Abstract W P211: Investigating the Cause for “Collateral Failure” in Stroke-in-Progression: Intracranial Pressure Elevation Reduces Flow Through Collateral Vessels

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Daniel Beard ◽  
Damian McLeod ◽  
Neil J Spratt
Keyword(s):  
Intracranial Pressure ◽  
Flow Velocity ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Minor Stroke ◽  
Collateral Flow ◽  
Mca Occlusion ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
Collateral Vessels

Background: Adequacy of the collateral circulation is a major determinant of outcome in stroke patients. Recent human imaging data indicates that collateral failure, rather than reperfusion-reocclusion is the most common cause for early progression in minor stroke. Our previous experimental data shows that intracranial pressure (ICP) rises transiently 24 h after even minor stroke. Herein, we investigated the effect of ICP manipulation on blood flow through collateral vessels during MCA occlusion. Methods: We developed and validated a method to quantify flow velocity and vessel diameter of anterior-middle cerebral artery (ACA-MCA) leptomeningeal collaterals in rats during stroke, using fluorescent microspheres. BIood flow velocity and diameter was quantified in individual collateral vessels and used to calculate absolute flow during MCA occlusion and reperfusion (n = 6). In separate experiments, ICP was increased after MCA occlusion by fluid infusion into the lateral ventricles and effects on relative collateral flow were determined (n = 4). Results: In vitro validation indicated accurate flow quantification (R 2 = 0.99, P<0.0001). Collateral flow was seen to switch from bidirectional to unidirectional flow (toward occluded vessel) and increase by 595 ± 134 % within 10 min of vessel occlusion. Direction and flow changes were variable after MCA reperfusion, however there was a mean flow reduction of 52 ± 15 % by 5 mins. Artificially elevating ICP during MCA occlusion caused a reduction of cerebral perfusion pressure which was strongly correlated with collateral flow reduction (R 2 = 0.90, p<0.0001). Discussion: Our method permits real time quantification of flow through individual collateral vessels during stroke and reperfusion. Intracranial pressure elevation reduced collateral flow, proportional to its effect on cerebral perfusion pressure. Coupled with our previous data indicating significant ICP elevation after even minor stroke, this suggests that transient ICP elevation is the possible cause of the collateral failure recently described in patients with stroke-in-progression.

scholarly journals Cerebral Blood Flow in Patients with Intracranial Pressure Elevation due to Traumatic Brain Edema

1976 ◽  
Vol 3 (1) ◽  
pp. 35-37 ◽  
Author(s):  
W. A. Tweed ◽  
Jørn Overgaard
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Monitoring And Control ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
And Control

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.

scholarly journals Intracranial Pressure Elevation Reduces Flow through Collateral Vessels and the Penetrating Arterioles they Supply. a Possible Explanation for ‘Collateral Failure’ and Infarct Expansion after Ischemic Stroke

2015 ◽  
Vol 35 (5) ◽  
pp. 861-872 ◽  
Author(s):  
Daniel J Beard ◽  
Damian D McLeod ◽  
Caitlin L Logan ◽  
Lucy A Murtha ◽  
Mohammad S Imtiaz ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Occlusion ◽  
Vessel Diameter ◽  
Experimental Stroke ◽  
Collateral Flow ◽  
Intracranial Pressure Elevation ◽  
Infarct Expansion ◽  
Flow Through ◽  
Collateral Vessels

Recent human imaging studies indicate that reduced blood flow through pial collateral vessels (‘collateral failure’) is associated with late infarct expansion despite stable arterial occlusion. The cause for ‘collateral failure’ is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by 4450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for ‘collateral failure’ in stroke-in-progression.

Transcranial Doppler ultrasonography in raised intra-cranial pressure and in intracranial circulatory arrest

1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski
Keyword(s):  
Intracranial Pressure ◽  
Brain Death ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Transcranial Doppler ◽  
Cerebral Perfusion ◽  
Doppler Ultrasonography ◽  
Perfusion Pressure ◽  
Circulatory Arrest ◽  
Transcranial Doppler Ultrasonography

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.

Effects of Head Posture on Cerebral Hemodynamics: Its Influences on Intracranial Pressure, Cerebral Perfusion Pressure, and Cerebral Oxygenation

Neurosurgery ◽  
2004 ◽  
Vol 54 (3) ◽  
pp. 593-598 ◽  
Author(s):  
Ivan Ng ◽  
Joyce Lim ◽  
Hwee Bee Wong
Keyword(s):  
Mean Arterial Pressure ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebral Oxygenation ◽  
Closed Head Injury ◽  
Head Posture ◽  
Head Elevation ◽  
Closed Head

Abstract OBJECTIVE Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 ± 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.

Intracranial pressure changes induced by sodium nitroprusside in patients with intracranial mass lesions

1978 ◽  
Vol 48 (3) ◽  
pp. 329-331 ◽  
Author(s):  
James E. Cottrell ◽  
Katie Patel ◽  
Herman Turndorf ◽  
Joseph Ransohoff
Keyword(s):  
Intracranial Pressure ◽  
Sodium Nitroprusside ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Intracranial Tumors ◽  
Cerebral Blood Vessels ◽  
Content Type ◽  
The Mean ◽  
Pressure Changes ◽  
Mass Lesions

✓ Because of the ability of sodium nitroprusside (SNP) to dilate cerebral blood vessels, intracranial pressure (ICP) should increase with its use. In patients with vascular intracranial tumors following SNP (0.01%) infusion, ICP increased from 14.58 ± 1.85 to 27.61 ± 3.33 torr (p > 0.0005) and cerebral perfusion pressure decreased from 89.32 ± 3.5 to 43.23 ± 4.60 torr (p < 0.0005) when the mean arterial pressure had reduced by 33%. These results suggest that SNP not be used in patients with raised ICP unless previous measures have been taken to improve intracranial compliance.

Attenuation of Haemodynamic Response to Placement of Mayfield Skull Pin Head Holder - Comparison of Dexmedetomidine Versus Propofol Infusion - A Randomized Interventional Trial Done in a Tertiary Centre in Central Kerala

2021 ◽  
Vol 8 (29) ◽  
pp. 2639-2643
Author(s):  
Sruthy Unni ◽  
Ranju Sebastian ◽  
Elizabeth Joseph ◽  
Remani Kelan Kamalakshi ◽  
Jamsheena Muthira Parambath
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Stress Response ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurosurgical Procedures ◽  
Sympathetic Nervous ◽  
The Brain ◽  
Group 1

BACKGROUND Anaesthesia for neurosurgery requires special considerations. The brain is enclosed in a rigid cranium, so the rise in intracranial pressure (ICP) which impairs cerebral perfusion pressure (CPP), results in irrepairable damage to various vital areas in the brain. Stable head position is required in long neurosurgical procedures. This is obtained with the use of clamps which fix the head rigidly. This is done usually under general anaesthesia because it produces intense painful stimuli leading to stimulation of sympathetic nervous system which in turn causes release of vasoconstrictive agents. This can impair perfusion in all organ systems. The increase in blood pressure due to sympathetic nervous system causes increase in blood flow. This causes increases in intracranial pressure which result in reduction in cerebral perfusion pressure once the auto regulatory limits are exceeded. We compared the effects of dexmedetomidine 1 µgm/kg and propofol 100 µgm/kg given as infusion over a period of 10 minutes before the induction of anaesthesia and continued till 5 minutes after pinning to attenuate the stress response while cranial pinning. In this study, we wanted to compare the effects of dexmedetomidine and propofol as infusion to attenuate the stress response while cranial pinning in patients undergoing neurosurgical procedures. METHODS This is a randomized interventional trial. Patients were divided into 2 groups of 20 each. Group 1 receiving dexmedetomidine and group 2 receiving propofol, both drugs given as infusion. Haemodynamic variables were monitored before and after cranial pinning. Data was analysed using IBM statistical package for social sciences (SPSS) statistics. The parameters recorded were analysed with the help of a statistician. RESULTS The two groups were comparable in demographic data. Incidence of tachycardia between group 1 and 2 showed that tachycardia to pinning was better controlled with propofol than dexmedetomidine (P < 0.05) which is statistically significant. There is no statistically significant difference in blood pressure values between group 1 and 2 after pinning. CONCLUSIONS From our study, we came to a conclusion that propofol was superior to dexmedetomidine in attenuating the heart rate response to cranial pinning. The effect of propofol and dexmedetomidine was comparable in attenuating the blood pressure response to cranial pinning. KEYWORDS Cranial Pinning, Dexmedetomidine, Propofol

Video microscopy of cerebrocortical capillary flow: response to hypotension and intracranial hypertension

1995 ◽  
Vol 268 (6) ◽  
pp. H2202-H2210 ◽  
Author(s):  
A. G. Hudetz ◽  
G. Feher ◽  
C. G. Weigle ◽  
D. E. Knuese ◽  
J. P. Kampine
Keyword(s):  
Cerebral Cortex ◽  
Intracranial Pressure ◽  
Flow Velocity ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Capillary Flow ◽  
Video Microscopy ◽  
Cell Counting ◽  
Correlation Technique ◽  
Cranial Window

Although autoregulation of cerebral blood flow is well established, the response of cerebral capillary circulation to reduced cerebral perfusion pressure (CPP) is unclear. The objective of this study was to determine whether red cell flow velocity in individual capillaries of the cerebral cortex is maintained during acute decreases in CPP. Microcirculation of the superficial parietal cerebral cortex of adult barbiturate-anesthetized artificially ventilated rats was visualized using a new design of closed-perfused cranial window and epifluorescent-intensified video microscopy. Fluorescein-isothiocyanate-labeled red blood cells (FRBC) injected intravenously were used as markers of capillary flow. CPP, defined as mean arterial pressure minus intracranial pressure, was reduced by controlled hemorrhage or by stepwise elevation of local intracranial pressure. The movement of FRBC in the parenchymal capillary network was video recorded at each pressure level, and FRBC velocity in each capillary was measured off-line with use of the dual-window digital cross-correlation technique. FRBC flux in the capillaries was measured by automated cell counting. FRBC velocity at normal perfusion pressure was 1.47 +/- 0.58 (SD) mm/s and changed little in the perfusion pressure range of 70-120 mmHg. The autoregulatory index in this pressure range was 0.0049 mm.s-1.mmHg-1. Opening of previously unperfused capillaries was not observed. FRBC flux correlated with FRBC velocity, but the latter was maintained in a narrower range than FRBC flux, suggesting a decrease in capillary diameter or hematocrit with decreasing perfusion pressure. The results suggest that flow autoregulation is associated with the maintenance of capillary flow velocity and that capillary recruitment does not contribute to flow autoregulation in the rat cerebral cortex.

Intratracheal Suctioning in Sick Preterm Infants: Prevention of Intracranial Hypertension and Cerebral Hypoperfusion by Muscle Paralysis

PEDIATRICS ◽  
1987 ◽  
Vol 79 (4) ◽  
pp. 538-543
Author(s):  
Sergio Fanconi ◽  
Gabriel Duc
Keyword(s):  
Heart Rate ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Preterm Infants ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Muscle Paralysis ◽  
Endotracheal Suctioning ◽  
Significant Difference ◽  
Transcutaneous Po2

In a prospective nonrandomized study, using each baby as his or her own control, we compared intracranial pressure (anterior fontanel pressure as measured with the Digilab pneumotonometer), cerebral perfusion pressure, BP, heart rate, transcutaneous Po2, and transcutaneous Pco2 before, during, and after endotracheal suctioning, with and without muscle paralysis, in 28 critically ill preterm infants with respiratory distress syndrome. With suctioning, there was a small but significant increase in intracranial pressure in paralyzed patients (from 13.7 [mean] ± 4.4 mm Hg [SD] to 15.8 ± 5.2 mm Hg) but a significantly larger (P &lt; .001) increase when they were not paralyzed (from 12.5 ± 3.6 to 28.5 ± 8.3 mm Hg). Suctioning led to a slight increase in BP with (from 45.3 ± 9.1 to 48.0 ± 8.7 mm Hg) and without muscle paralysis (from 45.1 ± 9.4 to 50.0 ± 11.7 mm Hg); but there was no significant difference between the two groups. The cerebral perfusion pressure in paralyzed infants did not show any significant change before, during, and after suctioning (31.5 ± 9.1 mm Hg before v 32.0 ± 8.7 mm Hg during suctioning), but without muscle paralysis cerebral perfusion pressure decreased (P &lt; .001) from 32.8 ± 9.7 to 21.3 ± 13.1 mm Hg. Suctioning induced a slight decrease in mean heart rate and transcutaneous Po2, but pancuronium did not alter these changes. There was no statistical difference in transcutaneous Pco2, before, during, and after suctioning with and without muscle paralysis. Our data demonstrate that muscle paralysis in sick preterm infants can significantly minimize the increase in intracranial pressure and can stabilize the cerebral perfusion pressure without having any effect on the BP increase during suctioning.

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