Background: Cranial dural arteriovenous fistulas with cortical venous drainage are rare lesions that can present with hemorrhage. A high rate of rebleeding in the early period following hemorrhage has been reported, but published long-term rates are much lower. No study has examined how risk of rebleeding changes over time. Our objective was to quantify the relative incidence of rebleeding in the early and later periods following hemorrhage. Methods: Patients with dural arteriovenous fistula and cortical venous drainage presenting with hemorrhage were identified from the multinational CONDOR (Consortium for Dural Fistula Outcomes Research) database. Natural history follow-up was defined as time from hemorrhage to first treatment, rebleed, or last follow-up. Rebleeding in the first 2 weeks and first year were compared using incidence rate ratio and difference. Results: Of 1077 patients, 250 met the inclusion criteria and had 95 cumulative person-years natural history follow-up. The overall annualized rebleed rate was 7.3% (95% CI, 3.2–14.5). The incidence rate of rebleeding in the first 2 weeks was 0.0011 per person-day; an early rebleed risk of 1.6% in the first 14 days (95% CI, 0.3–5.1). For the remainder of the first year, the incidence rate was 0.00015 per person-day; a rebleed rate of 5.3% (CI, 1.7–12.4) over 1 year. The incidence rate ratio was 7.3 (95% CI, 1.4–37.7; P , 0.026). Conclusions: The risk of rebleeding of a dural arteriovenous fistula with cortical venous drainage presenting with hemorrhage is increased in the first 2 weeks justifying early treatment. However, the magnitude of this increase may be considerably lower than previously thought. Treatment within 5 days was associated with a low rate of rebleeding and appears an appropriate timeframe.
Carotid Plaques From Symptomatic Patients With Mild Stenosis Is Associated With Intraplaque Hemorrhage
Carotid plaque vulnerability features beyond the degree of stenosis may play a key role in the pathogenesis and recurrence of ischemic cerebrovascular events. This study sought to compare intraplaque hemorrhage (IPH) as a marker of plaque vulnerability in symptomatic patients with mild (<50%), moderate (50%–69%), and severe (≥70%) carotid artery stenosis. We included patients who experienced ischemic cerebrovascular events with no other identifiable sources and underwent carotid endarterectomy for mild (n=32), moderate (n=47), and severe (n=58) carotid artery stenosis. The degree of stenosis and imaging hallmarks were assessed by computed tomography angiography or magnetic resonance angiography. Plaque specimens were stained with hematoxylin and eosin and Movat pentachrome staining. Carotid plaques of patients with mild stenosis had a higher extent of IPH (%) on tissue analysis compared with patients with moderate (mild, 15.7% [interquartile range, 7.8%–26.7%]; moderate, 3.9% [0.0%–9.2%]; P <0.001) and severe carotid artery stenosis (mild, 15.7% [interquartile range, 7.8%–26.7%]; severe, 2.5% [interquartile range, 0.0%–11.2%]; P <0.001). When considering the degree of carotid artery stenosis as a continuous variable, a lower lumen narrowing was associated with higher extent of IPH ( P <0.001; R, −0.329). Our major finding is the association of IPH with mild carotid artery stenosis based on histological analysis. The current study may suggest that IPH potentially plays a role in the mechanism of stroke in patients with nonobstructive carotid stenosis.
Carotid Artery Plaque Calcifications: Lessons From Histopathology to Diagnostic Imaging
The role of calcium in atherosclerosis is controversial and the relationship between vascular calcification and plaque vulnerability is not fully understood. Although calcifications are present in ≈50% to 60% of carotid plaques, their association with cerebrovascular ischemic events remains unclear. In this review, we summarize current understanding of carotid plaque calcification. We outline the role of calcium in atherosclerotic carotid disease by analyzing laboratory studies and histopathologic studies, as well as imaging findings to understand clinical implications of carotid artery calcifications. Differences in mechanism of calcium deposition express themselves into a wide range of calcification phenotypes in carotid plaques. Some patterns, such as rim calcification, are suggestive of plaques with inflammatory activity with leakage of the vasa vasourm and intraplaque hemorrhage. Other patterns such as dense, nodular calcifications may confer greater mechanical stability to the plaque and reduce the risk of embolization for a given degree of plaque size and luminal stenosis. Various distributions and patterns of carotid plaque calcification, often influenced by the underlying systemic pathological condition, have a different role in affecting plaque stability. Modern imaging techniques afford multiple approaches to assess geometry, pattern of distribution, size, and composition of carotid artery calcifications. Future investigations with these novel technologies will further improve our understanding of carotid artery calcification and will play an important role in understanding and minimizing stroke risk in patients with carotid plaques.
Flow Diversion for Middle Cerebral Artery Aneurysms: An International Cohort Study
Abstract BACKGROUND Open surgery has traditionally been preferred for the management of bifurcation middle cerebral artery (MCA) aneurysms. Flow diverting stents present a novel endovascular strategy for aneurysm treatment. OBJECTIVE To add to the limited literature describing the outcomes and complications in the use of flow diverters for the treatment of these complex aneurysms. METHODS This is a multicenter retrospective review of MCA bifurcation aneurysms undergoing flow diversion. We assessed post-treatment radiological outcomes and both thromboembolic and hemorrhagic complications. RESULTS We reviewed the outcomes of 54 aneurysms treated with flow diversion. Four (7.4%) of the aneurysms had a history of rupture (3 remote and 1 acute). Fourteen (25.9%) of the aneurysms already underwent either open surgery or coiling prior to flow diversion. A total of 36 out of the 45 aneurysms (80%) with available follow-up data had adequate aneurysm occlusion with a median follow-up time of 12 mo. There were no hemorrhagic complications but 16.7% (9/54) had thromboembolic complications. CONCLUSION Flow diverting stents may be a viable option for the endovascular treatment of complex bifurcation MCA aneurysms. However, compared to published series on the open surgical treatment of this subset of aneurysms, flow diversion has inferior outcomes and are associated with a higher rate of complications.
Outcome Following Hemorrhage From Cranial Dural Arteriovenous Fistulae
Background and Purpose: Dural arteriovenous fistulae can present with hemorrhage, but there remains a paucity of data regarding subsequent outcomes. We sought to use the CONDOR (Consortium for Dural Arteriovenous Fistula Outcomes Research), a multi-institutional registry, to characterize the morbidity and mortality of dural arteriovenous fistula–related hemorrhage. Methods: A retrospective review of patients in CONDOR who presented with dural arteriovenous fistula–related hemorrhage was performed. Patient characteristics, clinical follow-up, and radiographic details were analyzed for associations with poor outcome (defined as modified Rankin Scale score ≥3). Results: The CONDOR dataset yielded 262 patients with incident hemorrhage, with median follow-up of 1.4 years. Poor outcome was observed in 17.0% (95% CI, 12.3%–21.7%) at follow-up, including a 3.6% (95% CI, 1.3%–6.0%) mortality. Age and anticoagulant use were associated with poor outcome on multivariable analysis (odds ratio, 1.04, odds ratio, 5.1 respectively). Subtype of hemorrhage and venous shunting pattern of the lesion did not affect outcome significantly. Conclusions: Within the CONDOR registry, dural arteriovenous fistula–related hemorrhage was associated with a relatively lower morbidity and mortality than published outcomes from other arterialized cerebrovascular lesions but still at clinically consequential rates.
Venous Causes of Pulsatile Tinnitus: Clinical Presentation, Clinical and Radiographic Evaluation, Pathogenesis, and Endovascular Treatments: A Literature Review
Abstract Tinnitus is an abnormal perception of a sound without external stimulation. Venous pulsatile tinnitus (VPT) is a specific form of tinnitus characterized by an objective and often subjective bruit that occurs as a result of localized venous abnormalities. Clinical evaluation relies on sound quality, duration, and precipitating factors. Idiopathic intracranial hypertension (IIH) and transverse sinus stenosis (TSS) are among the most common causes of VPT. Other causes include sigmoid sinus wall abnormalities (SSWAs), jugular vein anomalies (JVAs), and emissary veins anomalies. These anomalies can be detected on magnetic resonance imaging, magnetic resonance angiography/magnetic resonance venography, and high-resolution temporal bone computed tomography. The pathogenesis behind the VPT includes turbulent blood flow as a result of luminal stenosis or abnormal dilation, amplification of internal sound due to temporal bone defects, and abnormal position of the venous sinus system structures adjacent to the bony structures of the auditive apparatus. Based on these theories, different interventional treatment modalities can be applied to treat the underlying causes. Endovascular treatments have shown high efficacy and safety among those treatments which include stenting of the lateral sinus stenosis in IIH and TSS, coiling of the SSWA and JVA, and embolization of emissary veins anomalies. Further studies are needed to understand the natural history of these anomalies and the efficacy of treatments of VPT, which—unlike other types of tinnitus—can be cured with proper treatment.
Background and Purpose: Pregnancy as a hemorrhage risk factor in women with cavernous malformations (CMs) is controversial. We describe prospective hemorrhage risk in women who become pregnant after an established CM diagnosis. Methods: Beginning in 2015, we recruited consecutive patients with radiologically confirmed CM of the brain or spinal cord to participate in a prospective registry. Participants underwent a baseline and annual medical record review, imaging review, and annual surveys to ascertain pregnancies, deliveries, and neurological complications. We collected prospective hemorrhage data on reproductive age women. We calculated prospective hemorrhage rates on childbearing age patients based on the number of hemorrhages occurring post-CM diagnosis during pregnancy and nonpregnancy, divided by the years of follow-up and censored at last follow-up, age 46, or surgery in sporadic-form CM. The hemorrhage rates were compared and the 95% CI presented with a P value of <0.05. Results: Of 160 women, 90 presented with CM under the age of 46 (average age 31.6 years; 25.6% familial form; 46.7% with hemorrhage; 24.4% brain stem location). These 90 patients had 136 pregnancies before CM diagnosis; 36 pregnancies occurred at or after the diagnosis of CM. Four patients had a hemorrhage while pregnant or postpartum leading to the first CM diagnosis. During 402.6 years of follow-up while not pregnant, 42 hemorrhages occurred prospectively yielding a 10.4% per year (95% CI, 7.5–14.0) risk of hemorrhage while not pregnant. No hemorrhages occurred during 32 prospective pregnancies (26 live births including 1 twinset and 7 nonviable fetuses) after CM diagnosis during 26.9 years of pregnancy time yielding a rate of 0% per year (95% CI, 0–13.6). We found no statistical difference in the rates of hemorrhage during pregnant and nonpregnant time ( P =0.09). No hemorrhage occurred during delivery. Conclusions: Our prospective data suggest that pregnancy does not increase the risk of hemorrhage in women with a known brain or spinal cord CM and that vaginal delivery is safe in appropriate candidates.
Clinical Reasoning: 63-Year-old woman with thoracic cavernous malformation and delayed worsening myelopathy