Long-term follow-up studies in patients with brain arteriovenous malformations (AVM) have yielded contradictory results regarding both risk factors for rupture and annual rupture rate. We performed a ...long-term follow-up study in an unselected, consecutive patient population with AVMs admitted to the Department of Neurosurgery at Helsinki University Central Hospital between 1942 and 2005.
Patients with untreated AVMs were followed from admission until death, occurrence of AVM rupture, initiation of treatment, or until the end of 2005. Patients with at least 1 month of follow-up were included in further analysis. Annual and cumulative incidence rates of AVM rupture as well as several potential risk factors for rupture were analyzed using Kaplan-Meier life table analyses and Cox proportional hazards regression models.
We identified 238 patients with a mean follow-up period of 13.5 years (range, 1 month-53.1 years). The average annual risk of hemorrhage from AVMs was 2.4%. The risk was highest during the first 5 years after diagnosis, decreasing thereafter. Risk factors predicting subsequent AVM hemorrhage in univariate analysis were young age, previous rupture, deep and infratentorial locations, and exclusively deep venous drainage. Previous rupture, large AVM size, and infratentorial and deep locations were independent risk factors according to multivariate models.
According to this long-term follow-up study, AVMs with previous rupture and large size, as well as with infratentorial and deep locations have the highest risk of subsequent hemorrhage. This risk is highest during the first few years after diagnosis but remains significant for decades.
Saccular intracranial aneurysms (sIA) are pouch-like pathological dilatations of intracranial arteries that develop when the cerebral artery wall becomes too weak to resist hemodynamic pressure and ...distends. Some sIAs remain stable over time, but in others mural cells die, the matrix degenerates, and eventually the wall ruptures, causing life-threatening hemorrhage. The wall of unruptured sIAs is characterized by myointimal hyperplasia and organizing thrombus, whereas that of ruptured sIAs is characterized by a decellularized, degenerated matrix and a poorly organized luminal thrombus. Cell-mediated and humoral inflammatory reaction is seen in both, but inflammation is clearly associated with degenerated and ruptured walls. Inflammation, however, seems to be a reaction to the ongoing degenerative processes, rather than the cause. Current data suggest that the loss of mural cells and wall degeneration are related to impaired endothelial function and high oxidative stress, caused in part by luminal thrombosis. The aberrant flow conditions caused by sIA geometry are the likely cause of the endothelial dysfunction, which results in accumulation of cytotoxic and pro-inflammatory substances into the sIA wall, as well as thrombus formation. This may start the processes that eventually can lead to the decellularized and degenerated sIA wall that is prone to rupture.
Rupture of a saccular intracranial artery aneurysm (IA) causes subarachnoid hemorrhage, a significant cause of stroke and death. The current treatment options, endovascular coiling and clipping, are ...invasive and somewhat risky. Since only some IAs rupture, those IAs at risk for rupture should be identified. However, to improve the imaging of rupture-prone IAs and improve IA treatment, IA wall pathobiology requires more thorough knowledge. Chronic inflammation has become understood as an important phenomenon in IA wall pathobiology, featuring inflammatory cell infiltration as well as proliferative and fibrotic remodulatory responses. We review the literature on what is known about inflammation in the IA wall and also review the probable mechanisms of how inflammation would result in the degenerative changes that ultimately lead to IA wall rupture. We also discuss current options in imaging inflammation and how knowledge of inflammation in IA walls may improve IA treatment.
Prospective studies on the risk factors for subarachnoid hemorrhage (SAH) are limited. Moreover, the effect of risk factors on the incidence rates of SAH is not well known about.
In this study, we ...aimed to identify risk factors for SAH and characterize subgroups in a population with a high incidence of SAH.
After recording multiple potential risk factors for SAH at the time of enrollment, first ever SAH events between 1972 and 2009 were recorded through the nationwide Causes of Death Register and Hospital Discharge Register for the population-based cohort of 64 349 participants, who participated in the National FINRISK Study between 1972 and 2007 in Finland.
During the follow-up time of 1.26 million person-years (median 17.9 years, range 0 to 37.9 years), 437 persons experienced fatal or non-fatal SAH. Crude SAH incidence was 34.8 (95% confidence interval: 31.7-38.2) per 100 000 person-years among ≥ 25-year-old persons. Female sex, high blood pressure values and current smoking were confirmed as risk factors for SAH. Previous myocardial infarction, history of premature stroke (any kind) in mother and elevated cholesterol levels in men were identified as new risk factors for SAH. Depending on the combination of risk factors, SAH incidence varied between 8 and 171 per 100 000 person-years.
New and previously reported risk factors appear to have a much stronger association with the incidence of SAH than is ordinarily seen in cardiovascular diseases. Risk factor assessments may facilitate the identification of high-risk persons who should be the focus of preventive interventions.
Introduction
Brain arteriovenous malformation (bAVM) might have a higher risk of rupture after partial embolization, and previous studies have shown that some metrics of vascular stability are ...related to bAVM rupture risk.
Objective
To analyze vascular stability of bAVM in patients after partial embolization.
Methods
Twenty‐four patients who underwent partial embolization were classified into the short‐term, medium‐term, and long‐term groups, according to the time interval between partial embolization and surgery. The control group consisted of 9 bAVM patients who underwent surgery alone. Hemodynamic changes after partial embolization were measured by angiogram. The inflammatory infiltrates and cell–cell junctions were evaluated by MMP‐9 and VE‐cadherin. At the protein level, the proliferative and apoptotic events of bAVMs were analyzed by immunohistochemical staining of VEGFA, eNOS, and caspase‐3. Finally, neovascularity and apoptotic cells were assessed by CD31 staining and TUNEL staining.
Results
Immediately after partial embolization, the blood flow velocity of most bAVMs increased. The quantity of MMP‐9 in the medium‐term group was the highest, and VE‐cadherin in the medium‐term group was the lowest. The expression levels of VEGFA, eNOS, and neovascularity were highest in the medium‐term group. Similarly, the expression level of caspase‐3 and the number of apoptotic cells were highest in the medium‐term group.
Conclusion
The biomarkers for bAVM vascular stability were most abnormal between 1 and 28 days after partial embolization.
Partial embolization plays a vital role in the management of bAVM. However, the optimal interval between nidal resection and preoperative adjuvant partial embolization in bAVM patients is still controversial. In addition, the prognostic impact of partial embolization on patients with bAVM has not been established. Our study is the first to systematically describe the changes in vascular stability biomarkers of bAVM after partial embolization. We provide the first evidence that these vascular stability‐related indexes are dynamic, varying with the time between embolization and resection. And, we first find that the biomarkers for bAVM vascular stability were most abnormal between 1 and 28 days after partial embolization. This may be a plausible explanation for the highest risk of rupture in the relatively early period after partial embolization in patients with bAVMs. Based on our results, we first provide a molecular biology level of evidence that support the viewpoint that resection surgery after partial embolization of bAVM patients should be performed early to avoid the high rupture risk period after partial embolization.
The lateral supraorbital (LSO) approach is a minimally invasive craniotomy widely used in the surgical treatment of intracranial aneurysms (IAs). A protective bypass is considered a safety measure in ...high-risk and complex clipping procedures to maintain distal cerebral flow. However, the protective bypass has so far only been applied through a pterional or larger craniotomy. We aimed to describe the characteristics of the superficial temporal artery to middle cerebral artery (STA-MCA) bypass through the LSO craniotomy to treat complex IAs.
We retrospectively identified six patients with complex IAs who underwent clipping and a protective STA-MCA bypass through the LSO approach between January 2016 and December 2020. The STA donor artery was harvested through the same curvilinear skin incision with a small extension, and it was anastomosed to the opercular segment of the MCA. Subsequently, aneurysm clipping followed standardized steps.
Anastomosis was successful in all patients. Despite requiring temporary occlusion of the parent artery, all aneurysms were successfully clipped without any neurological deterioration.
A protective STA-MCA bypass is feasible through the LSO approach with certain technical modifications. This technique helps protect distal cerebral flow for safe clip placement in the treatment of complex IAs with the associated benefits of a less invasive craniotomy.
•This study highlights the application of protective bypass through the lateral supraorbital craniotomy.•We present the characteristics of the procedure and delineate the technical aspects.•All bypass grafts were successfully anastomosed in our case series of complex intracranial aneurysms.•STA-MCA bypass is feasible through the lateral supraorbital approach with certain technical modifications.
Background and purpose
Moyamoya angiopathy (MMA) is a chronic progressive disorder, but imaging changes observed over time are not yet characterized in European populations. We analyzed the ...progression of MMA with magnetic resonance imaging and angiography (MRI and MRA) in our Finnish MMA registry. Stage classification based on MRA findings was used to evaluate the progress of the disease.
Methods
32 patients with MMA were evaluated with MRI and MRA and compared to previous imaging. The follow-up imaging was done 103 (range 6–380) months after the MMA diagnosis, and 64 (range 6–270) months after the previous imaging. We graded the disease stage according to the previously described MRA grading scale.
Results
No acute lesions, including silent ischemic strokes were found in the follow-up image compared to latest available previous image. One patient had an asymptomatic intracerebral hemorrhage since the last imaging. Ivy sign was observed in 22% of the patients in the follow-up image. Six percent (
n
= 2) had microhemorrhages and 9% (
n
= 3) white matter lesions in the follow-up imaging. The MRA grade was evaluated from the follow-up images and it was 3 and 2.5 points (right and left, respectively). Fifty-six percent (
n
= 18) had old ischemic lesions in the follow-up image. Majority (71%) of the old ischemic lesions were large anterior circulation infarcts.
Conclusions
A slow progression of MMA-related changes on MRI/MRA was found, being in line with our previous reports suggesting a rather benign course of the disease in the Finnish population.
Saccular intracranial aneurysm (sIA) aneurysm causes intracranial hemorrhages that are associated with high mortality. Lipid accumulation and chronic inflammation occur in the sIA wall. A major ...mechanism for lipid clearance from arteries is adenosine triphosphate-binding cassette A1 (ABCA1)-mediated lipid efflux from foam cells to apolipoprotein A-I (apoA-I). We investigated the association of wall degeneration, inflammation, and lipid-related parameters in tissue samples of 16 unruptured and 20 ruptured sIAs using histology and immunohistochemistry. Intracellular lipid accumulation was associated with wall remodeling (p = 0.005) and rupture (p = 0.020). Foam cell formation was observed in smooth muscle cells, in addition to CD68- and CD163-positive macrophages. Macrophage infiltration correlated with intracellular lipid accumulation and apolipoproteins, including apoA-I. ApoA-I correlated with markers of lipid accumulation and wall degeneration (p = 0.01). ApoA-I-positive staining colocalized with ABCA1-positive cells particularly in sIAs with high number of smooth muscle cells (p = 0.003); absence of such colocalization was associated with wall degeneration (p = 0.017). Known clinical risk factors for sIA rupture correlated inversely with apoA-I. We conclude that lipid accumulation associates with sIA wall degeneration and risk of rupture, possibly via formation of foam cells and subsequent loss of mural cells. Reduced removal of lipids from the sIA wall via ABCA1-apoA-I pathway may contribute to this process.
Arteriovenous malformations (AVMs) of the brain are relatively rare congenital developmental vascular lesions. They may cause hemorrhagic stroke, epilepsy, chronic headache, or focal neurologic ...deficits, and the incidence of asymptomatic AVMs is increasing due to widespread availability of noninvasive imaging methods. Since the most severe complication of an AVM is hemorrhagic stroke, most epidemiologic studies have concentrated on the hemorrhage risk and its risk factors. In this article, the authors discuss the epidemiology, presenting symptoms, and hemorrhage risk associated with brain AVMs.
The object of this study was to evaluate cases of subarachnoid hemorrhage (SAH) from ruptured blood blister-like aneurysms (BBAs) of the internal carotid artery (ICA) trunk.
The authors performed a ...single-center, retrospective study. Data analyzed were patient age, sex, Hunt and Hess grade, Fisher grade, time from SAH to hospitalization, aneurysm size and location, collateral capacity of the circle of Willis, time from hospitalization to aneurysm repair, type of aneurysm repair, complications, and Glasgow Outcome Scale (GOS) score at follow-up.
A total of 211 patients suffered SAH from ICA aneurysms. Of these, 14 patients (6.6%) had ICA trunk BBAs; 6 men and 8 women. The median age was 47.8 years (range 29.9-67.7 years). The Hunt and Hess grade was IV or V in 7 cases, and SAH was Fisher Grade 3 + 4 in 6. All aneurysms were small (< 1 cm), without relation to vessel bifurcations, and usually located anteromedially on the ICA trunk. Three patients were treated with coil placement and 11 with clip placement. Of the 7 patients in whom the ICA was preserved, only 1 had poor outcome (GOS Score 2). In contrast, cerebral infarcts developed in all patients treated with ICA sacrifice, directly postoperatively in 2 and after delay in 5. Six patients died, 1 survived in poor condition (GOS Score 3; p < 0.001).
Internal carotid BBAs are rare, small, and difficult to treat endovascularly, with only 2 of 14 patients successfully treated with coil placement. The BBAs rupture easily during surgery (ruptured in 6 of 11 surgical cases). Intraoperative aneurysm rupture invariably led to ICA trap ligation. Sacrifice of the ICA within 48 hours of an SAH led to very poor outcome, even in patients with adequate collateral capacity on preoperative angiograms, probably because of vasospasm-induced compromise of the cerebral collaterals.
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