Cerebral small vessel disease (CSVD) is a major cause of vascular cognitive impairment and functional loss in elderly patients. Progressive remodeling of cerebral microvessels due to arterial hypertension or other vascular risk factors, such as aging, can cause dementia or stroke. Typical imaging characteristics of CSVD include cerebral microbleeds (CMB), brain atrophy, small subcortical infarctions, white matter hyperintensities (WMH), and enlarged perivascular spaces (EPVS). Nevertheless, no animal models that reflect all the different aspects of CSVD have been identified. Here, we generated a new CSVD animal model using D-galactose (D-gal) combined with cerebral hypoperfusion in spontaneously hypertensive rats (SHR), which showed all the hallmark pathological features of CSVD and was based on vascular risk factors. SHR were hypodermically injected with D-gal (400 mg/kg/d) and underwent modified microcoil bilateral common carotid artery stenosis surgery. Subsequently, neurological assessments and behavioral tests were performed, followed by vascular ultrasonography, electron microscopy, flow cytometry, and histological analyses. Our rat model showed multiple cerebrovascular pathologies, such as CMB, brain atrophy, subcortical small infarction, WMH, and EPVS, as well as the underlying causes of CSVD pathology, including oxidative stress injury, decreased cerebral blood flow, structural and functional damage to endothelial cells, increased blood-brain barrier permeability, and inflammation. The use of this animal model will help identify new therapeutic targets and subsequently aid the development and testing of novel therapeutic interventions. Main process of the study: Firstly, we screened for optimal conditions for mimicking aging by injecting D-gal into rats for 4 and 8 weeks. Subsequently, we performed modified microcoil BCAS intervention for 4 and 8 weeks in rats to screen for optimal hypoperfusion conditions. Finally, based on these results, we combined D-gal for 8 weeks and modified microcoil BCAS for 4 weeks to explore the changes in SHR.

Orthostatic hypotension (OH) is a form of orthostatic intolerance (OI) and a key physiological indicator of autonomic dysfunction that is associated with an increased risk of major cerebrocardiovascular events. Symptoms of cerebral hypoperfusion have been reported in patients with OH, which worsens symptoms and increases the risk of syncope. Since pharmacological interventions increase blood pressure (BP) independent of posture and do not restore normal baroreflex control, nonpharmacological treatments are considered the foundation of OH management. While reductions in cerebral blood flow velocity (CBFv) during orthostatic stress are associated with a decrease in end-tidal CO2 (EtCO2) and hypocapnia in patients with OI, their contribution to the severity of OH is not well understood. These measures have been physiological targets in a wide variety of biofeedback interventions. This study explored the relationship between cardiovascular autonomic control, EtCO2 and cerebral hypoperfusion in patients (N = 72) referred for OI. Patients with systolic OH were more likely to be male, older, demonstrate reduced adrenal and vagal baroreflex sensitivity, and reduced cardiovagal control during head-up tilt (HUT) than patients without systolic OH. Greater reduction in CBFv during HUT was associated with a larger reduction in ETCO2 and systolic BP during HUT. While deficits in cardiovascular autonomic control played a more important role in systolic OH, reduced EtCO2 was a major contributor to orthostatic cerebral hypoperfusion. These findings suggest that biofeedback treatments targeting both the autonomic nervous system and EtCO2 should be part of nonpharmacological interventions complementing the standard of care in OH patients with symptoms of cerebral hypoperfusion.

The BIS value may decrease by cerebral hypoperfusion. We report a case in which the BIS value suddenly decreased during cervical spine surgery, which led us to find cervical screws compressing the vertebral arteries. In a 79-year-old man undergoing cervical spine surgery, the BIS suddenly decreased from about 40 to 10-20, about 4 h after the start of surgery. Intraoperative 3-dementional computed tomography indicated that both the two tips of cervical screws inserted in the 6th cervical vertebra were within bilateral transverse foramens. These cervical screws were removed, and the BIS increased immediately. The cervical screws were re-inserted again thorough the same vertebra into the bilateral transverse foramens, and the BIS decreased immediately. Postoperatively, cerebral hypoperfusion due to compression of bilateral vertebral arteries by two cervical screws was identified. The BIS may be a useful to detect cerebral hypoperfusion due to compression of the vertebral artery by a cervical screw.

UNASSIGNED: In Moyamoya angiopathy (MMA), mechanisms underlying cognitive impairment remain debated. We aimed to assess the association of cognitive impairment with the degree and the topography of cerebral hypoperfusion in MMA.
UNASSIGNED: A retrospective analysis of neuropsychological and perfusion MRI data from adults with MMA was performed. Ischemic and haemorrhagic lesion masks were created to account for cerebral lesions in the analysis of cerebral perfusion. Whole brain volume of hypoperfused parenchyma was outlined on perfusion maps using different Tmax thresholds from 4 to 12 s. Regional analysis produced mean Tmax values at different regions of interest. Analyses compared perfusion ratios in patients with and without cognitive impairment, with multivariable logistic regression analysis to identify predictive factors.
UNASSIGNED: Cognitive impairment was found in 20/48 (41.7%) patients. Attention/processing speed and memory were equally impaired (24%) followed by executive domain (23%). After adjustment, especially for lesion volume, hypoperfused parenchyma volume outlined by Tmax > 4 s or Tmax > 5 s thresholds was an independent factor of cognitive impairment (OR for Tmax > 4 s = 1.06 [CI 95% 1.008-1.123]) as well as attention/processing speed (OR for Tmax > 4 s = 1.07 [CI 95% 1.003-1.133]) and executive domains (OR for Tmax > 5 s = 1.08 [CI 95% 1.004-1.158]). Regarding cognitive functions, patients with processing speed and flexibility impairment had higher frontal Tmax compared to other ROIs and to patients with normal test scores.
UNASSIGNED: Cerebral hypoperfusion emerged as an independent factor of cognitive impairment in MMA particularly in attention/processing speed and executive domains, with a strong contribution of frontal areas.
UNASSIGNED: Considering this association, revascularization surgery could improve cognitive impairment.

Atrial fibrillation (AF) is closely related to abnormal cerebral blood flow. Inflammation and oxidative stress have always been important factors in the pathophysiology of AF. It remains unknown whether inflammation and oxidative stress are correlated to hippocampal perfusion in patients with AF.Sixty-three patients with AF with normal hippocampal blood perfusion (NHBP) were compared to 71 patients with AF with abnormal hippocampal blood perfusion (AHBP) using a case-control study design. The serum levels of inflammation and oxidative stress were measured. The hippocampal perfusion was detected. (1) The serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and oxidized low-density lipoprotein (ox-LDL) were statistically higher in the AHBP group than in the NHBP group. In the AHBP subgroup analysis, the serum levels of hs-CRP and IL-6 were statistically higher in patients with persistent AF than those with paroxysmal AF. (2) The relative cerebral blood volume (rCBV), mean transit time (MTT), and the time-to-peak (TTP) were statistically higher in the AHBP group than in the NHBP group. Moreover, cerebral blood flow (rCBF) was statistically lower in the AHBP group than in the NHBP group. (3) relative cerebral blood volume (rCBV), rCBF, MTT, and TTP were passively associated with serum hs-CRP and IL-6; rCBV, rCBF, and MTT were positively associated with ox-LDL. The serum levels of hs-CRP, IL-6, and ox-LDL were associated with AHBP in patients with AF after multivariate logistic regression analysis.Oxidative stress and inflammatory biomarkers were increased in patients with AF with AHBP, in which the serum levels of hs-CRP and IL-6 in the persistent AF group were statistically higher than those in the paroxysmal AF group. The serum levels of hs-CRP, IL-6, and ox-LDL were associated with AHBP in patients with AF.

Ascending aortic dissection is typically characterized by severe chest or back pain. However, its presentation can be atypical, leading to diagnostic challenges, especially in settings where classic symptomatology may not be evident. In this report, we described the case of a 74-year-old woman who presented to the emergency room of a rural community hospital with chief complaints of vertigo, nausea, and vomiting, without the classic symptoms of chest or back pain associated with aortic dissection. Despite initial treatment for autonomic dysregulation, the patient\'s symptoms persisted. Subsequent comprehensive assessments, including computed tomography angiography, revealed an ascending aortic dissection extending to the bilateral common carotid arteries. This atypical presentation, characterized by cerebral hypoperfusion and systemic hypotension without tachycardia, emphasizes the need to maintain a high suspicion index, even in the absence of hallmark symptoms. This case underscores the importance of considering the possibility of ascending aortic dissection in patients with nontraditional symptoms. Recognizing these atypical presentations is crucial for timely intervention, especially in rural settings with limited advanced diagnostic tools. This case also highlights potential sex disparities in symptom presentation, emphasizing the need for clinicians to recognize nontraditional symptoms in women. Rapid identification, evaluation, and management are imperative to prevent severe outcomes, and a multidisciplinary approach has proven to be the most effective in such cases.

Carotid cross-clamping during carotid endarterectomy might lead to intraoperative neurologic deficits, increasing stroke/death risk. If deficits are detected, carotid shunting has been recommended to reduce the risk of stroke. However, shunting may sustain a specific chance of embolic events and subsequently incurring harm. Current evidence is still questionable regarding its clear benefit. The aim is to determine whether a policy of selective shunt impacts the complication rate following an endarterectomy.
From January 2013 to May 2021, all patients undergoing carotid endarterectomy under regional anesthesia with intraoperative neurologic alteration were retrieved. Patients submitted to selective shunt were compared to a non-shunt group. A 1:1 propensity score matching (PSM) was performed. Differences between the groups and clinical outcomes were calculated, resorting to univariate analysis.
Ninety-eight patients were selected, from which 23 were operated on using a shunt. After PSM, 22 non-shunt patients were compared to 22 matched shunted patients. Concerning demographics and comorbidities, both groups were comparable to pre and post-PSM, except for chronic heart failure, which was more prevalent in shunted patients (26.1%, P=0.036) in pre-PSM analysis. Regarding 30-day stroke and score Clavien-Dindo ≥2, no significant association was found (P=0.730, P=0.635 and P=0.942, P=0.472, correspondingly, for pre and post-PSM).
In this cohort, resorting to shunting did not demonstrate an advantage regarding 30-day stroke or a Clavien-Dindo ≥ 2 rates. Nevertheless, additional more extensive studies are mandatory to achieve precise results concerning the accurate utility of carotid shunting in this subset of patients under regional anesthesia.

暂无摘要。

Multiple sclerosis (MS) is a common neurological disease, especially among people of young working age, and the number of MS cases registered in the world and in the Russian Federation tends to increase. The pathogenesis of MS is based on the theory of damage to its own myelin sheath as a result of activation of autoreactive T cells, which also leads to damage to both oligodendrocytes and axons. In addition, the role of vascular factor in the pathogenesis of MS is discussed in the literature periodically and several areas of research of vascular dysfunction in patients are identified. This article provides a retrospective analysis of the available literature dating from the 19th century to the present time in order to find the relationship between MS and changes in venous circulation.
Рассеянный склероз (РС) является распространенным неврологическим заболеванием, особенно у лиц молодого трудоспособного возраста, и имеет тенденцию к увеличению количества случаев, зарегистрированных в мире и в Российской Федерации. В основе патогенеза РС рассматривают теорию повреждения собственной миелиновой оболочки в результате активации аутореактивных Т-клеток, что приводит также к повреждению и олигодендроцитов, и аксонов. Кроме того, в литературе периодически обсуждается роль сосудистого фактора в патогенезе РС и выделяют несколько направлений изучения сосудистой дисфункции у пациентов. В данной статье проведен ретроспективный анализ доступной литературы за обширный период с XIX века по наше время с целью нахождения взаимосвязи между РС и изменениями венозного кровообращения.

Vascular cognitive impairment and dementia (VCID) is a series of cognitive dysfunction associated with cerebrovascular diseases and currently lacks effective treatments. The white matter, which is essential for neuronal information processing and integration, is nourished by a network of capillaries and is vulnerable to chronic hypoperfusion. Here, we show that metformin, a widely used drug for the treatment of type 2 diabetes, alleviates the white matter damage and improves cognitive impairment in a mouse model of VCID established by bilateral carotid artery stenosis (BCAS)-induced chronic hypoperfusion. Mechanistically, metformin restores the dysfunctions of oligodendrocyte precursor cells (OPCs) under hypoxia. Metformin up-regulates prolyl hydroxylases 2 via activating the AMP-activated protein kinase pathway, leading to hypoxia-inducible factor-1α (HIF-1α) degradation in OPCs. These findings suggest that metformin may have a promising therapeutic role in alleviating cognitive abnormalities by ameliorating white matter damage of VCID.