The risk of ischemic stroke due to carotid artery stenosis has long been assessed mainly based on luminal morphological characteristics such as stenosis and ulceration using angiography. Characteristics of the arterial wall itself have been revealed to play key roles in ischemic events with the recent development of vessel wall imaging (VWI) using modalities such as ultrasonography, computed tomography, and magnetic resonance imaging. In fact, some high-risk lesions in patients with nonstenotic carotid atherosclerosis could turn out to be ideal for surgical treatment.

Presently, stricter indications for carotid vascular surgery are required in accordance with the development of diagnostic VWI and improvements in multifaceted medical treatment, including intensive management of risk factors for atherosclerosis and lifestyle modifications. Treatment strategies for symptomatic low-grade stenosis and the development of diagnostic tools for asymptomatic vulnerable plaques have thus become new challenges.

This review article covers topics related to intraplaque hemorrhage, expansive remodeling, and radiation-induced atherosclerosis, with regard to carotid plaque assessment using VWI.

Carotid endarterectomy (CEA) and carotid artery stenting (CAS) are performed to revascularize internal carotid artery (ICA) stenosis. A comparative study between the two procedures has shown CEA to be more effective, and it is the first-line treatment for ICA stenosis. However, the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy trial showed the non-inferiority of CAS in the patient group at a high risk for CEA, among patients aged ≥ 70 years with contralateral carotid stenosis, pulmonary dysfunction, or a high cervical lesion. At our institution, the treatment outcomes and clinical characteristics of CEA efficacy and safety were classified based on age groups. We enrolled patients who underwent CEA at our hospital between January 2014 and December 2020. The patients were divided into the following age groups: ≤ 69 years, 70–79 years, and ≥ 80 years. The groups were analyzed for underlying disease, perioperative outcomes within 30 days, and the frequency of positive findings on postoperative diffusion-weighted magnetic resonance imaging. Changes in modified Rankin Scale (mRS) scores from admission to discharge were analyzed in the hyperacute (≤ 2 days), acute (3–7 days), subacute (8–30 days), and delayed (≥ 31 days) phases. In the young age group (≤ 69 years), diabetes and hypertension were the common comorbidities, while cardiac and renal issues were common for the middle (70–79 years) and older (≥ 80 years) age groups. The middle and older age groups were treated during the acute onset phase due to high acute cerebral infarction incidence arising from severe hemodynamic stroke. The mean mRS scores of these groups thereon improved. In cases of ICA stenosis due to severe hemodynamic stroke, acute revascularization procedure was observed to be effective, including by CEA, even when patients were ≥ 70 years.

Aneurysms at the proximal segment (A1) of the anterior cerebral artery are rare, accounting for 1–2% of all cerebral aneurysms. They are also known for the challenges they pose to treatment because of their proximity to the perforating arteries. In this study, we retrospectively reviewed ten cases of A1 aneurysms and reported their clinical characteristics and treatment strategies. Of the 1, 520 cases of cerebral aneurysms treated at our hospital, 10 (0.6%) were A1 aneurysms including nine unruptured and one ruptured. These aneurysms were located distal to A1 in six cases, proximal in three cases, and the middle in one case. A1 aneurysms were treated by clipping and coil embolization in four cases, and by wrapping in one case. One patient with a giant thrombosed aneurysm was treated via STA-STA-A3 bypass and trapping. There were no treatment-related complications or damage to the perforating arteries. Clipping is safe and effective in the treatment of A1 aneurysms while preserving the perforating arteries. However, endovascular treatment has been widely reported in recent years. As in the giant thrombosed A1 aneurysm case, bypass surgery is required for effective surgical management of the aneurysm.

We describe a case of impending ruptured aneurysm that developed oculomotor nerve palsy due to an internal carotid–posterior communicating (ICPC) aneurysm with a height of only 2.5 mm. A 65-year-old woman presented with ptosis and diplopia due to right oculomotor nerve palsy from 1 week ago. Cerebral angiography revealed a right ICPC aneurysm with bleb formation. The height of the aneurysm was as small as 2.5 mm; however, as the aneurysm could be confirmed at a position close to the oculomotor nerve through Fast imaging using steady state acquisition, we diagnosed it as oculomotor nerve palsy due to the impending ruptured aneurysm of ICPC and performed emergency surgery. The oculomotor nerve could be compressed by the aneurysm due to tortuosity of the internal carotid artery, even if the aneurysm is small; thus, performing neuroimaging and promptly considering a neurosurgical procedure for the ICPC aneurysm are necessary.

Spontaneous thrombosis of a giant intracranial aneurysm is a known occurrence; however, this aneurysm is rare wherein the thrombus extends to the parent artery and leads to occlusion. We report a case of a giant intracavernous internal carotid artery aneurysm with thrombosis and pseudo-occlusion of the internal carotid artery. A 55-year-old woman was incidentally found with a giant cerebral aneurysm; however, she had no symptoms. An angiogram and balloon occlusion test (BOT) were performed. The first angiogram revealed no thrombus in the aneurysm. Seven days after the BOT, the patient suddenly developed symptoms such as headache, vomiting, right eye pain, and right ptosis. The second angiogram showed an aneurysm that was barely visible and a slow flow of the internal carotid artery. Magnetic resonance imaging (MRI) revealed an infarction in the right middle cerebral artery territory. We considered the infarction as embolic because the collateral circulation was sufficient in this case. As the BOT showed a slight flow reduction (90% on the contralateral side), we performed a ligation of the internal carotid artery combined with superficial temporal artery to the middle cerebral artery branch M4 (STA-M4) bypass. Postoperatively, the right eye pain and ptosis disappeared. No neurological deficits and infarctions were observed. In this case, the temporary occlusion of the internal carotid artery through the BOT may have caused hemodynamic changes and affected thrombus formation.

Background: In the acute phase treatment of cerebral infarction due to internal carotid artery (ICA) dissection, endovascular treatment is not yet established. Bypass surgery is therefore used, with low-flow bypass being the most common for ICA dissection. We report a case in which the flow volume of low-flow bypass was insufficient for ICA occlusion, and thus, high-flow bypass was performed.

Case: A 48-year-old man presented with sudden right paralysis and aphasia. Urgent mechanical thrombectomy was performed due to left internal carotid artery occlusion; however, no recanalization was obtained. Consecutively, left internal carotid artery ligation and left superficial temporal artery–middle cerebral artery double anastomoses were performed. On the day after surgery, MRI revealed an enlargement of the cerebral infarction, and CT perfusion revealed an extensive ischemic penumbra region in the left cerebral hemisphere. Therefore, left external carotid artery–radial artery–middle cerebral artery anastomosis was performed. It stopped the progression of the cerebral infarction.

Conclusion: We experienced a case in which the flow volume of low-flow bypass was insufficient for treating ICA occlusion. In general, high-flow bypass is avoided in the acute phase of cerebral infarction; however, it should be considered and could be necessary in some cases.

Introduction: As revascularization of the anterior cerebral artery (A3) requires a longer graft than that of the middle cerebral artery, the design of the skin incision requires some ingenuity. Bilateral frontal craniotomy and a superficial temporal artery–anterior cerebral artery (A3) anastomosis were performed using a bicoronal skin incision right above the frontal branches of the bilateral superficial temporal arteries.

Case: A 73-year-old woman presented with a right distal anterior cerebral artery aneurysm and severe stenosis of the bilateral anterior cerebral arteries. Clipping and revascularization of the bilateral anterior cerebral arteries [A3–A3 bypass and left superficial temporal artery–anterior cerebral artery (A3) anastomosis] were performed. No facial nerve paralysis was observed in the postoperative period.

Conclusion: Facial nerve paralysis is unlikely with a skin incision above the Pitanguy’s line, and a bicoronal skin incision right above the frontal branches of the bilateral superficial temporal arteries is useful for the bilateral frontal craniotomy and anterior cerebral artery (A3) anastomosis.

We report a case of high-flow bypass (HFB) using a saphenous vein graft (SVG) for a giant cavernous carotid artery aneurysm in which the graft was occluded and the anastomosis with the middle cerebral artery (MCA) became an aneurysm.

The patient was a 70-year-old woman. She underwent internal carotid artery (IC) ligation and HFB [external carotid artery (EC)-SVG-middle cerebral artery (MCA)] for bilateral giant cavernous carotid aneurysms. First, left IC ligation and HFB (EC-SVG-MCA) were performed. Six months later, right IC ligation and HFB (EC-SVG-MCA) were performed. One year and 4 months after the second surgery, we confirmed occlusion of the right HFB and blind-end anastomosis between the HFB and MCA. Four years after the occlusion, neck clipping of the SVG aneurysm (SVGA) was performed because the blind end of the SVG slowly enlarged and changed the aneurysm.

Pathological observation of the SVG showed concentric thickening of the intima and tunica media, and marked lumen narrowing. Reactive fibrous thickening of the outer membrane was also observed, indicating that the SVG intima underwent atherosclerotic changes, possibly due to mechanical stimulation during anastomosis and exposure to arterial pressure.

In this case, the SVG used for the HFB was occluded, and the blind end of the anastomosis with the MCA changed the aneurysm. If the SVG is occluded during follow-up, knowing that the anastomosis with the MCA may become an aneurysm is necessary.

Radial artery grafts (RAGs) and great saphenous vein grafts (SVGs) are used for high-flow bypass (HFB). We report a case in which bypass replacement with a RAG was an adequate treatment for an enlarged saphenous vein graft aneurysm (SVGA). At the age of 36 years, he had a subarachnoid hemorrhage due to a ruptured C2 dissecting aneurysm of the right ICA. The patient underwent right ICA trapping following HFB using an SVG through the suprazygomatic route. At the age of 49 years, SVGA was noted, and enlargement was observed. The SVG was kinked angularly at the inlet where the SVAG was located. The maximum diameter of SVGA was 12.3 mm. Because SVGA enlarges over time, we decided to perform a surgical intervention. As a surgical strategy, an alternative HFB was created through the infrazygomatic route between the right ECA and right MCA M2 anterior branch using the RAG. The SVG was then trapped in the intracranial and cervical regions. The SVGA was thrombosed postoperatively. He was discharged with mRS 0 on postoperative day 20. Bypass replacement using RAG is considered an effective method for treating SVGA after HFB.

Infectious intracranial aneurysm is one of the complications of infective endocarditis (IE). However, few reported cases where several different types of bacteria were identified as responsible for its rupture exist. The present case is of a 75-year-old Japanese man who experienced an infectious intracranial aneurysm rupture 1 week after aortic valve replacement due to septic embolism from IE. CT angiography performed on onset revealed a 7-mm saccular aneurysm at the M1–M2 junction of the right middle cerebral artery. The patient had a history of aneurysmal clipping close to the lesion 9 years prior. The ruptured aneurysmal wall was resected for pathological examination after surgical obliteration of the aneurysm. Pathological findings revealed multiple bacteria, including Cryptococcus, Aspergillus, and colony formation of Gram-positive cocci. This case highlights the importance and challenge of identifying the responsible bacteria that caused the formation and rupture of infectious intracranial aneurysm.

Aneurysms buried in the brain at the distal M3 segment of the middle cerebral artery (MCA) cannot be recognized. They frequently have nonsaccular morphology that necessitates bypass and trapping of the superficial temporal artery (STA) to the M4 segment of the MCA (M4); however, identification of the recipient M4 is difficult. We introduce the “flash fluorescence” technique using indocyanine green-videoangiography (ICG-V) to identify an appropriate recipient M4. This technique is based on the analysis of differences in the timing of filling of M4 observed on serial ICG-V. First, correct identification of the M3 as the proximal artery for the aneurysm is necessary during preoperative cerebral angiography. Second, a wide dissection of the Sylvian fissure should be performed to expose the proximal M3. Under temporary clipping of the proximal M3, the candidate recipient M4 is not enhanced. After removing the temporary clip, the M4 is enhanced and identified as the recipient M4 for STA-M4 bypass.

A combination of clipping, removal of hematoma, and decompressive craniectomy is effective for the ruptured cerebral aneurysm with Sylvian hematoma. However, the postoperative degree of brain swelling varies among individual patients, and decompressive craniotomy may cause sinking flap syndrome (SFS) or require renewed cranioplasty. Therefore, surgeons may intraoperatively face a dilemma whether to concomitantly perform decompressive craniectomy. Here, we report the usefulness of an innovative approach, in which during wound closure, the autologous bone flap, thinned by cutting the internal plate, was returned to perform cranioplasty in one stage while applying decompression.

When the wound was closed, the dura mater was formed using a pericranial flap. The internal plate of the autologous bone flap was cut with a drill to reduce its thickness by half. The autologous bone flap was then fixed with a titanium plate. This contrivance is not a suitable alternative for conventional decompressive craniectomy. However, in case of mild brain swelling, this contrivance could contribute to the reduction of increased intracranial pressure and maintenance of cerebral hemodynamics while avoiding postoperative SFS or additional surgical stress.

Curative transarterial embolization (TAE) using liquid embolic material for intracranial dural arteriovenous fistulas (DAVF) can cause scalp necrosis, especially in patients who have undergone a previous craniotomy. Herein, we describe a case of recurrent superior sagittal sinus (SSS) DAVF associated with previous craniotomy successfully treated with the shield technique that can obliterate and “shield” extracranial feeders using calcium phosphate cements.

A 68-year-old man developed generalized convulsive seizures. He was diagnosed with SSS DVAF (Cognard type IIB) and a pial arteriovenous fistula (AVF) in the left parietal lobe. A TAE of the bilateral middle meningeal arteries was performed. Subsequently, a U-shaped skin incision was made beyond the midline, followed by a left parietal craniotomy and flow reduction of the SSS DVAF/pial AVF. The patient was seizure-free postoperatively. At 70 years of age, the patient presented with gait disturbances. Angiography revealed cerebral venous congestion due to a recurrent SSS DAVF. An H-shaped skin incision was made using the previous skin incision, followed by bilateral parietal craniotomy and coagulation of the dural arteries. The symptoms improved postoperatively; however, they recurred at the age of 71 years. Angiography revealed a marked arteriovenous shunt due to recurrent SSS DAVF, mainly via extracranial feeders that passed through small bone defects along the cranial bone flaps. Given the risk of scalp necrosis, extracranial feeders were obliterated using the shield technique. After the previous H-shaped skin incision was reopened, the bilateral parietal bone surfaces were widely exposed. The bone cortex was drilled to a depth of 5 mm. Calcium phosphate cement was applied to the drilled bone surface to “shield” future arteriovenous shunts via the extracranial feeders. The symptoms improved postoperatively. The postoperative course was uneventful without wound complications. Postoperative angiography revealed a substantial decrease in the arteriovenous shunt. The patient had no clinical events for two years and six months after the last surgery.

This method may be a useful therapeutic option for recurrent DAVF, especially in patients with a previous craniotomy.