放射線誘発頭蓋内血管狭窄に対する治療方針決定におけるMRI Vessel Wall Imagingの有用性
2026 年 48 巻 1 号 p. 49-55
詳細
2026 年 48 巻 1 号 p. 49-55
Radiotherapy is a recognized risk factor for vascular stenosis in patients with head and neck cancer. However, the treatment for radiation-induced vascular stenosis remains undefined because of its distinct pathophysiology from that of atherosclerotic disease. Herein, we present a case of radiation-induced stenosis successfully treated with balloon dilatation, guided by the assessment of vessel wall thickness using contrast-enhanced vessel wall imaging (CE-VWI). A 49-year-old woman presented with transient left hemiparesis at an outpatient clinic. The patient had a right cavernous sinus meningioma and had undergone tumor resection followed by radiotherapy for residual tumor 2 years earlier. Magnetic resonance imaging revealed right cerebral infarction caused by severe stenosis of the right middle cerebral artery, leading to a diagnosis of radiation-induced vasculopathy. Percutaneous transluminal angioplasty was planned after CE-VWI demonstrated significant wall thickening at the stenosis site. The procedure resulted in clinical improvement, and the patient remained recurrence-free during follow-up. CE-VWI is a valuable tool for assessing vessel wall integrity and for determining the feasibility of angioplasty in patients with radiation-induced vascular stenosis.
Surgery is the primary treatment for meningiomas. However, achieving total resection can be challenging, particularly for high-grade tumors, necessitating postoperative radiotherapy as an alternative or adjunctive treatment strategy [1]. Since the revision of medical reimbursement policies in Japan in 2008, advanced techniques such as intensity-modulated radiation therapy (IMRT) have been covered by insurance, leading to their widespread adoption in brain tumor management [2]. Despite these advancements, radiotherapy carries inherent risks, including late-onset effects in children such as vascular disorders, brain hemorrhage, and stroke [3, 4].
Treatment for radiation-induced stenosis typically begins with conservative management using antiplatelet agents or statins aimed at reducing the thrombotic risk and controlling cholesterol levels [5, 6]. However, when medical therapy is insufficient, endovascular therapy, such as percutaneous transluminal angioplasty (PTA), stent placement, and bypass surgery, may be considered [6]. Nevertheless, definitive treatment guidelines have not been established because of the limited evidence and variability in individual cases.
Intracranial stenotic lesions can be caused by a variety of conditions, including atherosclerosis, cerebral artery dissection, vasculitis, vasospasm, and moyamoya disease. Contrast-enhanced vascular wall MRI (VWI) enables detailed visualization of vessel wall characteristics at the site of the lesion, thereby facilitating a better understanding of the underlying pathology and aiding in differential diagnosis. Notably, in cases of atherosclerosis or vasculitis with positive remodeling, significant luminal stenosis may not be apparent on conventional magnetic resonance angiography (MRA), whereas VWI can detect vessel wall abnormalities that are otherwise difficult to identify. Since many vascular diseases can present with similar luminal imaging findings, VWI serves as a valuable adjunct to luminal imaging, enhancing diagnostic accuracy and supporting the differentiation of various intracranial vasculopathies [7, 8].
Radiation-induced fibrosis can cause vessel wall thinning, increasing the risk of complications, such as rupture or restenosis, during endovascular therapy [9, 10]. Contrast-enhanced vessel wall imaging (CE-VWI) is a non-invasive procedure for assessing vessel wall integrity and safely guiding therapeutic decisions. We present a case in which vessel wall imaging (VWI) provided valuable insights into the underlying pathology of intracranial arterial stenosis.
A 49-year-old woman had undergone tumor resection 2 years earlier for right cavernous sinus meningioma. Postoperatively, the patient received IMRT at a total dose of 54 Gy targeting the residual tumor (Figure 1, A). Follow-up magnetic resonance imaging (MRI) performed 18 months after radiotherapy revealed significant stenosis in the right middle cerebral artery (MCA) within the irradiated region. Antiplatelet therapy was initiated to prevent cerebral infarction.
Despite medical management, the patient presented to our outpatient clinic with transient left hemiparesis. At the time of admission, more than 24 hours had passed since the onset of symptoms. MRI revealed a right cerebral infarction and progression of arterial stenosis (Figure 1, B, C and D). High signal intensity was also observed on Fluid Attenuated Inversion Recovery (FLAIR), suggesting that this was not an ultra-acute phase, and it may have been a Transient Ischemic Attack (TIA). However, given the presence of a cerebral infarction in the watershed area between the middle cerebral artery (MCA) and the anterior cerebral artery (ACA), as well as reduced cerebral blood flow in the right MCA territory on cerebral perfusion scintigraphy, significant hemodynamic ischemia was strongly suspected, and the risk of recurrence was considered extremely high. MRA also revealed severe stenosis of the right M1 segment, with relatively poor visualization of the peripheral circulation compared to the contralateral side. Based on the angiographic findings showing no calcification (Figure 1, E), incomplete obstruction, and a short lesion segment classified as Mori type A, revascularization was deemed feasible.
The thickness at the stenotic segment in this case was 1.2 mm, and since the average thickness reported in previous studies was 1.0 mm, no thinning was observed [11] (Figure 1, F and G). Furthermore, wall thickening was found to be centripetal on CE-VWI, and based on the course of radiation exposure and the timing and location of stenosis, radiation-induced stenosis was considered likely. Percutaneous transluminal angioplasty (PTA) was performed for this case. The lesion was crossed using a CHIKAI 14 micro guidewire and an SL-10 microcatheter. As the vessel diameter at the stenotic segment was 1.85 mm, a Gateway 1.5 × 10 mm balloon catheter was selected. The SL-10 was exchanged for the balloon, and angioplasty was performed with inflation at 6 atm for 30 seconds.
The ultimate goal of this PTA was not to restore the vessel diameter to normal, but rather to achieve peripheral reperfusion. Post-dilatation imaging showed improved perfusion in the middle cerebral artery (with time 1.5 seconds), followed by mild recoil after 10 minutes. No further recoil was observed after an additional 5 minutes. (Figure 1, H and I).
Magnetic resonance angiography (MRA) showed blood flow signals in the stenotic area, and the peripheral circulation of the right MCA was well depicted compared to the preoperative images. Single photon Emission computed tomography (SPECT) also showed improvement in postoperative blood flow in the right anterior circulation, which had been impaired before endovascular therapy. (Figure 1, J, K, L, M). Postoperatively, the patient remained free of recurrent ischemic events.
Radiotherapy for meningioma can cause intracranial artery stenosis. The primary mechanism underlying intracranial vascular stenosis is often attributed to atherosclerosis; however, radiation exposure is also a significant contributing factor [12, 13]. Brain tumors located near the Willis polygon are associated with intracranial artery stenosis following radiation therapy [14, 15]. Radiation doses exceeding 25 Gy can induce vascular damage in 14–60 months posttreatment [9]. Approximately 12–21% of patients undergoing radiotherapy develop intracranial vascular complications, including cerebral hemorrhage and ischemic stroke [4, 9].
The mechanism of wall thickening in radiation-induced vascular stenosis has been reported to involve early endothelial damage, intimal fibrosis, and intimal accumulation of fibrin and hyaline granules, based on pathological findings in studies using rats [15].
The pathophysiological differences between radiation-induced vascular stenosis and stenosis associated with atherosclerotic arteriosclerosis are as follows. Radiation-induced stenosis develops over several months after irradiation, resulting in progressive endothelial damage that ultimately leads to endothelial proliferation, thickening of the basement membrane, and fibrosis of the outer layer [4]. The resulting wall thickening tends to be rich in macrophages and is often associated with plaque hemorrhage [4].
In contrast, atherosclerotic arteriosclerosis begins with the deposition and oxidation of LDL cholesterol in the subendothelial layer of the vessel wall, which triggers an inflammatory response, leading to the formation of macrophage-derived foam cells and proliferation of smooth muscle cells [16]. This process results in plaque formation and its destabilization, ultimately causing narrowing of the vascular lumen [16].
In radiation therapy-induced arterial stenosis, circumferential arterial wall thickening and strong enhancement are generally reported as common findings [17]. According to a report by Tanyildizi et al comparing radiation therapy-induced arterial stenosis and atherosclerotic thrombosis, circumferential thickening was observed in 16.6% of atherosclerotic thrombotic cerebral infarction cases, whereas it was present in 58.3% of radiation-induced arterial stenosis cases [19]. The addition of contrast-enhanced vessel wall imaging (VWI) may aid in understanding the pathophysiology and in evaluating disease activity, potentially assisting in treatment selection.
Contrast-enhanced vessel wall imaging (CE-VWI) can be effectively used to evaluate the vessel wall thickness of a radiation-induced stenosis. CE-VWI enables evaluation of intracranial vessel walls, which are normally difficult to evaluate. The scan protocol included a standard 3D Time-Of-Flight magnetic resonance angiography (TOF-MRA), with a matrix of 256 × 256, Field of view (FoV) of 180 × 180 mm, and section thickness of 0.50 mm (reconstructed), which was centered in the Circle of Willis for lumenographic identification of any stenosis. Multi planar reconstruction (MPR) was also performed. Some reports indicate that the normal MCA wall is 0.2–0.3 mm thick, which is smaller than the Vessel wall MRI (VW-MRI) voxel size. However, since intracranial vessels can suppress signals generated by adjacent blood and cerebrospinal fluid, it is possible to image the arterial wall, and pathological changes (thickening and enhancement effects) can be detected sufficiently [17].
Regarding the vascular enhancement effect, two methods have been proposed, according to Lindenholz et al: one involves acquiring reaction images before and after contrast-enhanced MRI, and the other involves evaluating the enhancement effect based on comparisons between the contrast-enhanced images and the signals from the contralateral vessels and brain tissue, as well as comparisons with the pituitary stalk [18]. In the present case, only contrast-enhanced images were available, and enhancement was observed in the lesion compared to the contralateral vessels.
This case presented with mildly elevated T-cho (224) and LDL (131) levels and was on rosuvastatin, but had no other risk factors for atherosclerosis, such as smoking or alcohol consumption. Although mild hypercholesterolemia was present, it was well controlled. The patient, who underwent radiation therapy with a total dose of 54 Gy for a right cavernous sinus meningioma, developed M1 stenosis at the central irradiation site 11 months after treatment, which progressed to symptomatic disease at 25 months, and was confined to the radiation field, with no stenosis or occlusion outside the radiation field. Given the consistency in timing and dose, the likelihood of radiation-induced stenosis was high.
The treatment of radiation-induced stenosis has not been well established, compared to atherosclerotic stenosis, because of differences in pathophysiology [19]. Medical treatment was initiated with cholesterol control and antiplatelet agents. However, this did not have a sufficient effect. Treatment was continued; however, the stenosis progressed, and the patient became symptomatic. Therefore, surgical treatment was considered.
The Mori classification is a system for classifying the morphology of intracranial arterial lesions based on angiographic findings, with the aim of evaluating the safety of endovascular treatment, as well as the difficulty and risk of recurrence. It is divided into three stages based on calcification and lesion size [20, 21]. Preoperative morphological assessment is used to assess the safety of endovascular therapy, and type A morphology is considered low-risk [22]. In the present case, the lesion was less than 5 mm in size, with symptomatic right MCA stenosis that was centripetal with Warfarin aspirin symptomatic intracranial disease (WASID) of 50% or more, no collateral branches, and no calcification; hence, the lesion was classified as Mori type A, allowing for a relatively safe therapeutic approach.
The risks associated with surgical treatment include vessel rupture during treatment and restenosis after treatment. The mechanisms underlying irradiation stenosis include atherosclerosis, vasculitis, and collagen vascular disorders [19]. Contrast-enhanced vessel wall imaging (CE-VWI) can evaluate vasculitis in an enhanced vessel wall and reveal the vessel in 0.5 mm slices of the x-, y-, and z-axes [23]. The patient had stenosis with an enhanced wall, which led to a diagnosis of radiation vasculopathy. Although a treatment strategy for this disease has not been established, in this case, endovascular therapy was performed relatively safely after confirming the absence of wall thinning by CE-VWI. In the intracranial artery, evaluation of the vessel wall is necessary to prevent vessel rupture during balloon dilatation because radiation may lead to weakening or thinning of the vessel wall [9]. Percutaneous transluminal angioplasty (PTA) was selected as the optimal treatment method for several reasons. First, CE-VWI showed no weakening or thinning of the vessel wall; therefore, there was a low risk of vessel rupture during balloon dilatation. Second, the extent of vascular stenosis was small, and PTA was considered possible. Finally, in this case, bypass surgery was impossible, as the patient had lost her superficial temporal artery during meningioma removal. Therefore, PTA was selected as the safest and most reliable method. If PTA had not provided effective vessel dilation, stent dilation may have been necessary; however, that procedure was not necessary in this case.
The management of radiation-induced intracranial artery stenosis, such as medial management and PTA, extends beyond the initial treatment phase owing to the ongoing risks of restenosis, vessel rupture, atherosclerosis, thromboembolism, rupture, fistula and aneurysm [10]. Despite a successful PTA, the long-term effects of radiation-induced vascular injury may persist, requiring comprehensive follow-up strategies using CE-VWI. In the present case, MRI scans were performed one week postoperatively, at three months, and at eight months, and no recurrence has been observed to date. We recommend follow-up at six-month to one-year intervals, similar to other vascular disorders.
Regarding the follow-up period, the restenosis rate after PTA for symptomatic MCA stenosis is reported to be 31.9%, with a median follow-up period of 63 months showing restenosis. Given that the incidence rate is reported to be significantly higher within the first five years after radiation therapy, imaging follow-up is recommended during this period. In long-term outcome and associated factors for imaging follow-up, attention should be paid to the progression of vascular stenosis on MRA, and VWI should be added as appropriate if stenosis progression or symptomatic cerebral infarction is detected.
Contrast-enhanced vessel wall imaging (CE-VWI) is an invaluable tool for evaluating vessel wall integrity in cases of radiation-induced vascular stenosis. PTA can be performed relatively safely in selected patients by confirming adequate wall thickness and ruling out thinning or weakening associated with fibrosis.
Conceptualization: Takuya Kishimoto, Takeru Umemura.
Investigation: Takuya Kishimoto.
Supervision: Takeru Umemura, Toru Kurokawa, Junkoh Yamamoto, Yuko Tanaka.
Writing-original draft: Takuya Kishimoto.
Writing-review & editing: Takuya Kishimoto, Takeru Umemura, Yuko Tanaka.
None
The authors declare no conflict of interest.
The data that support the findings of this study are available upon request from the corresponding author and are not publicly available because they contain information that could compromise the privacy of the research participants.
Not applicable.
Written informed consent was obtained from the patient for publication of this case report and any accompanying images.
