Neuroendoscopic cyst fenestration for delayed enlargement of perianeurysmal cyst formation through long-term follow-up after endovascular treatment: A case report and review of literature.

Background: Perianeurysmal cyst formation after endovascular treatment of cerebral aneurysms is a rare complication; however, the number of reports has gradually increased in recent years due to the development of several endovascular treatments. Case Description: We present a case of delayed perianeurysmal cyst enlargement 8 years after endovascular treatment for multiple recurrences of a large cerebral aneurysm in the anterior communicating artery. The patient presented with obstructive hydrocephalus caused by an enlarged perianeurysmal cyst. The patient underwent cyst fenestration using neuroendoscopy and ventriculoperitoneal shunting, recovered from the clinical symptoms, and had a good prognosis. Histopathological findings showed that the cyst wall contained a fibrotic layer under the monoependymal layer with hemosiderosis without evidence of neovascularization or inflammatory cell infiltration. These findings suggest that the origin of the perianeurysmal cyst wall is not the aneurysm itself but the adjacent brain tissue. Conclusion: Perianeurysmal cysts can develop during long-term follow-up, and clinicians should consider surgical treatment, including cyst fenestration, using neuro-endoscopy if the cyst presents with clinical symptoms.

A Case of a Perianeurysmal Cyst Following Stent-Assisted Coil Embolization of an Unruptured Vertebral Artery Aneurysm.

Objective: To report the rare case of a patient with a perianeurysmal cyst following stent-assisted coil embolization of an unruptured vertebral artery aneurysm. Case Presentation: A 63-year-old woman underwent stent-assisted coil embolization for an unruptured vertebral artery aneurysm embedded in the brainstem (pons). Complete occlusion of the aneurysm was successfully achieved. However, subsequent magnetic resonance imaging (MRI) conducted 8 months after the procedure showed perilesional edematous changes surrounding the aneurysm, and at 20 months, cyst formation was observed in the vicinity of the aneurysm. Progressive enlargement of the cyst eventually led to the development of paralysis and dysphagia, necessitating cyst fenestration surgery. Although postoperative reduction in the cyst size was achieved, the patient experienced complications in the form of aspiration pneumonia and bacterial meningitis, which resulted in a life-threatening condition. Conclusion: Aneurysms embedded in the brain parenchyma should be carefully followed up, recognizing the risk of perianeurysmal cyst formation after coil embolization.

Symptomatic perianeursymal cyst development 20 years after endovascular treatment of a ruptured giant aneurysm: Case report and updated review.

Perianeurysmal cysts are a rare and poorly understood finding in patients both with treated and untreated aneurysms. While the prior literature suggests that a minority of perianeurysmal cysts develop 1-4 years following endovascular aneurysm treatment, this updated review demonstrates that nearly half of perianeurysmal cysts were diagnosed following aneurysm coiling, with the other half diagnosed concurrently with an associated aneurysm prior to treatment. 64% of perianeurysmal cysts were surgically decompressed, with a 39% rate of recurrence requiring re-operation. We report a case of a 71-year-old woman who presented with vertigo and nausea and was found to have a 3.4 cm perianeurysmal cyst 20 years after initial endovascular coiling of a ruptured giant ophthalmic aneurysm. The cyst was treated with endoscopic fenestration followed by open fenestration upon recurrence. The case represents the longest latency from initial aneurysm treatment to cyst diagnosis reported in the literature and indicates that the diagnosis of perianeurysmal cyst should remain on the differential even decades after treatment. Based on a case discussion and updated literature review, this report highlights proposed etiologies of development and management strategies for a challenging lesion.

Unique image findings around "kissing" distal anterior cerebral artery aneurysms in addition to perianeurysmal edema: A case report.

Background: Some aneurysms cause edema formation in the surrounding brain parenchyma and are thought to reflect various phenomena occurring in the aneurysm. Some authors highlighted perianeurysmal edema (PAE) as a finding that indicates higher risk of rupture of the aneurysm. On the other hand, there are no reports of image changes in the surrounding brain parenchyma of aneurysm other than edema formation. Case Description: We describe a 63-year-old man with unique signal change in the surrounding brain parenchyma of "kissing" distal anterior cerebral artery aneurysms completely different from PAE. The large and partially thrombosed aneurysm presented well-defined signal change surrounding brain parenchyma in addition to PAE. Intraoperative findings revealed the signal change as a space of retaining serous fluid. Drain the fluid and clipping was made for the both anterior cerebral artery aneurysms. The postoperative course was uneventful and his headache was improved the day after the surgery. The perianeurysmal signal change was also disappeared immediately after the surgery except for the PAE. Conclusion: This case demonstrates a rare phenomenon of signal change around the aneurysm, and there is a possibility that the unique finding exists as an early manifestation of intracerebral hematoma associated with aneurysm rupture.

Case report: Unruptured small middle cerebral artery aneurysm with perianeurysmal edema.

Background: Perianeurysmal edema (PAE) has a tendency to occur in embolized aneurysms but also in partially thrombosed, large, or giant aneurysms. However, there are only a few cases recorded in which PAE was detected in untreated or small aneurysms. We suspected that PAE might be an impending sign of aneurysm rupture in these cases. Herein, we presented a unique case of PAE that was related to an unruptured small middle cerebral artery aneurysm. Case description: A 61-year-old woman was referred to our institute due to a newly formed abnormal fluid-attenuated inversion recovery (FLAIR) hyperintense lesion in the right medial temporal cortex. Upon admission, the patient did not present with any symptoms or complaints; however, FLAIR and CT angiography (CTA) suggested an increased risk of aneurysm rupture. Aneurysm clipping was conducted, and no evidence of subarachnoid hemorrhage and hemosiderin deposits around the aneurysm and brain parenchyma was noted. The patient was discharged home without any neurological symptoms. MRI taken at eight months post-clipping revealed complete regression of the FLAIR hyperintense lesion around the aneurysm. Conclusion: PAE in unruptured, small aneurysm is thought to be an impending sign of aneurysm rupture. Early surgical intervention is critical even for small aneurysms with PAE.

Perianeurysmal parenchymal cysts - Case series and literature review.

•Intracranial cysts are associated with a number of vascular lesions.•They predominantly occur in larger, partially-thrombosed aneurysms and in older patients.•There is a trend towards enlargement over time if untreated and a likelihood of recurrence following treatment.•We hypothesise the cysts arise either from dilated Virchow-Robin spaces and/or inflammatory processes.

Perianeurysmal cyst formation in the brainstem after coil embolization: illustrative case.

BACKGROUND: Perianeurysmal cysts in the brainstem after endovascular coil embolization are rare, and their underlying mechanism remains unclear. The authors reported a case of a postcoiling perianeurysmal cyst that developed 6 years after endovascular coil embolization for a ruptured aneurysm and reviewed the related literature. OBSERVATIONS: A 77-year-old woman had a history of subarachnoid hemorrhage 6 years earlier. The ruptured large left vertebral artery-posterior inferior cerebellar artery aneurysm was treated with endovascular coil embolization. Two years later, the aneurysm regrew and perianeurysmal brainstem edema was detected on magnetic resonance imaging (MRI); stent-assisted coil embolization combined with low-flow bypass was performed. Follow-up MRI showed that the perianeurysmal edema gradually transformed into a perianeurysmal cyst over the next 3 years. Finally, the perianeurysmal cyst caused gait disturbance with ataxia, and the patient received cyst puncture. After surgery, the symptom was immediately improved. LESSONS: The authors reported, for the first time, postcoiling of perianeurysmal cyst formation treated by cyst puncture. If perianeurysmal edema is detected after endovascular coil embolization, especially for large aneurysms, it is necessary to consider progression to cyst formation and follow up over time. In addition, cyst puncture is effective, depending on the symptoms and the lesion.

Obstructive hydrocephalus secondary to a perianeurysmal cyst: a case report.

Perianeurysmal cysts are an extremely rare association with cerebral aneurysms. We report the case of a 64 year old male who presented with obstructive hydrocephalus due to a perianeurysmal cyst. The cyst originated in association with a thrombosed, right-sided, terminal internal carotid artery aneurysm. Definitive management was offered with craniotomy and surgical clipping of the aneurysm together with endoscopic cyst fenestration. The patient made a full recovery and was asymptomatic at 3-month follow-up. We review the literature and discuss the potential mechanisms of cyst formation.

Large Parenchymal Perianeurysmal Cyst: A Case Report.

Parenchymal perianeurysmal cysts are rare. We report a case of 50-year-old woman who presented with persistent headaches and episodes of vomiting for the last 2 months. Magnetic resonance imaging of the brain showed a well-defined solitary cystic lesion with a mural nodule measuring 5.4 × 5.2 × 4.6 cm in the right basifrontal region. The mural nodule was cortically based. It was hypointense on T2-weighted fluid-attenuated inversion recovery and showed intense contrast enhancement with few nonenhancing areas-no evidence of diffusion restriction. The cyst wall was nonenhancing, and magnetic resonance angiogram was unremarkable. Differential diagnoses included intra-axial gliomas such as ganglioglioma and pleomorphic xanthoastrocytoma. Right pterional craniotomy and a transcortical approach were made. Subtotal excision of cyst and clipping of right middle cerebral artery bifurcation thrombosed aneurysm were done. After 6 months of follow-up, patient is stable without any deficits. A parenchymal perianeurysmal cyst is a rare entity; it is crucial to be considered a differential diagnosis in any cystic lesion with the mural nodule.

Hemodynamic features of an intracranial aneurysm rupture predicted by perianeurysmal edema: A case report.

BACKGROUND: Perianeurysmal edema (PAE) has been suggested as an indicator of potential aneurysm rupture; however, the hemodynamic features of these aneurysms are still unknown. A computational fluid dynamic (CFD) analysis was performed to evaluate the hemodynamic features of a very rare case of a ruptured middle cerebral artery (MCA) aneurysm with PAE. CASE DESCRIPTION: A 65-year-old woman presented with disturbed consciousness. A subarachnoid hemorrhage due to an azygos anterior cerebral artery (ACA) aneurysm rupture was suspected. An unruptured MCA aneurysm with PAE was identified in the left temporal lobe. Although the ACA aneurysm was clipped to prevent re-bleeding, the MCA aneurysm subsequently ruptured 6 days later. Clipping of the MCA aneurysm was performed, and hemosiderin deposits suggestive of sentinel bleeding were found on the surface of the aneurysm dome. CFD analysis revealed unstable hemodynamic stress at the expanded bleb area after rupture, localized to the rupture site. Moreover, this analysis revealed flow impingement with pressure elevation and low wall shear stress, which indicated increased inflammation and aneurysm wall thinning that likely led to rupture. CONCLUSION: Hemosiderin deposits at the aneurysm wall and PAE indicates leakage from a cerebral aneurysm. Hemodynamic stress at the aneurysm may promote an inflammatory response and lead to wall weakening accompanied by PAE. Based on our findings, we recommend that surgical intervention should be considered as the first line of treatment for such aneurysms to prevent rupture.

Peri-Aneurysmal Brain Edema in Native and Treated Aneurysms: The Role of Thrombosis.

Cerebral peri-aneurysmal edema (PE) is typically associated with giant partially-thrombosed aneurysms and less frequently with smaller aneurysms treated with endovascular embolization. An understanding of the pathophysiologic mechanism of PE is still limited. We report 3 cases of cerebral aneurysms associated with PE. We describe 2 cases of giant partially thrombosed aneurysms surrounded by vasogenic edema with apposition of an intramural and juxtamural thrombus. Our third case is a smaller aneurysm inciting vasogenic edema several years after coil embolization. Vessel-wall magnetic resonance imaging (MRI) showed avid wall enhancement and an enhancing thrombus embedded within the coils, reflecting inflammation of the aneurysm wall and proliferation of the vasa vasorum. Thrombosis within the aneurysmal sac and walls, both in native and treated aneurysms, may promote inflammatory changes and sustain the occurrence of PE. Vessel-wall MRI has a potential role in the evaluation process of this subgroup of aneurysms.

Exacerbation of immunoglobulin G4-related inflammatory abdominal aortic aneurysm after endovascular repair.

A 78-year-old male was admitted to our hospital with lumbar pain and was found to have an abdominal aortic aneurysm (AAA) and femoral artery aneurysm (FAA). Initially, the patient underwent endovascular aneurysm repair (EVAR) for the AAA and aneurysmectomy for the FAA. The FAA was diagnosed by histology as immunoglobulin G4-related disease (IgG4-RD). The preoperative serum IgG4 level was within the normal range, although a slight serum interleukin-6 (IL-6) elevation was observed. Four years later, the AAA-sac diameter had expanded and the serum levels of both IgG4 and IL-6 levels had increased. Six years after the initial EVAR, aneurysmorrhaphy of AAA-sac was performed. The resected specimen revealed adventitial fibrosis and prominent lymphoplasmacytic infiltrate with regulatory T cells, satisfying histological diagnostic criteria for IgG4-RD. Immunoreactive matrix metalloproteinases (MMPs), particularly MMP-2 and MMP-9, and IL-6 were detected within numerous spindle cells in the adventitia of both the FAA and the AAA-sac. Five months after the aneurysmorrhaphy, the residual AAA-sac was again enlarged with a thickened wall that accumulated [18 F] fluoro-2-deoxy-D-glucose (FDG-PET) on positron emission tomography; these findings were paralleled by increased levels of serum IgG4 and IL-6. Therefore, persistent inflammation after EVAR may be attributed to the inflammatory sequelae of IgG4-RD.

Non-traumatic subdural hemorrhage: beware of ruptured intracranial aneurysm.

Acute subdural hemorrhage (SDH) is commonly encountered by emergency radiologists in the setting of trauma. When history or imaging evidence of trauma is absent, the differential diagnosis for SDH should be expanded. Intracranial aneurysm rupture is a rare and underrecognized cause of SDH which may present without concurrent subarachnoid hemorrhage. The mechanism of aneurysmal SDH is controversial, but understanding the anatomic microenvironment of the aneurysm provides insight and clarifies aneurysm features predisposing to subdural compartment rupture. Aneurysmal SDH is a neurosurgical emergency and its treatment strategies differ from traumatic SDH. Outcomes are poor if treatment is delayed; thus, radiologists play a central role in recognizing this uncommon but potentially devastating complication of aneurysm rupture. The goal of this article is to familiarize radiologists with clinical and imaging characteristics of aneurysmal SDH and review pertinent anatomy, risk factors, and potential etiologies. Aneurysmal rupture can easily be overlooked in the routine workup of atraumatic SDH, and radiologists must know when to recommend vascular imaging to avoid the catastrophic consequences of a missed diagnosis.

Treatment and outcome of thrombosed aneurysms of the middle cerebral artery: institutional experience and a systematic review.

Thrombosed aneurysms of the middle cerebral artery (MCA) usually show large dimension and complex morphology with neck sclerosis and perforating vessels originating from the sac. Only limited experiences from case reports or small mixed series including thrombosed aneurysms in different locations are available in literature. To systematically review all the pertinent literature, a comprehensive literature review with the search terms "MCA, aneurysm, and thrombosis" and a pooled analysis including our institutional series were performed. We evaluated demographics, ruptured status, aneurysm morphology, topography and size, thrombosis extension, treatment, complications, final occlusion rate, and clinical outcome at follow-up. Data were individually extracted for each patient and included in a pool for the statistical analysis. Forty-two articles published between 1992 and 2016 were selected, including a total of 115 patients. Most of thrombosed aneurysms were saccular (67.6%), large or giant (86.7%), and located at the MCA bifurcation (67.3%). The treatment of choice was surgery in more than 80% of cases compared with the endovascular techniques, though the overall percentage of complications reported in the two groups was similar and around 20% of cases. Clinical outcome was favorable in more than 85% of patients after treatment. This is the first systematic review focusing on treatment and outcome of thrombosed MCA aneurysms. Our data depict their main angioarchictectural and clinical characteristics, proving the feasibility of their treatment with good prognosis in a high percentage of patients. However, complication and mortality rates of about 20 and 3.5%, respectively, are not negligible.

Temporary Worsening of Perianeurysmal Edema Following Clipping of a Partially Thrombosed Giant Pericallosal Artery Aneurysm.

We present a case of a partially thrombosed giant aneurysm of the pericallosal artery that experienced a temporary worsening of perianeurysmal edema after clipping. A 66-year-old man presented with progressive weakness of the right leg. Imaging studies revealed a partially thrombosed giant aneurysm at the bifurcation of the left pericallosal artery with concomitant perianeurysmal edema. The aneurysm was thought responsible for the symptoms of the patient, and he agreed to undergo clipping surgery. The aneurysmal neck was clipped using two long aneurysm clips without dissecting the aneurysmal dome. The patient woke up from anesthesia with the right-sided hemiparesis, which progressed to hemiplegia by 12 h after surgery. Brain computed tomography revealed worsening of the perianeurysmal edema. Fortunately, his symptoms resolved completely by 2 weeks after surgery with conservative management. Perianeurysmal edema is frequently observed in patients with partially thrombosed giant aneurysms. Although worsening of perianeurysmal edema is a relatively common complication of endovascular procedures, its occurrence after clipping has rarely been reported. The worsening may have been induced by release of inflammatory cytokines from aneurysm wall, which was rendered ischemic due to obliteration of the vasa vasorum by the clips. Perianeurysmal edema may develop or worsen after clipping of a partially thrombosed giant aneurysm if the interface between the aneurysm and surrounding brain is not fully dissected.

Imaging appearance of fibrosing diseases of the retroperitoneum: can a definitive diagnosis be made?

PURPOSE: To assess the frequency with which previously reported characteristic findings of retroperitoneal fibrosis (RPF) (a circumferential or almost circumferential peri-aortic mass centered at L4, which does not displace the abdominal aorta or proximal common iliac arteries) are present in patients with RPF, in patients with other fibrosing diseases, and in cancer patients referred to a subspecialty clinic with a suspected diagnosis of RPF, in order to determine whether diagnostic percutaneous biopsy can be avoided in some patients. METHODS: This HIPAA-compliant Institutional Review Board-approved retrospective study assessed clinical and CT and MR imaging abnormalities on imaging studies in 92 patients referred to a subspecialty clinic with suspected RPF over a 14-year period. Two reviewers, in consensus, determined the frequency of different CT and MRI findings in three groups of patients (Group 1: those with an eventual diagnosis of RPF, Group 2: those with a fibrosing disease associated with vascular or urologic abnormalities, and Group 3: those with cancer). Assessed imaging features included the presence of retroperitoneal masses, whether masses were single or multiple, whether such masses were circumferential or nearly circumferential, whether they displaced the aorta away from the spine (with the degree of such displacement measured), and whether there were abnormalities outside of the peri-aortic region of the retroperitoneum. The frequency with which findings previously reported as characteristic of RPF were present was determined for each of the three groups. Imaging results were correlated with the final diagnoses. RESULTS: Of 68 subjects eventually diagnosed with retroperitoneal fibrosis (RPF) (Group 1), 47 had peri-aortic retroperitoneal masses, 18 of which displaced the aorta anteriorly away from the spine. Of 12 subjects with fibrosing abnormalities related to vascular or urologic disease (Group 2), six had retroperitoneal masses, none of which displaced the aorta away from the spine. Of 12 subjects with malignancies (Group 3), six had peri-aortic retroperitoneal masses only two of whom had aortic displacement. Only 34 of 68 Group 1 subjects had peri-aortic masses characteristic of RPF, compared with six Group 2 subjects and one Group 3 subject. Subjects with characteristic retroperitoneal masses were significantly more likely to have benign disease than cancer (p = 0.009). CONCLUSION: Many patients with RPF do not have characteristic imaging findings. Contrary to prior publications, absence of aortic displacement is not seen in all patients with RPF and is seen in some cancer patients. Nonetheless, when infiltrative peri-aortic retroperitoneal soft tissue that does not displace the aorta is encountered on CT or MRI, RPF can be diagnosed with a high degree of confidence, obviating the need for biopsy.

Extensive bone erosion caused by pseudotumoral aneurysm growth.

Carotid ophthalmic aneurysms constitute 0.9-6.5% of the aneurysms of the ICA with up to 20% of the cases presenting with visual symptoms. We report a case of an adult woman, presented with chronic headaches and protracted visual alterations progressing to left eye amaurosis. Neuroradiological exams, revealed a giant partially thrombosed carotid ophthalmic aneurysm extending anteriorly, causing pseudotumoral spheno-orbital bone erosion. The patient underwent surgical clipping, evacuation of the thrombotic mass and decompression of the optic pathways with rapid recovery of the vision. This unusual case, contributes to the available body of evidence on aneurysms growth.

Endovascular Treatment of Inflammatory Infrarenal Aortic Aneurysms.

OBJECTIVES: The aim of this study was to evaluate short- and midterm outcomes of endovascular aneurysm repair in patients with inflammatory abdominal aortic aneurysm (IAAA) focusing on changes in perianeurysmal inflammation and hydronephrosis. METHODS: A retrospective study was performed considering data prospectively gathered from 1998 to 2013 in 3 centers. Patient demographics, preoperative clinical characteristics, clinical presentation, preoperative imaging measurements, procedural, and postoperative data were collected. Main outcome was to define evolution of periaortic fibrosis and hydronephrosis at computed tomography angiography (CTA) during follow-up. RESULTS: A total of 22 patients (male n = 20; mean age 70.9 years ± 9.3) were included (mean AAA diameter: 58 mm ± 11, symptomatic: 50%, ruptured: 9.1%). Hydroureteronephrosis was preoperatively diagnosed by CTA in 6 (27.3%) cases. Median clinical follow-up was 2.2 years (range 0.1-14.5). Nine patients died during follow-up. At 1, 2, 4, and 6 years, overall survival was 85.4%, 74.3%, 56.6%, and 49.5%, respectively. Among these 13 patients with CTA follow-up, the mean AAA diameter was 56.2 mm ± 15.5, and progression of sac diameter was detected in 1 (7.7%) patient. Median maximum thickness of perianeurysmal inflammation was 5 mm (range 2-11) and decreased/remained unchanged in 92.3% of patients. Regression of hydroureteronephrosis occurred in 3 of 5 patients available for follow-up. There were no cases of de novo hydroureteronephrosis. CONCLUSION: Endovascular treatment of IAAA has comparable short-term outcomes with non-IAAA. During midterm follow-up, aneurysm sac progression is rare, and perianeurysmal fibrosis decreases or remains unchanged in most cases. Hydronephrosis regression can occur in some but not all instances and thus warrants close surveillance.

Perianeurysmal edema in giant intracranial aneurysms in relation to aneurysm location, size, and partial thrombosis.

OBJECT: The underlying mechanisms causing intracranial perianeurysmal edema (PAE) are still poorly understood. Since PAE is most frequently observed in giant intracranial aneurysms (GIAs), the authors designed a study to examine the occurrence of PAE in relation to the location, size, and partial thrombosis (PT) of GIAs along with the clinical impact of PAE. METHODS: Magnetic resonance imaging data for patients with a diagnosis of unruptured GIA from the international multicenter Giant Intracranial Aneurysm Registry were retrospectively analyzed with regard to location and size of the GIA, PAE volume, and the presence of PT. The occurrence of PAE was correlated to clinical findings. RESULTS: Imaging data for 69 GIAs were eligible for inclusion in this study. Perianeurysmal edema was observed in 33.3% of all cases, with the highest frequency in GIAs of the middle cerebral artery (MCA; 68.8%) and the lowest frequency in GIAs of the cavernous internal carotid artery (ICA; 0.0%). Independent predictors of PAE formation were GIA volume (OR 1.13, p = 0.02) and the occurrence of PT (OR 9.84, p = 0.04). Giant intracranial aneurysm location did not predict PAE occurrence. Giant aneurysms with PAE were larger than GIAs without PAE (p < 0.01), and GIA volume correlated with PAE volume (rs = 0.51, p = 0.01). Perianeurysmal edema had no influence on the modified Rankin Scale score (p = 0.30 or the occurrence of aphasia (p = 0.61) or hemiparesis (p = 0.82). CONCLUSIONS: Perianeurysmal edema was associated with GIA size and the presence of PT. As no PAE was observed in cavernous ICA aneurysms, even though they exerted mass effect on the brain and also displayed PT, the dura mater may serve as a barrier protecting the brain from PAE formation.