Alterations In Cerebral Perfusion Research Articles

Asymmetry in cerebral perfusion from circle of Willis arterial variations in normal population.

Angiographic and cadaveric studies have evidenced variations in the circle of Willis (CoW). Age-related changes in cerebral hemodynamics may be attributable to vascular variations. The objective is to assess interdependence of completeness of CoW with age using non-invasive MRA and cerebral perfusion using arterial spin labeling (ASL). This single-center, prospective study segregated 189 subjects into three groups: ≤5, 5 to 18, and >18years. Angiographic (complete CoW and vascular asymmetry index) using TOF and contrast-enhanced- (CE-) MRA, and perfusion (perfusion asymmetry index) data using ASL were obtained. One hundred and six (56.08%) subjects showed complete CoW on TOF and 100 (52.91%) on CE-MRA. Anterior and posterior collateral pathways were more prevalent in the younger population. Completeness of CoW decreased with increasing age, group 1 (54/60, 90% TOF; 51/60, 85% CE), group 2 (39/64, 60% TOF; 37/64, 56.92% CE), and group 3 (13/65, 20.31% TOF; 12/65, 18.75% CE); p-value < .0001. A statistically significant decrease in cerebral and cerebellar perfusion with increasing age was seen. Cerebellar to frontal perfusion change was higher in group 1. Fetal posterior cerebral artery (PCA) led to ipsilateral low and contralateral hyperperfusion flow asymmetries between occipital lobes. This study shows that a complete CoW is commoner in pediatrics than adults and with increasing age, the completeness of CoW decreases paralleled by decrease in cerebral and cerebellar perfusion. There is age-related shift of perfusion from hindbrain to forebrain and the regression of PCoA occurs with increasing age leading to alterations in cerebral perfusion and hemodynamics.

Association between Cognitive Decline and Altered Cerebral Perfusion in Adults with Moyamoya Disease after Revascularization

Introduction: Certain studies have observed that patients with moyamoya disease (MMD) have cognitive decline after revascularization. Thus, this study analyzed the relationship between cognitive decline and altered cerebral perfusion after revascularization. Methods: Here, 313 adult patients with MMD underwent single unilateral revascularization. First, cognitive function was scored using a Mini-Mental Scale (MMSE) and Montreal cognitive function scale (MoCA) before and 3 months after the operation (superficial temporal artery-middle cerebral artery anastomosis with encephalo-myo-synangiosis). Then, computed tomography perfusion was performed before and 1 week after the operation to assess the cerebral perfusion. Results: Our data showed that cognitive function decreased in 55 cases (17.6%) after revascularization. Furthermore, the incidence of cerebral hyperperfusion (CHP) was significantly higher in the cognitive decline group (49/55) than in the cognitive nondecline group (89.1% vs. 5.4%, p < 0.001). Results also showed that although all 55 patients had postoperative cognitive decline, 47 experienced relative cerebral blood flow (CBF) decrease at a relatively distant area of the anastomosis compared with that before the operation, which was significantly higher than in patients without cognitive decline (85.5% vs. 1.94%, p < 0.001). In addition, 41 patients had a simultaneous occurrence of local CHP and paradoxical CBF decrease at a relatively distant anastomosis area, which indicated the incident of watershed shift (WS). As observed, WS occurred in 74.5% of patients with cognitive decline, significantly higher than in patients without cognitive decline (74.5% vs. 0%, p < 0.0001). Through multiple logistic regression analysis, WS was also observed to be a strong independent risk factor for predicting postoperative cognitive decline 3 months after revascularization (odds ratio 17.780, 95% confidence interval 1.668–18.564; p = 0.017). Conclusion: Therefore, cognitive decline in patients with MMD after revascularization is related to WS, leading to an uneven distribution of CBF.

Brain vasculature disturbance in schizophrenia.

The vascular hypothesis of schizophrenia (SZ) postulates that brain endothelial dysfunction contributes to brain pathophysiology. This review discusses recent evidence for and against this hypothesis, including data related to blood-brain barrier (BBB), brain endothelium, and brain blood supply, to provide a critical weighed update. Different studies report a consistent proportion of SZ patients showing increased BBB permeability, reflected by higher levels of albumin in the cerebral spinal fluid. Of note, this was not a result of antipsychotic medication. The high inflammatory profile observed in some SZ patients is strongly associated with increased BBB permeability to circulating immune cells, and with more severe cognitive deficiencies. Also, sex was found to interact with BBB integrity and permeability in SZ. The strongest independent genetic association with SZ has been identified in FZD1, a hypoxia-response gene that is 600-fold higher expressed in early development endothelium as compared to adult brain endothelium. Regarding brain blood supply, there is evidence to suggest alterations in proper brain perfusion in SZ. Nonetheless, ex-vivo experiments suggested that widely used antipsychotics favor vasoconstriction; thus, alterations in cerebral perfusion might be related to the patients' medication. In some patients with SZ, a vulnerable brain endothelium may be interacting with environmental stressors, such as inflammation or hypoxia, converging into a more severe SZ symptomatology. Gene expression and performance of human brain endothelium could vary along with development and the establishment of the BBB; therefore, we encourage to investigate its possible contribution to SZ considering this dynamic context.

The fetal lamb model of congenital diaphragmatic hernia shows altered cerebral perfusion using contrast enhanced ultrasound

BackgroundNeurodevelopmental impairment is common in survivors of congenital diaphragmatic hernia (CDH). Altered cerebral perfusion in utero may contribute to abnormal brain development in CDH patients. Methods5 fetal lambs with surgical left-CDH and 5 controls underwent transuterine cranial Doppler and contrast enhanced ultrasound (CEUS). Global and regional perfusion metrics were obtained. Biometric and perfusion data were compared between groups via nonparametric Mann Whitney U test and Spearman's rank order correlation. ResultsNo significant differences in cerebral Doppler measurements were identified between groups. By CEUS, CDH animals demonstrated significantly decreased global brain perfusion and increased transit time. With focal regions-of-interest (ROIs), there was a tendency towards decreased perfusion in the central/thalamic region in CDH but not in the peripheral brain parenchyma. Transit time was significantly increased in both ROIs in CDH, whereas flux rate was decreased in the central/thalamic region but not the peripheral brain parenchyma. Biometric CDH severity was correlated to perfusion deficit. There was no difference in cardiomyocyte histology. ConclusionThe fetal lamb model of CDH shows altered cerebral perfusion as measured by CEUS, correlating to disease severity. This suggests a physiological abnormality in fetal cerebrovascular perfusion that may contribute to abnormal brain development and neurodevelopmental impairment in survivors.

Cerebral Blood Flow Alterations in Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis of Arterial Spin Labeling Studies

ObjectiveArterial spin labeling (ASL) studies have revealed inconsistent regional cerebral blood flow (CBF) alterations in patients with type 2 diabetes mellitus (T2DM). The aim of this systematic review and meta-analysis was to identify concordant regional CBF alterations in T2DM.MethodsA systematic review was conducted to the published literatures comparing cerebral perfusion between patients with T2DM and healthy controls using ASL. The seed-based d mapping (SDM) was further used to perform quantitative meta-analysis on voxel-based literatures and to estimate the regional CBF alterations in patients with T2DM. Metaregression was performed to explore the associations between clinical characteristics and cerebral perfusion alterations.ResultsA total of 13 studies with 14 reports were included in the systematic review and 7 studies with 7 reports were included in the quantitative meta-analysis. The qualitative review found widespread CBF reduction in cerebral lobes in T2DM. The meta-analysis found increased regional CBF in right supplementary motor area and decreased regional CBF in bilateral middle occipital gyrus, left caudate nucleus, right superior parietal gyrus, and left calcarine fissure/surrounding cortex in T2DM.ConclusionThe patterns of cerebral perfusion alterations, characterized by the decreased CBF in occipital and parietal lobes, might be the neuropathology of visual impairment and cognitive aging in T2DM.

Alteration of cerebral perfusion and cortical thickness in depression episodes: a comparative MRI study

Aim: We aimed to determine the difference between cerebral perfusion and cortical thickness between first attack and recurrent in major depression patients.&#x0D; Material and Method: Our study was conducted prospectively between 01.03.2017-03.03.2018 in Izzet Baysal University Psychiatry department. 40 patients (21 first episodes and 19 recurrent episodes) diagnosed with depression according to DSM 5 by the American Psychiatric Association and a control group of 16 healthy individuals were evaluated for cerebral blood flow and cortical thickness with Perfusion MRI. Patients were also evaluated by Hamilton depression rating scale.&#x0D; Findings: The cortical thickness was significantly decreased in recurrent attacks.There was no significant difference of CBF in first episode and recurrent episodes, except cingulate cortex, which showed significantly reduced CBF values in recurrent group. In patients with higher Hamilton depression scale points, the CBF values of insular cortex were decreased.&#x0D; Conclusion: These findings suggests that cortical atrophy and activation of default mode network in recurrent episodes which leads to decreased response to treatment.

Association of compromised cerebral perfusion with lenticulostriate artery impairments in the subacute phase of branch atheromatous disease.

Background Purpose:Whether altered cerebral perfusion is associated with the pathogenesis of single subcortical infarctions (SSIs) in the lenticulostriate artery (LSA) territory remains unclear.Objective:We aimed to assess whether cerebral perfusion abnormalities are related to LSA impairments in the subacute phase of SSIs and then to examine their correlations with etiological subtypes of SSIs.Methods:A total of 110 patients with acute SSIs in the LSA territory were prospectively recruited between July 2017 and October 2021, and they underwent magnetic resonance perfusion-weighted imaging (PWI) and whole-brain vessel-wall imaging (VWI) within 7 days of stroke onset. Based on VWI, patients were assigned to one of two SSI subtypes: branch atheromatous disease (BAD, n = 78, 70.9%) or lacunar infarction related to cerebral small vessel disease (CSVD-related LI, n = 32, 29.1%). Perfusion maps and LSA morphology were also quantitatively assessed.Results:Based on PWI, 22 patients (20%) had hypoperfusion and 88 (80%) showed normal perfusion. Compared with normal individuals, patients with hypoperfusion showed shorter average LSA length (23.48 ± 4.81 mm versus 25.47 ± 3.74 mm, p = 0.037). Compared with patients with CSVD-related LI, patients with BAD had significantly lower relative cerebral blood flow [0.95 (IQR 0.81–1.12) versus 1.04 (IQR 0.92–1.22); p = 0.036] and cerebral blood volume [0.95 (IQR 0.84–1.15) versus 1.14 (IQR 0.97–1.27); p = 0.020] after adjusting for hypertension, number of LSA branches, and infarct volume.Conclusion:Compromised cerebral perfusion is associated with impairments in the LSA and with BAD pathogenesis. Perfusion magnetic resonance imaging can provide important insights into acute SSI pathophysiology, and it may be useful for determining the clinical significance of perfusion abnormalities in BAD occurrence.

Perfusion heterogeneity of cerebral small vessel disease revealed via arterial spin labeling MRI and machine learning

Cerebral small vessel disease (CSVD) is associated with altered cerebral perfusion. However, global and regional cerebral blood flow (CBF) are highly heterogeneous across CSVD patients. The aim of this study was to identify subtypes of CSVD with different CBF patterns using an advanced machine learning approach. 121 CSVD patients and 53 healthy controls received arterial spin label MRI, T1 structural MRI and clinical measurements. Regional CBF were used to identify distinct perfusion subtypes of CSVD via a semi-supervised machine learning algorithm. Statistical analyses were used to explore alterations in CBF, clinical measures, gray and white matter volume between healthy controls and different subtypes of CSVD. Correlation analysis was used to assess the association between clinical measures and altered CBF in each CSVD subtype. Three subtypes of CSVD with distinct CBF patterns were found. Subtype 1 showed decreased CBF in the temporal lobe and increased CBF in the parietal and occipital lobe. Subtype 2 exhibited decreased CBF in the right hemisphere of the brain, and increased CBF in the left cerebrum. Subtype 3 demonstrated decreased CBF in the posterior part of the brain, and increased CBF in anterior part of the brain. The three subtypes also differed significantly in gender (p = 0.005), the proportion of subjects with lacune (p = 0.002), with periventricular white matter hyperintensity (p = 0.043), and CSVD burden score (p = 0.048). In subtype 3, it was found that widespread decreased CBF was correlated with total CSVD burden score (r = -0.324, p = 0.029). Compared with healthy controls, the three CSVD subtypes also showed distinct volumetric patterns of white matter. The current results associate different subtypes with different clinical and imaging phenotypes, which can improve the understanding of brain perfusion alterations of CSVD and can facilitate precision diagnosis of CSVD.

Neurocardiovascular coupling in congenital diaphragmatic hernia patients undergoing different types of surgical treatment.

BACKGROUNDThe effect of peri-operative management on the neonatal brain is largely unknown. Triggers for perioperative brain injury might be revealed by studying changes in neonatal physiology peri-operatively.OBJECTIVETo study neonatal pathophysiology and cerebral blood flow regulation peri-operatively using the neuro-cardiovascular graph.DESIGNObservational, prospective cohort study on perioperative neuromonitoring. Neonates were included between July 2018 and April 2020.SETTINGMulticentre study in two high-volume tertiary university hospitals.PATIENTSNeonates with congenital diaphragmatic hernia were eligible if they received surgical treatment within the first 28 days of life. Exclusion criteria were major cardiac or chromosomal anomalies, or syndromes associated with altered cerebral perfusion or major neurodevelopmental impairment. The neonates were stratified into different groups by type of peri-operative management.INTERVENTIONEach patient was monitored using near-infrared spectroscopy and EEG in addition to the routine peri-operative monitoring. Neurocardiovascular graphs were computed off-line.MAIN OUTCOME MEASURESThe primary endpoint was the difference in neurocardiovascular graph connectivity in the groups over time.RESULTSThirty-six patients were included. The intraoperative graph connectivity decreased in all patients operated upon in the operation room (OR) with sevoflurane-based anaesthesia (P < 0.001) but remained stable in all patients operated upon in the neonatal intensive care unit (NICU) with midazolam-based anaesthesia. Thoracoscopic surgery in the OR was associated with the largest median connectivity reduction (0.33 to 0.12, P < 0.001) and a loss of baroreflex and neurovascular coupling. During open surgery in the OR, all regulation mechanisms remained intact. Open surgery in the NICU was associated with the highest neurovascular coupling values.CONCLUSIONNeurocardiovascular graphs provided more insight into the effect of the peri-operative management on the pathophysiology of neonates undergoing surgery. The neonate's clinical condition as well as the surgical and the anaesthesiological approach affected the neonatal physiology and CBF regulation mechanisms at different levels.TRIAL REGISTRATIONNL6972, URL: https://www.trialre-gister.nl/trial/6972.

Digoxin Ameliorates Glymphatic Transport and Cognitive Impairment in a Mouse Model of Chronic Cerebral Hypoperfusion.

The glymphatic system plays a pivotal role in maintaining cerebral homeostasis. Chronic cerebral hypoperfusion, arising from small vessel disease or carotid stenosis, results in cerebrometabolic disturbances ultimately manifesting in white matter injury and cognitive dysfunction. However, whether the glymphatic system serves as a potential therapeutic target for white matter injury and cognitive decline during hypoperfusion remains unknown. Here, we established a mouse model of chronic cerebral hypoperfusion via bilateral common carotid artery stenosis. We found that the hypoperfusion model was associated with significant white matter injury and initial cognitive impairment in conjunction with impaired glymphatic system function. The glymphatic dysfunction was associated with altered cerebral perfusion and loss of aquaporin 4 polarization. Treatment of digoxin rescued changes in glymphatic transport, white matter structure, and cognitive function. Suppression of glymphatic functions by treatment with the AQP4 inhibitor TGN-020 abolished this protective effect of digoxin from hypoperfusion injury. Our research yields new insight into the relationship between hemodynamics, glymphatic transport, white matter injury, and cognitive changes after chronic cerebral hypoperfusion.

Altered cerebral perfusion and microstructure in advanced Parkinson’s disease and their associations with clinical features

ABSTRACT Objective To explore the whole cerebral perfusion and microstructure alteration patterns in Parkinson’s disease (PD) and the associations of these patterns with clinical features. Methods Forty-one subjects [20 PD patients and 21 healthy controls (HCs)] underwent arterial spin labeling (ASL), diffusion tensor imaging (DTI) and 3D T1-weighted imaging (T1WI) MRI. The cerebral blood flow (CBF) of the whole brain and the fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD) and mean diffusivity (MD) of subcortical and cerebellar regions were measured and compared between groups. Pearson’s correlation was calculated between MRI measurements and clinical features [Unified Parkinson’s Disease Rating Scale (UPDRS), UPDRS III, Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA) and olfactory test scores]. Results Compared to HCs, PD patients showed lower CBF in the frontal, parietal and temporal lobes but higher CBF in bilateral hippocampi, red nuclei, right substantia nigra, thalamus and most cerebellar regions. The MD in the right thalamus and several regions in the cerebellum increased in PD compared to HCs. In PD patients, the total UPDRS, UPDRS III, MoCA, MMSE and olfactory test scores were related to FA or CBF in cerebellum. (all p < 0.05) Conclusion Hypoperfusion in cortical regions, together with hyperperfusion in subcortical and cerebellar regions may be the characteristic perfusion pattern in advanced PD patients. The microstructures of the right thalamus and cerebellum were changed in PD patients. The cognitive, motor and olfactory performance of PD patients is closely related to the perfusion and microstructure of the brain, especially the cerebellum.

Correlation between Head Computed Tomography Scan, Pre-operative Blood Lactate, and Pre-operative Glucose Level in Acute Traumatic Subdural Hematoma

Acute traumatic subdural hematoma (SDH) is a focal brain injury resulting in alteration of cerebral perfusion and glucose metabolism, which would also results in hyperglicemia-induced-hyperlactatemia. A cross-sectional study was performed to analyze acute traumatic SDH patients by head CT scan and observe the effect on pre-operative blood lactate and blood glucose levels in 40 acute traumatic SDH patients at Dr. Hasan Sadikin Hospital, Bandung, Indonesia during the period of July-September 2013. Somers' D correlation were used in the analysis with a p-value of ≤0.05 considered as significant with 95% confidence interval. The mean values of pre-operative blood lactate and blood glucose levels were 3.16±1.49 mmol/L and 155.85±32.95 mg/dl, respectively with a strong positive correlation between the hematoma thickness and the increase in blood lactate (r= 0.656; p= 0.021) and a moderate positive correlation with increased blood glucose (r= 0.556; p= 0.025). In addition, the compressed cistern also had a very weak positive correlation with increase in blood lactate (r =0.156; p=0.043) and very weak positive correlation with increase in blood glucose (r= 0.139; p=0.056) while the midline shift had a weak positive correlation with increased blood lactate (r=0.353; p= 0.041) and a weak positive correlation with increased blood glucose (r = 0.333; p= 0.046). In conclusion, increased hematoma thickness, compressed cistern, and midline shift seen on head CT scan correlate with increasing blood lactate and glucose levels in acute traumatic SDH. Head CT scan, blood lactate level, and blood glucose level can be considered as one of the routine examinations to determine acute traumatic SDH severity at the macroscopic and cellular level.

Cerebral perfusion responses to active standing are attenuated in patients with vasovagal syncope

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Irish Research Council (IRC): Government of Ireland Postgraduate Scholarship Programme 2018, Dublin, Ireland Fundació Universitària Agustí Pedro i Pons, Universitat de Barcelona, Barcelona, Spain Background Syncope is a transient loss of consciousness due to cerebral hypoperfusion. While traditionally peripheral haemodynamics are monitored during clinical assessment of syncope, relatively little is known about cerebrovascular haemodynamics during orthostasis in patients with syncope. Purpose Here we investigated whether young patients with syncope present an altered cerebral perfusion when compared to healthy controls. Given potential hyper-reactivity of the autonomic nervous system previously reported in these patients, we hypothesise that an overly active cerebral autoregulation will be present in patients with syncope. Methods Consecutive patients were prospectively recruited from a National Falls and Syncope Unit, and a convenience sample of young healthy community dwelling adults was recruited from a local university (16-30 years). Participants performed a 3 minute active stand test with continuous measurement of beat-to-beat peripheral haemodynamics (blood pressure (BP), heart rate (HR)) and changes in concentration of oxygenated Δ[O2Hb] and deoxygenated Δ[HHb] haemoglobin were derived from a near-infrared spectroscopy (NIRS) monitor. Baseline, steady state and other time domain features were derived for Δ[O2Hb] (nadir, overshoot, overshoot-to-nadir, overshoot-to-nadir recovery rate) and Δ[HHb] (peak, trough, peak-to-trough, peak-to-trough recovery rate) and multiple linear regression was used to compare differences between the two groups correcting for covariates (p &amp;lt; 0.05 significant). Results Patients (n = 40) were younger (20(5.5) vs 23(1) years, p = 0.003) than controls (n = 17) and were well matched in gender, weight, height, BMI and resting haemodynamics. Patients had a smaller Δ[O2Hb] overshoot-to-nadir difference (β: -0.749, CI:(-1.593 0.094), p = 0.08), a slower Δ[O2Hb] recovery rate (β: -0.186, CI:(-0.388 0.016), p = 0.071), and smaller Δ[HHb] peak-to-trough difference (β: -0.530, CI:( -0.921 0.138), p = 0.018) and slower Δ[HHb] recovery rate (β: -0.151, CI: (0.244 0.057), p = 0.008). Conclusion Patients with syncope had signs of an attenuated cerebral oxygenation response to an AS when compared to controls. We hypothesise that this is due to hyper-reactive cerebral autoregulation mechanism, which might be related to a hyper-sensitive autonomic system. Furthering our understanding of vasovagal syncope physiology can help inform future interventions and treatments. This study shows the clinical value of measuring cerebral perfusion using NIRS, an easy to use and readily applicable tool, in the assessment of syncope. Abstract Figure. Cerebral oxygenation upon standing

Neonatal Music Therapy and Cerebral Oxygenation in Extremely and Very Preterm Infants: a Pilot Study

Music therapy is a novel intervention that may minimize neonatal stress. The mechanism of action is still largely unknown. We hypothesized that one mechanism of action regards altered brain oxygenation (either due to altered cerebral perfusion or altered cerebral oxygen consumption). We measured cerebral oxygenation before, during and after music therapy sessions using Near-Infrared Spectroscopy (NIRS). We extracted data on cerebral oxygen saturation (rcSO2) and calculated cerebral fractional tissue oxygen extraction (cFTOE). In addition, we measured heart rate. We included 20 infants, receiving 44 music therapy sessions. Median gestational age was 27 weeks, the majority were males. We identified two distinct reactions: in one group rcSO2 increased and cFTOE decreased during therapy compared with before therapy, whereas in the other group rcSO2 decreased and cFTOE increased during therapy compared with before therapy. The first may indicate a sedative effect, whereas the second may reflect a hyperalert state. The observed changes in heart rate may contribute to these observations through altered cerebral perfusion. The clinical significance of these two distinct reactions for music processing and (future) neurological functioning in these infants warrants further investigation.

The Use of Near-Infrared Spectroscopy and/or Transcranial Doppler as Non-Invasive Markers of Cerebral Perfusion in Adult Sepsis Patients With Delirium: A Systematic Review.

Background:Several studies have previously reported the presence of altered cerebral perfusion during sepsis. However, the role of non-invasive neuromonitoring, and the impact of altered cerebral perfusion, in sepsis patients with delirium remains unclear.Methods:We performed a systematic review of studies that used near-infrared spectroscopy (NIRS) and/or transcranial Doppler (TCD) to assess adults (≥18 years) with sepsis and delirium. From study inception to July 28, 2020, we searched the following databases: Ovid MedLine, Embase, Cochrane Library, and Web of Science.Results:Of 1546 articles identified, 10 met our inclusion criteria. Although NIRS-derived regional cerebral oxygenation was consistently lower, this difference was only statistically significant in one study. TCD-derived cerebral blood flow velocity was inconsistent across studies. Importantly, both impaired cerebral autoregulation during sepsis and increased cerebrovascular resistance were associated with delirium during sepsis. However, the heterogeneity in NIRS and TCD devices, duration of recording (from 10 seconds to 72 hours), and delirium assessment methods (e.g., electronic medical records, confusion assessment method for the intensive care unit), precluded meta-analysis.Conclusion:The available literature demonstrates that cerebral perfusion disturbances may be associated with delirium in sepsis. However, future investigations will require consistent definitions of delirium, delirium assessment training, harmonized NIRS and TCD assessments (e.g., consistent measurement site and length of recording), as well as the quantification of secondary and tertiary variables (i.e., Cox, Mxa, MAPOPT), in order to fully assess the relationship between cerebral perfusion and delirium in patients with sepsis.

Altered cerebral perfusion in response to chronic mild hypercapnia and head-down tilt Bed rest as an analog for Spaceflight.

Following prolonged stays on the International Space Station (ISS), some astronauts exhibit visual acuity changes, ophthalmological findings, and mildly elevated intracranial pressures as part of a novel process called spaceflight-associated neuro-ocular syndrome (SANS). To determine the pathophysiology of SANS, NASA conducted a multi-investigator study in which 11 healthy participants underwent head-down tilt bed rest, mimicking microgravity-induced cephalad fluid shifts, combined with elevated ambient CO2 levels similar to those on the ISS (HDT+CO2). As part of that study, we examined the effects of HDT+CO2 on cerebral perfusion. Using arterial spin labeling, we compared cerebral perfusion before, during, and after HDT+CO2 in participants who developed SANS (n = 5) with those who did not (n = 6). All participants demonstrated a decrease in perfusion during HDT+CO2 (mean decrease of 25.1% at HDT7 and 16.2% at HDT29); however, the timing and degree of change varied between the groups. At day 7 of HDT+CO2, the SANS group experienced a greater reduction in perfusion than the non-SANS group (p =.05, 95% CI:-0.19 to 16.11, d=.94, large effect). Conversely, by day 29 of HDT+CO2, the SANS group had significantly higher perfusion (approaching their baseline) than the non-SANS group (p = .04, 95% CI:0.33 to 13.07, d=1.01, large effect). Compared with baseline and recovery, HDT+CO2 resulted in reduced cerebral perfusion which varied based on SANS status. Further studies are needed to unravel the relative role of HDT vs hypercapnia, to determine if these perfusion changes are clinically relevant, and whether perfusion changes contribute to the development of SANS during spaceflight.

Regional cerebral perfusion alterations in subjective cognitive decline measured by arterial spin labeling MRI

AbstractBackgroundIndividuals with subjective cognitive decline (SCD) are at high risk of developing Alzheimer's disease (AD) (Jessen et al., 2014). Changes in cerebral perfusion, particularly cerebral blood flow (CBF), are a feature of AD and has also been shown in pre‐dementia stages (Binnewijzend et al., 2016). This study investigates regional CBF and its association with cognition in individuals with SCD and healthy older adults.MethodCognitive performance and cerebral perfusion were assessed in 81 individuals with SCD (age 68±5 years) and 46 healthy controls (age 71±6 years). Regional CBF (mL/100g/min) was assessed by arterial spin labeling MRI and quantified in AD‐vulnerable regions (Wirth et al., 2016). The preclinical Alzheimer’s cognitive composite (PACC5) and composite scores for selected cognitive domains were calculated. General linear models were conducted to assess group differences in regional CBF as well as associations between regional CBF and cognitive performance. Interaction effect of group and regional CBF on cognitive performance was determined using the same method. All analyses were adjusted for potential confounders (including sex, age, and body mass index).ResultParticipants with SCD showed decreased CBF in the hippocampus (p=.038) and the basal ganglia (p=.014) compared to healthy controls. Moreover, participants with SCD exhibited greater CBF in the inferior temporal gyrus than healthy controls (p=.006). Across all participants, CBF in the basal ganglia was positively associated with executive function (p=.016), memory (p=.018), and PACC5 (p=.001). Exploratory investigations within each group revealed these associations only in healthy controls (p=.032, .037, .004, respectively). However, no effect of group was found on the relationship between regional CBF and cognitive performance.ConclusionOur findings indicate that alterations of cerebral perfusion are already detectable in the stage of SCD, in particular in the hippocampus, basal ganglia, and inferior temporal gyrus. In addition, cognitive performance was positively associated with CBF in the basal ganglia across all subjects; however, this effect was mainly driven by the healthy controls. Thus, our findings may point towards early pathological changes affecting the association between regional CBF and cognition in SCD, which needs to be evaluated in further studies.

Neurodevelopmental Outcomes in Congenital Heart Disease: A Review

We review the etiologies of neurodevelopmental outcomes in patients with congenital heart disease. Developmental delays have been identified in patients with congenital heart disease (CHD). Though historically neurodevelopmental morbidity in patients with CHD was thought to be surgically related, recent advances in imaging technology and the ability to prospectively provide longitudinal follow-up indicate multiple complex etiologies of neurodevelopmental delay in this group. It has been suggested that alterations in cerebral perfusion is related to cerebral dysgenesis and immaturity. Additionally, while there has been significant improvement in surgical technique, the brain is still vulnerable to ischemia and injury, further placing the patient at risk for developmental delays. The neurodevelopmental and cognitive delays span many domains and may not be detected until adolescence when cognitive and neurobehavioral demands increase. Given these comorbidities, there is a need for early and frequent multidisciplinary assessments of the patient and early identification of delays to provide access to resources to improve these patients’ quality of life.

Altered cerebral perfusion in bipolar disorder: A pCASL MRI study.

Neurovascular abnormalities are relevant to the pathophysiology of bipolar disorder (BD), which can be assessed using cerebral blood flow (CBF) imaging. CBF alterations have been identified in BD, but studies to date have been small and inconclusive. We aimed to determine cortical gray matter CBF (GM-CBF) differences between BD and healthy controls (HC) and to identify relationships between CBF and clinical or cognitive measures. Cortical GM-CBF maps were generated using Pseudo-Continuous Arterial Spin Labeling (pCASL) for 109 participants (BD, n=61; HC, n=48). We used SnPM13 to perform non-parametric voxel-wise two-sample t-tests comparing CBF between groups. We performed multiple linear regression to relate GM-CBF with clinical and cognitive measures. Analysis was adjusted for multiple comparisons with 10,000 permutations. Significance was set at a voxel level threshold of P<.001 followed by AlphaSim cluster-wise correction of P<.05. Compared to HCs, BD patients had greater GM-CBF in the left lateral occipital cortex, superior division and lower CBF in the right lateral occipital, angular and middle temporal gyrus. Greater GM-CBF in the left lateral occipital cortex correlated with worse working memory, verbal memory, attention and speed of processing. We found using voxel-wise regression that decreased gray matter CBF in the bilateral thalamus and cerebellum, and increased right fronto-limbic CBF were associated with worse working memory. No clusters were associated with clinical variables after FDR correction. Cortical GM-CBF alterations are seen in BD and may be related to cognitive function, which suggest neurovascular unit dysfunction as a possible pathophysiologic mechanism.

Brain perfusion during manic episode and at 6-month follow-up period in bipolar disorder patients: Correlation with cognitive functions.

BackgroundPatterns of altered cerebral perfusion and cognitive dysfunction have been described in Bipolar Disorder (BD) acute episodes and euthymia. Knowledge of the relationship between cognitive function and perfusion in a manic state and status when followed up is still limited.ObjectiveTo describe brain perfusion alterations and its relationship with cognitive impairment in patients with BD during manic episodes and after 6 months.MethodsObservational‐prospective study in 10 type I BD adults during moderate‐severe manic episodes. We assessed sociodemographic data and clinical variables as well as cognitive function through Screening for Cognitive Impairment in Psychiatry (SCIP‐S). Finally, we performed a Brain Perfusion SPECT using a Tc99m‐ethyl cysteine dimer.ResultsDuring manic episodes, patients showed cognitive impairment with a mean SCIP‐S score of 63.8 ± 17.16. This was positively correlated with perfusion measured as relative reuptake index (RRI) at the right temporal pole (ρ = 0.65 p = .0435) and negatively correlated with right the orbitofrontal cortex (ρ = −0.70 p = .0077) and the right subgenual cingulate cortex (ρ = −0.70 p = .0256). Episode severity measured by the Young Mania Rating Scale (YMRS) positively correlated with RRI at the right temporal pole (ρ = 0.75, p = .01). At follow‐up, six patients were taking treatment and were euthymic, we found a negative correlation with the YMRS and RRI at the bilateral orbitofrontal cortex (ρ = −0.8827, p = .019). They did not show significant improvement in cognitive performance at SCIP‐S, and there was negative correlation with the following of the SCIP‐S subscales; processing speed with the bilateral dorsolateral prefrontal, the bilateral medial prefrontal, the left temporal pole cortex RRI, and verbal fluency with the bilateral anterior cingulate cortex RRI.ConclusionCognitive impairment was correlated with brain perfusion patterns at baseline and follow‐up. Large sample size studies with longer follow‐up are needed to describe the changes in perfusion and cognitive functions in BD.