Cerebral autoregulation following head injury

2001 ◽  
Vol 95 (5) ◽  
pp. 756-763 ◽  
Author(s):  
Marek Czosnyka ◽  
Piotr Smielewski ◽  
Stefan Piechnik ◽  
Luzius A. Steiner ◽  
John D. Pickard
Keyword(s):  
Head Injury ◽  
Cerebral Autoregulation ◽  
Perfusion Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Head Injured ◽  
The Mean ◽  
Injured Patients ◽  
The Relationship ◽  
Fine Print

Object. The goal of this study was to examine the relationship between cerebral autoregulation, intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral perfusion pressure (CPP) after head injury by using transcranial Doppler (TCD) ultrasonography. Methods. Using ICP monitoring and TCD ultrasonography, the authors previously investigated whether the response of flow velocity (FV) in the middle cerebral artery to spontaneous variations in ABP or CPP provides reliable information about cerebral autoregulatory reserve. In the present study, this method was validated in 187 head-injured patients who were sedated and receiving mechanical ventilation. Waveforms of ICP, ABP, and FV were recorded over intervals lasting 20 to 120 minutes. Time-averaged mean FV and CPP were determined. The correlation coefficient index between FV and CPP (the mean index of autoregulation [Mx]) was calculated over 4-minute epochs and averaged for each investigation. The distribution of averaged mean FV values converged with the shape of the autoregulatory curve, indicating lower (CPP < 55 mm Hg) and upper (CPP > 105 mm Hg) thresholds of autoregulation. The relationship between the Mx and either the CPP or ABP was depicted as a U-shaped curve. Autoregulation was disturbed in the presence of intracranial hypertension (ICP ≥ 25 mm Hg) and when mean ABP was too low (ABP < 75 mm Hg) or too high (ABP > 125 mm Hg). Disturbed autoregulation (p < 0.005) and higher ICP (p < 0.005) occurred more often in patients with unfavorable outcomes than in those with favorable outcomes. Conclusions. Autoregulation not only is impaired when associated with a high ICP or low ABP, but it can also be disturbed by too high a CPP. The Mx can be used to guide intensive care therapy when CPP-oriented protocols are used.

Relationship of perfusion pressure and size to risk of hemorrhage from arteriovenous malformations

1992 ◽  
Vol 76 (6) ◽  
pp. 918-923 ◽  
Author(s):  
Robert F. Spetzler ◽  
Ronald W. Hargraves ◽  
Patrick W. McCormick ◽  
Joseph M. Zabramski ◽  
Richard A. Flom ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Feeding Artery ◽  
Content Type ◽  
Arterial Blood ◽  
The Mean ◽  
Feeding Pressure ◽  
Risk Of Hemorrhage ◽  
Relationship Of ◽  
The Relationship ◽  
Fine Print

✓ The relationship between the size of an arteriovenous malformation (AVM) and its propensity to hemorrhage is unclear. Although nidus volume increases geometrically with respect to AVM diameter, hemorrhages are at least as common, in small AVM's compared to large AVM's. The authors prospectively evaluated 92 AVM's for nidus size, hematoma size, and arterial feeding pressure to determine if these variables influence the tendency to hemorrhage. Small AVM's (diameter ≤ 3 cm) presented with hemorrhage significantly more often (p < 0.001) than large AVM's (diameter > 6 cm), the incidence being 82% versus 21%. Intraoperative arterial pressures were recorded from the main feeding vessel(s) in 24 of the 92 patients in this series: 10 presented with hemorrhage and 14 presented with other neurological symptoms. In the AVM's that had hemorrhaged, the mean difference between mean arterial blood pressure and the feeding artery pressure was 6.5 mm Hg (range 2 to 15 mm Hg). In the AVM's that did not rupture, this difference was 40 mm Hg (range 17 to 63 mm Hg). Smaller AVM's had significantly higher feeding artery pressures (p < 0.05) than did larger AVM's, and they were associated with large hemorrhages. It is suggested that differences in arterial feeding pressure may be responsible for the observed relationship between the size of AVM's and the frequency and severity of hemorrhage.

Cerebral autoregulation following minor head injury

1997 ◽  
Vol 86 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Elisabeth C. Jünger ◽  
David W. Newell ◽  
Gerald A. Grant ◽  
Anthony M. Avellino ◽  
Saadi Ghatan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Head Injury ◽  
Cerebral Autoregulation ◽  
Minor Head Injury ◽  
Lower Blood Pressure ◽  
Content Type ◽  
Lower Blood ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI). Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.

Effect of stable xenon inhalation on intracranial pressure during measurement of cerebral blood flow in head injury

1994 ◽  
Vol 81 (6) ◽  
pp. 822-828 ◽  
Author(s):  
Jan Plougmann ◽  
Jens Astrup ◽  
Jens Pedersen ◽  
Carsten Gyldensted
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Stable Xenon ◽  
The Mean ◽  
Injured Patients ◽  
Fine Print

✓ Xenon-enhanced computerized tomography (CT) is well suited for measurements of cerebral blood flow (CBF) in head-injured patients. Previous studies indicated divergent results on whether inhalation of xenon may cause a clinically relevant increase in intracranial pressure (ICP). The authors employed Xe-enhanced CT/CBF measurements to study the effect of 20 minutes of inhalation of 33% xenon in oxygen on ICP, cerebral perfusion pressure (CPP), and arteriovenous oxygen difference (AVDO2) in 13 patients 3 days (mean 1 to 5 days) after severe head injury (Glasgow Coma Scale score ≤ 7). The patients were moderately hyperventilated (mean PaCO2 4.3 kPa or 32.3 mm Hg). Six patients were studied before and during additional hyperventilation. All 13 patients reacted with an increase in ICP and 11 with a decrease in CPP. The mean ICP increment was 6.9 ± 7.7 (range 2 to 17 mm Hg). The mean CPP decrement was −9.7 ± −14.6 (range 17 to 47 mm Hg). The time course of the ICP changes indicated that ICP increased rapidly during the first 5 to 6 minutes, then declined to a plateau (peak-plateau type in four of 13 patients), remained at a plateau (plateau type in six of 13), or continued to increase in three of 13, indicating individual variance in xenon reactivity. Additional hyperventilation had no effect on the xenon-induced increments in ICP but these occurred at lower ICP and higher CPP baseline levels. The AVDO2 values, an index of flow in relation to metabolism, indicated a complex effect of xenon on CBF as well as on metabolism. This study indicates that xenon inhalation for Xe-CT CBF measurements in head-injured patients according to our protocol causes clinically significant increments in ICP and decrements in CPP. It is suggested that the effect of xenon is analogous to anesthesia induction. Individual variations were observed indicating possible individual tolerance, possible influence of type and extent of the cerebral injury, disturbances in cerebrovascular reactivity, and possible influence of medication. These effects of xenon suggest that hyperventilation should be ensured in patients with evidence of reduced compliance or high ICP. On the other hand, inhalation of stable xenon is not believed to pose a risk because no signs of cerebral oligemia or ischemia were indicated in the AVDO2 values.

Impairment of helper T-cell function and lymphokineactivated killer cytotoxicity following severe head injury

1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  
Keyword(s):  
T Cell ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cell Cytotoxicity ◽  
Content Type ◽  
Lak Cell ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

High-risk mild head injury

1997 ◽  
Vol 87 (2) ◽  
pp. 234-238 ◽  
Author(s):  
John N. K. Hsiang ◽  
Theresa Yeung ◽  
Ashley L. M. Yu ◽  
Wai S. Poon
Keyword(s):  
Head Injury ◽  
High Risk ◽  
Mild Head Injury ◽  
Radiographic Findings ◽  
Content Type ◽  
Head Injured ◽  
Definition Of ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

✓ The generally accepted definition of mild head injury includes Glasgow Coma Scale (GCS) scores of 13 to 15. However, many studies have shown that there is a heterogeneous pathophysiology among patients with GCS scores in this range. The current definition of mild head injury is misleading because patients classified in this category can have severe sequelae. Therefore, a prospective study of 1360 head-injured patients with GCS scores ranging from 13 to 15 who were admitted to the neurosurgery service during 1994 and 1995 was undertaken to modify the current definition of mild head injury. Data regarding patients' age, sex, GCS score, radiographic findings, neurosurgical intervention, and 6-month outcome were collected and analyzed. The results of this study showed that patients with lower GCS scores tended to have suffered more serious injury. There was a statistically significant trend across GCS scores for percentage of patients with positive acute radiographic findings, percentage receiving neurosurgical interventions, and percentage with poor outcome. The presence of postinjury vomiting did not correlate with findings of acute radiographic abnormalities. Based on the results of this study, the authors divided all head-injured patients with GCS scores ranging from 13 to 15 into mild head injury and high-risk mild head injury groups. Mild head injury is defined as a GCS score of 15 without acute radiographic abnormalities, whereas high-risk mild head injury is defined as GCS scores of 13 or 14, or a GCS score of 15 with acute radiographic abnormalities. This more precise definition of mild head injury is simple to use and may help avoid the confusion caused by the current classification.

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors

1992 ◽  
Vol 77 (5) ◽  
pp. 694-699 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Claramae H. Miller ◽  
Franklin C. Wagner ◽  
Sally J. DeNardo ◽  
Gerald L. DeNardo ◽  
...  
Keyword(s):  
Head Injury ◽  
Cellular Immunity ◽  
Severe Head Injury ◽  
Normal Subjects ◽  
Lymphocyte Function ◽  
Serum Factors ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factors) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immmunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

Effect of apolipoprotein E genotype on hematoma volume after trauma

2002 ◽  
Vol 96 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Imran Liaquat ◽  
Laurence T. Dunn ◽  
James A. R. Nicoll ◽  
Graham M. Teasdale ◽  
John D. Norrie
Keyword(s):  
Head Injury ◽  
Ct Scan ◽  
Injury Severity ◽  
Univariate Analysis ◽  
Hematoma Volume ◽  
Patient Age ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The apolipoprotein E-ϵ4 (APOE-ϵ4) allele is associated with poor outcome after head injury and spontaneous intracerebral hemorrhage (SICH). The aims of this study were to determine if patients in whom one or more APOE-ϵ4 alleles are present are more likely to sustain intracranial mass lesions after head injury and to determine whether there is an isoform-specific effect on the size of the intracranial hematoma. Methods. The authors performed a computerized volumetric analysis of 142 hematomas visible on computerized tomography (CT) scans obtained in 129 patients. The APOE genotype was determined by subjecting buccal smear samples to polymerase chain reaction and restriction enzyme digestion. Allele frequencies were similar in head-injured patients with and without intracranial hematomas (p = 0.36). Univariate analysis revealed that in those patients with one or more APOE-ϵ4 alleles hematoma volume was greater (cube root—transformed values) than that found in patients without the APOE-ϵ4 allele (3.1 cm compared with 2.5 cm, p = 0.0039). The results of univariate analysis also suggested significant effects of patient age, injury severity (mild, moderate, or severe according to admission Glasgow Coma Scale scores) and hematoma location (extraaxial, intraaxial, or both) on hematoma volume. The mechanism of injury (assault, fall, or other) was marginally associated with hematoma volume (p = 0.052). Time from injury to CT scan, hypoxia, and hypotension had no significant effect on hematoma volume. The results of multiple linear regression analysis showed that the presence of an APOE-ϵ4 allele and an extraaxial hematoma location were independent predictors of hematoma volume, after adjusting for patient age, hours between injury and CT scan, injury severity, and injury mechanism. Conclusions. Larger hematomas were found in head-injured patients with one or more APOE-ϵ4 alleles than in patients without the allele. This may contribute to the poorer outcomes observed in these patients.

Efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia

2003 ◽  
Vol 99 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Yoshikazu Nakajima ◽  
Mamoru Taneda ◽  
Osamu Tasaki ◽  
Yoshiaki Inoue ◽  
...  
Keyword(s):  
Intracranial Hypertension ◽  
Mild Hypothermia ◽  
Brain Temperature ◽  
Moderate Hypothermia ◽  
Content Type ◽  
Arterial Blood ◽  
Cell Counts ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. This study was performed to determine whether moderate hypothermia (31°C) improves clinical outcome in severely head injured patients whose intracranial hypertension cannot be controlled using mild hypothermia (34°C). Methods. Twenty-two consecutive severely head injured patients who fulfilled the following criteria were included in this study: an intracranial pressure (ICP) that remained higher than 40 mm Hg despite the use of mild hypothermia combined with conventional therapies; and a Glasgow Coma Scale score of 8 or less on admission. After the failure of mild hypothermia in combination with conventional therapies; patients were exposed to moderate hypothermia as quickly as possible. As brain temperature was reduced from 34 to 31°C, the volume of intravenous fluid infusion was increased significantly from 1.9 ± 0.9 to 2.6 ± 1.2 mg/kg/hr (p < 0.01), and the dose of dopamine infusion increased significantly from 4.3 ± 3.1 to 8.2 ± 4.4 µg/kg/min (p < 0.01). Nevertheless, mean arterial blood pressure and heart rate decreased significantly from 97.1 ± 13.1 to 85.1 ± 10.5 mm Hg (p < 0.01) and from 92.2 ± 13.8 to 72.2 ± 14.3 beats/minute at (p < 0.01) at 34 and 31°C, respectively. Arterial base excess was significantly aggravated from −3.3 ± 4 at 34°C to −5.6 ± 5.4 mEq/L (at 31°C; p < 0.05). Likewise, serum potassium concentration, white blood cell counts, and platelet counts at 31°C decreased significantly compared with those at 34°C (p < 0.01). In 19 (86%) of 22 patients, elevation of ICP could not be prevented using moderate hypothermia. In the remaining three patients, ICP was maintained below 40 mm Hg by inducing moderate hypothermia; however, these three patients died of multiple organ failure. These results clearly indicate that moderate hypothermia induces complications more severe than those induced by mild hypothermia without improving outcomes. Conclusions. The authors concluded that moderate hypothermia is not effective in improving clinical outcomes in severely head injured patients whose ICP remains higher than 40 mm Hg after treatment with mild hypothermia combined with conventional therapies.

Determination of threshold levels of cerebral perfusion pressure and intracranial pressure in severe head injury by using receiver operating—characteristic curves: an observational study in 291 patients

2001 ◽  
Vol 94 (3) ◽  
pp. 412-416 ◽  
Author(s):  
Iain Robert Chambers ◽  
Lynne Treadwell ◽  
A. David Mendelow
Keyword(s):  
Cerebral Perfusion ◽  
Operating Characteristic ◽  
Perfusion Pressure ◽  
Roc Curves ◽  
Content Type ◽  
Head Injured ◽  
Mass Lesions ◽  
Injured Patients ◽  
Fine Print

Object. Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) are frequently monitored in severely head injured patients. To establish which one (ICP or CPP) is more predictive of outcome and to examine whether there are significant threshold levels in the determination of outcome, receiver—operating characteristic (ROC) curves were used to analyze data in a large series of head-injured patients. Methods. Data were obtained from a total of 291 severely head injured patients (207 adults and 84 children). Outcome was categorized as either independent (good recovery or moderate disability) or poor (severely disabled, vegetative, or dead) by using the Glasgow Outcome Scale; patients were also grouped according to the Marshall computerized tomography scan classification. Conclusions. The maximum value of a 2-minute rolling average of ICP readings (defined as ICPmax) and the minimum value of the CPP readings (CPPmin) were then used to calculate the sensitivity and specificity of the ROC curves over a range of values. Using ROC curves, a threshold value for CPPmin of 55 mm Hg and for ICPmax of 35 mm Hg appear to be the best predictors in adults. For children the levels appear to be 43 to 45 mm Hg for CPPmin and 35 mm Hg for ICPmax. Higher levels of CPPmin seem important in adults with mass lesions. These CPP thresholds (45 mm Hg for children and 55 mm Hg for adults) are lower than previously predicted and may be clinically important, especially in children, in whom a lower blood pressure level is normal. Also, CPP management at higher levels may be more important in adults with mass lesions. A larger observational series would improve the accuracy of these predictions.

Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study

2001 ◽  
Vol 95 (2) ◽  
pp. 222-232 ◽  
Author(s):  
Jae Hong Lee ◽  
Daniel F. Kelly ◽  
Matthias Oertel ◽  
David L. McArthur ◽  
Thomas C. Glenn ◽  
...  
Keyword(s):  
Head Injury ◽  
Scale Score ◽  
Transcranial Doppler ◽  
Brain Lesions ◽  
Content Type ◽  
Head Injured ◽  
Metabolic Suppression ◽  
Injured Patients ◽  
Pressure Autoregulation ◽  
Fine Print

Object. Contemporary management of head-injured patients is based on assumptions about CO2 reactivity, pressure autoregulation (PA), and vascular reactivity to pharmacological metabolic suppression. In this study, serial assessments of vasoreactivity of the middle cerebral artery (MCA) were performed using bilateral transcranial Doppler (TCD) ultrasonography. Methods. Twenty-eight patients (mean age 33 ± 13 years, median Glasgow Coma Scale score of 7) underwent a total of 61 testing sessions during postinjury Days 0 to 13. The CO2 reactivity (58 studies in 28 patients), PA (51 studies in 23 patients), and metabolic suppression reactivity (35 studies in 16 patients) were quantified for each cerebral hemisphere by measuring changes in MCA velocity in response to transient hyperventilation, arterial blood pressure elevation, or propofol-induced burst suppression, respectively. One or both hemispheres registered below normal vasoreactivity scores in 40%, 69%, and 97% of study sessions for CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.0001), respectively. Intracranial hypertension, classified as intracranial pressure (ICP) greater than 20 mm Hg at the time of testing, was associated with global impairment of CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.05). A low baseline cerebral perfusion pressure (CPP) was also predictive of impaired CO2 reactivity and PA (p < 0.01). Early postinjury hypotension or hypoxia was also associated with impaired CO2 reactivity (p < 0.05), and hemorrhagic brain lesions in or overlying the MCA territory were predictive of impaired metabolic suppression reactivity (p < 0.01). The 6-month Glasgow Outcome Scale score correlated with the overall degree of impaired vasoreactivity (p < 0.05). Conclusions. During the first 2 weeks after moderate or severe head injury, CO2 reactivity remains relatively intact, PA is variably impaired, and metabolic suppression reactivity remains severely impaired. Elevated ICP appears to affect all three components of vasoreactivity that were tested, whereas other clinical factors such as CPP, hypotensive and hypoxic insults, and hemorrhagic brain lesions have distinctly different impacts on the state of vasoreactivity. Incorporation of TCD ultrasonography—derived vasoreactivity data may facilitate more injury- and time-specific therapies for head-injured patients.

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