Arterial carbon dioxide (PaCO2) and posture influence the middle (MCAv) and posterior (PCAv) cerebral artery blood velocitiesbut there is paucity of data about their interaction and need for an integrated model of their effects, including dynamic cerebral autoregulation (dCA). In 22 participants (11 male, age 30.2 ± 14.3 years), blood pressure (BP, Finometer), dominant MCAv and non-dominant PCAv (transcranial Doppler ultrasound), end-tidal CO2 (EtCO2, capnography) and heart rate (HR, ECG) were recorded continuously. Two recordings (R) were taken when the participant was supine (R1, R2), two taken when the participant was sitting (R3, R4), and two taken when the participant was standing (R5, R6). R1, R3 and R5 consisted of 3 minutes of 5% CO2 through a mask and R2, R4 and R6 consisted of 3 minutes of paced hyperventilation. The effects of PaCO2 were expressed with a logistic curve model (LCM) for each parameter. dCA was expressed by the autoregulation index (ARI), dervived by transfer function analysis. Standing shifted LCM to the left for MCAv (p<0.001), PCAv (p<0.001), BP (p=0.03) and ARI (p=0.001); downwards for MCAv and PCAv (both p<0.001), and upwards for HR (p<0.001). For BP, LCM was shifted downwards by sitting and standing (p=0.024). For ARI, the hypercapnic range of LCM was shifted upwards during standing (p<0.001). A more complete mapping of the combined effects of posture and arterial CO2 on the cerebral circulation and peripheral variables can be obtained with the LCM over a broad physiological range of EtCO2 values.

OBJECTIVE: Cerebral vasomotor reactivity (VMR) is vital for regulating brain blood flow and maintaining neurological function. Impaired cerebral VMR is linked to a higher risk of stroke and poor post-stroke outcomes. This study explores the relationship between statin treatment intensity and VMR in patients with ischemic stroke.
METHODS: Seventy-four consecutive patients (mean age 69.3 years, 59.4% male) with recent ischemic stroke were included. VMR levels were assessed 4 weeks after the index stroke using transcranial Doppler, measuring the breath-holding index (BHI) as an indicator of the percentage increase in middle cerebral artery blood flow (higher BHI signifies higher VMR). Multistep multivariable regression models, adjusted for demographic and cerebrovascular risk factors, were employed to examine the association between statin intensity treatment and BHI levels.
RESULTS: Forty-one patients (55%) received high-intensity statins. Patients receiving high-intensity statins exhibited a mean BHI of 0.85, whereas those on low-intensity statins had a mean BHI of 0.67 (mean difference 0.18, 95% confidence interval: 0.13-0.22, p-value<.001). This significant difference persisted in the fully adjusted model (adjusted mean values: 0.84 vs. 0.68, p-value: .008). No significant differences were observed in BHI values within patient groups on high-intensity or low-intensity statin therapy (all p-values>.05). Furthermore, no significant association was found between baseline low-density lipoprotein (LDL) levels and BHI.
CONCLUSIONS: High-intensity statin treatment post-ischemic stroke is linked to elevated VMR independent of demographic and clinical characteristics, including baseline LDL level. Further research is needed to explore statin therapy\'s impact on preserving brain vascular function beyond lipid-lowering effects.

IIH is a severe form of headache that often has superimposed migraine and often it is very difficult to distinguish the two forms of headache. Intracranial hemodynamics is a relatively unexplored means of distinguishing between the two forms of headache.
We aimed to study intracranial flow dynamics using Transcranial Doppler in patients with IIH, migraine, and normal controls.
It was a hospital-based observational study that included 51 people with IIH, 87 people with migraine, and 101 healthy controls and all were subjected to TCD study after detailed clinical examination.
Mean age of patients in three groups were similar with the mean age in IIH being 33.41 ± 10.75 (age in years ± SD). Vision loss was present in 66.67% of patients with IIH, and most common field defect was generalized constriction (27.5%). Neuroimaging was abnormal in 94.11% of patients of IIH with mean CSF pressure was 31.27±5.32 cm of water. Of all the TCD-measured velocities, mean flow velocity (MFV) showed a significant difference in all three groups with (p-value <0.001). The pulsatility index, both for middle cerebral arteries as well as ophthalmic arteries showed a significant difference in the three groups with the highest values in IIH patients (p-value<.001). The mean VMR in IIH (1.11±0.32) was lower than the mean VMR in migraine (1.34±0.43) as well as controls (1.49±0.46).
TCD parameters like MFV and PI are useful parameters that show considerable variation and can be used to differentiate between IIH and migraine.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily affects the respiratory system but can also lead to neurological complications. Among COVID-19 patients, the endothelium is considered the Achilles heel. A variety of endothelial dysfunctions may result from SARS-CoV-2 infection and subsequent endotheliitis, such as altered vascular tone, oxidative stress, and cytokine storms. The cerebral hemodynamic impairment that is caused is associated with a higher probability of severe disease and poor outcomes in patients with COVID-19. This review summarizes the most relevant literature on the role of vasomotor reactivity (VMR) in COVID-19 patients. An overview of the research articles is presented. Most of the studies have supported the hypothesis that endothelial dysfunction and cerebral VMR impairment occur in COVID-19 patients. Researchers believe these alterations may be due to direct viral invasion of the brain or indirect effects, such as inflammation and cytokines. Recently, researchers have concluded that viruses such as the Human Herpes Virus 8 and the Hantavirus predominantly affect endothelial cells and, therefore, affect cerebral hemodynamics. Especially in COVID-19 patients, impaired VMR is associated with a higher risk of severe disease and poor outcomes. Using VMR, one can gain valuable insight into a patient\'s disease progression and make more informed decisions regarding appropriate treatment options. A new pandemic may develop with the COVID-19 virus or other viruses, making it essential that healthcare providers and researchers remain focused on developing new strategies for improving survival in such patients, particularly those with cerebrovascular risk factors.

Cerebral autoregulation (CA) is a physiological mechanism that maintains constant cerebral blood flow regardless of changes in cerebral perfusion pressure and prevents brain damage caused by hypoperfusion or hyperperfusion. In recent decades, researchers have investigated the range of systemic blood pressures and clinical management strategies over which cerebral vasculature modifies intracranial hemodynamics to maintain cerebral perfusion. However, proposed clinical interventions to optimize autoregulation status have not demonstrated clear clinical benefit. As future trials are designed, it is crucial to comprehend the underlying cause of our inability to produce robust clinical evidence supporting the concept of CA-targeted management. This article examines the technological advances in monitoring techniques and the accuracy of continuous assessment of autoregulation techniques used in intraoperative and intensive care settings today. It also examines how increasing knowledge of CA from recent clinical trials contributes to a greater understanding of secondary brain injury in many disease processes, despite the fact that the lack of robust evidence influencing outcomes has prevented the translation of CA-guided algorithms into clinical practice.

Cerebral small vessel disease is a common manifestation among patients with Fabry disease (FD). As a biomarker of cerebral small vessel disease, the prevalence of impaired cerebral autoregulation as assessed by transcranial Doppler (TCD) ultrasonography was evaluated in FD patients and healthy controls.
TCD was performed to assess pulsatility index (PI) and vasomotor reactivity expressed by breath-holding index (BHI) for the middle cerebral arteries of included FD patients and healthy controls. Prevalence of increased PI (>1.2) and decreased BHI (<0.69) and ultrasound indices of cerebral autoregulation were compared in FD patients and controls. The potential association of ultrasound indices of impaired cerebral autoregulation with white matter lesions and leukoencephalopathy on brain MRI in FD patients was also evaluated.
Demographics and vascular risk factors were similar in 23 FD patients (43% women, mean age: 51 ± 13 years) and 46 healthy controls (43% women, mean age: 51 ± 13 years). The prevalence of increased PI (39%; 95% confidence interval [CI]: 20%-61%), decreased BHI (39%; 95% CI: 20%-61%), and the combination of increased PI and/or decreased BHI (61%; 95% CI: 39%-80%) was significantly (p < .001) higher in FD patients compared to healthy controls (2% [95% CI: 0.1%-12%], 2% [95% CI: 0.1%-12%], and 4% [95% CI: 0.1%-15%], respectively). However, indices of abnormal cerebral autoregulation were not associated independently with white matter hyperintensities and presented a low-to-moderate predictive ability for the discrimination of FD patients with and without white matter hyperintensities.
Impaired cerebral autoregulation as assessed by TCD appears to be highly more prevalent among FD patients compared to healthy controls.

Remote photoplethysmography (rPPG) is a promising contactless technology that uses videos of faces to extract health parameters, such as heart rate. Several methods for transforming red, green, and blue (RGB) video signals into rPPG signals have been introduced in the existing literature. The RGB signals represent variations in the reflected luminance from the skin surface of an individual over a given period of time. These methods attempt to find the best combination of color channels to reconstruct an rPPG signal. Usually, rPPG methods use a combination of prepossessed color channels to convert the three RGB signals to one rPPG signal that is most influenced by blood volume changes. This study examined simple yet effective methods to convert the RGB to rPPG, relying only on RGB signals without applying complex mathematical models or machine learning algorithms. A new method, GRGB rPPG, was proposed that outperformed most machine-learning-based rPPG methods and was robust to indoor lighting and participant motion. Moreover, the proposed method estimated the heart rate better than well-established rPPG methods. This paper also discusses the results and provides recommendations for further research.

OBJECTIVE: There has been increasing awareness that micro-vascular alteration or vascular inflammation has been associated with levodopa-induced dyskinesia in PD. Vascular endothelial function assessed by flow mediated dilation (FMD) is known to reflect early microvascular change. We compare the impact of levodopa or dopamine agonist treatment on the change of FMD in de novo PD patients.
METHODS: This retrospective study used a selected sample from registry. We identified de-novo PD patients who underwent FMD at baseline, and follow-up FMD after 1 year (± 2 month) of levodopa (n = 18) or dopamine agonist (n = 18) treatment.
RESULTS: FMD decreased after levodopa (8.60 ± 0.46 to 7.21 ± 0.4, p = 0.002) but there were no significant changes after DA treatment (8.33 ± 0.38 to 8.22 ± 0.33, p = 0.26). Homocysteine rose (11.52 ± 0.45 to 14.33 ± 0.68, p < 0.05) during levodopa treatment, but dopamine agonist had no effect (10.59 ± 0.38 to 11.38 ± 0.67, p = 0.184). Correlation analysis revealed that the changes in homocysteine level had non-significant correlation with FMD change (r =  - 0.30, p = 0.06). FMD change was not associated with age (p = 0.47), disease duration (p = 0.81), baseline motor UPDRS (p = 0.43), motor UPDRS change (p = 0.64), levodopa equivalent dose change (p = 0.65).
CONCLUSIONS: We found that 1-year levodopa treatment may adversely affect vascular endothelial function in de novo PD. Further studies are needed to clarify the exact pathogenesis and clinical implication of levodopa-induced endothelial dysfunction in PD.

BACKGROUND: The prevalence and significance of abnormal epicardial coronary vasomotor reactivity (ACVR) in patients with symptoms compatible with myocardial ischaemia remains ill-defined. Our diagnostic strategy is to perform a provocative test (PT) in every patient presenting with chest pain at rest, for whom coronary angiography does not reveal significant epicardial coronary artery disease (≥70% stenosis by visual assessment).
OBJECTIVE: To evaluate such a strategy in terms of incidence of ACVR, PT safety and patient outcomes.
METHODS: The present study was a retrospective observational study with a median clinical follow-up of 5years. The primary outcome was incidence of ACVR in patients with PT. Risk factors for ACVR and clinical follow-up were obtained, and the rate of major adverse cardiovascular and cerebrovascular events (MACCE; death, cardiovascular mortality, myocardial infarction, stroke and coronary revascularization) was reported.
RESULTS: ACVR was documented in 294 (12.4%) of the 2379 patients with PT, out of the 13,654 patients undergoing angiography. Patients with ACVR were more often female (43.9% vs. 30.0%; P<0.0001), current smokers (37.4% vs. 8.7%; P<0.0001) and had a suspected acute coronary syndrome (36.7% vs. 29.1%; P=0.005) at admittance compared with patients without ACVR. During clinical follow-up, MACCE occurred more frequently in patients with (9.8%) than in those without (3.7%) ACVR (hazard ratio [HR] 4.15, 95% confidence interval [CI] 2.62-6.57; P<0.0001), including more myocardial infarctions (4.0% vs. 0.4%; HR 17.8, 95% CI 6.41-49.5; P<0.0001) and more myocardial revascularizations (6.1% vs. 1.1%; HR 9.36, 95% CI 4.67-18.74; P<0.0001) compared with patients with normal PT at baseline.
CONCLUSIONS: ACVR is frequent in patients with symptoms compatible with myocardial ischaemia at rest, with no significant coronary stenosis. PT is a safe strategy to identify a population at high risk of recurrent ischaemic events.

Cerebrovascular dysfunction has been suggested as a physiomarker of Alzheimer\'s disease (AD)-associated neuronal degeneration, but the underlying mechanisms are still debated. Herein cerebral vasomotor reactivity (VMR, breath-hold index: BHI), metabolic activity (lobar SUVs, FDG PET MRI), amyloid load (Centiloid score, Flutemetamol PET MRI), hemispheric cortical thickness, white matter lesion load and cerebral blood flow (ASL) were studied in 43 consecutive subjects (mean age: 64 years, female 13), diagnosed with subjective cognitive impairment (SCI, n = 10), amnestic mild cognitive impairment (aMCI, n = 15), and probable Alzheimer\'s dementia (AD, n = 18). BHI was significantly reduced in AD and aMCI patients compared to SCI subjects. A highly significant inverse correlation was found between BHI and the centiloid score (r = -0.648, p < 0.001). There was moderate positive correlation between BHI and frontal, temporal and parietal FDG SUV and ASL values, and a borderline negative correlation with age and white matter lesion volume. The link between amyloid burden and VMR was independent and strong in linear regression models where all these parameters were included (β from -0.580 to -0.476, p < 0.001). In conclusion, our study confirms the negative association of cerebral amyloid accumulation and vasomotor reactivity in Alzheimer\'s disease with the most direct data to date in humans.