Cerebral blood flow and vasoresponsivity within and around cerebral contusions

1996 ◽  
Vol 85 (5) ◽  
pp. 871-876 ◽  
Author(s):  
Mark R. McLaughlin ◽  
Donald W. Marion

✓ There is increasing evidence that regional ischemia plays a major role in secondary brain injury. Although the cortex underlying subdural hematomas seems particularly vulnerable to ischemia, little is known about the adequacy of cerebral blood flow (CBF) or the vasoresponsivity within the vascular bed of contusions. The authors used the xenon-enhanced computerized tomography (CT) CBF technique to define the CBF and vasoresponsivity of contusions, pericontusional parenchyma, and the remainder of the brain 24 to 48 hours after severe closed head injury in 10 patients: six patients with one contusion and four with two contusions, defined as mixed or high-density lesions on CT scanning. The CBF within the contusions (29.3 ± 16.4 ml/100 g/minute, mean ± standard deviation) was significantly lower than both that found in the adjacent 1-cm perimeter of normal-appearing tissue (42.5 ± 15.8 ml/100 g/minute) and the mean global CBF (52.5 ± 17.5 ml/100 g/minute) (p < 0.004, repeated-measures analysis of variance). A subset of seven patients (10 contusions) also underwent a second Xe-CT CBF study during mild hyperventilation (a PaCO of 24–32 mm Hg). In only two of these 10 contusions was vasoresponsivity less than 1% (range 0%–7.6%); in the rim of normal-appearing pericontusional tissue, it was 0.4% to 9.1%. The authors conclude that CBF within intracerebral contusions is highly variable and is often above 18 ml/100 g/minute, the reported threshold for irreversible ischemia. Intracontusional CBF is significantly reduced relative to surrounding brain parenchyma, and CO2 vasoresponsivity is usually present. In the contusion and the surrounding parenchyma, vasoresponsivity may be nearly three times normal, suggesting hypersensitivity to hyperventilation therapy. Given this possible hypersensitivity and relative hypoperfusion within and around cerebral contusions, these lesions are particularly vulnerable to secondary injury such as that which may be caused by hypotension or aggressive hyperventilation.

1989 ◽  
Vol 71 (1) ◽  
pp. 63-71 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Anthony Marmarou ◽  
Antonio A. F. DeSalles ◽  
John D. Ward ◽  
Richard S. Zimmerman ◽  
...  

✓ The literature suggests that in children with severe head injury, cerebral hyperemia is common and related to high intracranial pressure (ICP). However, there are very few data on cerebral blood flow (CBF) after severe head injury in children. This paper presents 72 measurements of cerebral blood flow (“CBF15”), using the 133Xe inhalation method, with multiple detectors over both hemispheres in 32 children aged 3 to 18 years (mean 13.6 years) with severe closed head injury (average Glasgow Coma Scale (GCS) score 5.4). In 25 of the children, these were combined with measurements of arteriojugular venous oxygen difference (AVDO2) and of cerebral metabolic rate of oxygen (CMRO2). In 30 patients, the first measurement was taken approximately 12 hours postinjury. In 18 patients, an indication of brain stiffness was obtained by withdrawal and injection of ventricular cerebrospinal fluid and calculation of the pressure-volume index (PVI) of Marmarou. The CBF and CMRO2 data were correlated with the GCS score, outcome, ICP, and PVI. Early after injury, CBF tended to be lower with lower GCS scores, but this was not statistically significant. This trend was reversed 24 hours postinjury, as significantly more hyperemic values were recorded the lower the GCS score, with the exception of the most severely injured patients (GCS score 3). In contrast, mean CMRO2 correlated positively with the GCS score and outcome throughout the course, but large standard deviations preclude making predictions based on CMRO2 measurements in individual patients. Early after injury, there was mild uncoupling between CBF and CMRO2 (CBF above metabolic demands, low AVDO2) and, after 24 hours, flow and metabolism were completely uncoupled with an extremely low AVDO2. Consistently reduced flow was found in only four patients; 28 patients (88%) showed hyperemia at some point in their course. This very high percentage of patients with hyperemia, combined with the lowest values of AVDO2 found in the literature, indicates that hyperemia or luxury perfusion is more prevalent in this group of patients. The three patients with consistently the highest CBF had consistently the lowest PVI: thus, the patients with the most severe hyperemia also had the stiffest brains. Nevertheless, and in contrast to previous reports, no correlation could be established between the course of ICP or PVI and the occurrence of hyperemia, nor was there a correlation between the levels of CBF and ICP at the time of the measurements. The authors argue that this lack of correlation is due to: 1) a definition of hyperemia that is too generous, and 2) the lack of a systematic relationship between CBF and cerebral blood volume. The implications of these findings for therapeutic modes of controlling ICP in children, such as hyperventilation and the use of mannitol, are discussed.


1998 ◽  
Vol 88 (6) ◽  
pp. 996-1001 ◽  
Author(s):  
Aram Ter Minassian ◽  
Eliane Melon ◽  
Caroline Leguerinel ◽  
Carlo Alberto Lodi ◽  
Françis Bonnet ◽  
...  

Object. The aim of this study was to reassess whether middle cerebral artery blood flow velocity (MCAv) variations measured by transcranial Doppler ultrasonography during acute PaCO2 manipulation adequately reflect cerebral blood flow (CBF) changes in patients with severe closed head injury. Methods. The study was performed by comparing MCAv variations to changes in CBF as assessed by measurements of the difference in the arteriovenous content in oxygen (AVDO2). The authors initiated 35 CO2 challenges in 12 patients with severe closed head injury during the acute stage. By simultaneous recording of systemic and cerebral hemodynamic parameters, 105 AVDO2 measurements were obtained. Patients were stratified into two groups, “high” and “low,” with respect to whether their resting values of MCAv were greater than 100 cm/second during moderate hyperventilation. Four patients displayed an elevated MCAv, which was related to vasospasm in three cases and to hyperemia in one case. The PaCO2 and intracranial pressure levels were not different between the two groups. The slope of the regression line between 1 divided by the change in (Δ)AVDO2 and ΔMCAv was not different from identity in the low group (1/ΔAVDO2 = 1.08 × ΔMCAv − 0.07, r = 0.93, p < 0.001) and significantly differed (p < 0.05) from the slope of the high group (1/ΔAVDO2 = 1.46 × ΔMCAv − 0.4, r = 0.83, p < 0.001). Conclusions. In patients with severe closed head injury, MCAv variations adequately reflect CBF changes as assessed by AVDO2 measurements in the absence of a baseline increase in MCAv. These observations indicate that both moderate variations in PaCO2 and variations in cerebral perfusion pressure do not act noticeably on the diameter of the MCA. The divergence from the expected relationship in the high group seems to be due to the heterogeneity of CO2-induced changes in cerebrovascular resistance between differing arterial territories.


2000 ◽  
Vol 93 (2) ◽  
pp. 265-274 ◽  
Author(s):  
Peter Vajkoczy ◽  
Harry Roth ◽  
Peter Horn ◽  
Thomas Lucke ◽  
Claudius Thomé ◽  
...  

Object. Current clinical neuromonitoring techniques lack adequate surveillance of cerebral perfusion. In this article, a novel thermal diffusion (TD) microprobe is evaluated for the continuous and quantitative assessment of intraparenchymal regional cerebral blood flow (rCBF).Methods. To characterize the temporal resolution of this new technique, rCBF measured using the TD microprobe (TD-rCBF) was compared with rCBF levels measured by laser Doppler (LD) flowmetry during standardized variations of CBF in a sheep model. For validation of absolute values, the microprobe was implanted subcortically (20 mm below the level of dura) into 16 brain-injured patients, and TD-rCBF was compared with simultaneous rCBF measurements obtained using stable xenon-enhanced computerized tomography scanning (sXe-rCBF). The two techniques were compared using linear regression analysis as well as the Bland and Altman method.Stable TD-rCBF measurements could be obtained throughout all 3- to 5-hour sheep experiments. During hypercapnia, TD-rCBF increased from 49.3 ± 15.8 ml/100 g/min (mean ± standard deviation) to 119.6 ± 47.3 ml/100 g/min, whereas hypocapnia produced a decline in TD-rCBF from 51.2 ± 12.8 ml/100 g/min to 39.3 ± 5.6 ml/100 g/min. Variations in mean arterial blood pressure revealed an intact autoregulation with pressure limits of approximately 65 mm Hg and approximately 170 mm Hg. After cardiac arrest TD-rCBF declined rapidly to 0 ml/100 g/min. The dynamics of changes in TD-rCBF corresponded well to the dynamics of the LD readings. A comparison of TD-rCBF and sXe-rCBF revealed a good correlation (r = 0.89; p <0.0001) and a mean difference of 1.1 ± 5.2 ml/100 g/min between the two techniques.Conclusions. The novel TD microprobe provides a sensitive, continuous, and real-time assessment of intraparenchymal rCBF in absolute flow values that are in good agreement with sXe-rCBF measurements. This study provides the basis for the integration of TD-rCBF into multimodal monitoring of patients who are at risk for secondary brain injury.


1993 ◽  
Vol 79 (5) ◽  
pp. 752-755 ◽  
Author(s):  
Michael D. Medlock ◽  
William C. Hanigan ◽  
Robert P. Cruse

✓ A 2-month-old infant demonstrated clinical brain death 48 hours after suffering a closed head injury accompanied by cardiac arrest. Two nuclear cerebral blood flow (CBF) studies demonstrated normal perfusion. On the 11th day following injury, cerebral electrical activity ceased and a normal glucose metabolic gradient between gray and white matter was documented on positron emission tomography. Autopsy revealed widespread necrosis with mononuclear cell infiltrates throughout all cerebral cortical layers. Nine children have previously been described with clinical brain death, electrocerebral silence, and evidence of CBF by radionuclide scan. The dissociation between cerebral electrical activity and blood flow may be explained by an increase in cranial volume allowed by the expansile neonatal skull, preventing both intracranial hypertension and a reduction in perfusion pressure. The persistence of glucose metabolism may be associated with the presence of inflammatory microglial cells in the ischemic cortex. The authors conclude that persistence of CBF and glucose metabolism in brain-dead children may not indicate neuronal survival. If repeated neurological examinations with or without electroencephalography support the diagnosis of brain death, the presence of CBF and glucose metabolism should not alter this conclusion.


1990 ◽  
Vol 72 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Jurg L. Jaggi ◽  
Walter D. Obrist ◽  
Thomas A. Gennarelli ◽  
Thomas W. Langfitt

✓ Cerebral blood flow (CBF) measurements were obtained acutely in 96 comatose patients with closed head injury, using the intravenous 133Xe technique. Arteriojugular venous oxygen differences and cerebral metabolic rate for oxygen (CMRO2) were determined in a subgroup of 66 patients. The relationship between each of these variables and outcome at 6 months was analyzed, using the Glasgow Outcome Scale. The CMRO2 was significantly depressed in patients who subsequently died or remained in a vegetative state, whereas higher values were obtained in patients who later regained consciousness. Although CBF was not predictive of outcome in the total sample, omission of patients with acute hyperemia resulted in a significant relationship that paralleled the metabolic findings. Follow-up studies in the survivors revealed a correlation between CBF and degree of functional recovery, the lowest blood flows being obtained among patients with severe disability. Age, initial Glasgow Coma Scale score, and occurrence of intracranial hypertension were each found to be predictive of outcome, thus confirming previous reports. When these variables were combined with CMRO2 in a logistic regression analysis, the probability of recovery was correctly predicted in 82% of the cases. The CMRO2 was relatively independent of the other prognostic indicators and, next to age, contributed most to the prediction.


1993 ◽  
Vol 79 (3) ◽  
pp. 354-362 ◽  
Author(s):  
Donald W. Marion ◽  
Walter D. Obrist ◽  
Patricia M. Earlier ◽  
Louis E. Penrod ◽  
Joseph M. Darby

✓ Animal research suggests that moderate therapeutic hypothermia may improve outcome after a severe head injury, but its efficacy has not been established in humans. The authors randomly assigned 40 consecutively treated patients with a severe closed head injury (Glasgow Coma Scale score 3 to 7) to either a hypothermia or a normothermia group. Using cooling blankets and cold saline gastric lavage, patients in the hypothermia group were cooled to 32° to 33°C (brain temperature) within a mean of 10 hours after injury, maintained at that temperature for 24 hours, and rewarmed to 37° to 38°C over 12 hours. Patients in the normothermia group were maintained at 37° to 38°C during this time. Deep-brain temperatures were monitored directly and used for all temperature determinations. Intracranial pressure (ICP), cerebral blood flow (CBF), and cerebral metabolic rate for oxygen (CMRO2) were measured serially for all patients. Hypothermia significantly reduced ICP (40%) and CBF (26%) during the cooling period, and neither parameter showed a significant rebound increase after patients were rewarmed. Compared to the normothermia group, the mean CMRO2 in the hypothermia group was lower during cooling and higher 5 days after injury. Three months after injury, 12 of the 20 patients in the hypothermia group had moderate, mild, or no disabilities; eight of the 20 patients in the normothermia group had improved to the same degree. Both groups had a similar incidence of systemic complications, including cardiac arrhythmias, coagulopathies, and pulmonary complications. It is concluded that therapeutic moderate hypothermia is safe and has sustained favorable effects on acute derangements of cerebral physiology and metabolism caused by severe closed head injury. The trend toward better outcome with hypothermia may indicate that its beneficial physiological and metabolic effects limit secondary brain injury.


1999 ◽  
Vol 90 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Leif Østergaard ◽  
Fred H. Hochberg ◽  
James D. Rabinov ◽  
A. Gregory Sorensen ◽  
Michael Lev ◽  
...  

Object. In this study the authors assessed the early changes in brain tumor physiology associated with glucocorticoid administration. Glucocorticoids have a dramatic effect on symptoms in patients with brain tumors over a time scale ranging from minutes to a few hours. Previous studies have indicated that glucocorticoids may act either by decreasing cerebral blood volume (CBV) or blood-tumor barrier (BTB) permeability and thereby the degree of vasogenic edema.Methods. Using magnetic resonance (MR) imaging, the authors examined the acute changes in CBV, cerebral blood flow (CBF), and BTB permeability to gadolinium-diethylenetriamine pentaacetic acid after administration of dexamethasone in six patients with brain tumors. In patients with acute decreases in BTB permeability after dexamethasone administration, changes in the degree of edema were assessed using the apparent diffusion coefficient of water.Conclusions. Dexamethasone was found to cause a dramatic decrease in BTB permeability and regional CBV but no significant changes in CBF or the degree of edema. The authors found that MR imaging provides a powerful tool for investigating the pathophysiological changes associated with the clinical effects of glucocorticoids.


2002 ◽  
Vol 97 (5) ◽  
pp. 1179-1183 ◽  
Author(s):  
Basar Atalay ◽  
Hayrunnisa Bolay ◽  
Turgay Dalkara ◽  
Figen Soylemezoglu ◽  
Kamil Oge ◽  
...  

Object. The goal of this study was to investigate whether stimulation of trigeminal afferents in the cornea could enhance cerebral blood flow (CBF) in rats after they have been subjected to experimental subarachnoid hemorrhage (SAH). Cerebral vasospasm following SAH may compromise CBF and increase the risks of morbidity and mortality. Currently, there is no effective treatment for SAH-induced vasospasm. Direct stimulation of the trigeminal nerve has been shown to dilate constricted cerebral arteries after SAH; however, a noninvasive method to activate this nerve would be preferable for human applications. The authors hypothesized that stimulation of free nerve endings of trigeminal sensory fibers in the face might be as effective as direct stimulation of the trigeminal nerve. Methods. Autologous blood obtained from the tail artery was injected into the cisterna magna of 10 rats. Forty-eight and 96 hours later (five rats each) trigeminal afferents were stimulated selectively by applying transcorneal biphasic pulses (1 msec, 3 mA, and 30 Hz), and CBF enhancements were detected using laser Doppler flowmetry in the territory of the middle cerebral artery. Stimulation-induced changes in cerebrovascular parameters were compared with similar parameters in sham-operated controls (six rats). Development of vasospasm was histologically verified in every rat with SAH. Corneal stimulation caused an increase in CBF and blood pressure and a net decrease in cerebrovascular resistance. There were no significant differences between groups for these changes. Conclusions. Data from the present study demonstrate that transcorneal stimulation of trigeminal nerve endings induces vasodilation and a robust increase in CBF. The vasodilatory response of cerebral vessels to trigeminal activation is retained after SAH-induced vasospasm.


2001 ◽  
Vol 95 (6) ◽  
pp. 1414-1421 ◽  
Author(s):  
Matthias Hübler ◽  
Jennifer E. Souders ◽  
Erin D. Shade ◽  
Nayak L. Polissar ◽  
Carmel Schimmel ◽  
...  

Background Perfluorocarbon (PFC) liquids are known to improve gas exchange and pulmonary function in various models of acute respiratory failure. Vaporization has been recently reported as a new method of delivering PFC to the lung. Our aim was to study the effect of PFC vapor on the ventilation/perfusion (VA/Q) matching and relative pulmonary blood flow (Qrel) distribution. Methods In nine sheep, lung injury was induced using oleic acid. Four sheep were treated with vaporized perfluorohexane (PFX) for 30 min, whereas the remaining sheep served as control animals. Vaporization was achieved using a modified isoflurane vaporizer. The animals were studied for 90 min after vaporization. VA/Q distributions were estimated using the multiple inert gas elimination technique. Change in Qrel distribution was assessed using fluorescent-labeled microspheres. Results Treatment with PFX vapor improved oxygenation significantly and led to significantly lower shunt values (P &lt; 0.05, repeated-measures analysis of covariance). Analysis of the multiple inert gas elimination technique data showed that animals treated with PFX vapor demonstrated a higher VA/Q heterogeneity than the control animals (P &lt; 0.05, repeated-measures analysis of covariance). Microsphere data showed a redistribution of Qrel attributable to oleic acid injury. Qrel shifted from areas that were initially high-flow to areas that were initially low-flow, with no difference in redistribution between the groups. After established injury, Qrel was redistributed to the nondependent lung areas in control animals, whereas Qrel distribution did not change in treatment animals. Conclusion In oleic acid lung injury, treatment with PFX vapor improves gas exchange by increasing VA/Q heterogeneity in the whole lung without a significant change in gravitational gradient.


2000 ◽  
Vol 92 (6) ◽  
pp. 1009-1015 ◽  
Author(s):  
Seiji Yamamoto ◽  
Weiyu Teng ◽  
Shigeru Nishizawa ◽  
Takeharu Kakiuchi ◽  
Hideo Tsukada

Object. The hydroxyl radical scavenger (±)-N,N′-propylenedinicotinamide (AVS) has been shown to ameliorate the occurrence of vasospasm following experimental subarachnoid hemorrhage (SAH) and to reduce the incidence of delayed ischemic neurological deficits (DINDs) in patients with SAH. The authors investigated whether prophylactic administration of AVS could improve cerebral blood flow (CBF) and cerebral glucose utilization (CGU) following SAH in rats.Methods. Anesthetized rats were subjected to intracisternal injection of blood (SAH group) or saline (control group). Either AVS (1 mg/kg/min) or saline (vehicle group) was continuously injected into the rat femoral vein. Forty-eight hours later, positron emission tomography scanning was used with the tracers 15O-H2O and 18F-2-fluoro-d-glucose to analyze quantitatively CBF and CGU, respectively, in the frontoparietal and occipital regions (12 regions of interest/group).In SAH rats receiving only vehicle, CBF decreased significantly (p < 0.05, Tukey's test) and CGU tended to decrease, compared with values obtained in control (non-SAH) rats receiving vehicle. In rats that were subjected to SAH, administration of AVS significantly (p < 0.05, Tukey's test) improved CBF and CGU in both the frontoparietal and occipital regions compared with administration of vehicle alone.Conclusions. Prophylactic administration of AVS improves CBF and CGU in the rat brain subjected to SAH, and can be a good pharmacological treatment for the prevention of DINDs following SAH.


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