OBJECTIVE: Many studies suggested that short-term exposure to fine particulate matter (PM2.5) and coarse particulate matter (PM2.5-10) was linked to elevated risk of cerebrovascular disease. However, little is known about the potentially differential effects of PM2.5 and PM2.5-10 on various types of cerebrovascular disease.
METHODS: We collected individual cerebrovascular death records for all residents in Shanghai, China from 2005 to 2021. Residential daily air pollution data were predicted from a satellite model. The associations between particulate matters (PM) and cerebrovascular mortality were investigated by an individual-level, time-stratified, case-crossover design. The data was analyzed by the conditional logistic regression combined with the distributed lag model with a maximum lag of 7 days. Furthermore, we explored the effect modifications by sex, age and season.
RESULTS: A total of 388,823 cerebrovascular deaths were included. Monotonous increases were observed for mortality of all cerebrovascular diseases except for hemorrhagic stroke. A 10 μg/m3 rise in PM2.5 was related to rises of 1.35% [95% confidence interval (CI): 1.04%, 1.66%] in mortality of all cerebrovascular diseases, 1.84% (95% CI: 1.25%, 2.44%) in ischemic stroke, 1.53% (95% CI: 1.07%, 1.99%) in cerebrovascular sequelae and 1.56% (95% CI: 1.08%, 2.05%) in ischemic stroke sequelae. The excess risk estimates per each 10 μg/m3 rise in PM2.5-10 were 1.47% (95% CI: 1.10%, 1.84%), 1.53% (95% CI: 0.83%, 2.24%), 1.93% (95% CI: 1.38%, 2.49%) and 2.22% (95% CI: 1.64%, 2.81%), respectively. The associations of both pollutants with all cerebrovascular outcomes were robust after controlling for co-pollutants. The associations were greater in females, individuals > 80 years, and during the warm season.
CONCLUSIONS: Short-term exposures to both PM2.5 and PM2.5-10 may independently increase the mortality risk of cerebrovascular diseases, particularly of ischemic stroke and stroke sequelae.

BACKGROUND: Existing studies have already shown a connection between nitrogen dioxide (NO2) exposure and cerebrovascular mortality. However, the differential effects of NO2 on cerebrovascular disease and its subtypes remain unclear and require further exploration.
METHODS: Daily stroke mortality data between 2013 and 2021 in Shanghai, China were collected. Residential daily air pollution data for each decedent were predicted from a satellite model. An individual-level, time-stratified, case-crossover design was applied to examine the relationship between NO2 exposure and cerebrovascular mortality. A combination of conditional logistic regression and distributed lag models with a maximum lag of 7 days was used for data analysis.
RESULTS: A total of 219,147 cases of cerebrovascular mortality were recorded. Among them, the proportion of sequelae of cerebrovascular disease, hemorrhagic stroke and ischemic stroke was 50.7%, 17.1% and 27.5%, respectively. The monotonic increases in mortality risks of cerebrovascular diseases, sequelae of cerebrovascular disease and ischemic stroke were observed, without any discernible thresholds. Each 10 μg/m3 increase in NO2 concentration was associated with increments of 3.62% [95% confidence interval (CI): 2.56%, 4.69%] for total cerebrovascular mortality, 4.29% (95% CI: 2.81%, 5.80%) for sequelae of cerebrovascular disease mortality and 4.30% (95% CI: 2.30%, 6.33%) for ischemic stroke mortality. No positive associations between NO2 exposure and hemorrhagic stroke mortality were observed. A greater risk of NO2 was observed in the warm season, in patients with less than 9 years of education and in those with single marital status. The effects of NO2 were robust to mutual adjustment of co-pollutants.
CONCLUSIONS: Short-term exposures to NO2 may increase the risk of cerebrovascular mortality, specifically for ischemic stroke and sequelae of cerebrovascular disease.

Moyamoya disease (MMD) is a rare yet progressive cerebrovascular disorder caused by the constriction of arteries, which leads to the twisting and tangling of small arteries in the brain, ultimately causing blockages. Although moyamoya angiopathy (MMA) has been known for almost six decades, its pathophysiology remains unknown, posing challenges to timely diagnosis. Moyamoya syndrome (MMS) refers to the association of MMA with various diseases, including infections, tumors, arteriovenous malformations, radiation treatment, and hereditary disorders. On the other hand, MMD, an idiopathic form, is now more frequently linked to genetic abnormalities. MMS is more common in people of Asian descent, but we encountered and aim to discuss a rare case of a 32-year-old Caucasian from Colombia who was diagnosed with it. The patient initially presented with unexplained symptoms of stroke, prompting doctors to conduct additional imaging. Fortunately, this led to her timely diagnosis. The report discusses the challenges that healthcare professionals face in diagnosis when presented with such uncommon cases. Through this case report, we try to review the presentation, diagnosis, and treatment used for this patient with MMS. The limited information available about the disease, especially the demographic data in countries outside Asia, often leads to delayed diagnoses, emphasizing the need for further exploration. Timelier diagnosis and heightened research into the disease\'s presentation and risk factors could lead to improved outcomes. Our report also briefly discusses the effectiveness of the current treatment protocol for patients. Currently, the patient is undergoing rehabilitation and showing promising progress.

BACKGROUND: Cerebral cavernous malformations (CCMs) are a major type of cerebrovascular lesions of proven genetic origin that occur in either sporadic (sCCM) or familial (fCCM) forms, the latter being inherited as an autosomal dominant condition linked to loss-of-function mutations in three known CCM genes. In contrast to fCCMs, sCCMs are rarely linked to mutations in CCM genes and are instead commonly and peculiarly associated with developmental venous anomalies (DVAs), suggesting distinct origins and common pathogenic mechanisms.
METHODS: A hemorrhagic sCCM in the right frontal lobe of the brain was surgically excised from a symptomatic 3 year old patient, preserving intact and pervious the associated DVA. MRI follow-up examination performed periodically up to 15 years after neurosurgery intervention demonstrated complete removal of the CCM lesion and no residual or relapse signs. However, 18 years after surgery, the patient experienced acute episodes of paresthesia due to a distant recurrence of a new hemorrhagic CCM lesion located within the same area as the previous one. A new surgical intervention was, therefore, necessary, which was again limited to the CCM without affecting the pre-existing DVA. Subsequent follow-up examination by contrast-enhanced MRI evidenced a persistent pattern of signal-intensity abnormalities in the bed of the DVA, including hyperintense gliotic areas, suggesting chronic inflammatory conditions.
CONCLUSIONS: This case report highlights the possibility of long-term distant recurrence of hemorrhagic sCCMs associated with a DVA, suggesting that such recurrence is secondary to focal sterile inflammatory conditions generated by the DVA.

BACKGROUND: Stroke is currently the second leading cause of death in the elderly population. Neuropsychiatric complications following stroke are common, can be overlooked, and are associated with low quality of life, increase in the burden of caregiving and impaired functional status.
METHODS: We report a case of poststroke psychosis in a woman without prior psychiatric history. In addition, a brief, nonsystematic review of the pertinent literature was performed.
RESULTS: Psychosis can present in almost 5% of stroke survivors. Many patients with poststroke psychosis have no previous psychiatric history and the most common lesion locations include the right frontal, temporal and parietal lobes, the white matter connecting those areas, as well as the right caudate nucleus. Compared to other stroke survivors, patients with poststroke psychosis are more likely to depend on assistance in their everyday lives, can have more difficulty coping with the sequelae of stroke, and have an increased 10-year mortality risk. Guidelines for diagnosing and managing poststroke psychosis are needed.
CONCLUSIONS: Psychosis is a possible complication of stroke and is associated with impairment and increased mortality. Guidelines for diagnosing and managing poststroke psychosis are currently lacking. To assure evidence-based care, further research is needed.
UNASSIGNED: GRUNDLAGEN: Der Schlaganfall ist heute die zweithäufigste Todesursache in der älteren Bevölkerung. Neuropsychiatrische Komplikationen nach einem Schlaganfall sind häufig, können übersehen werden und sind mit geringer Lebensqualität, erhöhter Pflegebelastung und eingeschränktem Funktionsstatus verbunden.
METHODS: In diesem Beitrag wird über einen Fall von Psychose nach Schlaganfall bei einer Frau ohne psychiatrische Vorgeschichte berichtet. Darüber hinaus erfolgte ein kurzes, nichtsystematisches Review der einschlägigen Literatur.
UNASSIGNED: Eine Psychose kann bei fast 5% der Schlaganfallüberlebenden auftreten. Viele Patienten mit einer Psychose nach Schlaganfall haben keine psychiatrische Vorgeschichte, und die häufigsten Läsionsorte sind der rechte Frontal‑, Temporal- und Parietallappen, die weiße Substanz, die diese Bereiche verbindet sowie der rechte Nucleus caudatus. Im Vergleich zu anderen Schlaganfallüberlebenden sind Patienten mit einer Psychose nach dem Schlaganfall im Alltag eher auf Hilfe angewiesen, haben größere Schwierigkeiten, die Folgen des Schlaganfalls zu bewältigen, und haben ein erhöhtes 10-Jahres-Mortalitätsrisiko. Leitlinien für die Diagnose und Behandlung von Psychosen nach einem Schlaganfall sind erforderlich.
UNASSIGNED: Eine Psychose ist eine mögliche Komplikation des Schlaganfalls und geht mit Beeinträchtigungen und einer erhöhten Sterblichkeit einher. Leitlinien für die Diagnose und Behandlung von Psychosen nach einem Schlaganfall fehlen derzeit. Um eine evidenzbasierte Versorgung zu gewährleisten, sind weitere Forschungsarbeiten notwendig.

Patients with intracranial artery stenosis show high incidence of stroke. Angiography reports contain rich but underutilized information that can enable the detection of cerebrovascular diseases. This study evaluated various natural language processing (NLP) techniques to accurately identify eleven intracranial artery stenosis from angiography reports. Three NLP models, including a rule-based model, a recurrent neural network (RNN), and a contextualized language model, XLNet, were developed and evaluated by internal-external cross-validation. In this study, angiography reports from two independent medical centers (9614 for training and internal validation testing and 315 as external validation) were assessed. The internal testing results showed that XLNet had the best performance, with a receiver operating characteristic curve (AUROC) ranging from 0.97 to 0.99 using eleven targeted arteries. The rule-based model attained an AUROC from 0.92 to 0.96, and the RNN long short-term memory model attained an AUROC from 0.95 to 0.97. The study showed the potential application of NLP techniques such as the XLNet model for the routine and automatic screening of patients with high risk of intracranial artery stenosis using angiography reports. However, the NLP models were investigated based on relatively small sample sizes with very different report writing styles and a prevalence of stenosis case distributions, revealing challenges for model generalization.

The aim of this study was to determine the differences in life expectancy and causes of death after primary intracerebral hemorrhage (ICH) relative to general population controls.
In a population-based setting, 963 patients from Northern Ostrobothnia who had their first-ever ICH between 1993 and 2008 were compared with a cohort of 2884 sex- and age-matched controls in terms of dates and causes of death as extracted from the Causes of Death Register kept by Statistics Finland and valid up to the end of 2017.
Of our 963 patients, 781 died during the follow-up time (mortality 81.1%). Cerebrovascular disease was the most common cause of death for these patients, 37.3% compared with 8.2% amongst the controls. The most common reasons for cerebrovascular mortality in the ICH patients were late sequelae of ICH in 12.8% (controls 0%) and new bleeding in 10.6% (controls 1.0%). The long-term survivors had a smaller ICH volume (median 12 ml) than those patients who died within 3 months (median 39 ml). The mortality rate of ICH patients during a follow-up between 12 and 24 years was still higher than that of their controls (hazard ratio 2.08, 95% confidence interval 1.58-2.74, p < 0.001).
Very long-term ICH survivors have a constant excess mortality relative to controls even 10 years after the index event. A significantly larger proportion of patients died of cerebrovascular causes and fewer because of cancer relative to the controls.

Cerebrovascular endothelial dysfunction is involved in the progression of leukoaraiosis. Asymmetric dimethylarginine is a competitive inhibitor of nitric oxide, which is highly expressed in patients with leukoaraiosis. Dimethylarginine dimethylaminohydrolase (DDAH) is a hydrolytic enzyme that is primarily responsible for eliminating asymmetric dimethylarginine, and it plays a role in the pathogenesis of cardiovascular and cerebrovascular diseases. The DDAH2 subtype is expressed in organs rich in induced nitric oxide synthase, including the heart, the placenta, and the cerebral endothelium during cerebral ischemia, in the stress state, or under neurotoxicity. Overexpression of the DDAH2 gene can inhibit asymmetric dimethylarginine-induced peripheral circulating endothelial cell dysfunction. However, it is unknown whether this polymorphism regulates plasma asymmetric dimethylarginine levels in patients with leukoaraiosis. In this double-blind study, we recruited 46 patients with leukoaraiosis and 46 healthy, matched controls. Plasma asymmetric dimethylarginine levels were determined using enzyme-linked immunoassays. Genomic DNA was isolated from whole blood samples, and polymerase chain reaction, SmaI restriction enzyme digestion, restriction fragment length polymorphisms, and agarose electrophoresis were used to detect DDAH2 (-449 G/C) gene polymorphisms. The results revealed that 95.65% of leukoaraiosis patients had recessive genetic models (GG and CG), while 89.13% of healthy control subjects had dominant genetic models (CC and CG). There was a significant difference in the genotype composition ratio between leukoaraiosis patients and healthy controls (P = 0.0002). The frequency of G alleles in the leukoaraiosis patients (71.74%) was significantly higher than in healthy controls, whereas the frequency of C alleles was lower (χ2 = 13.9580, P = 0.0002). Furthermore, asymmetric dimethylarginine concentrations in subjects with the GG genotype were significantly higher than in subjects with the CG and CC genotypes (Kruskal-Wallis H = 24.5955, P < 0.0001). In addition, the GG genotype of DDAH2 (-449 G/C) was more common in patients with leukoaraiosis. These findings suggest that the G allele of DDAH2 (-449 G/C) is a risk factor for leukoaraiosis morbidity and is correlated with high levels of asymmetric dimethylarginine. This study was approved by the Institutional Ethics Committee of The 2nd Affiliated Hospital of Harbin Medical University of China (approval No. KY2016-177) on July 28, 2016.

With the ubiquity of susceptibility weighted imaging (SWI), cerebral microbleeds (CMBs) are fast becoming a prevalent phenomenon. They are tightly associated with age, neurodegeneration and diverse vascular etiologies. CMBs have a unique radiological signature. Their morphology, number and topology are quite informative. They also pose a therapeutic conundrum, as they are associated with the risk of cerebral hemorrhage. We present the case of an 86-year-old woman who has a vascular dementia, Binswanger\'s syndrome, and coronary artery disease, who presented with more than five CMBs. We present this case in order to highlight the dilemma of anti-platelet therapy in this group of patients and we demonstrate the cardinal radiologic features of CMBs. We then segue into the pathologic correlates of CMBs and associated risk factors. We finally analyze the risk of anti-platelet therapy in the presence of CMBs, and we unfold the latest data on CMB number and anti-platelet therapy.

BACKGROUND: There is still no consensus among researchers on the impact of opium dependency on cerebrovascular stenosis. Some studies suggest that opium may be a risk factor for ischemic stroke. This study compared carotid intima-media thickness (CIMT) and cerebrovascular reactivity between opium-dependent and healthy people.
METHODS: This case-control study was done among opium addicts at Shafa hospital in Kerman, Iran, in year 2018. People with systemic disease or who took any medicine were excluded from our study. The control group were selected from healthy non-addicted volunteers. The control group was matched in age and sex with the case group. Cerebrovascular reactivity of middle cranial artery and intima-media thickness of carotid artery were measured for all in both groups. The results were analyzed using chi-square, independent samples t, and logistic regression tests.
RESULTS: 47 opium addicts and 47 healthy people entered this study. 88% of them were men and 12% were women. 68.1% of the case group and 31.9% of the control group were cigarette smokers; this difference was statistically significant. Comparison of cerebrovascular reactivity and CIMT between the two groups was statistically significant (P < 0.001). This relationship remained significant for the CIMT after removing confounding factors (P = 0.018).
CONCLUSIONS: Overall, our findings show that opium dependency affects the carotid intima-media thickness as an indicator of cerebral atherosclerosis.