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Intracranial aneurysm (IA) is a common cerebrovascular disease in which sacral aneurysms occurring in the Wills ring region can lead to devastating subarachnoid hemorrhage. Despite advances in research, the underlying mechanisms of IA formation and rupture remain incompletely understood, hindering early diagnosis and effective treatment. This review comprehensively summarizes the current landscape of IA biomarkers, encompassing genetic markers, DNA, RNA, inflammatory molecules, oxidative stress proteins, and extracellular matrix (ECM) components. Accumulating evidence suggests that various biomarkers are associated with different stages of IA pathogenesis, including initiation, progression, and rupture. Aberrant ECM composition and remodeling have been observed in IA patients, and extracellular matrix-degrading enzymes are implicated in IA growth and rupture. Biomarker research in IA holds great potential for improving clinical outcomes. Future studies should focus on validating the existing biomarkers, identifying novel ones, and investigating their underlying mechanisms to facilitate the development of personalized preventive and therapeutic strategies for IA.

BackgroundUnruptured intracranial aneurysms (UIAs) are increasingly diagnosed and are commonly treated using endovascular treatment or microsurgical clipping. The safety and efficacy of treatments have not been compared in a randomised trial. How to treat patients with UIAs suitable for both options remains unknown.MethodsWe randomly allocated clipping or coiling to patients with one or more 3–25 mm UIAs judged treatable both ways. The primary outcome was treatment failure, defined as: initial failure of aneurysm treatment, intracranial haemorrhage or residual aneurysm on 1-year imaging. Secondary outcomes included neurological deficits following treatment, hospitalisation >5 days, overall morbidity and mortality and angiographic results at 1 year.ResultsThe trial was designed to include 260 patients. An analysis was performed for slow accrual: 136 patients were enrolled from 2010 through 2016 and 134 patients were treated. The 1-year primary outcome, available for 104 patients, was reached in 5/48 (10.4% (4.5%–22.2%)) patients allocated surgical clipping, and 10/56 (17.9% (10.0%–29.8%)) patients allocated endovascular coiling (OR: 0.54 (0.13–1.90), p=0.40). Morbidity and mortality (modified Rankin Scale>2) at 1 year occurred in 2/48 (4.2% (1.2%–14.0%)) and 2/56 (3.6% (1.0%–12.1%)) patients allocated clipping and coiling, respectively. New neurological deficits (15/65 vs 6/69; OR: 3.12 (1.05–10.57), p=0.031), and hospitalisations beyond 5 days (30/65 vs 6/69; OR: 8.85 (3.22–28.59), p=0.0001) were more frequent after clipping.ConclusionSurgical clipping or endovascular coiling of UIAs did not show differences in morbidity at 1 year. Trial continuation and additional randomised evidence will be necessary to establish the supposed superior efficacy of clipping.

The evolution of imaging techniques and their increased use in clinical practice have led to a higher detection rate of unruptured intracranial aneurysms. The diagnosis of an unruptured intracranial aneurysm is a source of significant stress to the patient because of the concerns for aneurysmal rupture, which is associated with substantial rates of morbidity and mortality. Therefore, it is important that decisions regarding optimum management are made based on the comparison of the risk of aneurysmal rupture with the risk associated with intervention. This review provides a comprehensive overview of the epidemiology, pathophysiology, natural history, clinical presentation, diagnosis, and management options for unruptured intracranial aneurysms based on the current evidence in the literature. Furthermore, the authors discuss the genetic abnormalities associated with intracranial aneurysm and current guidelines for screening in patients with a family history of intracranial aneurysms. Since there is significant controversy in the optimum management of small unruptured intracranial aneurysms, we provided a systematic approach to their management based on patient and aneurysm characteristics as well as the risks and benefits of intervention.

Abstract Flow diverters have drastically changed the landscape of intracranial aneurysm treatment and are now considered first-line therapy for select lesions. Their mechanism of action relies on intrinsic alteration in hemodynamic parameters, both at the parent artery and within the aneurysm sac. Moreover, the device struts act as a nidus for endothelial cell growth across the aneurysm neck ultimately leading to aneurysm exclusion from the circulation. In silico computational analyses and investigations in preclinical animal models have provided valuable insights into the underlying biological basis for flow diverter therapy. Here, we review the present understanding pertaining to flow diverter biology and mechanisms of action, focusing on stent design, induction of intra-aneurysmal thrombosis, endothelialization, and alterations in hemodynamics.

Hemorrhage from a recurrent aneurysm is a major concern after coiling for intracranial aneurysms. We aimed to identify aneurysm recurrence patterns associated with hemorrhage. We investigated radiological data of patients who underwent coiling for intracranial aneurysms in 2008-2016 and were followed-up for at least 6 months. Aneurysm recurrence patterns were classified as: type Ⅰ, enlargement of aneurysm neck; type Ⅱ, recurrent cavity within the coil mass; type Ⅲ, recurrent cavity along the aneurysm wall; and type Ⅳ, formation of a daughter sac. We evaluated the incidence of various recurrence patterns with or without hemorrhage. Of the 173 aneurysms included in the study (mean follow-up period, 32 months; range, 6-99 months), 22 (13%) recurred and required re-treatment. The recurrence patterns included type Ⅰ, Ⅱ, Ⅲ, and Ⅳ in 7 (4%), 4 (2%), 9 (5%), and 2 (1%) cases, respectively. Most of the type Ⅰ, Ⅱ, and Ⅲ recurrences occurred within 1 year, and type Ⅳ occurred at 7 years after coiling. Three aneurysms exhibited hemorrhage, one with type Ⅲ and two with type Ⅳ pattern. The two aneurysms with type Ⅳ recurrence initially occurred as type Ⅰ; however, the recurrent neck enlarged gradually, resulting in new sac formation. We recommend prompt re-treatment for aneurysms recurring with type Ⅲ or Ⅳ patterns, as such patterns were associated with hemorrhage. Furthermore, we need a special care to type Ⅰ recurrence with enlargement of recurrent neck because this specific pattern may develop to type Ⅳ.

Aneurysmal subarachnoid hemorrhage is diagnosed by computed tomography of the head and by CT angiography, catheter angiography, or both. Randomized trials suggest that aneurysms treatable by either open surgery or endovascular intervention are usually better treated by the latter.

Intracranial aneurysms (IA) are local dilatations in cerebral arteries that predominantly affect the circle of Willis. Occurring in approximately 2–5% of adults, these weakened areas are susceptible to rupture, leading to subarachnoid hemorrhage (SAH), a type of hemorrhagic stroke. Due to its early age of onset and poor prognosis, SAH accounts for > 25% of years lost for all stroke victims under the age of 65. In this review, we describe the cerebrovascular pathology associated with intracranial aneurysms. To understand IA genetics, we summarize syndromes with elevated incidence, genome-wide association studies (GWAS), whole exome studies on IA-affected families, and recent research that established definitive roles for Thsd1 (Thrombospondin Type 1 Domain Containing Protein 1) and Sox17 (SRY-box 17) in IA using genetically engineered mouse models. Lastly, we discuss the underlying molecular mechanisms of IA, including defects in vascular endothelial and smooth muscle cells caused by dysfunction in mechanotransduction, Thsd1/FAK (Focal Adhesion Kinase) signaling, and the Transforming Growth Factor β (TGF-β) pathway. As illustrated by THSD1 research, cell adhesion may play a significant role in IA.

Background: Intracranial aneurysm with and without subarachnoid haemorrhage (SAH) is a relevant health problem: The overall incidence is about 9 per 100,000 with a wide range, in some countries up to 20 per 100,000. Mortality rate with conservative treatment within the first months is 50–60%. About one third of patients left with an untreated aneurysm will die from recurrent bleeding within 6 months after recovering from the first bleeding. The prognosis is further influenced by vasospasm, hydrocephalus, delayed ischaemic deficit and other complications. The aim of these guidelines is to provide comprehensive recommendations on the management of SAH with and without aneurysm as well as on unruptured intracranial aneurysm. Methods: We performed an extensive literature search from 1960 to 2011 using Medline and Embase. Members of the writing group met in person and by teleconferences to discuss recommendations. Search results were graded according to the criteria of the European Federation of Neurological Societies. Members of the Guidelines Committee of the European Stroke Organization reviewed the guidelines. Results: These guidelines provide evidence-based information on epidemiology, risk factors and prognosis of SAH and recommendations on diagnostic and therapeutic methods of both ruptured and unruptured intracranial aneurysms. Several risk factors of aneurysm growth and rupture have been identified. We provide recommendations on diagnostic work up, monitoring and general management (blood pressure, blood glucose, temperature, thromboprophylaxis, antiepileptic treatment, use of steroids). Specific therapeutic interventions consider timing of procedures, clipping and coiling. Complications such as hydrocephalus, vasospasm and delayed ischaemic deficit were covered. We also thought to add recommendations on SAH without aneurysm and on unruptured aneurysms. Conclusion: Ruptured intracranial aneurysm with a high rate of subsequent complications is a serious disease needing prompt treatment in centres having high quality of experience of treatment for these patients. These guidelines provide practical, evidence-based advice for the management of patients with intracranial aneurysm with or without rupture. Applying these measures can improve the prognosis of SAH.

A 15-month-old infant presented with an episode of acute agitation, characterized by crying, refusal to feed, and a focal seizure involving the left arm and leg lasting 1–2 min. Following the seizure, the infant fell asleep but experienced another brief seizure during transport to the hospital. Initial assessment at a private hospital in Mersin, Turkey, led to a referral to our center, where imaging revealed an intraparenchymal hemorrhage in the left frontobasal region. The hemorrhage extended into all ventricles and the right retrosellar area, with notable rightward shift and ventricular enlargement. CTA confirmed a ruptured Acom aneurysm with a bleb. Diagnostic angiography was performed, and an endovascular stent coiling procedure was performed without hematoma evacuation. At 1-year follow-up, patients' symptoms improved without neurological sequelae, and MR angiography revealed no residual filling in the aneurysm.