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Background: In recent years, cases of dystextia (texting disabilities) and dystypia (typing disabilities) have been reported. However, reports describing isolated dystextia without aphasia or other cognitive impairments are rare, and the detailed pathophysiology is not fully understood. Most Japanese people use the alphabetical spelling system (Romaji) for texting and typing. Herein, we report the case of a man with isolated dystextia and dystypia resulting from Romaji conversion difficulties. Case presentation: A 48-year-old, right-handed Japanese man developed texting and typing difficulties. The standard neuropsychological tests showed no signs of aphasia or other cognitive impairments, except for slight executive dysfunction. Thus, isolated dystextia and dystypia were diagnosed. Furthermore, the patient experienced Romaji conversion difficulties. Magnetic resonance imaging revealed a subcortical infarction in the left cerebral hemisphere. Single photon emission tomography revealed hypoperfusion, including in the left dorsolateral frontal cortex. Conclusions: The left dorsolateral frontal cortex may be related to Romaji conversion in Japanese individuals. Therefore, diaschisis of the left dorsolateral frontal cortex due to subcortical lesions may have impaired Romaji conversion, leading to dystextia and dystypia, in this patient. [ABSTRACT FROM AUTHOR]

Mature myelinating oligodendrocytes, the cells that produce the myelin sheath that insulates axons in the central nervous system, have distinct energetic and metabolic requirements compared to neurons. Neurons require substantial energy to execute action potentials, while the energy needs of oligodendrocytes are directed toward building the lipid‐rich components of myelin and supporting neuronal metabolism by transferring glycolytic products to axons as additional fuel. The utilization of energy metabolites in the brain parenchyma is tightly regulated to meet the needs of different cell types. Disruption of the supply of metabolites can lead to stress and oligodendrocyte injury, contributing to various neurological disorders, including some demyelinating diseases. Understanding the physiological properties, structures, and mechanisms involved in oligodendrocyte energy metabolism, as well as the relationship between oligodendrocytes and neighboring cells, is crucial to investigate the underlying pathophysiology caused by metabolic impairment in these disorders. In this review, we describe the particular physiological properties of oligodendrocyte energy metabolism and the response of oligodendrocytes to metabolic stress. We delineate the relationship between oligodendrocytes and other cells in the context of the neurovascular unit, and the regulation of metabolite supply according to energetic needs. We focus on the specific bioenergetic requirements of oligodendrocytes and address the disruption of metabolic energy in demyelinating diseases. We encourage further studies to increase understanding of the significance of metabolic stress on oligodendrocyte injury, to support the development of novel therapeutic approaches for the treatment of demyelinating diseases. [ABSTRACT FROM AUTHOR]

Background: Selective antegrade cerebral perfusion (sACP) is a crucial cerebral protection technique employed during aortic dissection surgeries involving cardiopulmonary bypass. However, postoperative neurological complications, particularly those related to cannulation issues and perfusion problems, remain a significant concern. Case Presentation: This case report details an unusual instance where a 38-year-old male patient with Marfan syndrome experienced cerebral hypoperfusion during emergency surgery for Stanford Type A aortic dissection. Despite following standard protocols, a significant drop in regional cerebral oxygen saturation (rSO2) and abnormal blood pressure fluctuations were observed shortly after initiating sACP via the innominate artery. After initial attempts to optimize perfusion flow proved ineffective, the cannulation position was adjusted, leading to improvements. Nevertheless, the patient subsequently exhibited signs of cerebral hypoperfusion and was found to have suffered a new cerebral infarction. Conclusions: This case report underscores the importance of precise cannula placement during sACP procedures and the dire consequences that can arise from improper positioning. It emphasizes the need for continuous monitoring and prompt intervention in cases of abnormal cerebral oxygenation and blood pressure, as well as the value of considering cannulation-related issues as potential causes of postoperative neurological complications. [ABSTRACT FROM AUTHOR]

Background/Objectives: Diabetic retinopathy (DR) is a common diabetes complication that can lead to blindness through vision-threatening complications like clinically significant macular edema and proliferative retinopathy. Identifying eyes at risk of progression using non-invasive methods could help develop targeted therapies to halt diabetic retinal disease progression. Methods: A set of 82 imaging and systemic features was used to characterize the progression of nonproliferative diabetic retinopathy (NPDR). These features include baseline measurements (static features) and those capturing the temporal dynamic behavior of these static features within one year (dynamic features). Interpretable models were trained to distinguish between eyes with Early Treatment Diabetic Retinopathy Study (ETDRS) level 35 and eyes with ETDRS levels 43–47. The data used in this research were collected from 109 diabetic type 2 patients (67.26 ± 2.70 years; diabetes duration 19.6 ± 7.26 years) and acquired over 2 years. Results: The characterization of the data indicates that NPDR progresses from an initial stage of hypoperfusion to a hyperperfusion response. The performance of the classification model using static features achieved an area under the curve (AUC) of the receiver operating characteristics equal to 0.84 ± 0.07, while the model using both static and dynamic features achieved an AUC of 0.91 ± 0.05. Conclusion: NPDR progresses through an initial hypoperfusion stage followed by a hyperperfusion response. Characterizing and automatically identifying this disease progression stage is valuable and necessary. The results indicate that achieving this goal is feasible, paving the way for the improved evaluation of progression risk and the development of better-targeted therapies to prevent vision-threatening complications. [ABSTRACT FROM AUTHOR]

Background: Spinal cord injury (SCI) disrupts intestinal barrier function, thereby increasing antigen permeation and leading to poor outcomes. Despite the intestinal tract's anatomic and physiologic heterogeneity, studies following SCI have not comprehensively addressed intestinal pathophysiology with regional specificity. Aims and Methods: We used an experimental model of high thoracic SCI to investigate (1) regional mucosal oxidative stress using dihydroethidium labeling; (2) regional paracellular permeability to small- and large-molecular probes via Ussing chamber; (3) regional intestinal tight junction (TJ) protein expression; and (4) hindgut perfusion via the caudal mesenteric artery. Results: Dihydroethidium staining was significantly elevated within duodenal mucosa at 3-day post-SCI. Molar flux of [14C]-urea was significantly elevated in duodenum and proximal colon at 3-day post-SCI, while molar flux of [3H]-inulin was significantly elevated only in duodenum at 3-day post-SCI. Barrier permeability was mirrored by a significant increase in the expression of pore-forming TJ protein claudin-2 in duodenum and proximal colon at 3-day post-SCI. Claudin-2 expression remained significantly elevated in proximal colon at 3-week post-SCI. Expression of the barrier-forming TJ protein occludin was significantly reduced in duodenum at 3-day post-SCI. Caudal mesenteric artery flow was unchanged by SCI at 3 days or 3 weeks despite significant reductions in mean arterial pressure. Conclusion: These data show that T3-SCI provokes elevated mucosal oxidative stress, altered expression of TJ proteins, and elevated intestinal barrier permeability in the proximal intestine. In contrast, mucosal oxidative stress and intestinal barrier permeability were unchanged in the hindgut after SCI. This regional heterogeneity may result from differential sensitivity to reduced mesenteric perfusion, though further studies are required to establish a causal link. Understanding regional differences in intestinal pathophysiology is essential for developing effective treatments and standards of care for individuals with SCI. [ABSTRACT FROM AUTHOR]

Background: Radioembolization with yttrium-90 (Y-90) is utilized to treat primary liver malignancies. The efficacy of this intra-arterial therapy in arterially hypoperfused tumors is not known. Methods: We reviewed data of patients with primary liver tumors treated with Y-90 prescription doses of at least 150 Gy. Baseline patient characteristics, treatment history, imaging-based tumor response assessments, and clinical outcome metrics were recorded. Tumors were classified as arterially hyperperfused versus hypoperfused on post-TARE Y-90 SPECT/CTs or pre-TARE hepatic perfusion SPECT/CTs. Perfusion status was correlated with tumor response assessments and clinical outcomes. Cox proportional hazards models were utilized to compare survival and progression-free survival. Inverse probability weighting was utilized to account for clinical factors and adjusted multivariable proportional hazards analyses to examine the relationship of quantitative perfusion and cancer outcomes. Results: Of 400 Y-90 treatments, 88 patients received a prescribed dose of at least 150 Gy and had pre- or post-treatment SPECT/CT images. 11 and 77 patients had arterially hypoperfused and hyperperfused lesions, respectively. On dedicated liver MRI or CT at 3 months after Y-90, the complete response rates were 5.6% and 16.5% in the hypoperfused and hyperperfused cohort, respectively (P = 0.60). When controlling for various clinical features, including tumor histology, patients with arterially hypoperfused tumors had significantly shorter progression-free survival (HR 1.87, 95% CI - 1.03 - 3.37, P = 0.039) and greater elsewhere liver (HR 3.36, 95% CI = 1.23 - 9.20, P = 0.019) and distant failure (HR 7.64 (2.71 - 21.54, P <0.001). In inverse probability weighted analysis, patients with arterially hypoperfused tumors had worse overall survival (P = 0.032). In the quantitative analysis, lower levels of lesion perfusion were also associated with worse clinical outcomes, again controlling for tumor histology. Conclusion: Compared to arterially hyperperfused tumors, hypoperfused primary liver tumors treated with Y-90 may have worse clinical outcomes. [ABSTRACT FROM AUTHOR]

Background: Preserving sufficient oxygen supply to the tissue is fundamental for maintaining organ function. However, our ability to identify those at risk and promptly recognize tissue hypoperfusion during abdominal surgery is limited. To address this problem, we aimed to develop a new method of perfusion monitoring that can be used during surgical procedures and aid surgeons' decision-making. Methods: In this experimental porcine study, thirteen subjects were randomly assigned one organ of interest [stomach (n = 3), ascending colon (n = 3), rectum (n = 3), and spleen (n = 3)]. After baseline perfusion recordings, using high-frequency, low-dose bolus injections with weight-adjusted (0.008 mg/kg) ICG, organ-supplying arteries were manually and completely occluded leading to hypoperfusion of the target organ. Continuous organ perfusion monitoring was performed throughout the experimental conditions. Results: After manual occlusion of pre-selected organ-supplying arteries, occlusion of the peripheral arterial supply translated in an immediate decrease in oscillation signal in most organs (3/3 ventricle, 3/3 ascending colon, 3/3 rectum, 2/3 spleen). Occlusion of the central arterial supply resulted in a further decrease or complete disappearance of the oscillation curves in the ventricle (3/3), ascending colon (3/3), rectum (3/3), and spleen (1/3). Conclusion: Continuous organ-perfusion monitoring using a high-frequency, low-dose ICG bolus regimen can detect organ hypoperfusion in real-time. [ABSTRACT FROM AUTHOR]

Aims: Hypoperfusion induces significant white matter injury in cerebral vascular disorders, including arteriosclerotic cerebral small vessel disease (aCSVD), which is prevalent among the elderly. Iron transport by blood vessel endothelial cells (BVECs) from the periphery supports oligodendrocyte maturation and white matter repair. This study aims to elucidate the association between iron homeostasis changes and white matter injury severity, and explore the crosstalk between BVECs and oligodendroglial lineage cells. Methods: In vivo: C57BL/6 mice were subjected to unilateral common carotid artery occlusion (UCCAO). In vitro: BVECs with myelin pretreatment were co‐cultured with oligodendrocyte progenitor cells (OPCs) or organotypic cerebellar slices subjected to oxygen and glucose deprivation. Results: Circulatory iron tends to be stored in aCSVD patients with white matter injury. Myelin debris endocytosis by BVECs impairs iron transport, trapping iron in the blood and away from the brain, worsening oligodendrocyte iron deficiency in hypoperfusion‐induced white matter injury. Iron accumulation in BVECs triggers ferroptosis, suppressing iron transport and hindering white matter regeneration. Intranasal holo‐transferrin (hTF) administration bypassing the BBB alleviates oligodendrocyte iron deficiency and promotes myelin regeneration in hypoperfusion‐induced white matter injury. Conclusion: The iron imbalance between BVECs and oligodendroglial lineage cells is a potential therapeutic target in hypoperfusion‐induced white matter injury. [ABSTRACT FROM AUTHOR]

Abstract Background Selective antegrade cerebral perfusion (sACP) is a crucial cerebral protection technique employed during aortic dissection surgeries involving cardiopulmonary bypass. However, postoperative neurological complications, particularly those related to cannulation issues and perfusion problems, remain a significant concern. Case Presentation This case report details an unusual instance where a 38-year-old male patient with Marfan syndrome experienced cerebral hypoperfusion during emergency surgery for Stanford Type A aortic dissection. Despite following standard protocols, a significant drop in regional cerebral oxygen saturation (rSO2) and abnormal blood pressure fluctuations were observed shortly after initiating sACP via the innominate artery. After initial attempts to optimize perfusion flow proved ineffective, the cannulation position was adjusted, leading to improvements. Nevertheless, the patient subsequently exhibited signs of cerebral hypoperfusion and was found to have suffered a new cerebral infarction. Conclusions This case report underscores the importance of precise cannula placement during sACP procedures and the dire consequences that can arise from improper positioning. It emphasizes the need for continuous monitoring and prompt intervention in cases of abnormal cerebral oxygenation and blood pressure, as well as the value of considering cannulation-related issues as potential causes of postoperative neurological complications.

PurposeTo assess if a novel automated method to spatially delineate and quantify the extent of hypoperfusion on multienergy CT angiograms can aid the evaluation of chronic thromboembolic pulmonary hypertension (CTEPH) disease severity.Materials and methodsMultienergy CT angiograms obtained between January 2018 and December 2020 in 51 patients with CTEPH (mean age, 47 years ± 17 [SD]; 27 women) were retrospectively compared with those in 110 controls with no imaging findings suggestive of pulmonary vascular abnormalities (mean age, 51 years ± 16; 81 women). Parenchymal iodine values were automatically isolated using deep learning lobar lung segmentations. Low iodine concentration was used to delineate areas of hypoperfusion and calculate hypoperfused lung volume (HLV). Receiver operating characteristic curves, correlations with preoperative and postoperative changes in invasive hemodynamics, and comparison with visual assessment of lobar hypoperfusion by two expert readers were evaluated.ResultsGlobal HLV correctly separated patients with CTEPH from controls (area under the receiver operating characteristic curve = 0.84; 10% HLV cutoff: 90% sensitivity, 72% accuracy, and 64% specificity) and correlated moderately with hemodynamic severity at time of imaging (pulmonary vascular resistance [PVR], ρ = 0.67; P < .001) and change after surgical treatment (∆PVR, ρ = -0.61; P < .001). In patients surgically classified as having segmental disease, global HLV correlated with preoperative PVR (ρ = 0.81) and postoperative ∆PVR (ρ = -0.70). Lobar HLV correlated moderately with expert reader lobar assessment (ρHLV = 0.71 for reader 1; ρHLV = 0.67 for reader 2).ConclusionAutomated quantification of hypoperfused areas in patients with CTEPH can be performed from clinical multienergy CT examinations and may aid clinical evaluation, particularly in patients with segmental-level disease.Keywords: CT-Spectral Imaging (Multienergy), Pulmonary, Pulmonary Arteries, Embolism/Thrombosis, Chronic Thromboembolic Pulmonary Hypertension, Multienergy CT, Hypoperfusion© RSNA, 2023.

Lipedema is a progressive connective tissue disease with enlargement of adipose tissue, fibrosis, fluid collection, and dermal thickening. Herein, we present a case of lipedema associated with skin hypoperfusion and ulceration in which soft tissue debulking with liposuction improved patients' symptoms. A 39-year-old female presented with asymmetric progressive initially unilateral lower limb swelling with severe pain with subsequent skin ulceration. Conservative management failed to improve her condition. After excluding other causes and detailed radiologic investigation, lipedema was diagnosed with an associated impaired skin perfusion. Trial of local wound care and compression therapy failed to improve the condition. Subsequent soft tissue debulking with circumferential liposuction and ulcer debridement and immediate compression showed dramatic improvement of the symptoms and skin perfusion. The unique nature of this case sheds light on lipedema as a loose connective tissue disease. Inflammation and microangiopathies explain the associated pain with hypoperfusion and ulceration being quite atypical and in part might be related to the large buildups of matrix proteins and sodium contents leading to fragility in microvessels with frequent petechiae and hematoma and subsequent tissue ischemia. Conservative measures like compression therapy plays a significant role in disease course. Surgical debulking with liposuction was shown to be efficacious in reducing the soft tissue load with improvement in limb pain, edema, circumference, and skin perfusion that was seen in our patient. Lipedema is a frequently misdiagnosed condition with disabling features. Skin involvement in lipedema with potential hypoperfusion was shown and it requires further investigation.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) is frequently complicated by delayed cerebral ischemia (DCI), leading to poor outcomes. Early diagnosis of DCI is crucial for improving survival and outcomes but remains challenging in comatose patients. In this study, we aimed to evaluate computed tomography with angiography and perfusion (P-CT) as a screening modality on postictal days four and eight for impending DCI after aSAH in comatose patients using vasospasm with hypoperfusion (hVS) as a surrogate and DCI-related infarction as an outcome measure. Two objectives were set: (1) to evaluate the screening's ability to accurately risk stratify patients and (2) to assess the validity of P-CT screening. Methods: We conducted a retrospective review of the records of comatose patients with aSAH from January 2019 to December 2021 who were monitored with P-CT scans on days four and eight. The event rates of DCI-related infarction, hVS, and endovascular rescue therapy (ERT) were analyzed, and the sensitivity, specificity, negative predictive value (NPV), and positive predictive value (PPV) for DCI were calculated. DCI-related infarction was defined as new secondary cerebral infarction > 48 h < 6 weeks post aSAH not attributable to other causes, and hVS was defined as arterial narrowing with corresponding hypoperfusion on P-CT. Results: Fifty-six comatose patients were included, and 98 P-CT scans were performed. The incidence of DCI-related infarction was 40%. Screening P-CT on days four and eight found vasospasm in 23% of all patients, including 11% with hVS. A positive hVS on day four or eight revealed a relative risk of 2.4 [95% confidence interval (CI) 1.13–5.11, p = 0.03], sensitivity of 23% (95% CI 8–45, p = 0.03), specificity of 95% (95% CI 36–100, p = 0.03), PPV of 0.83 (95% CI 0.36–1.00, p = 0.03), and NPV of 0.65 (95% CI 0.50–0.78). Six positive P-CT scans led to digital subtraction angiography in five patients, three of whom received ERT. All ERT-intervened patients developed DCI-related infarction. Conclusions: P-CT resulted in few interventions and often resulted in late detection of DCI at an irreversible stage. Although a positive P-CT result accurately predicts impending DCI-related infarction, screening on days four and eight alone in comatose patients with aSAH often fails to timely detect impending DCI. Based on our analysis, we cannot recommend P-CT as a screening modality. P-CT is likely best used as a confirmatory test prior to invasive interventions when guided by continuous multimodal monitoring; however, prospective studies with comparison groups are warranted. The need for a reliable continuous screening modality is evident because of the high rate of deterioration and narrow treatment window. [ABSTRACT FROM AUTHOR]

Background: Although laser Doppler imaging (LDI) accurately delineates a hypoperfused area to help target hyaluronidase treatment, laser speckle contrast imaging (LSCI) is more appropriate for assessing microvascular hemodynamics and has greater reproducibility than LDI. This study investigated the use of LSCI in the evaluation and treatment of six patients who developed vascular complications after facial dermal filler injections. Methods: The areas of vascular occlusion were accurately defined in real time by LSCI and were more precise than visual inspections or photographic evidence for guiding needling and hyaluronidase treatment. Results: All patients had achieved satisfactory outcomes as early as Day 2 of treatment and no procedure-related complications were reported after a median follow-up of 9.5 (7–37) days. Conclusion: LSCI accurately and noninvasively delineated vascular occlusions in real time among patients experiencing complications of facial dermal filler injections. Moreover, LSCI was more accurate than visual and photographic evaluations. Clinicians can use LSCI to reliably follow-up therapeutic outcomes after salvage interventions for vascular occlusions. Level of Evidence IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266. [ABSTRACT FROM AUTHOR]

Abdominal aortic aneurysm (AAA) is a vascular disease that involves aortic wall dilation. Cigarette smoking is an established risk factor and rupture, and nicotine may be a major contributor to the onset of AAA. In humans the condition is associated with stenosis of the vasa vasorum (VV), which may be caused by nicotine. In this study, we evaluated the effects of nicotine on VV pathology. After 4 weeks of nicotine administration to rats using an osmotic pump, the VV patency rate in the nicotine administration group was significantly lower than that in the control group. The levels of Ki-67, a cell proliferation marker, were significantly increased in the regions containing VV in the nicotine group, as were hypoxia inducible factor-α levels. Collagen levels around VV were significantly lower in the nicotine group than in the controls. Our data suggest that nicotine can cause VV stenosis by inducing abnormal proliferation of smooth muscle cells in the VV. The increased risk of AAA development due to cigarette smoking may be partially explained by nicotine-induced VV denaturation and collagen fiber degradation. [ABSTRACT FROM AUTHOR]

Lipedema is a progressive connective tissue disease with enlargement of adipose tissue, fibrosis, fluid collection, and dermal thickening. Herein, we present a case of lipedema associated with skin hypoperfusion and ulceration in which soft tissue debulking with liposuction improved patients' symptoms. A 39-year-old female presented with asymmetric progressive initially unilateral lower limb swelling with severe pain with subsequent skin ulceration. Conservative management failed to improve her condition. After excluding other causes and detailed radiologic investigation, lipedema was diagnosed with an associated impaired skin perfusion. Trial of local wound care and compression therapy failed to improve the condition. Subsequent soft tissue debulking with circumferential liposuction and ulcer debridement and immediate compression showed dramatic improvement of the symptoms and skin perfusion. The unique nature of this case sheds light on lipedema as a loose connective tissue disease. Inflammation and microangiopathies explain the associated pain with hypoperfusion and ulceration being quite atypical and in part might be related to the large buildups of matrix proteins and sodium contents leading to fragility in microvessels with frequent petechiae and hematoma and subsequent tissue ischemia. Conservative measures like compression therapy plays a significant role in disease course. Surgical debulking with liposuction was shown to be efficacious in reducing the soft tissue load with improvement in limb pain, edema, circumference, and skin perfusion that was seen in our patient. Lipedema is a frequently misdiagnosed condition with disabling features. Skin involvement in lipedema with potential hypoperfusion was shown and it requires further investigation. [ABSTRACT FROM AUTHOR]

INTRODUCTION: Transport of neonates from peripheral health centres to advanced neonatal intensive care units which are concentrated in urban areas is a necessity in India. The transport of newborn baby by a skilled and organised team reduces neonatal mortality and morbidity. Among the various pretransport and posttransport neonatal assessment scores, TOPS score, a bedside score to assess acute physiological parameters was chosen for the study. AIMS: To study the correlation of TOPS Score with survival rate among referred neonates. MATERIALS AND METHODS: TOPS score was assessed for 101 outborn neonates referred to tertiary teaching hospital during the study period. RESULTS: Among the study population, 67% were male, 57% were term, 60% had normal birth weight. At time of admission, 38% neonates had hypoxia, 12% had hypoperfusion, 10% had hypothermia, 2% had hypoglycaemia. TOPS score <2 was associated with survival and >2 was associated with significant mortality. CONCLUSION: TOPS score is a simple, bedside test to determine prognosis of referred neonates. It also helps to monitor care received by the neonates during transport. Appropriate care during transport is essential to decrease neonatal mortality. [ABSTRACT FROM AUTHOR]

CT perfusion (CTP) images can be easily and rapidly obtained on all modern CT scanners and have become part of the routine imaging protocol of patients with aneurysmal subarachnoid haemorrhage (aSAH). There is a growing body of evidence supporting the use of CTP imaging in these patients, however, there are significant differences in the software packages and methods of analysing CTP. In. addition, no quantitative threshold values for tissue at risk (TAR) have been validated in this patients’ population. Here we discuss the contribution of the technique in the identification of patients at risk of aSAH-related delayed cerebral ischemia (DCI) and in the assessment of the response to endovascular rescue therapy (ERT). We also address the limitations and pitfalls of automated CTP postprocessing that are specific to aSAH patients as compared to acute ischemic stroke (AIS).

BackgroundRadioembolization with yttrium-90 (Y-90) is utilized to treat primary liver malignancies. The efficacy of this intra-arterial therapy in arterially hypoperfused tumors is not known.MethodsWe reviewed data of patients with primary liver tumors treated with Y-90 prescription doses of at least 150 Gy. Baseline patient characteristics, treatment history, imaging-based tumor response assessments, and clinical outcome metrics were recorded. Tumors were classified as arterially hyperperfused versus hypoperfused on post-TARE Y-90 SPECT/CTs or pre-TARE hepatic perfusion SPECT/CTs. Perfusion status was correlated with tumor response assessments and clinical outcomes. Cox proportional hazards models were utilized to compare survival and progression-free survival. Inverse probability weighting was utilized to account for clinical factors and adjusted multivariable proportional hazards analyses to examine the relationship of quantitative perfusion and cancer outcomes.ResultsOf 400 Y-90 treatments, 88 patients received a prescribed dose of at least 150 Gy and had pre- or post-treatment SPECT/CT images. 11 and 77 patients had arterially hypoperfused and hyperperfused lesions, respectively. On dedicated liver MRI or CT at 3 months after Y-90, the complete response rates were 5.6% and 16.5% in the hypoperfused and hyperperfused cohort, respectively (P = 0.60). When controlling for various clinical features, including tumor histology, patients with arterially hypoperfused tumors had significantly shorter progression-free survival (HR 1.87, 95% CI - 1.03 - 3.37, P = 0.039) and greater elsewhere liver (HR 3.36, 95% CI = 1.23 - 9.20, P = 0.019) and distant failure (HR 7.64 (2.71 - 21.54, P < 0.001). In inverse probability weighted analysis, patients with arterially hypoperfused tumors had worse overall survival (P = 0.032). In the quantitative analysis, lower levels of lesion perfusion were also associated with worse clinical outcomes, again controlling for tumor histology.ConclusionCompared to arterially hyperperfused tumors, hypoperfused primary liver tumors treated with Y-90 may have worse clinical outcomes.

This article discusses the concept of the Laffer curve, which was popularized by economist Arthur Laffer in the 1970s. The Laffer curve illustrates the relationship between tax rates and tax revenue, suggesting that there is an optimal tax rate that maximizes government revenue. The article then applies this concept to the study of lactate kinetics in physiology. Lactate is produced by cells during anaerobic metabolism and is used as a measure of tissue perfusion. The article suggests that there may be two states of perfusion that result in the same blood lactate concentration, which could have implications for the interpretation of lactate levels in clinical practice. [Extracted from the article]

Purpose: To explore the relationship between obstructive sleep apnea (OSA) and hypoperfusion during ultra-early acute cerebral infarction. Patients and methods: Data were retrospectively collected from patients admitted to our hospital with acute cerebral infarction between January 2020 and January 2022, who underwent comprehensive whole-brain computed tomography perfusion imaging and angiography examinations within 6 h of onset. The F-stroke software automatically assessed and obtained relevant data (Tmax). The patients underwent an initial screening for sleep apnea. Based on their Apnea-Hypopnea Index (AHI), patients were categorized into an AHI ≤15 (n = 22) or AHI >15 (n = 25) group. The pairwise difference of the time-to-maximum of the residue function (Tmax) > 6 s volume was compared, and the correlation between AHI, mean pulse oxygen saturation (SpO2), oxygen desaturation index (ODI), percentage of time with oxygen saturation < 90% (T90%), and the Tmax >6 s volume was analyzed. Results: The Tmax >6 s volume in the AHI > 15 group was significantly larger than that in the AHI ≤ 15 group [109 (62–157) vs. 59 (21–106) mL, p = 0.013]. Spearman’s correlation analysis revealed Tmax >6 s volume was significantly correlated with AHI, mean SpO2, ODI, and T90% in the AHI > 15 group, however, no significant correlations were observed in the AHI ≤ 15 group. Controlling for the site of occlusion and Multiphase CT angiography (mCTA) score, AHI (β = 0.919, p < 0.001), mean SpO2 (β = −0.460, p = 0.031), ODI (β = 0.467, p = 0.032), and T90% (β =0.478, p = 0.026) remained associated with early hypoperfusion in the AHI > 15 group. Conclusion: In patients with acute cerebral infarction and AHI > 15, AHI, mean SpO2, ODI and T90% were associated with early hypoperfusion. However, no such relationship exists among patients with AHI ≤ 15. [ABSTRACT FROM AUTHOR]

Dementia is a devastating disorder that commonly affects people over the age of 65. Alzheimer’s disease and vascular dementia are the most common forms of dementias, A number of studies have implicated cardiovascular risks as important factors in the development of dementia. Loss of cognitive function and vascular risk factor produce pathological changes into the brain. Changes are Infarcts, Ischemia hypoperfusion, Hemoragic Brain and Atrophy (Degeneration of cells), Neurofibrillary tangles impairment. Bilateral Common Carotid Artery occlusion (BCCAO) has been considered as a critical cause for the development of cognitive decline and dementia of vascular origin. In our study hypoperfusion reduced oxidative stress, nitric oxide level, Acetylcholine, SOD (Superoxide Dismutase). TRPV1 Receptors have been reported to be beneficial in improving memory deterioration. Aim of this study is to explore the role of capsaicin in Bilateral Common Carotid Artery occlusion (BCCAO) induced vascular dementia .In clinical research capsaicin role is of antioxidant and other one shows anti-inflammatory actions. It showed significant cognitive deficits, cholinergic dysfunction (increased acetyl cholinesterase-AChE) activity along with increased brain oxidative stress (brain thiobarbituric acid reactive species), glutathione, as well as superoxide dismutase with an increase in malondialdehyde levels) and TTC (2,3,5 Triphenyltetrazolium chloride staining). Furthermore, treatment of capsaicin reduced BCCAO induced learning and memory deficits.(Morris water maze-MWM), locomotion (Actophotometer), and limited cholinergic dysfunction, oxidative stress, and tissue damage, Estimation of Brain Total Protein, infarct volume suggesting that capsaicin TRPV1 Receptors may provide benefits in BCCAO induced VaD. [ABSTRACT FROM AUTHOR]

AbstractBackgroundMethods/case reportResultsConclusionsWatershed infarcts (WIs) are a distinct type of stroke with a varying clinical presentation that affects the border areas between the territories of two cerebral arteries and are typically associated with hemodynamic impairment and internal carotid artery stenosis. However, there is a paucity of data concerning its association with the history of recreational substance and drug abuse.This case report presents a unique instance of bilateral internal watershed infarcts in a 23-year-old male with a history of polysubstance abuse, including methadone and cocaine. The patient’s presentation included confusion, lower limb weakness, and systemic complications such as acute liver injury and myonecrosis, underlying the complexity of the clinical scenario.The investigation revealed no evidence of arterial stenosis or thrombosis, leading to the conclusion that the infarctions were likely precipitated by a total loss of consciousness due to substance abuse-related cerebral hypoperfusion and vasoconstriction. Methadone and cocaine, both implicated in vasoconstriction, lowering the seizure threshold and contributing to QTc prolongation, thus leading to loss of consciousness, were identified as potential triggers for the episode.In the young adult population, it is important to consider drug abuse as an etiological trigger for watershed infarcts, whereas the multi-system involvement and atypical presentation highlight the need for a comprehensive approach. [ABSTRACT FROM AUTHOR]

Introduction: In the perioperative period, regional analgesia techniques may play an increasingly important role in "Enhanced Recovery After Surgery (ERAS)" programs, as they can facilitate recovery. We hypothesized that Erector Spinae Plane (ESP) block could improve regional perfusion, thereby limiting blood lactate increase. Therefore, we aimed to evaluate the effect of ESP block on intraoperative blood lactate levels in patients scheduled for elective on-pump cardiac surgery with ERAS protocol. Methods: A total of 68 adult patients scheduled for on-pump cardiac surgery were included. All patients were randomized to the ESP group and the non-ESP group. Blood lactate analyses were performed at intraoperative five-time points. C-Reactive protein (CRP) values were also measured. Results: Blood lactate values were significantly lower in the ESP group than in the Non-ESP group, at the end of CPB [1.78 (1.23–2.78) mmol L−1 to 2.63 (1.70–3.12) mmol L−1] and during the sternal closure period [1.78 (1.27–2.42) mmol L−1 to 2.40 (2.14–2.80) mmol L−1] (p = 0.039, p = 0.009). In addition, CRP values were significantly lower in the ESP group in the postoperative period [0.048 (0.036–0.105) g L−1 to 0.090 (0.049–0.154) g L−1] (p = 0.035). Conclusions: This study showed that preoperative bilateral single-shot ESP block significantly reduces intraoperative final blood lactate and postoperative CRP values. We consider that these results are related to the attenuation of intraoperative hypoperfusion and the alleviation of surgery-related postoperative inflammation. ERAS programs aim to achieve the rapid recovery of patients, a decrease in inflammation, and high-quality analgesia with less opioid consumption. Therefore, our results also prove that it is easier to reach the primary goals of ERAS programs with the application of ESP block in cardiac surgery. [ABSTRACT FROM AUTHOR]

Clinical populations with basal ganglia pathologies may present with language production impairments, which are often described in combination with comprehension measures or attributed to motor, memory, or processing-speed problems. In this systematic review and meta-analysis, we studied word production in four (vascular and non-vascular) pathologies of the basal ganglia: stroke affecting the basal ganglia, small vessel disease, Parkinson's disease, and Huntington's disease. We compared scores of these clinical populations with those of matched cognitively unimpaired adults on four well-established production tasks, namely picture naming, category fluency, letter fluency, and past-tense verb inflection. We conducted a systematic search in PubMed and PsycINFO with terms for basal ganglia structures, basal ganglia disorders and language production tasks. A total of 114 studies were included, containing results for one or more of the tasks of interest. For each pathology and task combination, effect sizes (Hedges' g) were extracted comparing patient versus control groups. For all four populations, performance was consistently worse than that of cognitively unimpaired adults across the four language production tasks (p-values < 0.010). Given that performance in picture naming and verb inflection across all pathologies was quantified in terms of accuracy, our results suggest that production impairments cannot be fully explained by motor or processing-speed deficits. Our review shows that while language production difficulties in these clinical populations are not negligible, more evidence is necessary to determine the exact mechanism that leads to these deficits and whether this mechanism is the same across different pathologies. [ABSTRACT FROM AUTHOR]

This systematic review, meta-analysis, and novel time course analysis examines microvascular failure in the treatment of acute ischemic stroke (AIS) patients undergoing endovascular therapy (EVT) and/or thrombolytic administration for stroke management. A systematic review and meta-analysis following PRIMSA-2020 guidelines was conducted along with a novel curve-of-best fit analysis to elucidate the time-course of microvascular failure. Scopus and PubMed were searched using relevant keywords to identify studies that examine recanalization and reperfusion assessment of AIS patients following large vessel occlusion. Meta-analysis was conducted using a random-effects model. Curve-of-best-fit analysis of microvascular failure rate was performed with a negative exponential model. Twenty-seven studies with 1151 patients were included. Fourteen studies evaluated patients within a standard stroke onset-to-treatment time window (≤6 hours after last known normal) and thirteen studies had an extended time window (>6 hours). Our analysis yields a 22% event rate of microvascular failure following successful recanalization (95% CI: 16–30%). A negative exponential curve modeled a microvascular failure rate asymptote of 28.5% for standard time window studies, with no convergence of the model for extended time window studies. Progressive microvascular failure is a phenomenon that is increasingly identified in clinical studies of AIS patients undergoing revascularization treatment. [ABSTRACT FROM AUTHOR]

The goal of reperfusion therapy for acute ischemic stroke (AIS) is to restore cerebral blood flow through recanalization of the occluded vessel. Unfortunately, successful recanalization does not always result in favorable clinical outcome. Post-recanalization perfusion deficits (PRPDs), constituted by cerebral hypo- or hyperperfusion, may contribute to lagging patient recovery rates, but its clinical significance remains unclear. This scoping review provides an overview of clinical and preclinical findings on post-ischemic reperfusion, aiming to elucidate the pattern and consequences of PRPD from a translational perspective. The MEDLINE database was searched for quantitative clinical and preclinical studies of AIS reporting PRPD based on cerebral circulation parameters acquired by translational tomographic imaging methods. PRPD and stroke outcome were mapped on a charting table, creating an overview of PRPD after AIS. Twenty-two clinical and twenty-two preclinical studies were included. Post-recanalization hypoperfusion is rarely reported in clinical studies (4/22) but unequivocally associated with detrimental outcome. Post-recanalization hyperperfusion is more commonly reported (18/22 clinical studies) and may be associated with positive or negative outcome. PRPD has been replicated in animal studies, offering mechanistic insights into causes and consequences of PRPD and allowing delineation of possible courses of PRPD. Complex relationships exist between PRPD and stroke outcome. Diversity in methods and lack of standardized definitions in reperfusion studies complicate the characterization of reperfusion patterns. Recommendations are made to advance the understanding of PRPD mechanisms and to further disentangle the relation between PRPD and disease outcome. [ABSTRACT FROM AUTHOR]

CCH, resulting from multiple cerebrovascular diseases, has been considered the primary cause of cognitive impairment in recent years. In this process, oxidative stress plays a critical role and damages hippocampal neurons. Research has shown that Salvia verticillata has a significant antioxidant and free radical-scavenging activity due to its polyphenolic compounds. Therefore, the present study aimed to evaluate the effect of Salvia verticillata on a rat model of chronic cerebral hypoperfusion. A total of 24 rats were subjected to Salvia verticillata or vehicle orally from one week before 2VO surgery for 14 days. Cerebral hypoperfusion was induced by the bilateral occlusion of the common carotid arteries (2VO, n = 12 and sham, n = 12). The cognition of rats was evaluated 1 week after surgery in the MWM. In the MWM test, 2VO rats showed longer escape latency time and swimming distance and spent a shorter time in the target quadrant (p < 0.05). Moreover, we observed that Salvia verticillata treatment significantly reduced escape latency time, shortened the swimming distance, and increased target quadrant time (p > 0.05). Our results indicated that Salvia verticillata treatment significantly improved cognitive deficits in cerebral ischemic rats, probably by reducing oxidative stress damage.

肢体抖动型短暂性脑缺血发作（limb-shaking transient ischemic attack，LS-TIA）是一种罕见的脑血管病类型，本文报道1例LS-TIA患者在双联抗血小板、调脂等常规治疗下仍反复出现不自主肢体抖动，但通过补液扩容使症状得到了改善。本文结合患者的影像学特点深入探讨脑血流灌注在LS-TIA发病机制中的作用，并对其治疗方式进行文献综述。 Abstract: Limb-shaking transient ischemic attack (LS-TIA) is a rare type of cerebrovascular disease. This study reports a case with LS-TIA who suffered from refractory involuntary limb shaking under routine stroke treatments such as dual antiplatelet therapy and lipid regulation. The involuntary limbs shaking was successfully attenuated after treatment with fluid resuscitation. This case report highlights the critical role of cerebral perfusion in the pathogenesis of LS-TIA and conducts a literature review on the related treatments.

Open in new tab Download slide OBJECTIVES Cardiopulmonary resuscitation (CPR) aggravates the pre-existing dismal prognosis of patients suffering from acute type A aortic dissection (ATAAD). We aimed to identify factors affecting survival and outcome in ATAAD patients requiring CPR at presentation at 2 European aortic centres. METHODS Data on 112 surgical candidates and undergoing preoperative CPR were retrospectively evaluated. Patients were divided into 2 groups according to 30-day mortality. A multivariable model identified predictors for 30-day mortality. RESULTS Preoperative death occurred in 23 patients (20.5%). In the remaining 89 surgical patients (79.5%) circulatory arrest time (41 ± 20 min in 30-day non-survivors vs 30 ± 13 min in 30-day survivor, P  = 0.003) as well as cardiopulmonary bypass time (320 ± 132 min in 30-day non-survivors vs 252 ± 140 min in 30-day survivor, P  = 0.020) time was significantly longer in patients with worse outcome. Thirty-day mortality of the total cohort was 61.6% (n  = 69) with cardiac failure in 48% and aortic rupture or haemorrhagic shock (28%) as predominant reasons of death. Age [odds ratio (OR) 1.04, 95% confidence interval (CI) 1.01–1.09, P  = 0.034], preoperative coronary (OR 3.42, 95% CI 1.34–9.26, p = 0.012) and spinal malperfusion (OR 12.49, 95% CI 1.83–225.02, P  = 0.028) emerged as independent predictors for 30-day mortality while CPR due to tamponade was associated with improved early survival (OR 0.29, 95% CI 0.091–0.81, P  = 0.023). CONCLUSIONS Assessment of underlying cause for CPR is mandatory. Pericardial tamponade, rapidly resolved with pericardial drainage, is a predictor for improved survival, while age and presence of coronary and spinal malperfusion are associated with dismal outcome in this high-risk patient group. [ABSTRACT FROM AUTHOR]

Open in new tab Download slide OBJECTIVES The aim of this study was to explore the prognostic value of brain computed tomography perfusion (CTP) for postoperative new stroke in acute type A aortic dissection (ATAAD) patients. METHODS Patients with ATAAD and suspected cerebral malperfusion who underwent brain CTP and surgical repair were retrospectively analysed. Brain perfusion was quantified mainly with the averaged cerebral blood flow. Significant clinical and imaging findings were identified through univariable and multivariable regression analysis. Furthermore, the added prognostic benefit of perfusion parameters was confirmed with the receiver operating characteristic curves in the entire cohort and subgroup analysis. RESULTS The incidence of postoperative new stroke was 30.8% (44/143). The independent adjusted predictors of postoperative new stroke included an impaired averaged cerebral blood flow (ml/100 ml/min) (odds ratio: 0.889; P  < 0.001), severe stenosis (odds ratio: 5.218; P  = 0.011) or occlusion (odds ratio: 14.697; P  = 0.048) of the true lumen in common carotid artery (CCA), hypotension on admission (odds ratio: 9.644; P  = 0.016) and a longer surgery time (odds ratio: 1.593; P  = 0.021). The area under the receiver operating characteristic curves significantly improved after adding perfusion parameters to clinical and computed tomography angiography characteristics (P  = 0.048). This benefit was more pronounced in patients with severe stenosis or occlusion in CCA true lumen (P  = 0.004). CONCLUSIONS Brain CTP could be a useful prognostic tool for surgically treated ATAAD patients and especially beneficial in patients with severe stenosis or occlusion of the CCA true lumen. [ABSTRACT FROM AUTHOR]

CCH, resulting from multiple cerebrovascular diseases, has been considered the primary cause of cognitive impairment in recent years. In this process, oxidative stress plays a critical role and damages hippocampal neurons. Research has shown that Salvia verticillata has a significant antioxidant and free radical-scavenging activity due to its polyphenolic compounds. Therefore, the present study aimed to evaluate the effect of Salvia verticillata on a rat model of chronic cerebral hypoperfusion. A total of 24 rats were subjected to Salvia verticillata or vehicle orally from one week before 2VO surgery for 14 days. Cerebral hypoperfusion was induced by the bilateral occlusion of the common carotid arteries (2VO, n = 12 and sham, n = 12). The cognition of rats was evaluated 1 week after surgery in the MWM. In the MWM test, 2VO rats showed longer escape latency time and swimming distance and spent a shorter time in the target quadrant (p < 0.05). Moreover, we observed that Salvia verticillata treatment significantly reduced escape latency time, shortened the swimming distance, and increased target quadrant time (p > 0.05). Our results indicated that Salvia verticillata treatment significantly improved cognitive deficits in cerebral ischemic rats, probably by reducing oxidative stress damage. [ABSTRACT FROM AUTHOR]

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In the neuroimaging workup of a suspected ischemic stroke, the involvement of more than one arterial territory without an anatomical substrate should raise the suspicion of a stroke mimic. We report the case of a 61-year-old male with a new-onset headache and transient phasic disturbances who presented a pattern of vascular abnormalities characterized by left-hemispheric leptomeningeal vessel paucity and hypoperfusion.

Abstract Background The vast majority of women with dementia are post-menopausal. Despite clinical relevance, menopause is underrepresented in rodent models of dementia. Before menopause, women are less likely than men to experience strokes, obesity, and diabetes—known risk factors for vascular contributions to cognitive impairment and dementia (VCID). During menopause, ovarian estrogen production stops and the risk of developing these dementia risk factors spikes. Here, we aimed to determine if menopause worsens cognitive impairment in VCID. We hypothesized that menopause would cause metabolic dysfunction and increase cognitive impairment in a mouse model of VCID. Methods We performed a unilateral common carotid artery occlusion surgery to produce chronic cerebral hypoperfusion and model VCID in mice. We used 4-vinylcyclohexene diepoxide to induce accelerated ovarian failure and model menopause. We evaluated cognitive impairment using behavioral tests including novel object recognition, Barnes maze, and nest building. To assess metabolic changes, we measured weight, adiposity, and glucose tolerance. We explored multiple aspects of brain pathology including cerebral hypoperfusion and white matter changes (commonly observed in VCID) as well as changes to estrogen receptor expression (which may mediate altered sensitivity to VCID pathology post-menopause). Results Menopause increased weight gain, glucose intolerance, and visceral adiposity. VCID caused deficits in spatial memory regardless of menopausal status. Post-menopausal VCID specifically led to additional deficits in episodic-like memory and activities of daily living. Menopause did not alter resting cerebral blood flow on the cortical surface (assessed by laser speckle contrast imaging). In the white matter, menopause decreased myelin basic protein gene expression in the corpus callosum but did not lead to overt white matter damage (assessed by Luxol fast blue). Menopause did not significantly alter estrogen receptor expression (ERα, ERβ, or GPER1) in the cortex or hippocampus. Conclusions Overall, we have found that the accelerated ovarian failure model of menopause caused metabolic impairment and cognitive deficits in a mouse model of VCID. Further studies are needed to identify the underlying mechanism. Importantly, the post-menopausal brain still expressed estrogen receptors at normal (pre-menopausal) levels. This is encouraging for any future studies attempting to reverse the effects of estrogen loss by activating brain estrogen receptors.

Background: Reduction in oxygen delivery to developing kidneys of premature infants may be an important source for acute kidney injury in premature infants. Purpose: To describe changes in continuous kidney oxygenation (RrSO2) measures before, during, and after routine diaper changes. Methods: Non–a priori analysis of a prospective cohort that received continuous measurement of RrSO2 with near-infrared spectroscopy (NIRS) over the first 14 days of life demonstrating acute RrSO2 drops surrounding diaper changes. Results: In total, 26 of 38 (68%) infants (≤1800 g) from our cohort exhibited acute drops in RrSO2 that temporally correlated with diaper changes. Mean (SD) RrSO2 baseline prior to each diaper change event was 71.1 (13.2), dropped to 59.3 (11.6) during diaper change, and recovered to 73.3 (13.2). There was a significant difference between means when comparing baseline to diaper change (P < .001; 95% CI, 9.9 to 13.8) and diaper change to recovery (P < .001; 95% CI, −16.9 to −11.2). The mean decrease in RrSO2 during diaper change averaged 12 points (17%) below 15-minute RrSO2 mean prior to diaper change, with quick recovery to prediaper change levels. No decreases in SpO2, blood pressure, or heart rate were documented during the intermittent kidney hypoxic events. Implications for Practice and Research: Routine diaper changes in preterm infants may increase the risk for acute reductions in RrSO2 as measured by NIRS; however, the impact on kidney health remains unknown. Larger prospective cohort studies assessing kidney function and outcomes related to this phenomenon are needed. [ABSTRACT FROM AUTHOR]

Chronic cerebral hypoperfusion due to carotid artery stenosis is a major cause of vascular cognitive impairment and dementia (VCID). Bilateral carotid artery stenosis (BCAS) in rodents is a well-established model of VCID where most studies have focused on white matter pathology and subsequent cognitive deficit. Therefore, our aim was to study the implication of adult hippocampal neurogenesis in hypoperfusion-induced VCID in mice, and its relationship with cognitive hippocampal deficits. Mice were subjected to BCAS; 1 and 3 months later, hippocampal memory and neurogenesis/cell death were assessed, respectively, by the novel object location (NOL) and spontaneous alternation performance (SAP) tests and by immunohistology. Hypoperfusion was assessed by arterial spin labeling-magnetic resonance imaging (ASL-MRI). Hypoperfused mice displayed spatial memory deficits with decreased NOL recognition index. Along with the cognitive deficit, a reduced number of newborn neurons and their aberrant morphology indicated a remarkable impairment of the hippocampal neurogenesis. Both increased cell death in the subgranular zone (SGZ) and reduced neuroblast proliferation rate may account for newborn neurons number reduction. Our data demonstrate quantitative and qualitative impairment of adult hippocampal neurogenesis disturbances associated with cerebral hypoperfusion-cognitive deficits in mice. These findings pave the way for novel diagnostic and therapeutic targets for VCID. [ABSTRACT FROM AUTHOR]

Blood pressure goals in the intensive care unit (ICU) have been extensively investigated in large datasets and have been associated with various harm thresholds at or greater than a mean pressure of 65 mm Hg. While it is difficult to perform interventional randomized trials of blood pressure in the ICU, important evidence does not support defense of a higher pressure, except in retrospective database analyses. Perfusion pressure may be a more important target than mean pressure, even more so in the vulnerable patient population. In the cardiac ICU, blood pressure targets are tailored to specific cardiac pathophysiology and patient characteristics. Generally, the goal is to maintain adequate blood pressure within a certain range to support cardiac function and to ensure end organ perfusion. Individualized targets demand the use of both invasive and noninvasive monitoring modalities and frequent titration of medications and/or mechanical circulatory support where necessary. In this review, we aim to identify appropriate blood pressure targets in the ICU, recognizing special patient populations and outlining the risk factors and predictors of end organ failure. [ABSTRACT FROM AUTHOR]

Background and purpose: Reduced cerebral perfusion has been observed in multiple sclerosis (MS) and may contribute to tissue loss both acutely and chronically. Here, we test the hypothesis that hypoperfusion occurs in MS and relates to the presence of irreversible tissue damage. Methods: In 91 patients with relapsing MS and 26 healthy controls (HC), gray matter (GM) cerebral blood flow (CBF) was assessed using pulsed arterial spin labeling. GM volume, T1 hypointense and T2 hyperintense lesion volumes (T1LV and T2LV, respectively), and the proportion of T2‐hyperintense lesion volume that appears hypointense on T1‐weighted magnetic resonance imaging (T1LV/T2LV) were quantified. GM CBF and GM volume were evaluated globally, as well as regionally, using an atlas‐based approach. Results: Global GM CBF was lower in patients (56.9 ± 12.3 mL/100 g/min) than in HC (67.7 ± 10.0 mL/100 g/min; p < 0.001), a difference that was widespread across brain regions. Although total GM volume was comparable between groups, significant reductions were observed in a subset of subcortical structures. GM CBF negatively correlated with T1LV (r = −0.43, p = 0.0002) and T1LV/T2LV (r = −0.37, p = 0.0004), but not with T2LV. Conclusions: GM hypoperfusion occurs in MS and is associated with irreversible white matter damage, thus suggesting that cerebral hypoperfusion may actively contribute and possibly precede neurodegeneration by hampering tissue repair abilities in MS. [ABSTRACT FROM AUTHOR]

Chronic cerebral hypoperfusion due to carotid artery stenosis is a major cause of vascular cognitive impairment and dementia (VCID). Bilateral carotid artery stenosis (BCAS) in rodents is a well-established model of VCID where most studies have focused on white matter pathology and subsequent cognitive deficit. Therefore, our aim was to study the implication of adult hippocampal neurogenesis in hypoperfusion-induced VCID in mice, and its relationship with cognitive hippocampal deficits. Mice were subjected to BCAS; 1 and 3 months later, hippocampal memory and neurogenesis/cell death were assessed, respectively, by the novel object location (NOL) and spontaneous alternation performance (SAP) tests and by immunohistology. Hypoperfusion was assessed by arterial spin labeling-magnetic resonance imaging (ASL-MRI). Hypoperfused mice displayed spatial memory deficits with decreased NOL recognition index. Along with the cognitive deficit, a reduced number of newborn neurons and their aberrant morphology indicated a remarkable impairment of the hippocampal neurogenesis. Both increased cell death in the subgranular zone (SGZ) and reduced neuroblast proliferation rate may account for newborn neurons number reduction. Our data demonstrate quantitative and qualitative impairment of adult hippocampal neurogenesis disturbances associated with cerebral hypoperfusion-cognitive deficits in mice. These findings pave the way for novel diagnostic and therapeutic targets for VCID.

Cardiogenic shock remains a time-critical, complex syndrome that continues to present challenges to clinicians and healthcare systems. Despite advances in the fields of cardiovascular and critical care medicine, mortality remains high. This article summarises the recent shock to survival document, which outlined the current and ideal future state of cardiogenic shock care nationally to improve patient outcomes. Shock to survival emphasises the need for education and training in the early recognition of the hypoperfusion that is pathognomomic of cardiogenic shock. Improved provision of focused cardiac ultrasound is essential to confirm a cardiac cause. Early identification of the patient with cardiogenic shock should be supported by access to defined pathways of care, including specialist shock centres and multiprofessional teams with domain expertise and the capability to manage the myriad of causative aetiologies. Given the absence of high-quality data to inform practice nationally, robust datasets are an unmet need to inform best practice, guide design of clinical services and pathways and drive innovation through research and clinical trials. [ABSTRACT FROM AUTHOR]

Watershed strokes have been described previously as ischemic strokes located in vulnerable border zones between brain tissue supplied by the anterior, posterior, and middle cerebral arteries in the distal junction between two non-anastomotic arterial territories. Ischemic strokes in border zones are well-recognized entities and well-described in terms of imaging features, but the pathophysiological mechanism of brain injury production is not fully defined. Border zone ischemia is caused by cerebral hypoperfusion through decreased cerebral blood flow and arterial embolism in unstable atheroma plaque. It is often difficult to say which mechanisms are fully responsible for producing cerebral ischemic lesions. This review aimed to highlight the imaging aspect of watershed strokes and to correlate the clinical characteristics of this type of stroke with the diagnostic algorithm for optimal therapeutic management. Neurologists should promptly recognize this type of stroke and investigate its etiology in the shortest possible time. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Aluminum phosphide poisoning may cause rare visual impairment. In a case, a 31‐year‐old female, visual loss was linked to shock‐induced hypoperfusion, causing oxygen lack and cerebral atrophy, emphasizing the need for identifying atypical symptoms. This case report describes the multidisciplinary evaluation of a 31‐year‐old female patient who suffered from visual impairment as a result of aluminum phosphide (AlP) poisoning. Phosphine, which is formed in the body when AlP reacts with water, cannot cross the blood–brain barrier; therefore, visual impairment seems unlikely to be the direct result of phosphine. To our knowledge, it is the first documented report of such impairment due to AlP. [ABSTRACT FROM AUTHOR]

Any acute and profound reduction in fetal oxygenation increases the risk of anaerobic metabolism in the fetal myocardium and, hence, the risk of lactic acidosis. On the contrary, in a gradually evolving hypoxic stress, there is sufficient time to mount a catecholamine-mediated increase in the fetal heart rate to increase the cardiac output and redistribute oxygenated blood to maintain an aerobic metabolism in the fetal central organs. When the hypoxic stress is sudden, profound, and sustained, it is not possible to continue to maintain central organ perfusion by peripheral vasoconstriction and centralization. In case of acute deprivation of oxygen, the immediate chemoreflex response via the vagus nerve helps reduce fetal myocardial workload by a sudden drop of the baseline fetal heart rate. If this drop in the fetal heart rate continues for >2 minutes (American College of Obstetricians and Gynecologists' guideline) or 3 minutes (National Institute for Health and Care Excellence or physiological guideline), it is termed a prolonged deceleration, which occurs because of myocardial hypoxia, after the initial chemoreflex. The revised International Federation of Gynecology and Obstetrics guideline (2015) considers the prolonged deceleration to be a "pathologic" feature after 5 minutes. Acute intrapartum accidents (placental abruption, umbilical cord prolapse, and uterine rupture) should be excluded immediately, and if they are present, an urgent birth should be accomplished. If a reversible cause is found (maternal hypotension, uterine hypertonus or hyperstimulation, and sustained umbilical cord compression), immediate conservative measures (also called intrauterine fetal resuscitation) should be undertaken to reverse the underlying cause. In reversible causes of acute hypoxia, if the fetal heart rate variability is normal before the onset of deceleration, and normal within the first 3 minutes of the prolonged deceleration, then there is an increased likelihood of recovery of the fetal heart rate to its antecedent baseline within 9 minutes with the reversal of the underlying cause of acute and profound reduction in fetal oxygenation. The continuation of the prolonged deceleration for >10 minutes is termed "terminal bradycardia," and this increases the risk of hypoxic-ischemic injury to the deep gray matter of the brain (the thalami and the basal ganglia), predisposing to dyskinetic cerebral palsy. Therefore, any acute fetal hypoxia, which manifests as a prolonged deceleration on the fetal heart rate tracing, should be considered an intrapartum emergency requiring an immediate intervention to optimize perinatal outcome. In uterine hypertonus or hyperstimulation, if the prolonged deceleration persists despite stopping the uterotonic agent, then acute tocolysis is recommended to rapidly restore fetal oxygenation. Regular clinical audit of the management of acute hypoxia, including the "the onset of bradycardia to delivery interval," may help identify organizational and system issues, which may contribute to poor perinatal outcomes. [ABSTRACT FROM AUTHOR]