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Background The primary aim was to determine to what extent continuously monitored neurointensive care unit (neuro-ICU) targets predict cerebral blood flow (CBF) and delivery of oxygen (CDO 2 ) after aneurysmal subarachnoid hemorrhage. The secondary aim was to determine whether CBF and CDO 2 were associated with clinical outcome. Methods In this observational study, patients with aneurysmal subarachnoid hemorrhage treated at the neuro-ICU in Uppsala, Sweden, from 2012 to 2020 with at least one xenon-enhanced computed tomography (Xe-CT) obtained within the first 14 days post ictus were included. CBF was measured with the Xe-CT and CDO 2 was calculated based on CBF and arterial oxygen content. Regional cerebral hypoperfusion was defined as CBF < 20 mL/100 g/min, and poor CDO 2 was defined as CDO 2  < 3.8 mL O 2 /100 g/min. Neuro-ICU variables including intracranial pressure (ICP), pressure reactivity index, cerebral perfusion pressure (CPP), optimal CPP, and body temperature were assessed in association with the Xe-CT. The acute phase was divided into early phase (day 1–3) and vasospasm phase (day 4–14). Results Of 148 patients, 27 had underwent a Xe-CT only in the early phase, 74 only in the vasospasm phase, and 47 patients in both phases. The patients exhibited cerebral hypoperfusion and poor CDO 2 for medians of 15% and 30%, respectively, of the cortical brain areas in each patient. In multiple regressions, higher body temperature was associated with higher CBF and CDO 2 in the early phase. In a similar regression for the vasospasm phase, younger age and longer pulse transit time (lower peripheral resistance) correlated with higher CBF and CDO 2 , whereas lower hematocrit only correlated with higher CBF but not with CDO 2 . ICP, CPP, and pressure reactivity index exhibited no independent association with CBF and CDO 2 . R 2 of these regressions were below 0.3. Lower CBF and CDO 2 in the early phase correlated with poor outcome, but this only held true for CDO 2 in multiple regressions. Conclusions Systemic and cerebral physiological variables exhibited a modest association with CBF and CDO 2 . Still, cerebral hypoperfusion and low CDO 2 were common and low CDO 2 was associated with poor outcome. Xe-CT imaging could be useful to help detect secondary brain injury not evident by high ICP and low CPP.

Higher intracranial pressure variability (ICPV) has been associated with a more favorable cerebral energy metabolism, lower rate of delayed ischemic neurologic deficits, and more favorable outcome in aneurysmal subarachnoid hemorrhage (aSAH). We have hypothesized that higher ICPV partly reflects more compliant and active cerebral vessels. In this study, the aim was to further test this by investigating if higher ICPV was associated with lower cerebrovascular resistance (CVR) and higher cerebral blood flow (CBF) after aSAH. In this observational study, 147 aSAH patients were included, all of whom had been treated in the Neurointensive Care (NIC) Unit, Uppsala, Sweden, 2012–2020. They were required to have had ICP monitoring and at least one xenon-enhanced computed tomography (Xe-CT) scan to study cortical CBF within the first 2 weeks post-ictus. CVR was defined as the cerebral perfusion pressure in association with the Xe-CT scan divided by the concurrent CBF. ICPV was defined over three intervals: subminute (ICPV-1m), 30-min (ICPV-30m), and 4 h (ICPV-4h). The first 14 days were divided into early (days 1–3) and vasospasm phase (days 4–14). In the vasospasm phase, but not in the early phase, higher ICPV-4h (β =  − 0.19, p < 0.05) was independently associated with a lower CVR in a multiple linear regression analysis and with a higher global cortical CBF (r = 0.19, p < 0.05) in a univariate analysis. ICPV-1m and ICPV-30m were not associated with CVR or CBF in any phase. This study corroborates the hypothesis that higher ICPV, at least in the 4-h interval, is favorable and may reflect more compliant and possibly more active cerebral vessels.

Abstract BACKGROUND We hypothesized that reduced cerebral blood flow (CBF) and/or energy metabolic disturbances exist in the tissue surrounding a surgically evacuated intracerebral hemorrhage (ICH). If present, such CBF and/or metabolic impairments may contribute to ongoing tissue injury and the modest clinical efficacy of ICH surgery. OBJECTIVE To conduct an observational study of CBF and the energy metabolic state in the perihemorrhagic zone (PHZ) tissue and in seemingly normal cortex (SNX) by microdialysis (MD) following surgical ICH evacuation. METHODS We evaluated 12 patients (median age 64; range 26-71 yr) for changes in CBF and energy metabolism following surgical ICH evacuation using Xenon-enhanced computed tomography (n = 10) or computed tomography perfusion (n = 2) for CBF and dual MD catheters, placed in the PHZ and the SNX at ICH surgery. RESULTS CBF was evaluated at a mean of 21 and 58 h postsurgery. In the hemisphere ipsilateral to the ICH, CBF improved between the investigations (36.6 ± 20 vs 40.6 ± 20 mL/100 g/min; P < .05). In total, 1026 MD samples were analyzed for energy metabolic alterations including glucose and the lactate/pyruvate ratio (LPR). The LPR was persistently elevated in the PHZ compared to the SNX region (P < .05). LPR elevations in the PHZ were predominately type II (pyruvate normal-high; indicating mitochondrial dysfunction) as opposed to type I (pyruvate low; indicating ischemia) at 4 to 48 h (70% vs 30%) and at 49 to 84 h (79% vs 21%; P < .05) postsurgery. CONCLUSION Despite normalization of CBF following ICH evacuation, an energy metabolic disturbance suggestive of mitochondrial dysfunction persists in the perihemorrhagic zone.

Introduction Effective noninvasive tests that can distinguish early-stage nonalcoholic steatohepatitis (NASH) from simple steatosis (SS) have long been sought. Our aim was to determine the possibility of noninvasively distinguishing early-stage NASH from SS. Materials and methods We used Fick’s principle and the Kety–Schmidt equation to determine the hepatic tissue blood flow (TBF) in 65 NASH patients who underwent xenon computed tomography (Xe-CT). We calculated the lambda value (LV), i.e., Xe gas solubility coefficient, in liver and blood. We assessed the histological severity of fatty changes and fibrosis on the basis of Brunt’s classification. Liver biopsy revealed SS in 9 patients and NASH in 56 patients. NASH stages 1 and 2 were classified as early-stage NASH (Ea-NASH; 38 patients) and stages 3 and 4 as advanced-stage NASH (Ad-NASH; 18 patients). We evaluated the differences in LV and TBF among the 3 groups. Results LV was significantly lower in the Ad-NASH group than in the SS and Ea-NASH groups. Portal venous TBF (PVTBF) was significantly lower in the Ea-NASH group than in the SS group, and PVTBF was lower in the Ad-NASH group than in the Ea-NASH group. Total hepatic TBF (THTBF) was significantly different between the SS and Ea-NASH groups and between the SS and Ad-NASH groups. Conclusions In conclusion, measurements of TBF and LV are useful for evaluating the pathophysiological progression of NASH. In addition, these measurements can facilitate the differential diagnosis of SS and Ea-NASH, which may not be distinguishable by other means.

Background : Delayed cerebral ischemia from cerebral arterial vasospasm following aneurysmal subarachnoid hemorrhage (aSAH) is associated with significant morbidity and mortality. Early recognition of the cerebral arterial vasospasm and institution of appropriate treatment can reduce the consequences. Aim : We investigated the association of transcranial Doppler (TCD) and Xe-CT with the characteristics of symptomatic vasospasm secondary to aneurysmal subarachnoid hemorrhage (SAH) in patients who underwent euvolemic treatment without sedation. Materials and Methods : Data collected prospectively in patients with aSAH admitted to a neurocritical care unit in a regional hospital were retrospectively analyzed. Out of the 98 consecutive patients with aSAH, 30 patients underwent paired Xe-CT (not sedated) and TCD studies. Correlation between cortical cerebral blood flow (CBF) and mean blood flow velocity in middle cerebral artery (MCA) territories was analyzed. The lowest cortical regional CBF and MCA velocity were compared between patients with and without symptomatic vasospasm. Results : Symptomatic vasospasm occurred in 12 patients. No correlation was found between CBF and mean blood flow velocity of the MCA territory. The differences between MCA velocity and lowest cortical CBF in patients with symptomatic vasospasm were significantly different from patients without symptoms. Conclusion : TCD does not help to predict regional CBF in the MCA territory in patients with aSAH on euvolemic treatment.

It is controversial whether a low cerebral blood flow (CBF) simply reflects the severity of injury or whether ischemia contributes to the brain's injury. It is also not clear whether posttraumatic cerebral hypoperfusion results from intracranial hypertension or from pathologic changes of the cerebral vasculature. The answers to these questions have important implications for whether and how to treat a low CBF. We performed a retrospective analysis of 77 patients with severe traumatic brain injury who had measurement of CBF within 12 hours of injury. CBF was measured using xenon-enhanced computed tomography (XeCT). Global CBF, physiological parameters at the time of XeCT, and outcome measures were analyzed. Average global CBF for the 77 patients was 36+/-16 mL/100 g/minutes. Nine patients had an average global CBF<18 (average 12+/-5). The remaining 68 patients had a global CBF of 39+/-15. The initial ICP was >20 mmHg in 90% and >30 mmHg in 80% of patients in the group with CBF<18, compared to 33% and 16%, respectively, in the patients with CBF>or=18. Mortality was 90% at 6 months postinjury in patients with CBF<18. Mortality in the patients with CBF>18 was 19% at 6 months after injury. In patients with CBF<18 mL/100 g/minutes, intracranial hypertension plays a major causative role in the reduction in CBF. Treatment would most likely be directed at controlling intracranial pressure, but the early, severe intracranial hypertension also probably indicates a severe brain injury. For levels of CBF between 18 and 40 mL/100 g/minutes, the presence of regional hypoperfusion was a more important factor in reducing the average CBF.

Delayed cerebral ischemia from cerebral arterial vasospasm following aneurysmal subarachnoid hemorrhage (aSAH) is associated with significant morbidity and mortality. Early recognition of the cerebral arterial vasospasm and institution of appropriate treatment can reduce the consequences. We investigated the association of transcranial Doppler (TCD) and Xe-CT with the characteristics of symptomatic vasospasm secondary to aneurysmal subarachnoid hemorrhage (SAH) in patients who underwent euvolemic treatment without sedation. Data collected prospectively in patients with aSAH admitted to a neurocritical care unit in a regional hospital were retrospectively analyzed. Out of the 98 consecutive patients with aSAH, 30 patients underwent paired Xe-CT (not sedated) and TCD studies. Correlation between cortical cerebral blood flow (CBF) and mean blood flow velocity in middle cerebral artery (MCA) territories was analyzed. The lowest cortical regional CBF and MCA velocity were compared between patients with and without symptomatic vasospasm. Symptomatic vasospasm occurred in 12 patients. No correlation was found between CBF and mean blood flow velocity of the MCA territory. The differences between MCA velocity and lowest cortical CBF in patients with symptomatic vasospasm were significantly different from patients without symptoms. TCD does not help to predict regional CBF in the MCA territory in patients with aSAH on euvolemic treatment.

Objective: The purpose of this study was to verify transhemispheric diaschisis in the early hours after an ischemic event. Methods: XeCT cerebral blood flow (CBF) studies within 8 h of stroke were studied in 23 patients. Mean CBF was evaluated in the ischemic area, contralateral hemisphere and ipsilateral cerebellum. Results: A severe CBF reduction was found in the ischemic area (mean 9 ± 3 ml/100 g/min). The mean CBF in the unaffected hemisphere (33 ± 10 ml/100 g/min) was 35% less compared to the normal mean value. CBF was decreased in the cerebellum ipsilateral to the stroke (mean 31 ± 12 ml/100 g/min) suggesting a blood flow depression of the whole brain. Conclusions: During the initial hours of cerebral ischemia, the asymptomatic hemisphere demonstrated CBF depression that was part of the global flow reduction.

Objective: The purpose of this study was to determine the relationship between cerebral blood flow (CBF) measurements in acute stroke and early clinical outcome. Material and Methods: The xenon-enhanced computed tomography (XeCT) CBF studies performed in 50 patients in the acute stage (within 8 h) of a hemispheric stroke were retrospectively analyzed. The mean CBF of the symptomatic vascular territory was compared to the corresponding territory in the contralateral hemisphere. Clinical assessment on admission and discharge was performed using the National Institutes of Health stroke scale (NIHSS). Results: Three groups were defined according to the degree of CBF asymmetry between the symptomatic and the contralateral asymptomatic vascular region. The CBF asymmetry was mild in group A (≤20%), moderate in group B (>20% and <60%) and severe in group C (≥60%). Patients in group A (n = 18) had a good outcome with a mean NIHSS score of 2 ± 2 at discharge. In group B, the patients (n = 22) had intermediate but variable outcomes: 2 patients died and the mean NIHSS score for the survivors was variable (mean NIHSS score: 9 ± 6). The patients in group C (n = 10) had a very poor outcome: 4 patients died and the survivors had a mean NIHSS score of 15 ± 1. Conclusions: Quantitative XeCT CBF measurements may be useful for selecting subgroups of stroke patients with different clinical outcomes. The possibility of predicting patient prognosis as early as in the first hours after the ischemic event may help to identify the appropriate target population that will benefit from aggressive stroke therapy.

INTRODUCTION The amplitude of contingent negative variation (CNV) has been reported to be decreased in dementia, 1 –3 parkinsonism 4 and elderly subjects. 5,6 There is a report on the correlation between the amplitude of CNV and global cerebral blood flow using the xenon-133 inhalation method, 7 but there is no report on the correlation between the amplitude of CNV and regional cerebral blood flow using the stable xenon computed tomography (CT) method. [...]we investigated the correlation between the amplitude of CNV and regional cerebral blood flow using the stable xenon CT method, which can measure the blood flows in the subcortical area more accurately than the xenon-133 inhalation method. 8 METHODS AND MATERIALS Seventeen cases of chronic multiple cerebral infarction in the perforating artery areas (vascular dementia, mean age 67.0), 6 cases of Alzheimer's disease (mean age 69.5) and 8 healthy controls (mean age 62.5) were studied. See PDF] Table 1 Amplitude of contingent negative variation in three groups (mean ± standard deviation) Vascular dementia Alzheimer's disease Healthy control amplitude of early CNV (μV) 8.7 ± 3.1* 10.2 ± 3.8 13.6 ± 4.5 amplitude of late CNV (μV) 12.6 ± 4.8 13.5 ± 5.1 14.3 ± 5.3 * P < 0.01 compared with healthy control group Figure 2 shows records of xenon CT in vascular dementia and for a healthy control. See PDF] Table 2 Regional cerebral blood flows (ml/100g/min, mean ± standard deviation) and correlation coefficients with amplitude of early CNV Vascular dementia Alzheimer's disease Healthy control Total subjects Frontal cortex 46.1 ± 12.1 45.6 ± 13.9 62.4 ±13.7 51.8 ± 14.6 r = 0.593 b r = 0.585 b r = 0.248 r = 0.537 b Temporal cortex 45.7 ± 10.4 41.5 ± 12.7 64.5 ± 14.8 49.8 ± 14.9 r = 0.121 r = 0.147 r = 0.243 r = 0.167 Parietal cortex 45.1 ± 9.5 a 42.6 ± 17.1 67.2 ± 12.6 48.3 ± 15.5 r = 0.325 r = 0.147 r = 0.139 r = 0.274 Occipital cortex 40.9 ± 8.8 37.8 ± 2.0 40.4 ± 8.9 39.7 ± 8.0 r = 0.152 r = 0.237 r = 0.214 r = 0.195 Frontal white matter 24.6 ± 8.9 25.3 ± 9.4 38.4 ± 9.6 29.4 ± 10.9 r = 0.083 r = 0.152 r = 0.062 r = 0.103 Temporal white matter 22.8 ± 8.8 21.8 ± 9.5 35.2 ± 9.7 26.8 ± 9.3 r = 0.146 r = 0.094 r = 0.154 r = 0.128 Occipital white matter 18.1 ± 5.0 18.0 ± 2.4 22.6 ± 4.7 18.2 ± 5.0 r = 0.163 r = 0.128 r = 0.131 r = 0.142 Caudate nucleus 51.7 ± 14.1 55.8 ± 17.3 66.2 ± 9.4 53.8 ±16.8 r = 0.128 r = 0.196 r = 0.053 r = 0.141 Putamen 53.7 ±13.9 53.9 ± 9.9 63.9 ± 9.8 55.7 ± 13.2 r = 0.096 r = 0.092 r = 0.094 r = 0.095 Thalamus 45.8 ± 8.4 a 46.0 ±13.2 64.7 ± 9.6 54.5 ± 17.8 r = 0.216 r = 0.132 r = 0.086 r = 0.115 a : P < 0.01 compared with healthy control group. b : P < 0.01 with amplitude of early CNV. The decrease in blood flow below the lower limit of normal range in the vascular dementia and Alzheimer's disease groups is considered to produce dementia and the decrease in amplitude of early CNV, while the decrease in blood flow within the normal range in healthy controls does not produce dementia nor the decrease in amplitude of early CNV.