THE EFFECTS OF HEMORRHAGE AND BRAIN INJURY ALONE, OR COMBINED, ON CEREBRAL BLOOD FLOW AND SUPERIOR SAGITTAL SINUS THROMBOXANE AND PROSTACYCLIN LEVELS

1991 ◽  
Vol 3 (3) ◽  
pp. 249
Author(s):  
D L Kong ◽  
D S Prough ◽  
D S DeWitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Superior Sagittal Sinus ◽  
Sagittal Sinus

scholarly journals Small vessel disease is associated with altered cerebrovascular pulsatility but not resting cerebral blood flow

2018 ◽  
Vol 40 (1) ◽  
pp. 85-99 ◽  
Author(s):  
Yulu Shi ◽  
Michael J Thrippleton ◽  
Gordon W Blair ◽  
David A Dickie ◽  
Ian Marshall ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Small Vessel Disease ◽  
Superior Sagittal Sinus ◽  
Small Vessel ◽  
Perivascular Spaces ◽  
Intracranial Volume ◽  
Vessel Disease ◽  
Sagittal Sinus ◽  
Intracranial Pulsatility

Cerebral small vessel disease (SVD) contributes to 25% of ischemic strokes and 45% of dementias. We aimed to investigate the role of cerebral blood flow (CBF) and intracranial pulsatility in SVD. We scanned 60 patients with minor ischemic stroke, representing a range of white matter hyperintensities (WMH). We rated WMH and perivascular spaces (PVS) using semi-quantitative scales and measured WMH volume. We measured flow and pulsatility in the main cerebral vessels and cerebrospinal fluid (CSF) using phase-contrast MRI. We investigated the association between flow, pulsatility and SVD features. In 56/60 patients (40 male, 67.8±8.3 years) with complete data, median WMH volume was 10.7 mL (range 1.4–75.0 mL), representing median 0.77% (0.11–5.17%) of intracranial volume. Greater pulsatility index (PI) in venous sinuses was associated with larger WMH volume (e.g. superior sagittal sinus, β = 1.29, P < 0.01) and more basal ganglia PVS (e.g. odds ratio = 1.38, 95% confidence interval 1.06, 1.79, per 0.1 increase in superior sagittal sinus PI) independently of age, sex and blood pressure. CSF pulsatility and CBF were not associated with SVD features. Our results support a close association of SVD features with increased intracranial pulsatility rather than with low global CBF, and provide potential targets for mechanistic research, treatment and prevention of SVD.

Cerebral blood flow and oxygen consumption in the newborn dog

1978 ◽  
Vol 234 (5) ◽  
pp. R209-R215
Author(s):  
M. J. Hernandez ◽  
R. W. Brennan ◽  
R. C. Vannucci ◽  
G. S. Bowman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Superior Sagittal Sinus ◽  
Venous Blood ◽  
Arterial Pco2 ◽  
Content Difference ◽  
Cerebral Metabolic Rate ◽  
Sagittal Sinus ◽  
Newborn Brain ◽  
Arterial Blood

Cerebral blood flow (CBF), CBF responses to changes in arterial CO2 tension, and cerebral metabolic rate for oxygen (CMRO2) were measured in newborn dogs, by means of a modification of the Kety and Schmidt technique employing 133Xe. Mongrel dogs of 1-7 days of age were paralyzed and passively ventilated with 70% N2O and 30% O2. CBF was derived by analysis of paired serial 20-microliter samples of arterial and of cerebral venous blood from the superior sagittal sinus. At an arterial PCO2 of 36.9 +/- 3.7 Torr and a mean arterial blood pressure of 62 +/- 10 Torr, CBF was 23 +/- 8 ml/min per 100 g. The arteriovenous oxygen content difference averaged 5.6 vol%, and CMRO2 was 1.13 +/- 0.30 ml O2/min per 100 g. CBF increased or decreased by 0.58 ml/min/100 g per Torr change in PCO2. Our results suggest that in the newborn, basal CBF and CBF responses to CO2 are considerably lower than in the adult and parallel the lower metabolic needs of the newborn brain.

scholarly journals Quantitative cerebral blood flow using xenon-enhanced CT after decompressive craniectomy in traumatic brain injury

2018 ◽  
Vol 129 (1) ◽  
pp. 241-246 ◽  
Author(s):  
Aditya Vedantam ◽  
Claudia S. Robertson ◽  
Shankar P. Gopinath
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Clinical Outcome ◽  
Decompressive Craniectomy ◽  
Decompressive Surgery ◽  
Hemodynamic Parameters ◽  
Enhanced Ct ◽  
The Mean

OBJECTIVEFew studies have reported on changes in quantitative cerebral blood flow (CBF) after decompressive craniectomy and the impact of these measures on clinical outcome. The aim of the present study was to evaluate global and regional CBF patterns in relation to cerebral hemodynamic parameters in patients after decompressive craniectomy for traumatic brain injury (TBI).METHODSThe authors studied clinical and imaging data of patients who underwent xenon-enhanced CT (XeCT) CBF studies after decompressive craniectomy for evacuation of a mass lesion and/or to relieve intractable intracranial hypertension. Cerebral hemodynamic parameters prior to decompressive craniectomy and at the time of the XeCT CBF study were recorded. Global and regional CBF after decompressive craniectomy was measured using XeCT. Regional cortical CBF was measured under the craniectomy defect as well as for each cerebral hemisphere. Associations between CBF, cerebral hemodynamics, and early clinical outcome were assessed.RESULTSTwenty-seven patients were included in this study. The majority of patients (88.9%) had an initial Glasgow Coma Scale score ≤ 8. The median time between injury and decompressive surgery was 9 hours. Primary decompressive surgery (within 24 hours) was performed in the majority of patients (n = 18, 66.7%). Six patients had died by the time of discharge. XeCT CBF studies were performed a median of 51 hours after decompressive surgery. The mean global CBF after decompressive craniectomy was 49.9 ± 21.3 ml/100 g/min. The mean cortical CBF under the craniectomy defect was 46.0 ± 21.7 ml/100 g/min. Patients who were dead at discharge had significantly lower postcraniectomy CBF under the craniectomy defect (30.1 ± 22.9 vs 50.6 ± 19.6 ml/100 g/min; p = 0.039). These patients also had lower global CBF (36.7 ± 23.4 vs 53.7 ± 19.7 ml/100 g/min; p = 0.09), as well as lower CBF for the ipsilateral (33.3 ± 27.2 vs 51.8 ± 19.7 ml/100 g/min; p = 0.07) and contralateral (36.7 ± 19.2 vs 55.2 ± 21.9 ml/100 g/min; p = 0.08) hemispheres, but these differences were not statistically significant. The patients who died also had significantly lower cerebral perfusion pressure (52 ± 17.4 vs 75.3 ± 10.9 mm Hg; p = 0.001).CONCLUSIONSIn the presence of global hypoperfusion, regional cerebral hypoperfusion under the craniectomy defect is associated with early mortality in patients with TBI. Further study is needed to determine the value of incorporating CBF studies into clinical decision making for severe traumatic brain injury.

The Influence of Inhaled Nitric Oxide on Cerebral Blood Flow and Metabolism in a Child with Traumatic Brain Injury

2001 ◽  
Vol 93 (2) ◽  
pp. 351-353 ◽  
Author(s):  
Monica S. Vavilala ◽  
Joan S. Roberts ◽  
Anne E. Moore ◽  
David W. Newell ◽  
Arthur M. Lam
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Inhaled Nitric Oxide

scholarly journals Virtual Simulation of the Effects of Intracranial Fluid Cavitation in Blast-Induced Traumatic Brain Injury

2015 ◽  
Author(s):  
Shivonne Haniff ◽  
Paul Taylor ◽  
Aaron Brundage ◽  
Damon Burnett ◽  
Candice Cooper ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cavitation Bubble ◽  
Superior Sagittal Sinus ◽  
Von Mises Stress ◽  
Bubble Collapse ◽  
Compressive Wave ◽  
Sagittal Sinus ◽  
Microscale Model ◽  
Von Mises

A microscale model of the brain was developed in order to understand the details of intracranial fluid cavitation and the damage mechanisms associated with cavitation bubble collapse due to blast-induced traumatic brain injury (TBI). Our macroscale model predicted cavitation in regions of high concentration of cerebrospinal fluid (CSF) and blood. The results from this macroscale simulation directed the development of the microscale model of the superior sagittal sinus (SSS) region. The microscale model includes layers of scalp, skull, dura, superior sagittal sinus, falx, arachnoid, subarachnoid spacing, pia, and gray matter. We conducted numerical simulations to understand the effects of a blast load applied to the scalp with the pressure wave propagating through the layers and eventually causing the cavitation bubbles to collapse. Collapse of these bubbles creates spikes in pressure and von Mises stress downstream from the bubble locations. We investigate the influence of cavitation bubble size, compressive wave amplitude, and internal bubble pressure. The results indicate that these factors may contribute to a greater downstream pressure and von Mises stress which could lead to significant tissue damage.

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