova, Cerenovus, Ceretrieve, CereVasc, Ceroflo, Deinde Medical, Gentuity, Imperative Care, Insera, Jacob’s Institute, Medtronic Neurovascular, Microvention/Terumo, Nuvascular, Q’Apel, Philips Healthcare, Scientia, Spryte Medical, Stryker Neurovascular, Surmodics (paid to institution). M.J.G. received consulting fees for Alembic LLC, BendIt Technologies, Cerenovus, Imperative Care, Jacob’s Institute, Maduro Medical, Medtronic Neurovascular, phenox GMbH, Philips Healthcare, Q’Apel, Scientia, Stryker Neurovascular, Stryker Sustainability Solutions, and honoraria from Spryte Medical. M.J.G. participates leadership or fiduciary role in SNIS Foundation Board and serves as JNIS Associate Editor, and holds stock or stock options of Imperative Care, Neurofine, Galaxy Therapeutics, Kapto, and Synchron. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Vlak MH, Algra A, Brandenburg R, et al. Prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis. Lancet Neurol 2011;10:626-36. [Crossref] [PubMed]
2. Kim BS. Unruptured Intracranial Aneurysm: Screening, Prevalence and Risk Factors. Neurointervention 2021;16:201-3. [Crossref] [PubMed]
3. Dayyani M, Sadeghirad B, Grotta JC, et al. Prophylactic Therapies for Morbidity and Mortality After Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Network Meta-Analysis of Randomized Trials. Stroke 2022;53:1993-2005. [Crossref] [PubMed]
4. Pobereskin LH. Incidence and outcome of subarachnoid haemorrhage: a retrospective population based study. J Neurol Neurosurg Psychiatry 2001;70:340-3. [Crossref] [PubMed]
5. Lv B, Lan JX, Si YF, et al. Epidemiological trends of subarachnoid hemorrhage at global, regional, and national level: a trend analysis study from 1990 to 2021. Mil Med Res 2024;11:46.
6. Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention. N Engl J Med 1998;339:1725-33. [Crossref] [PubMed]
7. UCAS Japan Investigators. The natural course of unruptured cerebral aneurysms in a Japanese cohort. N Engl J Med 2012;366:2474-82. [Crossref] [PubMed]
8. Juvela S, Porras M, Poussa K. Natural history of unruptured intracranial aneurysms: probability of and risk factors for aneurysm rupture. J Neurosurg 2000;93:379-87. [Crossref] [PubMed]
9. Juvela S, Poussa K, Lehto H, et al. Natural history of unruptured intracranial aneurysms: a long-term follow-up study. Stroke 2013;44:2414-21. [Crossref] [PubMed]
10. Sonobe M, Yamazaki T, Yonekura M, et al. Small unruptured intracranial aneurysm verification study: SUAVe study, Japan. Stroke 2010;41:1969-77. [Crossref] [PubMed]
11. Wiebers DO, Whisnant JP, Huston J 3rd, et al. Unruptured intracranial aneurysms: natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 2003;362:103-10. [Crossref] [PubMed]
12. Etminan N, Beseoglu K, Barrow DL, et al. Multidisciplinary consensus on assessment of unruptured intracranial aneurysms: proposal of an international research group. Stroke 2014;45:1523-30. [Crossref] [PubMed]
13. Beck J, Rohde S, Berkefeld J, et al. Size and location of ruptured and unruptured intracranial aneurysms measured by 3-dimensional rotational angiography. Surg Neurol 2006;65:18-25; discussion 25-7. [Crossref] [PubMed]
14. Ohashi Y, Horikoshi T, Sugita M, et al. Size of cerebral aneurysms and related factors in patients with subarachnoid hemorrhage. Surg Neurol 2004;61:239-45; discussion 245-7. [Crossref] [PubMed]
15. Frösen J, Piippo A, Paetau A, et al. Remodeling of saccular cerebral artery aneurysm wall is associated with rupture: histological analysis of 24 unruptured and 42 ruptured cases. Stroke 2004;35:2287-93. [Crossref] [PubMed]
16. Wadghiri YZ, Hoang DM, Leporati A, et al. High-resolution Imaging of Myeloperoxidase Activity Sensors in Human Cerebrovascular Disease. Sci Rep 2018;8:7687. [Crossref] [PubMed]
17. Gounis MJ, van der Marel K, Marosfoi M, et al. Imaging Inflammation in Cerebrovascular Disease. Stroke 2015;46:2991-7. [Crossref] [PubMed]
18. Mortazavi MM, Quadri SA, Khan MA, et al. Subarachnoid Trabeculae: A Comprehensive Review of Their Embryology, Histology, Morphology, and Surgical Significance. World Neurosurg 2018;111:279-90. [Crossref] [PubMed]
19. Jun YJ, Hwang DK, Lee HS, et al. Flow Diverter Performance Comparison of Different Wire Materials for Effective Intracranial Aneurysm Treatment. Bioengineering (Basel) 2024;11:76. [Crossref] [PubMed]
20. Koskinas KC, Ughi GJ, Windecker S, et al. Intracoronary imaging of coronary atherosclerosis: validation for diagnosis, prognosis and treatment. Eur Heart J 2016;37:524-35a-c.
21. Gerbaud E, Weisz G, Tanaka A, et al. Multi-laboratory inter-institute reproducibility study of IVOCT and IVUS assessments using published consensus document definitions. Eur Heart J Cardiovasc Imaging 2016;17:756-64. [Crossref] [PubMed]
22. Chen CJ, Kumar JS, Chen SH, et al. Optical Coherence Tomography: Future Applications in Cerebrovascular Imaging. Stroke 2018;49:1044-50. [Crossref] [PubMed]
23. Gounis MJ, Ughi GJ, Marosfoi M, et al. Intravascular Optical Coherence Tomography for Neurointerventional Surgery. Stroke 2019;50:218-23. [Crossref] [PubMed]
24. Huang D, Swanson EA, Lin CP, et al. Optical coherence tomography. Science 1991;254:1178-81. [Crossref] [PubMed]
25. Swanson EA, Fujimoto JG. The ecosystem that powered the translation of OCT from fundamental research to clinical and commercial impact Biomed Opt Express 2017;8:1638-64. [Invited].
26. Tearney GJ, Brezinski ME, Bouma BE, et al. In vivo endoscopic optical biopsy with optical coherence tomography. Science 1997;276:2037-9. [Crossref] [PubMed]
27. Tearney GJ, Regar E, Akasaka T, et al. Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. J Am Coll Cardiol 2012;59:1058-72. [Crossref] [PubMed]
28. Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2025;151:e771-862. [Crossref] [PubMed]
29. Vrints C, Andreotti F, Koskinas KC, et al. 2024 ESC Guidelines for the management of chronic coronary syndromes. Eur Heart J 2024;45:3415-537. [Crossref] [PubMed]
30. Ozaki Y, Tobe A, Onuma Y, et al. CVIT expert consensus document on primary percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS) in 2024. Cardiovasc Interv Ther 2024;39:335-75. [Crossref] [PubMed]
31. Adler DC, Chen Y, Huber R, et al. Three-dimensional endomicroscopy using optical coherence tomography. Nature Photonics 2007;1:709-16.
32. Leitgeb R, Hitzenberger C, Fercher A. Performance of fourier domain vs. time domain optical coherence tomography. Opt Express 2003;11:889-94. [Crossref] [PubMed]
33. Choma M, Sarunic M, Yang C, et al. Sensitivity advantage of swept source and Fourier domain optical coherence tomography. Opt Express 2003;11:2183-9. [Crossref] [PubMed]
34. Yabushita H, Bouma BE, Houser SL, et al. Characterization of human atherosclerosis by optical coherence tomography. Circulation 2002;106:1640-5. [Crossref] [PubMed]
35. Nakamura D, Wijns W, Price MJ, et al. New Volumetric Analysis Method for Stent Expansion and its Correlation With Final Fractional Flow Reserve and Clinical Outcome: An ILUMIEN I Substudy. JACC Cardiovasc Interv 2018;11:1467-78. [Crossref] [PubMed]
36. Stone GW, Christiansen EH, Ali ZA, et al. Intravascular imaging-guided coronary drug-eluting stent implantation: an updated network meta-analysis. Lancet 2024;403:824-37. [Crossref] [PubMed]
37. Kuno T, Kiyohara Y, Maehara A, et al. Comparison of Intravascular Imaging, Functional, or Angiographically Guided Coronary Intervention. J Am Coll Cardiol 2023;82:2167-76. [Crossref] [PubMed]
38. Kawase Y, Suzuki Y, Ikeno F, et al. Comparison of nonuniform rotational distortion between mechanical IVUS and OCT using a phantom model. Ultrasound Med Biol 2007;33:67-73. [Crossref] [PubMed]
39. Gounis MJ, Ughi GJ, Marosfoi M, et al. Intravascular Optical Coherence Tomography for Neurointerventional Surgery. Stroke 2019;50:218-23. [Crossref] [PubMed]
40. Bezerra HG, Costa MA, Guagliumi G, et al. Intracoronary optical coherence tomography: a comprehensive review clinical and research applications. JACC Cardiovasc Interv 2009;2:1035-46. [Crossref] [PubMed]
41. Ughi GJ, Wang H, Gerbaud E, et al. Clinical Characterization of Coronary Atherosclerosis With Dual-Modality OCT and Near-Infrared Autofluorescence Imaging. JACC Cardiovasc Imaging 2016;9:1304-14. [Crossref] [PubMed]
42. Wang H, Gardecki JA, Ughi GJ, et al. Ex vivo catheter-based imaging of coronary atherosclerosis using multimodality OCT and NIRAF excited at 633 nm. Biomed Opt Express 2015;6:1363-75. [Crossref] [PubMed]
43. Lopes DK, Johnson AK. Evaluation of cerebral artery perforators and the pipeline embolization device using optical coherence tomography. J Neurointerv Surg 2012;4:291-4. [Crossref] [PubMed]
44. Quimby DL Jr, Rothstein ES, Richmond HCT, et al. Efficacy and Safety of High-Frequency Optical Coherence Tomography (HF-OCT) for Coronary Imaging: A Multicenter Study. J Soc Cardiovasc Angiogr Interv 2025;4:102577. [Crossref] [PubMed]
45. Bezerra HG, Quimby DL Jr, Matar F, et al. High-Frequency Optical Coherence Tomography (HF-OCT) for Preintervention Coronary Imaging: A First-in-Human Study. JACC Cardiovasc Imaging 2023;16:982-4. [Crossref] [PubMed]
46. Ughi GJ, Marosfoi MG, King RM, et al. A neurovascular high-frequency optical coherence tomography system enables in situ cerebrovascular volumetric microscopy. Nat Commun 2020;11:3851. [Crossref] [PubMed]
47. Brezinski ME, Tearney GJ, Bouma BE, et al. Optical coherence tomography for optical biopsy. Properties and demonstration of vascular pathology. Circulation 1996;93:1206-13. [Crossref] [PubMed]
48. Pereira VM, Lylyk P, Cancelliere N, et al. Volumetric microscopy of cerebral arteries with a miniaturized optical coherence tomography imaging probe. Sci Transl Med 2024;16:eadl4497. [Crossref] [PubMed]
49. Hariri LP, Bouma BE, Waxman S, et al. An automatic image processing algorithm for initiating and terminating intracoronary OFDI pullback. Biomed Opt Express 2010;1:566-73. [Crossref] [PubMed]
50. Ali ZA, Karimi Galougahi K, Mintz GS, et al. Intracoronary optical coherence tomography: state of the art and future directions. EuroIntervention 2021;17:e105-23. [Crossref] [PubMed]
51. Roleder T, Jąkała J, Kałuża GL, et al. The basics of intravascular optical coherence tomography. Postepy Kardiol Interwencyjnej 2015;11:74-83. [Crossref] [PubMed]
52. King RM, Peker A, Epshtein M, et al. Active drug-coated flow diverter in a preclinical model of intracranial stenting. J Neurointerv Surg 2024;16:731-6. [Crossref] [PubMed]
53. Anagnostakou V, Epshtein M, Ughi GJ, et al. Transvascular in vivo microscopy of the subarachnoid space. J Neurointerv Surg 2022;14:neurintsurg-2021-018544.
54. Tearney GJ, Yabushita H, Houser SL, et al. Quantification of macrophage content in atherosclerotic plaques by optical coherence tomography. Circulation 2003;107:113-9. [Crossref] [PubMed]
55. Ughi GJ, Adriaenssens T, Sinnaeve P, et al. Automated tissue characterization of in vivo atherosclerotic plaques by intravascular optical coherence tomography images. Biomed Opt Express 2013;4:1014-30. [Crossref] [PubMed]
56. Caroff J, King RM, Ughi GJ, et al. Longitudinal Monitoring of Flow-Diverting Stent Tissue Coverage After Implant in a Bifurcation Model Using Neurovascular High-Frequency Optical Coherence Tomography. Neurosurgery 2020;87:1311-9. [Crossref] [PubMed]
57. King RM, Peker A, Anagnostakou V, et al. High-frequency optical coherence tomography predictors of aneurysm occlusion following flow diverter treatment in a preclinical model. J Neurointerv Surg 2023;15:919-23. [Crossref] [PubMed]
58. Rouchaud A, Ramana C, Brinjikji W, et al. Wall Apposition Is a Key Factor for Aneurysm Occlusion after Flow Diversion: A Histologic Evaluation in 41 Rabbits. AJNR Am J Neuroradiol 2016;37:2087-91. [Crossref] [PubMed]
59. Zoppo CT, Epshtein M, Gounis MJ, et al. Longitudinal healing flow diverting stents with phosphorylcholine surface modification. J Neurointerv Surg 2024;16:582-6. [Crossref] [PubMed]
60. Zoppo CT, Kolstad JW, King RM, et al. A novel intrasaccular aneurysm device with high complete occlusion rate: initial results in a rabbit model. J Neurointerv Surg 2024;16:928-33. [Crossref] [PubMed]
61. Vardar Z, King RM, Kraitem A, et al. High-resolution image-guided WEB aneurysm embolization by high-frequency optical coherence tomography. J Neurointerv Surg 2021;13:669-73. [Crossref] [PubMed]
62. Malle C, Tada T, Steigerwald K, et al. Tissue characterization after drug-eluting stent implantation using optical coherence tomography. Arterioscler Thromb Vasc Biol 2013;33:1376-83. [Crossref] [PubMed]
63. Ughi GJ, Steigerwald K, Adriaenssens T, et al. Automatic characterization of neointimal tissue by intravascular optical coherence tomography. J Biomed Opt 2014;19:21104. [Crossref] [PubMed]
64. De Cock D, Tu S, Ughi GJ, et al. Development of 3D IVOCT Imaging and Co-Registration of IVOCT and Angiography in the Catheterization Laboratory. Current Cardiovascular Imaging Reports 2014;7:9290.
65. Chandra RV, Maingard J, Slater LA, et al. A Meta-Analysis of Rupture Risk for Intracranial Aneurysms 10 mm or Less in Size Selected for Conservative Management Without Repair. Front Neurol 2021;12:743023. [Crossref] [PubMed]
66. Ishibashi T, Murayama Y, Urashima M, et al. Unruptured intracranial aneurysms: incidence of rupture and risk factors. Stroke 2009;40:313-6. [Crossref] [PubMed]
67. Chung CY, Peterson RB, Howard BM, et al. Imaging Intracranial Aneurysms in the Endovascular Era: Surveillance and Posttreatment Follow-up. Radiographics 2022;42:789-805. [Crossref] [PubMed]
68. Howard BM, Hu R, Barrow JW, et al. Comprehensive review of imaging of intracranial aneurysms and angiographically negative subarachnoid hemorrhage. Neurosurg Focus 2019;47:E20. [Crossref] [PubMed]
69. Martin AJ, Hetts SW, Dillon WP, et al. MR imaging of partially thrombosed cerebral aneurysms: characteristics and evolution. AJNR Am J Neuroradiol 2011;32:346-51. [Crossref] [PubMed]
70. Nadel L, Braun IF, Kraft KA, et al. Intracranial vascular abnormalities: value of MR phase imaging to distinguish thrombus from flowing blood. AJR Am J Roentgenol 1991;156:373-80. [Crossref] [PubMed]
71. Edjlali M, Gentric JC, Régent-Rodriguez C, et al. Does aneurysmal wall enhancement on vessel wall MRI help to distinguish stable from unstable intracranial aneurysms? Stroke 2014;45:3704-6. [Crossref] [PubMed]
72. Vakil P, Ansari SA, Cantrell CG, et al. Quantifying Intracranial Aneurysm Wall Permeability for Risk Assessment Using Dynamic Contrast-Enhanced MRI: A Pilot Study. AJNR Am J Neuroradiol 2015;36:953-9. [Crossref] [PubMed]
73. Ishii D, Nakagawa D, Zanaty M, et al. Quantitative Susceptibility Mapping and Vessel Wall Imaging as Screening Tools to Detect Microbleed in Sentinel Headache. J Clin Med 2020;9:979. [Crossref] [PubMed]
74. Larsen N, von der Brelie C, Trick D, et al. Vessel Wall Enhancement in Unruptured Intracranial Aneurysms: An Indicator for Higher Risk of Rupture? High-Resolution MR Imaging and Correlated Histologic Findings. AJNR Am J Neuroradiol 2018;39:1617-21. [Crossref] [PubMed]
75. van den Berg R. Intracranial aneurysm wall enhancement: fact or fiction? Neuroradiology 2020;62:269-70.
76. Zedde M, Sette MD, Quatrale R, et al. Intracranial vessel wall lesions on MRI: anatomical and pathological issues. Neurol Sci 2025;46:4851-73. [Crossref] [PubMed]
77. Bender MT, Wendt H, Monarch T, et al. Shifting Treatment Paradigms for Ruptured Aneurysms from Open Surgery to Endovascular Therapy Over 25 Years. World Neurosurg 2017;106:919-24. [Crossref] [PubMed]
78. Abecassis IJ, Zeeshan Q, Ghodke BV, et al. Surgical Versus Endovascular Management of Ruptured and Unruptured Intracranial Aneurysms: Emergent Issues and Future Directions. World Neurosurg 2020;136:17-27. [Crossref] [PubMed]
79. Fox AJ, Millar J, Raymond J, et al. Dangerous advances in measurements from digital subtraction angiography: when is a millimeter not a millimeter? AJNR Am J Neuroradiol 2009;30:459-61. [Crossref] [PubMed]
80. Elisevich K, Cunningham IA, Assis L. Size estimation and magnification error in radiographic imaging: implications for classification of arteriovenous malformations. AJNR Am J Neuroradiol 1995;16:531-8.
81. Hochmuth A, Spetzger U, Schumacher M. Comparison of three-dimensional rotational angiography with digital subtraction angiography in the assessment of ruptured cerebral aneurysms. AJNR Am J Neuroradiol 2002;23:1199-205.
82. Brinjikji W, Cloft H, Lanzino G, et al. Comparison of 2D digital subtraction angiography and 3D rotational angiography in the evaluation of dome-to-neck ratio. AJNR Am J Neuroradiol 2009;30:831-4. [Crossref] [PubMed]
83. Shah Kajol, Csore J, Roy TL. Approaches and considerations for optimal vessel sizing in peripheral vascular interventions. JVS-Vascular Insights. 2024;2:100092.
84. Caroff J, Tamura T, King RM, et al. Phosphorylcholine surface modified flow diverter associated with reduced intimal hyperplasia. J Neurointerv Surg 2018;10:1097-101. [Crossref] [PubMed]
85. King RM, Marosfoi M, Caroff J, et al. High frequency optical coherence tomography assessment of homogenous neck coverage by intrasaccular devices predicts successful aneurysm occlusion. J Neurointerv Surg 2019;11:1150-4. [Crossref] [PubMed]
86. Zoppo CT, Kolstad JW, King RM, et al. A novel intrasaccular aneurysm device with high complete occlusion rate: initial results in a rabbit model. J Neurointerv Surg 2024;16:928-33. [Crossref] [PubMed]
87. King RM, Brooks OW, Langan ET, et al. Communicating malapposition of flow diverters assessed with optical coherence tomography correlates with delayed aneurysm occlusion. J Neurointerv Surg 2018;10:693-7. [Crossref] [PubMed]
88. King RM, Peker A, Anagnostakou V, et al. High-frequency optical coherence tomography predictors of aneurysm occlusion following flow diverter treatment in a preclinical model. J Neurointerv Surg 2023;15:919-23. [Crossref] [PubMed]
89. Al-Mufti F, Cohen ER, Amuluru K, et al. Bailout Strategies and Complications Associated with the Use of Flow-Diverting Stents for Treating Intracranial Aneurysms. Interv Neurol 2020;8:38-54. [Crossref] [PubMed]
90. Hohenstatt S, Ulfert C, Herweh C, et al. Acute Intraprocedural Thrombosis After Flow Diverter Stent Implantation: Risk Factors and Relevance of Standard Observation Time for Early Detection and Management. Clin Neuroradiol 2023;33:343-51. [Crossref] [PubMed]
91. Hoffmann T, Boese A, Saalfeld S, et al. Intravascular optical coherence tomography (OCT) as an additional tool for the assessment of stent structures. Current Directions in Biomedical Engineering 2015;1:257-60.
92. King RM, Peker A, Epshtein M, et al. Active drug-coated flow diverter in a preclinical model of intracranial stenting. J Neurointerv Surg 2024;16:731-6. [Crossref] [PubMed]
93. Linn FH, Wijdicks EF, van der Graaf Y, et al. Prospective study of sentinel headache in aneurysmal subarachnoid haemorrhage. Lancet 1994;344:590-3. [Crossref] [PubMed]
94. Wan Z, Meng H, Xu N, et al. Clinical characteristics associated with sentinel headache in patients with unruptured intracranial aneurysms. Interv Neuroradiol 2021;27:497-502. [Crossref] [PubMed]
95. Nakagawa D, Kudo K, Awe O, et al. Detection of microbleeds associated with sentinel headache using MRI quantitative susceptibility mapping: pilot study. J Neurosurg 2019;130:1391-7. [Crossref] [PubMed]
96. Oda S, Shimoda M, Hirayama A, et al. Neuroradiologic Diagnosis of Minor Leak prior to Major SAH: Diagnosis by T1-FLAIR Mismatch. AJNR Am J Neuroradiol 2015;36:1616-22. [Crossref] [PubMed]
97. Oda S, Shimoda M, Hirayama A, et al. Retrospective review of previous minor leak before major subarachnoid hemorrhage diagnosed by MRI as a predictor of occurrence of symptomatic delayed cerebral ischemia. J Neurosurg 2018;128:499-505. [Crossref] [PubMed]
98. Valavanis A. Environment of aneurysms and endovascular considerations. Interv Neuroradiol 2008;14:48-9. [Crossref] [PubMed]
99. Vinas FC, Dujovny M, Fandino R, et al. Microsurgical anatomy of the infratentorial trabecular membranes and subarachnoid cisterns. Neurol Res 1996;18:117-25. [Crossref] [PubMed]
100. Vinas FC, Dujovny M, Fandino R, et al. Microsurgical anatomy of the arachnoidal trabecular membranes and cisterns at the level of the tentorium. Neurol Res 1996;18:305-12. [Crossref] [PubMed]
101. Lü J, Zhu X. Microsurgical anatomy of the interpeduncular cistern and related arachnoid membranes. J Neurosurg 2005;103:337-41. [Crossref] [PubMed]
102. Lü J. Arachnoid membrane: the first and probably the last piece of the roadmap. Surg Radiol Anat 2015;37:127-38. [Crossref] [PubMed]
103. Matsuno H, Rhoton AL Jr, Peace D. Microsurgical anatomy of the posterior fossa cisterns. Neurosurgery 1988;23:58-80. [Crossref] [PubMed]
104. Anagnostakou V, Epshtein M, Peker A, et al. New frontiers in intracranial imaging with HF-OCT: Ex vivo human cerebrovasculature evaluation and in vivo intracranial arteries dynamic visualization. Frontiers in Photonics 2022;3: [Crossref]
105. Lu S, Brusic A, Gaillard F. Arachnoid Membranes: Crawling Back into Radiologic Consciousness. AJNR Am J Neuroradiol 2022;43:167-75. [Crossref] [PubMed]
106. Backes D, Rinkel GJE, Greving JP, et al. ELAPSS score for prediction of risk of growth of unruptured intracranial aneurysms. Neurology 2017;88:1600-6. [Crossref] [PubMed]
107. Hacein-Bey L, Varelas PN. Pedunculated basilar terminus aneurysm with pseudo-septation due to anterior herniation through a perforated membrane of Liliequist. AJNR Am J Neuroradiol 2009;30:1688-90. [Crossref] [PubMed]