PubMed Health⌕ Search

Biomedical subjects

Marek Czosnyka

Publications and source records attributed to Marek Czosnyka.

At least 19 recordsLinked to original sources
PubMed2006

Nonlinear analysis of cerebral hemodynamic and intracranial pressure signals for characterization of autoregulation.

The objective of this study was to determine whether or not the underlying physiological systems that generates spontaneous arterial blood pressure (ABP), cerebral blood flow velocity (CBFV), and intracranial pressure signals could be adequately approximated as a linear stochastic process. Furthermore, a new measure (C) capable of capturing the degree of nonlinear dependency between two ABP and CBFV signals (including a time-varying situation) was proposed for quantifying the degree of cerebral blood flow autoregulation. A surrogate data test of fifteen ABP, CBFV, and intracranial pressure (ICP) segments was conducted for detecting whether there exists a statistically significant deviation from the null hypothesis of linear signals. The extension of the established block computation method of C measure to an adaptive one was achieved. This new algorithm was then applied to study the C evolution using brain injury patients data from a hyperventilation study and two propofol studies. Nonlinearity has not been detected for all the fifteen recordings, neither has nonlinear dependency between CBFV and ABP. However, their presences in some of the signal segments justified the adoption of a nonlinear measure of dependency capable of characterizing both linear and nonlinear correlations for inferring autoregulation status. C measure started to decrease with the introduction of hypocapnia state indicating that hyperventilation may reduce the dependency of CBFV on ABP fluctuations. On the other hand, complex patterns of C measure evolution were observed among 14 cases of propofol data indicating a nontrivial effect of propofol on the dependency of CBFV on ABP.

Adaptation, Physiological↗
PubMed2006

Impact of intracranial pressure and cerebral perfusion pressure on severe disability and mortality after head injury.

OBJECTIVE: To investigate the relationships between intracranial pressure (ICP), cerebral perfusion pressure (CPP), and outcome after traumatic brain injury. MATERIAL AND METHODS: A retrospective analysis of prospectively recorded data from 429 patients after head injury requiring intensive treatment on the Neuroscience Intensive Annex and the Neuro Critical Care Unit, Cambridge, UK. ICP, CPP, and arterial blood pressure (ABP) were continuously recorded. Mean values of pressures were compared to outcome assessed at 6 months after injury (using the Glasgow Outcome Scale). RESULTS: The mortality rate was greater in those having mean ICP greater than 20 mmHg (17% below versus 47% above; p < 0.0001). The mortality rate was dramatically increased for CPP below 55 mmHg (81% below versus 23% above; p < 0.0001). For values of CPP greater than 95 mmHg, favorable outcome was less frequent (50% below versus 28% above; p < 0.033). The rate of severe disability showed the tendency to increase with CPP ( r = 0.87; p = 0.02), suggesting that a higher CPP does not help in achieving favorable outcomes. ICP was greater in those who died in comparison to those who survived (27 +/- 19 mmHg versus 16 +/- 6 mmHg; p < 0.10 - 7), and CPP was lower (68 +/- 21 versus 76 +/- 10 mmHg; p < 0.0002). There was no difference between mean ICP and CPP in good/moderate and severe disability outcome groups. CONCLUSION: High ICP is strongly associated with fatal outcome. Excessive CPP seems to reduce the probability of achieving a favorable outcome following head trauma.

Adolescent↗
PubMed2005

Analysis of intracranial pressure during and after the infusion test in patients with communicating hydrocephalus.

The cerebrospinal fluid (CSF) infusion test is used to evaluate the dynamics of CSF circulation in patients with communicating hydrocephalus and is based on constant-rate infusion of the normal saline into cerebrospinal fluid space. The aim of the study was to refine methods of the analysis of intracranial pressure (ICP) recorded during and after the infusion test. The mathematical model of cerebrospinal fluid circulation was extended by the equation describing ICP decrease after the infusion. The nonlinear least-squares method of Levenberg-Marquardt was used to estimate the parameters describing the CSF compensatory mechanisms. Twenty-seven infusion tests were studied. Both phases of the test-the increase and the decrease of ICP-were recorded and the compensatory parameters were calculated for each of them. ICP often does not return to the resting level after the infusion test within the period equivalent to the time of infusion in all cases. In 20 tests the differences between post- and pre-infusion resting ICP (DeltaICP) was higher than 1 mmHg, which was considered as significant. The mean value of DeltaICP for 20 infusion tests was 3.0 +/- 0.7 mmHg. The cerebral elasticity evaluated during the infusion was greater than the elasticity estimated from the decreasing phase after the infusion (0.24 +/- 0.07 ml(-1) versus 0.14 +/- 0.03 ml(-1); p < 0.01).

Adult↗
PubMed2005

Effects of acute treatment with pravastatin on cerebral vasospasm, autoregulation, and delayed ischemic deficits after aneurysmal subarachnoid hemorrhage: a phase II randomized placebo-controlled trial.

BACKGROUND AND PURPOSE: Statins may improve cerebral vasomotor reactivity through cholesterol-dependent and -independent mechanisms. A phase II randomized controlled trial was conducted to examine the hypothesis that acute pravastatin treatment could improve cerebrovascular autoregulation and reduce vasospasm-related complications after aneurysmal subarachnoid hemorrhage (SAH). METHODS: A total of 80 aneurysmal SAH (aSAH) patients (18 to 84 years of age) within 72 hours from the ictus were randomized equally to receive either oral pravastatin (40 mg) or placebo daily for up to 14 days. Primary end points were the incidence, duration, and severity of cerebral vasospasm, and duration of impaired autoregulation estimated from transcranial Doppler ultrasonography. Secondary end points were the incidence of vasospasm-related delayed ischemic deficits (DIDs) and disability at discharge. RESULTS: Prerandomization characteristics were balanced between the 2 groups. No treatment-related complication was observed. The incidences of vasospasm and severe vasospasm were reduced by 32% (P=0.006) and 42% (P=0.044), respectively, and the duration of severe vasospasm was shortened by 0.8 days (P=0.068) in the pravastatin group. These measurements were maximal on the ipsilateral side of ruptured aneurysms. The duration of impaired autoregulation was shortened bilaterally (P< or =0.01), and the incidence of vasospasm-related DIDs and mortality were decreased by 83% (P<0.001) and 75% (P=0.037), respectively, in the pravastatin group. CONCLUSIONS: Acute treatment with pravastatin after aSAH is safe and ameliorates cerebral vasospasm, improves cerebral autoregulation, and reduces vasospasm-related DID. Unfavorable outcome at discharge was reduced primarily because of a reduction in overall mortality. This is the first demonstration of clinical benefits with immediate statin therapy for an acute cerebrovascular disorder.

Adolescent↗
PubMed2005

Age, intracranial pressure, autoregulation, and outcome after brain trauma.

OBJECT: The object of this study was to investigate whether a failure of cerebrovascular autoregulation contributes to the relationship between age and outcome in patients following head injury. METHODS: Data obtained from continuous bedside monitoring of intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral perfusion pressure (CPP = ABP - ICP) in 358 patients with head injuries and intermittent monitoring of transcranial Doppler blood flow velocity (FV) in the middle cerebral artery in 237 patients were analyzed retrospectively. Indices used to describe cerebral autoregulation and pressure reactivity were calculated as correlation coefficients between slow waves of systolic FV and CPP (autoregulation index [ARI]) and between ABP and ICP (pressure reactivity index [PRI]). Older patients had worse outcomes after brain trauma than younger patients (p = 0.00001), despite the fact that the older patients had higher initial Glasgow Coma Scale scores (p = 0.006). When age was considered as an independent variable, it appeared that ICP decreased with age (p = 0.005), resulting in an increasing mean CPP (p = 0.0005). Blood FV was not dependent on age (p = 0.58). Indices of autoregulation and pressure reactivity demonstrated a deterioration in cerebrovascular control with advancing age (PRI: p = 0.003; ARI: p = 0.007). CONCLUSIONS: An age-related decline in cerebrovascular autoregulation was associated with a relative deterioration in outcome in elderly patients following head trauma.

Adolescent↗
PubMed2004

Sustained moderate reductions in arterial CO2 after brain trauma time-course of cerebral blood flow velocity and intracranial pressure.

OBJECTIVE: In healthy volunteers cerebral blood flow starts to recover towards baseline within a few minutes of continued hyperventilation due to normalisation of perivascular pH. We investigated the time-course of changes in middle cerebral artery mean flow velocity (FVm) and intracranial pressure (ICP) in head-injured patients during sustained moderate reductions in arterial partial pressure of CO(2) (PaCO(2)). DESIGN: Observational study. PATIENTS: Twenty-seven sedated, mechanically ventilated patients with severe head injury. INTERVENTIONS: Measurements were made during and after routine determination of CO(2)-reactivity: an acute 20% increase in respiratory minute volume was followed by a 10-min stabilisation period and 50 min of continued moderate hyperventilation at a constant PaCO(2) (>3.5 kPa). MEASUREMENTS AND RESULTS: FVm was monitored with transcranial Doppler, ICP was monitored with intraparenchymal probes. During the 50-min period with stable PaCO(2) FVm increased in 36% of patients. All other patients showed a decline in FVm over the same time period. Overall FVm recovery was -0.03+/-0.14%.min(-1). The time-course of ICP changes was significantly different from that of FVm, with ICP reaching its lowest value earlier than FVm (23+/-12 vs 37+/-20 min; P = 0.001) and returning more rapidly towards baseline than FVm (0.23+/-0.23 vs -0.03+/-0.14%.min(-1); P< 0.0001). CONCLUSIONS: Head-injured patients may adapt differently to hyperventilation than healthy volunteers. Potentially harmful reductions in cerebral blood flow may persist beyond the duration of useful ICP reduction.

Adolescent↗
PubMed2004

Critical closing pressure in subarachnoid hemorrhage: effect of cerebral vasospasm and limitations of a transcranial Doppler-derived estimation.

BACKGROUND AND PURPOSE: Critical closing pressure (CCP) is thought to be jointly influenced by intracranial pressure and cerebrovascular tone. We examined how CCP is affected by cerebral vasospasm after subarachnoid hemorrhage (SAH). METHODS: In 15 patients with vasospasm of the middle cerebral artery, CCP was calculated using 2 methods previously reported (ad modem Aaslid and Michel, indexed CCP(Aaslid) and CCP(Michel), respectively) based on data of arterial blood pressure and flow velocity (FV) as assessed by transcranial Doppler. RESULTS: CCP decreased significantly (P<0.05) during vasospasm (CCP(Aaslid)=6.3+/-22.9 mm Hg, CCP(Michel)=14.9+/-16.5 mm Hg, mean+/-SD) as compared with baseline (CCP(Aaslid)=24.4+/-20.3 mm Hg, CCP(Michel)=27.8+/-19.4 mm Hg). This was not attributable to ICP, which remained unaffected by vasospasm. In addition, CCP was significantly lower on the side of vasospasm (CCP(Aaslid)=11.9+/-24.2 mm Hg, CCP(Michel)=18.4+/-19.6 mm Hg) as compared with the contralateral nonvasospastic side (CCP(Aaslid)=24.7+/-22.3 mm Hg, CCP(Michel)=28.2+/-18.0 mm Hg). CONCLUSIONS: Assuming that autoregulation-related distal vasodilatation outweighs proximal vasospasm, CCP should decrease. Alternatively, CCP might have increased during vasospasm as the tension of big vessels increase, but the turbulence occurring during vasospasm may have impaired the linear relationship between pressure and FV, thus leading to a marked underestimation of CCP. In conclusion, interpretation of CCP in vasospasm is difficult and may be overshadowed by nonlinear hemodynamic effects.

Adult↗
PubMed2004

Pattern of white matter regional cerebral blood flow and autoregulation in normal pressure hydrocephalus.

The mean cerebral blood flow (CBF) has generally been demonstrated to be lower in normal pressure hydrocephalus (NPH) than in normal controls. We investigated the distribution of the regional peri- and paraventricular white matter CBF (WM CBF) in NPH at baseline and during a controlled rise in intracranial pressure (ICP). Twelve patients with idiopathic NPH (mean age 69 years) underwent a CSF infusion study. CBF was measured by H2(15)O PET at baseline and then during the steady-state plateau of raised ICP. The PET images were co-registered and resliced to 3D structural T1-weighted MRIs. Ten healthy normal volunteers served as control subjects for baseline CBF determination only. Profiles of the regional distribution of the baseline WM CBF and of the percentage change in WM CBF as a function of distance from the ventricles were plotted. The global mean baseline CBF in patients (28.4 +/- 5.2 ml/100 ml/min) was lower than in the control subjects (33 +/- 5.4 ml/100 ml/min) (P < 0.005). In patients, the profile of the regional WM CBF at baseline showed an increase with distance from the ventricles (P < 0.0001), with a maximal reduction adjacent to the ventricles and progressive normalization with distance, whereas in controls no relationship was apparent (P = 0.0748). In 10 patients, the rise in ICP during the infusion produced a fall in cerebral perfusion pressure (CPP) and a significant decrease of the global mean CBF from 27.6 +/- 3.1 to 24.5 +/- 2.9 ml/100 ml/min (P < 0.0001). The profile of the percentage changes in regional WM CBF in patients showed a U-shaped relationship with distance from the ventricles (P = 0.0007), with a maximal decrease skewed on the side of the lateral ventricles at around a mean distance of 9 mm. The WM CBF is reduced in NPH, with an abnormal gradient from the lateral ventricles towards the subcortical WM. An excessive decrease in CBF is brought about by reductions in CPP and appears to be maximal in the paraventricular watershed region. These results are discussed in the light of previous hypotheses concerning the aetiology of periventricular CBF reduction in NPH.

Aged↗
PubMed2004

Cerebrospinal fluid dynamics.

Hydrocephalus is far more complicated than a simple disorder of CSF circulation. Historically, it has been diagnosed using clinical and psychomotor assessment plus brain imaging. The role of physiological measurement to aid diagnosis becomes more appreciated in current clinical practice. This has been reflected by recently formulated guidelines for the management of normal pressure hydrocephalus. Clinical measurement in hydrocephalus is mainly related to intracranial pressure (ICP) and cerebral blood flow. This review lists and discusses most common forms of the methods: CSF infusion study, overnight ICP monitoring, assessment of slow ICP waves, testing pressure reactivity, cerebral autoregulation, CO2 reactivity and PET-CBF studies combined with MRI co-registration. The basics of CSF dynamics modelling are presented and the principles of the assessment of functioning of the implanted hydrocephalus shunts are also discussed. The descriptions of multiple forms of measurement along with clinical illustrations are mainly based on in-house experience of a multidisciplinary group of scientists and clinicians from Cambridge, UK.

Brain↗
PubMed2004

Changes in cerebral blood flow during cerebrospinal fluid pressure manipulation in patients with normal pressure hydrocephalus: a methodological study.

The combination of cerebral blood flow measurement using (15)O-water positron emission tomography with magnetic resonance coregistration and CSF infusion studies was used to study the global and regional changes in CBF with changes in CSF pressure in 15 patients with normal pressure hydrocephalus. With increases in CSF pressure, there was a variable increase in arterial blood pressure between individuals and global CBF was reduced, including in the cerebellum. Regionally, mean CBF decreased in the thalamus and basal ganglia, as well as in white matter regions. These reductions in CBF were significantly correlated with changes in the CSF pressure and with proximity to the ventricles. A three-dimensional finite-element analysis was used to analyze the effects on ventricular size and the distribution of stress during infusion. To study regional cerebral autoregulation in patients with possible normal pressure hydrocephalus, a sensitive CBF technique is required that provides absolute, not relative normalized, values for regional CBF and an adequate change in cerebral perfusion pressure must be provoked.

Aged↗
PubMed2004

Direct comparison of cerebrovascular effects of norepinephrine and dopamine in head-injured patients.

OBJECTIVE: To directly compare the cerebrovascular effects of norepinephrine and dopamine in patients with acute traumatic brain injury. DESIGN: Prospective randomized crossover trial. SETTING: Neurosciences critical care unit of a university hospital. PATIENTS: Ten acutely head-injured patients requiring vasoactive drugs to maintain a cerebral perfusion pressure of 65 mm Hg. INTERVENTIONS: Patients were randomized to start the protocol with either norepinephrine or dopamine. Using an infusion of the allocated drug, cerebral perfusion pressure was adjusted to 65 mm Hg. After 20 mins of data collection, cerebral perfusion pressure was increased to 75 mm Hg by increasing the infusion rate of the vasoactive agent. After 20 mins of data collection, cerebral perfusion pressure was increased to 85 mm Hg and again data were collected for 20 mins. Subsequently, the infusion rate of the vasoactive drug was reduced until a cerebral perfusion pressure of 65 mm Hg was reached and the drug was exchanged against the other agent. The protocol was then repeated. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure and intracranial pressure were monitored and cerebral blood flow was estimated with transcranial Doppler. Norepinephrine led to predictable and significant increases in flow velocity for each step increase in cerebral perfusion pressure (57.5+/-19.9 cm x sec, 61.3+/-22.3 cm x sec, and 68.4+/-24.8 cm x sec at 65, 75, and 85 mm Hg, respectively; p <.05 for all three comparisons), but changes with dopamine were variable and inconsistent. There were no differences between absolute values of flow velocity or intracranial pressure between the two drugs at any cerebral perfusion pressure level. CONCLUSIONS: Norepinephrine may be more predictable and efficient to augment cerebral perfusion in patients with traumatic brain injury.

Adult↗
PubMed2004

Normal pressure hydrocephalus and cerebral blood flow: a PET study of baseline values.

Regional cerebral blood flow (CBF) was studied with O(15)-water positron emission tomography and anatomic region-of-interest analysis on co-registered magnetic resonance in patients with idiopathic (n = 12) and secondary (n = 5) normal pressure hydrocephalus (NPH). Mean CBF was compared with values obtained from healthy volunteers (n = 12) and with clinical parameters. Mean CBF was significantly decreased in the cerebrum and cerebellum of patients with NPH. The regional analysis demonstrated that CBF was reduced in the basal ganglia and the thalamus but not in white matter regions. The results suggest that the role of the basal ganglia and thalamus in NPH may be more prominent than currently appreciated. The implications for theories regarding the pathogenesis of NPH are discussed.

Aged↗
PubMed2004

Slight elevation of baseline intracranial pressure after fluid infusion into CSF space in patients with hydrocephalus.

OBJECTIVE: To investigate the elevation of resting cerebrospinal fluid (CSF) pressure recorded after a CSF infusion test in patients with hydrocephalus. MATERIAL AND METHODS: Fifty patients (30 men and 20 women, mean age 68 +/- 13 years) with ventriculomegaly and clinical symptoms of normal pressure hydrocephalus have been studied. Lumbar (56%) or intraventricular (44%) computerized infusion studies were performed to investigate the hydrodynamics of CSF. After infusion, the fall in ICP was recorded until a steady-state level was achieved and the difference between pre- and post-infusion resting ICP was calculated (DeltaICP). RESULTS: A positive difference (>2 mm Hg) between post- and pre-infusion resting ICP was identified in 31 infusion tests (62%). The mean value of the difference was 6.7 with an SD of 3.5 mm Hg. The patients who demonstrated this phenomenon had a greater elastance coefficient (p>0.05); DeltaICP was positively correlated with age (R=0.27; p=0.03), with the size of the brain's ventricles (R=0.63, p=0.03) and inversely with the severity of clinical impairment (Stein-Langfitt score R=-0.61, p=0.02; normal pressure hydrocephalus score: R=0.54; p<0.05). DeltaICP was independent of the site of infusion (lumbar or ventricular). CONCLUSION: In patients with a 'stiffer' brain, ICP returns to the resting level after the infusion test at a slightly higher level than before the test. The magnitude of this increase is greater when ventricles are more dilated and clinical symptoms are less severe.

Adult↗
PubMed2004

Continuous assessment of cerebral autoregulation in subarachnoid hemorrhage.

UNLABELLED: Cerebral vasospasm remains a leading cause of morbidity and mortality after subarachnoid hemorrhage (SAH). Cerebral ischemia may ensue when autoregulation fails to compensate for spasm. We examined how autoregulation is affected by vasospasm by using transcranial Doppler. The moving correlation coefficient between slow changes of arterial blood pressure and mean or systolic flow velocity (FV), termed "Mx" and "Sx," respectively, was used to characterize cerebral autoregulation. Vasospasm was declared when the mean FV increased to more than 120 cm/s and the Lindegaard ratio was more than 3. This occurred in 15 of 32 SAH patients. On the basis of the bilateral transcranial Doppler recordings of the middle cerebral artery in vasospastic patients, Mx and Sx were calculated for baseline and vasospasm. Mx increased during vasospasm (0.46 +/- 0.32; mean +/- SD) and was significantly higher (P = 0.021) than at baseline (0.21 +/- 0.24). Sx was also increased (0.22 +/- 0.26 vs 0.05 +/- 0.21 at baseline; P = 0.03). Mx correlated with mean FV (r = 0.577; P = 0.025) and the Lindegaard ratio (r = 0.672; P < 0.006). Mx (P = 0.006) and Sx (P = 0.044) were higher on the vasospastic side (Mx, 0.44 +/- 0.27; Sx, 0.24 +/- 0.23) when compared with the contralateral side (Mx, 0.34 +/- 0.29; Sx, 0.16 +/- 0.25). The increased Mx and Sx during cerebral vasospasm demonstrate impaired cerebral autoregulation. Mx and Sx provide additional information on changes in autoregulation in SAH patients. IMPLICATIONS: The moving correlation coefficients between slow changes of arterial blood pressure and mean or systolic flow velocity, termed "Mx" and "Sx," respectively, characterize cerebral autoregulation but have not been applied to subarachnoid hemorrhage. A study in 15 patients revealed that Mx and Sx were significantly increased, indicating impaired autoregulation during vasospasm as compared with baseline, as well as on the side of vasospasm in comparison with the contralateral side.

Adult↗
PubMed2004

Pressure autoregulation and positron emission tomography-derived cerebral blood flow acetazolamide reactivity in patients with carotid artery stenosis.

OBJECTIVE: Testing autoregulation is of importance in predicting risk of stroke and managing patients with occlusive carotid arterial disease. The use of small spontaneous changes in arterial blood pressure and transcranial Doppler (TCD) flow velocity can be used to assess autoregulation noninvasively without the need for a cerebrovascular challenge. We have previously described an index (called "Mx") that achieves this. Negative or low positive values (<0.4) indicate intact pressure autoregulation, whereas an Mx greater than 0.4 indicates diminished autoregulation. The objective of this study was to compare acetazolamide reactivity of positron emission tomography (PET)-derived cerebral blood flow (CBF) with Mx in patients with carotid arterial disease. METHODS: In 40 patients with carotid arterial disease, we used bilateral TCD recordings of the middle cerebral artery to derive Mx and compared this with PET-derived CBF measurements of acetazolamide reactivity. RESULTS: Mx correlated inversely with baseline PET CBF (P = 0.042, R = -0.349) but not with postacetazolamide CBF or cerebrovascular reactivity to acetazolamide. This may reflect discordance between pressure autoregulation and acetazolamide reactivity. Mx correlated significantly with degree of internal carotid artery stenosis (P = 0.022, R = 0.38), whereas CBF reactivity to acetazolamide did not correlate with Mx (P = 0.22). After the administration of acetazolamide, slow-wave activity in blood pressure and TCD flow velocity recordings was seen to diminish, rendering the calculation of Mx unreliable after acetazolamide. CONCLUSION: The measurement of Mx offers a noninvasive, safe technique for assessing abnormalities of pressure autoregulation in patients with carotid arterial disease.

Acetazolamide↗
PubMed2003

Assessment of cerebrovascular autoregulation in head-injured patients: a validation study.

BACKGROUND AND PURPOSE: Cerebrovascular autoregulation is frequently measured in head-injured patients. We attempted to validate 4 bedside methods used for assessment of autoregulation. METHODS: PET was performed at a cerebral perfusion pressure (CPP) of 70 and 90 mm Hg in 20 patients. Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) were determined at each CPP level. Patients were sedated with propofol and fentanyl. Norepinephrine was used to control CPP. During PET scanning, transcranial Doppler (TCD) flow velocity in the middle cerebral artery was monitored, and the arterio-jugular oxygen content difference (AJDo2) was measured at each CPP. Autoregulation was determined as the static rate of autoregulation based on PET (SROR(PET)) and TCD (SROR(TCD)) data, based on changes in AJDo2, and with 2 indexes based on the relationship between slow waves of CPP and flow velocity (mean velocity index, Mx) and between arterial blood pressure and intracranial pressure (pressure reactivity index, PRx) RESULTS: We found significant correlations between SROR(PET) and SROR(TCD) (r2=0.32; P<0.01) and between SROR(PET) and PRx (r2=0.31; P<0.05). There were no significant associations between PET data and autoregulation as assessed by changes in AJDo2. Global CMRo2 was significantly lower at the higher CPP (P<0.01). CONCLUSIONS: Despite some variability, SROR(TCD) and PRx may provide useful approximations of autoregulation in head-injured patients. At least with our methods, CMRo2 changes with the increase in CPP; hence, flow-metabolism coupling may affect the results of autoregulation testing.

Adolescent↗