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Spontaneous intracranial artery dissection is an uncommon and probably underdiagnosed cause of stroke that is defined by the occurrence of a haematoma in the wall of an intracranial artery. Patients can present with headache, ischaemic stroke, subarachnoid haemorrhage, or symptoms associated with mass effect, mostly on the brainstem. Although intracranial artery dissection is less common than cervical artery dissection in adults of European ethnic origin, intracranial artery dissection is reportedly more common in children and in Asian populations. Risk factors and mechanisms are poorly understood, and diagnosis is challenging because characteristic imaging features can be difficult to detect in view of the small size of intracranial arteries. Therefore, multimodal follow-up imaging is often needed to confirm the diagnosis. Treatment of intracranial artery dissections is empirical in the absence of data from randomised controlled trials. Most patients with subarachnoid haemorrhage undergo surgical or endovascular treatment to prevent rebleeding, whereas patients with intracranial artery dissection and cerebral ischaemia are treated with antithrombotics. Prognosis seems worse in patients with subarachnoid haemorrhage than in those without.

Up to 12% of patients with stroke have intracranial arterial dolichoectasia (IADE) and the basilar artery is affected in 80% of these cases. Diagnostic criteria and prognosis studies of IADE are based on basilar artery diameter, which is a good quantitative marker for the severity of the disease. The pathophysiology is largely unknown, but IADE can be viewed as a common final pathway of arterial wall response or damage in the tunica media due to various mechanisms, such as matrix metalloproteinase dysfunction or muscle cell or elastic fibre injury. No randomised controlled trials have been undertaken in IADE and thus little high-level evidence is available on which to base treatment guidelines. IADE management depends on clinical presentation and disease severity, and includes blood pressure control, antithrombotic treatments, endovascular procedures, and surgery. Further studies are needed to better define IADE in the general population, to establish its prevalence and pathophysiology, to identify subgroups at risk of life-threatening complications, and to offer effective treatment options.

Stroke occurs across the lifespan with unique issues in the fetus, neonate, and child. The past decade has seen substantial advances in paediatric stroke research and clinical care, but many unanswered questions and controversies remain. The pathobiology of perinatal stroke needs to be better understood if prevention strategies are to be realised. Similarly, enhanced understanding of the mechanisms underlying childhood stroke, including cerebral arteriopathies, could inform the development of mechanism-specific treatments. Emerging clinical trials, including studies of neonatal sinovenous thrombosis and childhood arterial stroke, offer the hope of evidence-based treatment options in the near future. Early recognition of stroke in children is a key educational target for both the public and health-care professionals, and has translational potential to advance the application of neuroprotective, thrombolytic, and antithrombotic interventions and rehabilitation strategies to the earliest possible timepoints after stroke onset, improving outcomes and quality of life for affected children and their families.

Lacunar lesions (LLs) and white matter lesions (WMLs) affect cognition. We assessed whether lesions located in specific white matter tracts were associated with cognitive performance taking into account total lesion burden. Within the Second Manifestations of ARTerial disease Magnetic Resonance (SMART-MR) study, cross-sectional analyses were performed on 516 patients with manifest arterial disease. We applied an assumption-free voxel-based lesion-symptom mapping approach to investigate the relation between LL and WML locations on 1.5 Tesla brain MRI and compound scores of executive functioning, memory and processing speed. Secondly, a multivariable linear regression model was used to relate the regional volume of LLs and WMLs within specific white matter tracts to cognitive functioning. Voxel-based lesion-symptom mapping identified several clusters of voxels with a significant correlation between WMLs and executive functioning, mostly located within the superior longitudinal fasciculus and anterior thalamic radiation. In the multivariable linear regression model, a statistically significant association was found between regional LL volume within the superior longitudinal fasciculus and anterior thalamic radiation and executive functioning after adjustment for total LL and WML burden. These findings identify the superior longitudinal fasciculus and anterior thalamic radiation as key anatomical structures in executive functioning and emphasize the role of strategically located vascular lesions in vascular cognitive impairment.

Intracranial arterial stenosis (ICAS) is the predominant cause of ischemic stroke and transient ischemic attack in Asia. Change of signal intensities (SI) across an ICAS on magnetic resonance angiography (MRA) may reflect its hemodynamic severity. In-patients with a symptomatic single ICAS detected on 3D time-of-flight MRA were recruited from 2 hospitals. Baseline and 1-year follow-up data were collected. Signal intensity ratio (SIR) [ =  (mean post-stenotic SI -mean background SI)/(mean pre-stenotic SI - mean background SI)] was evaluated on baseline MRA to represent change of SIs across an ICAS. Acute infarct volume was measured on baseline diffusion-weighted images (DWI). Relationships between SIR and baseline characteristics as well as 1y outcomes were evaluated. Thirty-six subjects (86.1% males, mean age 55.0) were recruited. Overall, mean SIR was 0.84±0.23. Mean SIRs were not significantly different between the 23 (63.9%) anatomically severe stenoses and the 13 (36.1%) anatomically moderate stenoses (0.80±0.23 versus 0.92±0.21, p = 0.126). SIR was significantly, linearly and negatively correlated to acute infarct volume on DWI (Spearman correlation coefficient -0.471, p = 0.011). Two patients (5.6%) had recurrent ischemic strokes at 1y, not related to SIR values. Change of signal intensities across an ICAS on MRA may reflect its hemodynamic and functional severity. Future studies are warranted to further verify the relationships between this index and prognosis of patients with symptomatic ICAS.

Purpose The features of intracranial arterial injury in tuberculous meningitis (TBM) are of important diagnostic and prognostic value. The study aimed to elucidate the high-resolution vessel wall imaging (HR-VWI) manifestations of intracranial arterial insults in TBM. Methods The clinical data, routine cranial magnetic resonance imaging, magnetic resonance angiography (MRA) and HR-VWI before and after contrast enhancement of intracranial arteries in clinically diagnosed TBM patients were retrospectively analyzed. Results In this study 27 TBM patients were included. Abnormalities in the intracranial arteries were detected in all patients using HR-VWI. Typical vessel insults included nodular or granular lesions, related thickness and prominent enhancement in the wall, and lumen narrowing or occlusion. The most frequently involved arteries were the C4 segment of the internal carotid artery and the P1 segment of the posterior cerebral artery. The lesions were consistent with disease stage and disease duration and correlated with infarction. Conclusion The use of HR-VWI revealed that cerebral artery involvement in patients with TBM is much more common and extensive than in previous radiological reports. The use of HR-VWI improves recognition of arterial pathologies and has diagnostic value in patients with TBM.

Abstract BACKGROUND: The limitations of the medical management of symptomatic intracranial arterial stenosis encourage the development of new therapeutic strategies such as intracranial stenting. OBJECTIVE: To report and analyze the results of a series of 42 patients treated with 3 different endovascular techniques: isolated angioplasty, balloon-expandable coronary stents, and the Wingspan self-expandable intracranial stent system. METHODS: Forty-two patients presenting with symptomatic intracranial arterial stenosis were treated with one of these techniques. Computed tomography angiography was performed 6 months after the procedure, and the clinical neurological statuses were categorized using the modified Rankin Scale and the National Institutes of Health Stroke Scale. RESULTS: A total of 42 lesions were treated: 9 with isolated angioplasty, 14 with balloon-expandable coronary stents, and 19 with Wingspan self-expandable intracranial stents. The mean patient age was 62.9 years, and the mean arterial diameter stenosis was 73.9%. Technical success was achieved in 97.6% of the patients. The overall incidence of procedural complications was 21.4%, and the postoperative permanent morbidity/mortality rate was 7.1%. There were 3 cases of in-stent thrombosis (1 fatal) and 5 cases of asymptomatic restenosis (11.9%), 3 in the isolated angioplasty group and 2 in the Wingspan self-expandable intracranial stent group (mean follow-up 20.4 months). The rate of restenosis was higher in the angioplasty group (33%) than in the coronary (0%) and Wingspan stent (10.5%) groups. CONCLUSION: Endovascular treatment of symptomatic intracranial stenosis has significant overall morbidity and mortality rates. Nevertheless, the very critical natural history of severe refractory lesions and the relatively favorable postoperative evolution suggest that it should be considered the first alternative strategy in cases in which medical therapy has failed.

The mechanism underlying atherosclerotic ischemic events within the middle cerebral artery (MCA) is unclear. High structural stress induced by blood pressure might be a potential aetiology as plaque rupture occurs when such mechanical loading exceeds its material strength. To perform reliable analyses quantifying the mechanical loading within a plaque, the local blood pressure is needed. However, data on MCA blood pressure is currently lacking. In this study, the arterial pressure proximal to the stenotic site in the MCA was measured in 15 patients scheduled for intervention. The relationships between these local measurements and pre-intervention and intra-intervention non-invasive arm measurements were assessed. The impact of luminal stenosis on the local blood pressure was quantified. Compared with the pre-intervention arm measurement, the intra-intervention arm pressure decreased significantly by 23.9 ± 11.8 and 9.3 ± 14.7 % at diastole and systole, respectively. The pressure proximal to the stenosis was much lower than the pre-intervention arm measurement (diastole: 65.3 ± 15.7 vs 82.0 ± 9.7, p < 0.01; systole: 81.1 ± 15.9 vs 133.9 ± 18.7, p < 0.01; unit: mmHg). The systolic pressure in the MCA in patients with stenosis <70 % (n = 6) was significantly higher than the value in patients with stenosis ≥70 % (n = 9) (92.0 ± 7.3 vs 73.9 ± 16.1, p = 0.02; unit: mmHg), as was pulse pressure (22.8 ± 6.4 vs 11.1 ± 8.3, p = 0.01; unit: mmHg). However, diastolic pressure remained unaffected (69.2 ± 9.3 vs 62.8 ± 19.0, p = 0.58; unit: mmHg). In conclusion, the obtained results are helpful in understanding the local hemodynamic environment modulated by the presence of atherosclerosis. The local pressure measurements can be used for computational analysis to quantify the critical mechanical condition within an MCA lesion.

The pathogenesis of intracranial arterial aneurysms (AA) remains unclear, despite their clinical importance. An improved understanding of this disease is important in choosing therapeutic options. In addition to the \"classical\" berry-type aneurysm, there are various other types of intracranial AA such as infectious, dissecting or giant, partially-thrombosed aneurysms. From the clinician's perspective, the hypothesis that some of these intracranial AA might be due to abluminal factors has been proposed for several years. Indeed, this hypothesis and the empirical use of anti-inflammatory drugs in giant intracranial aneurysms have been confirmed by recent studies reporting that an enzyme involved in the inflammatory cascade (5-lipoxygenase or 5-LO) promotes the pathogenesis of specific aneurysms in humans. 5-LO generates different forms of leukotrienes which are potent mediators of inflammation. Adventitial inflammation leads to a weakening of the media from the abluminal part of the vessel wall due to the release of proinflammatory factors that invade the media, thereby degrading the extracellular matrix, the elastic lamina of the vascular wall, and, finally, the integrity of the vessel lumen. This in turn results in a dilation of the vessel and aneurysm formation. Moreover, neoangiogenesis of vasa vasorum is found in close proximity to 5-LO activated macrophages. In addition to this biological cascade, we argue that repeated subadventitial haemorrhages from the new vasa vasorum play an important role in aneurysm pathogenesis, due to a progressive increase in size mediated by the apposition of new layers of intramural haematoma within the vessel wall. Intracranial giant AA can therefore be regarded as a proliferative disease of the vessel wall induced by extravascular activity. Considering certain aneurysmal vasculopathies as an abluminal disease might alter current therapeutic strategies. Therapy should not only be aimed at the intraluminal repair of the artery, but also cross the vessel wall to reach the vasa vasorum. Drug-eluting stents placed proximal to the lesion and targeted to the origin of the vasa vasorum could be considered as a potential future option. \"Intelligent\" MRI contrast agents (i.e., macrophage marking) could be used to detect vasa vasorum proliferation and weakening of the vessel wall in vivo.

The role of angioplasty/stenting procedures, neurointerventionist experience, vascular risk factors, medical treatment and blood flow velocities were analysed to identify possible causes of intra-stent restenosis (ISR) following stenting of cervical and/or intracranial arteries, assuming progressive atherosclerosis to be the shared mechanism in both territories. Patients. 26 cerebrovascular patients subjected to stenting of severe (≥85%) symptomatic or asymptomatic carotid stenoses or moderate-to-severe (≥50%) intracranial or vertebral stenoses were included. Clinical, radiological and ultrasonographic follow-up data were analysed retrospectively. Overall, stenting of the internal carotid artery (ICA) induced significant reductions in peak systolic velocities at 2 years (96±31cm/s vs. 358.2±24.9cm/s at baseline). The procedure-related ischemic complications rate was 7.4% (one hemispheric stroke and one TIA). The rate of ISR≤50% was 8% in the ICA at 2 years; was 50% in the common carotid artery (CCA) at 1 year, with concomitant distal ICA stenosis in 75% of CCA stenting, but all ISR were asymptomatic. Patients with ISR of the ICA were significantly younger (56.8±4.5 vs. 71.3±3.6 years, P=0.042) and had significantly more risk factors (5.5±0.9 vs. 3±0.3, P=0.012). No ISR≥70% was detected. ISR is relatively infrequent and, when present, it is mild and asymptomatic. Restenosis is more frequent in younger patients and those with several risk factors, and it may also be related to stenting of previous carotid endarterectomy.