scholarly journals Cerebrovascular pathology in patients with hemorrhagic fever

2021 ◽  
Vol XXX (3-4) ◽  
pp. 19-21
Author(s):  
L. B. Novikova

It was performed complex ultrasound investigation of 50 patients with hemorragic fever at different stages of disease. Analysis of dopplerographic parameters showed, that in acute stage of disease the following patterns of changed cerebral blood flow can be determined: poor cerebral perfusion, stenosis and venous discirculation. In reconvalescent patients in comparison with the control group reliable deviations retained, presented mostly by autoregulatory disorders. For prognostic risk development evaluation of late neurologic complications in patients, having had hemorrhagic fever, cerebro-renal index was suggested.


2020 ◽  
Author(s):  
Joseph P Archie

AbstractIntroductionIn patients with 70% to 99% diameter carotid artery stenosis cerebral blood flow reserve may be protective of future ischemic cerebral events. Reserve cerebral blood flow is created by brain auto-regulation. Both cerebral blood flow reserve and cerebrovascular reactivity can be measured non-invasively. However, the factors and variables that determine the availability and magnitude and of reserve blood flow remain poorly understood. The availability of reserve cerebral blood flow is a predictor of stroke risk. The aim of this study is to employ a hemodynamic model to predict the variables and functional relationships that determine cerebral blood flow reserve in patients with significant carotid stenosis.MethodsA basic one-dimensional, three-unit (carotid, collateral and brain) energy conservation fluid mechanics blood flow model is employed. It has two distinct but adjacent blood flow components with normal cerebral blood flow at the interface. In the brain auto-regulated blood flow component cerebral blood flow is maintained normal by reserve flow. In the brain pressure dependent blood flow component cerebral blood flow is below normal because cerebral perfusion pressure is below the lower threshold value for auto-regulation. Patient specific values of collateral vascular resistance are determined from a model solution using clinically measured systemic and carotid arterial stump pressures. Collateral vascular resistance curves illustrate the model solutions for reserve and actual cerebral blood flow as a function of percent diameter carotid artery stenosis and mean systemic arterial pressure. The threshold cerebral perfusion pressure value for auto-regulation is assumed to be 50 mmHg. Normal auto-regulated regional cerebral blood flow is assumed to be 50 ml/min/100g. Cerebral blood flow and reserve blood flow solutions are given for systemic arterial pressures of 80, 90, 100, 110 and 120 mmHg and for three patient specific collateral vascular resistance values, Rw = 1.0 (mean patient value), Rw = 0.5 (lower 1 SD) and Rd = 3.0 (upper 1 SD).ResultsReserve cerebral blood flow is only available when a patients cerebral perfusion pressure is in the normal auto-regulatory range. Both actual and reserve cerebral blood flows are primarily from the carotid circulation when carotid stenosis is less than 60% diameter. Between 60% and 75% stenosis the remaining carotid blood flow reserve is utilized and at higher degrees of stenosis all reserve flow is from the collateral circulation. The primary independent variables that determine actual and reserve cerebral blood flow are mean systemic arterial pressure, degree of carotid stenosis and patient specific collateral vascular resistance. Approximate 16% of patients have collateral vascular resistance greater than 5.0 and are predicted to be at high risk of cerebral ischemia or infarction with progression to severe carotid stenosis or occlusion. The approximate 50% of patients with a collateral vascular resistance less than 1.0 are predicted to have adequate cerebral blood flow with progression to carotid occlusion, and most maintain some reserve. Clinically measured values of cerebral blood flow reserve or cerebrovascular reactivity are predicted to be unreliable without consideration of systemic arterial pressure and degree of carotid stenosis. Reserve cerebral blood flow values measured in patients with only moderate 60% to 70% carotid stenosis are in general too high and variable to be of clinical value, but are most reliable when measured near 80% diameter stenosis and considered as percent of the maximum reserve blood flow. Patient specific measured reserve blood flow values can be inserted into the model to calculate the collateral vascular resistance.ConclusionsPredicting cerebral blood flow reserve in patients with significant carotid stenosis is complex and multifactorial. A simple cerebrovascular model predicts that patient specific collateral vascular resistance is an excellent predictor of reserve cerebral blood flow in patients with significant carotid stenosis. Cerebral blood flow reserve measurements are of limited value without accounting for systemic pressure and actual percent carotid stenosis. Asymptomatic patients with severe carotid artery stenosis and a collateral vascular resistance greater than 1.0 are at increased risk of cerebral ischemia and may benefit from carotid endarterectomy.



2007 ◽  
Vol 28 (2) ◽  
pp. 412-419 ◽  
Author(s):  
Meike W Vernooij ◽  
Aad van der Lugt ◽  
Mohammad Arfan Ikram ◽  
Piotr A Wielopolski ◽  
Henri A Vrooman ◽  
...  

Reduced cerebral perfusion may contribute to the development of cerebrovascular and neurodegenerative diseases. Little is known on cerebral perfusion in the general population, as most measurement techniques are too invasive for application in large groups of healthy individuals. Total cerebral blood flow (tCBF) can be noninvasively measured by magnetic resonance imaging (MRI) but is highly correlated with brain volume. We calculated total brain perfusion by dividing tCBF by brain volume, and we investigated determinants of total brain perfusion in comparison with tCBF. Secondly, we studied whether persons with a low tCBF or low total brain perfusion have a larger volume of white matter lesions (WML). This study is based on 892 persons aged 60 to 91 years from the Rotterdam Study, a population-based cohort study. We performed two-dimensional (2D) phase-contrast MRI for tCBF measurement. Brain volume and WML volume were quantitatively assessed. Cardiovascular determinants were assessed by interview and physical examination. We assessed associations between cardiovascular determinants and flow measures with linear regression models, adjusted for age and sex. Associations between tCBF or total brain perfusion and WML volume were assessed using general linear models. We found that determinants of tCBF and total brain perfusion differed largely due to the large influence of brain volume on tCBF values. Persons with low total brain perfusion had a significantly larger WML volume compared with those with high total brain perfusion. Prospective studies are required to unravel whether hypoperfusion contributes to WML formation or that tissue damage, manifested by WML, leads to brain hypoperfusion.



Author(s):  
Carl Waldmann ◽  
Andrew Rhodes ◽  
Neil Soni ◽  
Jonathan Handy

Dealing with neurological critically ill patients is one of the most challenging situations in intensive care. The range of conditions can go from carbon dioxide narcosis to status epilepticus or hypoxic or traumatic brain injuries. The key difficulty is the neurological assessment of these patients while they require general anaesthesia. This chapter discusses neurological monitoring and includes discussion on intracranial pressure (ICP) monitoring (including indications for ICP monitoring, methods of measuring ICP, complications of ICP monitoring, and ICP in normal and pathological conditions), intracranial perfusion (regulation of cerebral perfusion and measurement of cerebral blood flow), electroencephalogram (EEG) and cerebral function analysing monitoring (CFAM) (EEG, cerebral function monitors (CFM)/CFAM, EEG terminology, and clinical use in the intensive care unit), and other forms of neurological monitoring (tissue metabolism, cerebral blood flow and metabolism, and peripheral nerve and muscle electrophysiology).



Author(s):  
Bryce Weir ◽  
Devidas Menon ◽  
Thomas Overton

SUMMARY:Seventy six regional cerebral blood flow (rCBF) studies were conducted on 32 patients who had a total of 39 aneurysms. Twenty three of these patients were studied pre- and post-operatively. Normal values were obtained from a control group of 33 subjects, each of whom underwent one rCBF study. Flow was reduced following subarachnoid hemorrhage (SAH); it increased significantly postoperatively. Lower flows were associated with poorer clinical grades. There was a greater variation in regional distribution of flow immediately following SAH than in normals or in patients who had recovered from the acute phase. rCBF studies correlated with CT scans demonstrated that a progressive increase in ventricular size was accompanied by a progressive reduction in flow. In addition, intraventricular hemorrhage (IVH) was associated with a significant reduction in cerebral blood flow (CBF). No significant correlation between CBF and spasm was demonstrable.



1993 ◽  
Vol 265 (4) ◽  
pp. H1243-H1248 ◽  
Author(s):  
K. Waschke ◽  
H. Schrock ◽  
D. M. Albrecht ◽  
K. van Ackern ◽  
W. Kuschinsky

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.



2019 ◽  
Vol 48 (3-6) ◽  
pp. 217-225 ◽  
Author(s):  
Masayuki Kameyama ◽  
Miki Fujimura ◽  
Ryosuke Tashiro ◽  
Kenichi Sato ◽  
Hidenori Endo ◽  
...  

Objective: Superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis is a standard surgical procedure for adult patients with moyamoya disease (MMD) and plays a role in preventing ischemic and/or hemorrhagic stroke. Cerebral hyperperfusion (CHP) syndrome is a potential complication of this procedure that can result in deleterious outcomes, such as delayed intracerebral hemorrhage, but the exact threshold of the pathological increase in postoperative cerebral blood flow (CBF) is unclear. Thus, we analyzed local CBF in the acute stage after revascularization surgery for adult MMD to predict CHP syndrome under modern perioperative management. Materials and Methods: Fifty-nine consecutive adult MMD patients, aged 17–66 years old (mean 43.1), underwent STA-MCA anastomosis with indirect pial synangiosis for 65 affected hemispheres. All patients were perioperatively managed by strict blood pressure control (systolic pressure of 110–130 mm Hg) to prevent CHP syndrome. Local CBF at the site of anastomosis was quantitatively measured using the autoradiographic method by N-isopropyl-p-[123I] iodoamphetamine single-photon emission computed tomography 1 and 7 days after surgery, in addition to the preoperative CBF value at the corresponding area. We defined CHP phenomenon as a local CBF increase over 150% compared to the preoperative value. Then, we investigated the correlation between local hemodynamic change and the development of CHP syndrome. Results: After 65 surgeries, 5 patients developed CHP syndrome, including 2 patients with delayed intracerebral hemorrhage (3.0%), 1 with symptomatic subarachnoid hemorrhage (1.5%), and 2 with focal neurological deterioration without hemorrhage. The CBF increase ratio was significantly higher in patients with CHP syndrome (270.7%) than in patients without CHP syndrome (135.2%, p = 0.003). Based on receiver operating characteristic analysis, the cutoff value for the pathological postoperative CBF increase ratio was 184.5% for CHP syndrome (sensitivity = 83.3%, specificity =  94.2%, area under the curve [AUC] value  =  0.825) and 241.3% for hemorrhagic CHP syndrome (sensitivity =  75.0%, specificity =  97.2%, AUC value  =  0.742). Conclusion: Quantitative measurement of the local CBF value in the early postoperative period provides essential information to predict CHP syndrome after STA-MCA anastomosis in patients with adult MMD. The pathological threshold of hemorrhagic CHP syndrome was as high as 241.3% by the local CBF increase ratio, but 2 patients (3.0%) developed delayed intracerebral hemorrhage in this series that were managed following the intensive perioperative management protocol. Thus, we recommend routine CBF measurement in the acute stage after direct revascularization surgery for adult MMD and satisfactory blood pressure control to avoid the deleterious effects of CHP.



1992 ◽  
Vol 262 (6) ◽  
pp. H1908-H1914 ◽  
Author(s):  
M. Ferrari ◽  
D. A. Wilson ◽  
D. F. Hanley ◽  
R. J. Traystman

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.



Author(s):  
W. A. Tweed ◽  
Jørn Overgaard

SUMMARY:The object of this study was to determine if traumatic brain edema (BE) and increased intracranial pressure (ICP) reduce cerebral blood flow (CBF). Two groups of patients were studied, one with slight BE and ICP less than 20 mm Hg., the other with pronounced BE and ICP over 20 mm Hg. Although ICP was higher and cerebral perfusion pressure lower in pro-nounced edema there was only a small and non-significant reduction in CBF and no difference in cerebro-vascular resistance. Since traumatic BE does not increase resistance to blood flow through the brain, cerebral perfusion can be maintained if an adequate perfusion pressure is established. This in turn, demands the monitoring and control of ICP.



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