BACKGROUND: We investigated the interactive associations between amyloid and hypertension on the entorhinal cortex (EC) tau and atrophy and the role of cerebral blood flow (CBF) as a shared mechanism by which amyloid and hypertension contribute to EC tau and regional white matter hyperintensities (WMHs).
METHODS: We analyzed data from older adults without dementia participating in the Add-Tau study (NCT02958670, n = 138) or Alzheimer\'s Disease Neuroimaging Initiative (ADNI) (n = 523) who had available amyloid-positron emission tomography (PET), tau-PET, fluid-attenuated inversion recovery (FLAIR), and T1-weighted magnetic resonance imaging (MRI). A subsample in both cohorts had available arterial spin labeling (ASL) MRI (Add-Tau: n = 78; ADNI: n = 89).
RESULTS: The detrimental effects of hypertension on AD pathology and EC thickness were more pronounced in the Add-Tau cohort. Increased amyloid burden was associated with decreased occipital gray matter CBF in the ADNI cohort. In both cohorts, lower regional gray matter CBF was associated with higher EC tau and posterior WMH burden.
CONCLUSIONS: Reduced cerebral perfusion may be one common mechanism through which hypertension and amyloid are related to increased EC tau and WMH volume.
CONCLUSIONS: Hypertension is associated with increased entorhinal cortex (EC) tau, particularly in the presence of amyloid. Decreased cortical cerebral blood flow (CBF) is associated with higher regional white matter hyperintensity volume. Increasing amyloid burden is associated with decreasing CBF in the occipital lobe. MTL CBF and amyloid are synergistically associated with EC tau.

BACKGROUND: The periaqueductal gray (PAG) is at the center of a powerful descending antinociceptive neuronal network, and is a key node in the descending pain regulatory system of pain. However, less is known about the altered perfusion of PAG in chronic migraine (CM).
OBJECTIVE: To measure the perfusion of PAG matter, an important structure in pain modulation, in CM with magnetic resonance (MR) perfusion without contrast administration.
METHODS: Three-dimensional pseudocontinuous arterial spin labeling (3D-PCASL) and brain structure imaging were performed in 13 patients with CM and 15 normal subjects. The inverse deformation field generated by brain structure image segmentation was applied to the midbrain PAG template to generate individualized PAG. Then the perfusion value of the PAG area of the midbrain was extracted based on the individual PAG mask.
RESULTS: Cerebral blood flow (CBF) value of PAG in CM patients (47.98 ± 8.38 mL/100 mg min) was significantly lower than that of the control group (59.87 ± 14.24 mL/100 mg min). Receiver operating characteristic (ROC) curve analysis showed that the area under the curve was 0.77 (95% confidence interval [CI], 0.60, 0.94), and the cutoff value for the diagnosis of CM was 54.83 mL/100 mg min with a sensitivity 84.60% and a specificity 60%.
CONCLUSIONS: Imaging evidence of the impaired pain conduction pathway in CM may be related with the decreased perfusion in the PAG, which could be considered as an imaging biomarker for the diagnosis and therapy evaluation.

Surgery of the aortic arch remains a complex procedure, with neurological events such as stroke remaining its most dreaded complications. Changes in surgical technique and the continuous innovation in neuroprotective strategies have led to a significant decrease in cerebral and spinal events. Different modes of cerebral perfusion, varying grades of hypothermia, and a number of pharmacological strategies all aim to reduce hypoxic and ischemic cerebral injury, yet there is no evidence indicating the clear superiority of one method over another. While surgical results continue to improve, novel hybrid and interventional techniques are just entering the stage and the question of optimal neuroprotection remains up to date. Within this perspective statement, we want to shed light on the current evidence and controversies of cerebral protection in aortic arch surgery, as well as what is on the horizon in this fast-evolving field. We further present our institutional approach as a large tertiary aortic reference center.

Shifts from deep to moderate hypothermic circulatory arrest (HCA) in aortic arch surgery necessitate an examination of their differential impacts on neurocognitive functions, especially structured verbal memory, given its significance for patient recovery and quality of life. This study evaluates and synthesizes evidence on the effects of deep (≤20.0 °C), low-moderate (20.1-24.0 °C), and high-moderate (24.1-28.0 °C) hypothermic temperatures on structured verbal memory preservation and overall cognitive health in patients undergoing aortic arch surgery. We evaluated the latest literature from major medical databases such as PubMed and Scopus, focusing on research from 2020 to 2024, to gather comprehensive insights into the current landscape of temperature management during HCA. This comparative analysis highlights the viability of moderate hypothermia (20.1-28.0 °C), supported by recent trials and observational studies, as a method to achieve comparable neuroprotection with fewer complications than traditional deep hypothermia. Notably, low-moderate and high-moderate temperatures have been shown to support substantial survival rates, with impacts on structured verbal memory preservation that necessitate careful selection based on individual surgical risks and patient profiles. The findings advocate for a nuanced approach to selecting hypothermic protocols in aortic arch surgeries, emphasizing the importance of tailoring temperature management to optimize neurocognitive outcomes and patient recovery. This study fills a critical gap in the literature by providing evidence-based recommendations for temperature ranges during HCA, calling for ongoing updates to clinical guidelines and further research to refine these recommendations. The implications of temperature on survival rates, complications, and success rates underpin the necessity for evolving cardiopulmonary bypass techniques and cerebral perfusion strategies to enhance patient outcomes in complex cardiovascular procedures.

BACKGROUND: Surgical repair of aortic arch hypoplasia in children requires a \"dry\" surgical field with reliable end-organ protection. Perfusion strategies commonly involve deep hypothermic circulatory arrest (DHCA) and variations of the continuous perfusion techniques, such as selective antegrade cerebral perfusion (SACP) and full-flow perfusion with double aortic cannulation (DAC). We aimed to evaluate the end-organ protection in the surgery of aortic arch hypoplasia in newborns and infants using DHCA and DAC.
METHODS: 66 newborns and infants with aortic arch hypoplasia and biventricular anatomy were enrolled in this prospective study. Patients were randomly assigned into two groups according to the perfusion strategy - DHCA (n = 33); and DAC (n = 33). Primary endpoint: acute kidney injury (AKI), graded according to the KDIGO score. Secondary endpoints: neurological sequelae (pre- and postoperative MRI), in-hospital mortality.
RESULTS: The lowest temperature was 32 (28; 34)°С in the DAC group and 23 (20; 25)°С in the DHCA group. The patients with DAC had lower incidence of AKI (6 patients (18.2%) versus 19 patients (57.6%); p = .017). In the multivariate analysis, the inotropic index at 48 h was identified as a risk factor, increasing the risk of AKI by 4%. The DHCA group was associated with a 3.8-fold increase in the risk of AKI. There was no difference in hospital mortality between the DAC and DHCA groups (1 patient (3%) versus 3 patients (9.1%); p = .61). Neurological sequelae by MRI scan were observed in 18 patients (54.5%) in the DHCA group compared to 5 patients (15.15%) in the DAC group (p = .026). The only risk factor identified in the multivariate analysis for neurological lesions on MRI scan was the DHCA group, which increased the risk by 8.8 times.
CONCLUSIONS: Surgical reconstruction of the aortic arch hypoplasia using the method of full-body perfusion reduces the incidence of neurological lesions and renal complications requiring renal replacement therapy compared with the deep hypothermic circulatory arrest in neonates and infants.

Background: Extracorporeal life support echniques as an Adjunct to Advanced Cardiac Life Support is usually suitable for complex heart surgery such as cardiopulmonary bypass (CPB). Cerebral perfusion is a clinically feasible neuroprotective strategy; however, the lack of a reliable small animal model.Methods: Based on the rat model of ECLS we evaluate the effects of ECLS-CP using HE staining, Nissl staining, TUNEL staining and ELISA.Result: We found that ECLS combined with the cerebral perfusion model did not cause brain injury and immune inflammation. There was no difference between the two by a left carotid artery or right carotid artery CP.Conclusion: These experimental results can provide the experimental basis for selecting blood vessels for ECLS patients and clinical CP to offers a trustworthy animal model for future exploration of applying brain perfusion strategies during ECLS-CP.

Cerebral perfusion is functionally regulated by neural mechanisms in addition to the systemic hemodynamic variation, vascular reactivity and cerebral metabolism. Although anesthesia is generally esteemed to suppress the overall brain neural activity and metabolism, a few inhalation anesthetics, such as isoflurane, can increase cerebral perfusion, thus heightening the risks of higher intracranial pressure, bleeding, and brain edema during surgery. With the aid of laser speckle contrast imaging, we observed a transient yet limited effect of cerebral perfusion enhancement in mice from awake to anesthetized conditions with different concentration of isoflurane. Retrograde and antegrade tracing revealed a higher proportion of parasympathetic control more than sympathetic innervation for the blood vessels. Surprisingly, isoflurane directly activated pterygopalatine ganglion (PPG) explants and induced FOS expression in the cholinergic neurons. Chemogenetic activation of cholinergic PPG neurons reduced isoflurane-related cerebral perfusion. On the contrary, ablation of the cholinergic PPG neurons resulted in further enhancement of cerebral perfusion induced by isoflurane. While blocking muscarinic cholinergic receptors resulted in the overall reduction upon isoflurane stimulation, the blockage of nicotinic cholinergic receptors enhanced the isoflurane-induced cerebral perfusion only when PPG neurons exist. Collectively, these results suggest that PPG play important roles in regulating cerebral perfusion under isoflurane inhalation.

BACKGROUND: Mannitol is widely used in neurosurgical units to mitigate raised intracranial pressure and cerebral edema, crucial in postoperative management. Its hyperosmolar properties reduce brain extracellular fluid, thereby altering cerebral perfusion and cardiac dynamics. However, the temporal and combined effects of mannitol on cardiovascular and cerebrovascular parameters remain inadequately explored in postoperative settings.
METHODS: This prospective observational study enrolled 20 adult patients who underwent elective craniotomies for tumor excision. Mannitol was administered to the patients at a dose of 0.5 mg/kg/dose as a bolus dose over 20 to 30 minutes. The time interval was eight hours between the doses (scheduled dosing). Patients received their first dose of mannitol in the ICU after eight hours of intraoperative dose. The patients were given mannitol for two postoperative days and followed up for two days in the postoperative period. Transthoracic echocardiography and transcranial color Doppler were used to assess cardiovascular and cerebrovascular parameters at multiple intervals post-mannitol administration.
RESULTS: Significant increases in mean flow velocities were observed bilaterally immediately post-mannitol administration on the first postoperative day, indicative of improved cerebral blood flow. However, these changes were transient, with no significant variations noted on the second postoperative day. Cerebrovascular resistance, as measured by the pulsatility index, showed non-significant changes bilaterally across both days. Cardiovascular parameters, including stroke volume and cardiac output, remained stable throughout the study period.
CONCLUSIONS: Mannitol administration at 0.5 g/kg in postoperative neurosurgical patients transiently improves cerebral perfusion without causing significant hemodynamic instability. This study underscores the importance of monitoring both cerebrovascular and cardiovascular parameters post-mannitol administration to optimize patient management and outcomes.

UNASSIGNED: Effect of stenosis of vertebrobasilar artery (VBA) on cognitive function is elusive.
UNASSIGNED: To investigate association of cerebral hypoperfusion and poor collaterals with vascular cognitive impairment (VCI) in severe VBA stenosis patients.
UNASSIGNED: We consecutively enrolled patients with severe VBA stenosis confirmed by digital subtraction angiography who underwent computed tomographic perfusion (CTP) and cognitive assessments. Patients were divided into poor or good collaterals groups according to the collateral circulation status, and were grouped into different perfusion groups according to CTP. Cognitive function was measured by Montreal Cognitive Assessment (MoCA), Clock Drawing Test, Stroop Color Word Test, Trail Making Test, Digital Span Test, Auditory Verbal Learning Test, and Boston Naming Test scales. The association of cerebral perfusion and collaterals with VCI were explored.
UNASSIGNED: Among 88 eligible patients, VCI occurred in 51 (57.9%) patients experienced. Poor collateral was present in 73 (83.0%) patients, and hypoperfusion in 64 (72.7%). Compared with normal perfusion patients, the odds ratio with 95% confidence interval for VCI was 12.5 (3.7-42.4) for overall hypoperfusion, 31.0 (7.1-135.5) for multiple site hypoperfusion, 3.3 (1.0-10.5) for poor collaterals, and 0.1 (0-0.6) for presence of posterior communicating artery (PcoA) compensated for posterior cerebral artery (PCA) and basilar artery (BA). Additionally, decreased scores of cognitive function tests occurred in patients with decompensated perfusion or poor collaterals.
UNASSIGNED: Hypoperfusion and poor collaterals were positively associated with cognitive impairment in patients with severe VBA. However, PcoA compensated for the PCA and BA had a protective role in cognitive impairment development.

UNASSIGNED: Cerebral small vessel disease (CSVD) causes between 25% and 30% of all ischemic strokes. In acute lacunar ischemic stroke, despite often mild initial symptoms, early neurological deterioration (END) occurs in approximately 15-20% of patients and is associated with poor functional outcome, yet its mechanisms are not well understood.
UNASSIGNED: In this review, we systematically evaluated data on: (1) definitions and incidence of END, (2) mechanisms of small vessel occlusion, (3) predictors and mechanisms of END, and (4) prospects for the prevention or treatment of patients with END.
UNASSIGNED: We identified 67 reports (including 13,407 participants) describing the incidence of END in acute lacunar ischemic stroke. The specified timescale for END varied from <24 h to 3 weeks. The rate of END ranged between 2.3% and 47.5% with a pooled incidence of 23.54% (95% confidence interval (CI) = 21.02-26.05) but heterogeneity was high (I2 = 90.29%). The rates of END defined by National Institutes of Health Stroke Scale (NIHSS) decreases of ⩾1, ⩾2, ⩾3, and 4 points were as follows: 24.17 (21.19-27.16)%, 22.98 (20.48-25.30)%, 23.33 (16.23-30.42)%, and 10.79 (2.09-23.13)%, respectively, with lowest heterogeneity and greatest precision for a cutoff of ⩾2 points. Of the 20/67 studies (30%) reporting associations of END with clinical outcome, 19/20 (95%) reported worse outcomes (usually measured using the modified Rankin score at 90 days or at hospital discharge) in patients with END. In a meta-regression analysis, female sex, hypertension, diabetes, and smoking were associated with END.
UNASSIGNED: END occurs in more than 20% of patients with acute lacunar ischemic stroke and might provide a novel target for clinical trials. A definition of an NIHSS ⩾2 decrease is most used and provides the best between-study homogeneity. END is consistently associated with poor functional outcome. Further research is needed to better identify patients at risk of END, to understand the underlying mechanisms, and to carry out new trials to test potential interventions.