Changes In Cerebral Physiology Research Articles

MR Assessment of Acute Changes of Cerebral Perfusion, Metabolism, and Blood-Brain Barrier Permeability in Response to Aerobic Exercise.

It remains unclear how a single bout of exercise affects brain perfusion, oxygen metabolism, and blood-brain barrier (BBB) permeability. Addressing this unresolved issue is essential to understand the acute changes in cerebral physiology induced by aerobic exercise. To dynamically monitor the acute changes in cerebral physiology subsequent to a single aerobic exercise training session using noninvasive MRI measurements. Prospective. Twenty-three healthy participants (18-35 years, 10 females/13 males) were enrolled and divided into 10-minute exercising (N = 10) and 20-minute exercising (N = 13) groups. 3.0 T/Phase Contrast (PC) MRI (gradient echo), T2-Relaxation-Under-Spin-Tagging (TRUST) MRI (gradient echo EPI), Water-Extraction-with-Phase-Contrast-Arterial-Spin-Tagging (WEPCAST) MRI (gradient echo EPI) and T1-weighted magnetization-prepared-rapid-acquisition-of-gradient-echo (MPRAGE) (gradient echo). A baseline MR measurement plus four repeated MR measurements immediately after 10 or 20 minutes moderate running exercise. MR measurements included cerebral blood flow (CBF) as measured by PC MRI, venous oxygenation (Yv) and cerebral metabolic rate of oxygen (CMRO2) as assessed by TRUST MRI, water extraction fraction (E), and BBB permeability-surface-area product (PS) as determined by WEPCAST MRI. The time dependence of the physiological parameters was studied with a linear mixed-effect model. Additionally, pairwise t-tests comparison of the physiological parameters at each time point was conducted. A P-value of <0.05 was considered statistically significant. There was an initial drop (8.22 ± 2.60%) followed by a recovery in CBF after exercise, while Yv revealed a significant decrease (6.37 ± 0.92%), i.e., an increased oxygen extraction, and returned to baseline at later time points. CMRO2 showed a trend of increase (5.68 ± 3.04%) and a significant interaction between time and group. In addition, E increased significantly (3.86% ± 0.89) and returned to baseline level at later time points, while PS remained elevated (13.33 ± 4.79%). A single bout of moderate aerobic exercise can induce acute alterations in cerebral perfusion, metabolism, and BBB permeability. 2 TECHNICAL EFFICACY: Stage 2.

Speech Therapy as a Component of Comprehensive Rehabilitation of Patients with Acute Impairment of Cerebral Circulation

The article reveals the essence of speech and speech therapy as a component of the rehabilitation process in restoring the health of patients who have suffered acute impairment of cerebral circulation. The concept of cerebral vascular insufficiency was analyzed, which refers to cerebral physiological changes in old age and associated conditions of speech impairment. Vascular diseases of the brain are not only a medical problem, but also a social one: they cause enormous damage to the economy, considering the costs of treatment, medical rehabilitation, and losses in production. The effectiveness of motor recovery after an ischemic stroke in the early recovery period depends largely on timely rehabilitation. Physical exercises have a positive effect on the recovery of the body systems of people who have had an ischemic stroke. The most frequent consequences of stroke in about 40-50% of the total number of patients are disorders of speech function, manifested in the form of aphasia and dysarthria, which are often combined with pathology of other higher mental functions (various types of agnosia and apraxia). Today, speech therapy is practiced by specialists both as a separate method and in combination with other techniques, and is used in individual and group work, including work with patients who have had an acute impairment of cerebral circulation.

Interactions of brain, blood, and CSF: a novel mathematical model of cerebral edema

BackgroundPrevious models of intracranial pressure (ICP) dynamics have not included flow of cerebral interstitial fluid (ISF) and changes in resistance to its flow when brain swelling occurs. We sought to develop a mathematical model that incorporates resistance to the bulk flow of cerebral ISF to better simulate the physiological changes that occur in pathologies in which brain swelling predominates and to assess the model’s ability to depict changes in cerebral physiology associated with cerebral edema.MethodsWe developed a lumped parameter model which includes a representation of cerebral ISF flow within brain tissue and its interactions with CSF flow and cerebral blood flow (CBF). The model is based on an electrical analog circuit with four intracranial compartments: the (1) subarachnoid space, (2) brain, (3) ventricles, (4) cerebral vasculature and the extracranial spinal thecal sac. We determined changes in pressure and volume within cerebral compartments at steady-state and simulated physiological perturbations including rapid injection of fluid into the intracranial space, hyperventilation, and hypoventilation. We simulated changes in resistance to flow or absorption of CSF and cerebral ISF to model hydrocephalus, cerebral edema, and to simulate disruption of the blood–brain barrier (BBB).ResultsThe model accurately replicates well-accepted features of intracranial physiology including the exponential-like pressure–volume curve with rapid fluid injection, increased ICP pulse pressure with rising ICP, hydrocephalus resulting from increased resistance to CSF outflow, and changes associated with hyperventilation and hypoventilation. Importantly, modeling cerebral edema with increased resistance to cerebral ISF flow mimics key features of brain swelling including elevated ICP, increased brain volume, markedly reduced ventricular volume, and a contracted subarachnoid space. Similarly, a decreased resistance to flow of fluid across the BBB leads to an exponential-like rise in ICP and ventricular collapse.ConclusionsThe model accurately depicts the complex interactions that occur between pressure, volume, and resistances to flow in the different intracranial compartments under specific pathophysiological conditions. In modelling resistance to bulk flow of cerebral ISF, it may serve as a platform for improved modelling of cerebral edema and blood–brain barrier disruption that occur following brain injury.

Metabolic brain measurements in the newborn: Advances in optical technologies.

Neonatal monitoring in neonatal intensive care is pushing the technological boundaries of newborn brain monitoring in order to improve patient outcome. There is an urgent need of a cot side, real time monitoring for assessment of brain injury severity and neurodevelopmental outcome, in particular for term newborn infants with hypoxic‐ischemic brain injury. This topical review discusses why brain tissue metabolic monitoring is important in this group of infants and introduces the currently used neuromonitoring techniques for metabolic monitoring in the neonatal intensive care unit (NICU). New optical techniques that can monitor changes in brain metabolism together with brain hemodynamics at the cot side are presented. Early studies from these emerging technologies have demonstrated their potential to deliver continuous information regarding cerebral physiological changes in sick newborn infants in real time. The promises of these new tools as well as their potential limitations are discussed.

Spatial and Temporal Pattern of Ischemia and Abnormal Vascular Function Following Traumatic Brain Injury

Ischemia is an important pathophysiological mechanism after traumatic brain injury (TBI), but its incidence and spatiotemporal patterns are poorly characterized. To comprehensively characterize the spatiotemporal changes in cerebral physiology after TBI. This single-center cohort study uses 15oxygen positron emission tomography data obtained in a neurosciences critical care unit from February 1998 through July 2014 and analyzed from April 2018 through August 2019. Patients with TBI requiring intracranial pressure monitoring and control participants were recruited. Cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral oxygen metabolism (CMRO2), and oxygen extraction fraction. Ratios (CBF/CMRO2 and CBF/CBV) were calculated. Ischemic brain volume was compared with jugular venous saturation and brain tissue oximetry. A total of 68 patients with TBI and 27 control participants were recruited. Results from 1 patient with TBI and 7 health volunteers were excluded. Sixty-eight patients with TBI (13 female [19%]; median [interquartile range (IQR)] age, 29 [22-47] years) underwent 90 studies at early (day 1 [n = 17]), intermediate (days 2-5 [n = 54]), and late points (days 6-10 [n = 19]) and were compared with 20 control participants (5 female [25%]; median [IQR] age, 43 [31-47] years). The global CBF and CMRO2 findings for patients with TBI were less than the ranges for control participants at all stages (median [IQR]: CBF, 26 [22-30] mL/100 mL/min vs 38 [29-49] mL/100 mL/min; P < .001; CMRO2, 62 [55-71] μmol/100 mL/min vs 131 [101-167] μmol/100 mL/min; P < .001). Early CBF reductions showed a trend of high oxygen extraction fraction (suggesting classical ischemia), but this was inconsistent at later phases. Ischemic brain volume was elevated even in the absence of intracranial hypertension and highest at less than 24 hours after TBI (median [IQR], 36 [10-82] mL), but many patients showed later increases (median [IQR] 6-10 days after TBI, 24 [4-42] mL; across all points: patients, 10 [5-39] mL vs control participants, 1 [0-3] mL; P < 001). Ischemic brain volume was a poor indicator of jugular venous saturation and brain tissue oximetry. Patients' CBF/CMRO2 ratio was higher than controls (median [IQR], 0.42 [0.35-0.49] vs 0.3 [0.28-0.33]; P < .001) and their CBF/CBV ratio lower (median [IQR], 7.1 [6.4-7.9] vs 12.3 [11.0-14.0]; P < .001), suggesting abnormal flow-metabolism coupling and vascular reactivity. Patients' CBV was higher than controls (median [IQR], 3.7 [3.4-4.1] mL/100 mL vs 3.0 [2.7-3.6] mL/100 mL; P < .001); although values were lower in patients with intracranial hypertension, these were still greater than controls (median [IQR], 3.7 [3.2-4.0] vs 3.0 [2.7-3.6] mL/100 mL; P = .002), despite more profound reductions in partial pressure of carbon dioxide (median [IQR], 4.3 [4.1-4.6] kPa vs 4.7 [4.3-4.9] kPa; P = .001). Ischemia is common early, detectable up to 10 days after TBI, possible without intracranial hypertension, and inconsistently detected by jugular or brain tissue oximetry. There is substantial between-patient and within-patient pathophysiological heterogeneity; ischemia and hyperemia commonly coexist, possibly reflecting abnormalities in flow-metabolism coupling. Increased CBV may contribute to intracranial hypertension but can coexist with abnormal CBF/CBV ratios. These results emphasize the need to consider cerebrovascular pathophysiological complexity when managing patients with TBI.

Bihemispheric Cerebral Oximetry Monitoring's Functionality in Suspected Cerebral Edema Diabetic Ketoacidosis With Therapeutic 3% Hyperosmolar Therapy in a Pediatric Emergency Department.

Suspected cerebral edema diabetic ketoacidosis (SCEDKA) is more common than perceived with symptoms including altered mentation, headache with vomiting, depressed Glasgow coma scale (GCS), abnormal motor or verbal responses, combativeness, and neurological depression. Suspected cerebral edema diabetic ketoacidosis has been associated with initial diabetic ketoacidosis (DKA) presentation and at start of DKA therapy.Cerebral oximetry (bihemispheric regional cerebral oxygen saturation [rcSO2] and cerebral blood volume index [CBVI]) can detect increased intracranial pressure (ICP)-induced altered bihemispheric cerebral physiology (rcSO2) (Crit Care Med 2006;34:2217-2223, J Pediatr 2013;163: 1111-1116, Curr Med Chem 2009;16:94-112, Diabetologia 1985;28:739-742, Pediatr Crit Care Med 2013;14:694-700). In pediatrics, rcSO2 of less than 60% or rcSO2 of greater than 85% reflects increased ICP and cerebral edema (Crit Care Med 2006;34:2217-2223, J Pediatr 2013;163: 1111-1116, Curr Med Chem 2009;16:94-112, Diabetologia 1985;28:739-742, Pediatr Crit Care Med 2013;14:694-700). Cerebral oximetry can detect increased ICP-induced altered bihemispheric cerebral physiology (rcSO2, CBVI) and cerebral physiological changes (rcSO2, CBVI changes) during therapeutic mechanical cerebral spinal fluid removal to decrease increased ICP (Crit Care Med 2006;34:2217-2223, J Pediatr 2013;163: 1111-1116, Curr Med Chem 2009;16:94-112, Diabetologia 1985;28:739-742, Pediatr Crit Care Med 2013;14:694-700).In the pediatric intensive care units, SCEDKA patients with nonbihemispheric cerebral oximetry showed an initial rcSO2 of greater than 90%. Bihemispheric rcSO2 with CBVI in SCEDKA patients has the potential to detect the abnormal cerebral physiology and disruptive autoregulation while detecting 3% hypertonic saline solution (HTS) effects on the SCEDKA altered cerebral physiology (rcSO2). The purposes of this study were to analyze and compare 3% HTS effect on bihemispheric rcSO2 readings, neurological and biochemical parameters in SCEDKA with 3% HTS infusion to non-SCEDKA patients in pediatric emergency department (PED). An observational retrospective comparative analysis study of bihemispheric rcSO2 readings, neurological and biochemical parameters in 2 groups of PED DKA patients were performed: PED DKA patients with SCEDKA +3% HTS infusions versus non-SCEDKA without 3% HTS infusions. From 2008 to 2013, of the 1899 PED DKA patients, 60 SCEDKA patients received 3% HTS (5 mL/kg via peripheral intravenous) infusion (median age of 5 years [range, 3.7-7 years]), with 42 new DKA insulin dependent diabetes mellitus onset. Suspected cerebral edema diabetic ketoacidosis patients had GCS of 11 (range, 11-12), with consistent SCEDKA signs and symptoms (severe headaches with vomiting, confusion, blurred vision, altered speech, lethargy, and combativeness). Suspected cerebral edema diabetic ketoacidosis patients' initial (0-5 minutes) left rcSO2 readings were 91.4% (range, 88.4%-94.1%) and right was 90.3% (range, 88.6%-94.1%) compared with non-SCEDKA patients' left rcSO2 readings of 73.2% (range, 69.7%-77.8%) and right of 73.2% (range, 67.6%-77%) (P < 0.0001). The rcSO2 monitoring time before 3% HTS infusion was 54.9 minutes (range, 48.3-66.8 minutes) with 3% HTS time effect change: pre-3% HTS (54.9 minutes [range, 48.3-66.8 minutes]). Before 3% HTS infusion, the left rcSO2 readings were 90.0% (range, 89%-95%) and right was 91% (range, 86%-95%). The 30 to 45 minutes post-3% HTS showed that left was 64% (range, 62%-69%) and right was 65.4% (range, 63%-70%) (P < 0.0001). rcSO2 Δ change for post-3% HTS (0-20 minutes) to pre-3% HTS was as follows: left, -26.58 (-29.5 to -23.7) (P < 0.0001); right, -25.2 (-27.7 to -22.6) (P < 0.0001). Post-3% HTS GCS (14,15) and biochemistry compared with pre-3% HTS infusions all improved (P < 0.001). In PED SCEDKA patients, the pre-3% HTS bihemispheric rcSO2 readings were greater than 90% and had lower GCS than non-SCEDKA patients. The post-3% HTS infusion rcSO2 readings showed within minutes a substantial reduction compared with non-SCEDKA patients, with no complications. Changes in rcSO2 readings after 3% HTS correlated with improved SCEDKA indicators (improved mental status, headache, and GCS) without any complications. We showed that cerebral oximetry in PED SCEDKA patients has shown an initial bihemispheric of greater than 90% readings signifying abnormal bihemispheric cerebral physiology. We also showed the cerebral oximetry's functionality in detecting 3% HTS therapeutic effects on SCEDKA's abnormal cerebral physiology and the beneficial therapeutic effects of 3% HTS infusion in SCEDKA patients. Using cerebral oximetry in pediatric DKA patients' initial cerebral assessment could have a significant impact in detecting SCEDKA patients. Further SCEDKA research using cerebral oximetry should be considered.

Sedatives in neurocritical care: an update on pharmacological agents and modes of sedation

In this article, the specific and general indications for sedatives in the neurocritical care unit are discussed, together with an overview on current insights in sedative protocols for these patients. In addition, physiological effects of sedative agents on the central nervous system are reviewed. In the general ICU population, a large body of evidence supports light protocolized sedation over indiscriminate deep sedation. Unfortunately, in patients with severe acute brain injury, the evidence from randomized controlled trials is scarce to nonexistent, and practice is supported by expert opinion, physiological studies and observational or small interventional trials. The different sedatives each have different beneficial effects and side-effects. Extrapolating the findings from studies in the general ICU population suggests to reserve deep continuous sedation in the neuro-ICU for specific indications. Although an improved understanding of cerebral physiological changes in patients with brain injury may be helpful to guide individualized sedation, we still lack the evidence base to make broad recommendations for specific patient groups.

CT-based Techniques for Brain Perfusion.

Recent rapid advances in endovascular treatment for acute ischemic stroke highlight the crucial role of neuroimaging especially multimodal computed tomography (CT) including CT perfusion in stroke triage and management decisions. With an increasing focus on changes in cerebral physiology along with time-based matrices in clinical decisions for acute ischemic stroke, CT perfusion provides a rapid and practical modality for assessment and identification of salvageable tissue at risk and infarct core and provides a better understanding of the changes in cerebral physiology. Although there are challenges with the lack of standardization and accuracy of quantitative assessment, CT perfusion is evolving as a cornerstone for imaging-based strategies in the rapid management of acute ischemic stroke.

Abstract 19890: Pre-operative Cerebral Hemodynamics From Birth Until Surgery in Neonates With Critical Congenital Heart Disease

Introduction: Neonates with critical congenital heart disease (CHD) exhibit a high prevalence of white matter injury (WMI). Recent work in neonates with hypoplastic left heart syndrome has shown that a longer wait from birth to surgery was associated with lower cerebral tissue oxygen saturations (StO2) on the morning of surgery and an increased risk for postoperative white matter injury (WMI). Understanding the daily preoperative changes in cerebral physiology during this vulnerable period may lead to new therapeutic algorithms aimed at prevention of WMI. Methods: Term neonates with critical CHD were recruited for this study. Frequency domain diffuse optical spectroscopy was employed to noninvasively quantify StO2. Daily StO2 measurements were made from day of recruitment until the day of surgery. Results: We studied 37 neonates with critical CHD. Operations were performed at 1-8 days of life. Non-elective reasons for timing of surgery resulted only in earlier surgery in this cohort. The subjects were placed in 2 groups depending on if they had a normal arch (N=20) or obstructed arch (N=17). In a linear mixed-effects model, StO2 decreased as a function of time from birth but was not specific to diagnostic group. Conclusions: Observed longitudinal daily decline in StO2 from birth until surgery supports our earlier findings and extends them to other groups of CHD. These results suggest that reported increases in risk for WMI with time-to-surgery could be due to mismatched oxygen delivery to metabolic demand. Therapeutic interventions such as increasing cerebral blood flow or decreasing cerebral oxygen demand may be considered when earlier surgery is not possible.

Sensitivity of near-infrared spectroscopy and diffuse correlation spectroscopy to brain hemodynamics: simulations and experimental findings during hypercapnia.

Near-infrared spectroscopy (NIRS) and diffuse correlation spectroscopy (DCS) are two diffuse optical technologies for brain imaging that are sensitive to changes in hemoglobin concentrations and blood flow, respectively. Measurements for both modalities are acquired on the scalp, and therefore hemodynamic processes in the extracerebral vasculature confound the interpretation of cortical hemodynamic signals. The sensitivity of NIRS to the brain versus the extracerebral tissue and the contrast-to-noise ratio (CNR) of NIRS to cerebral hemodynamic responses have been well characterized, but the same has not been evaluated for DCS. This is important to assess in order to understand their relative capabilities in measuring cerebral physiological changes. We present Monte Carlo simulations on a head model that demonstrate that the relative brain-to-scalp sensitivity is about three times higher for DCS (0.3 at 3 cm) than for NIRS (0.1 at 3 cm). However, because DCS has higher levels of noise due to photon-counting detection, the CNR is similar for both modalities in response to a physiologically realistic simulation of brain activation. Even so, we also observed higher CNR of the hemodynamic response during graded hypercapnia in adult subjects with DCS than with NIRS.

Simultaneous quantitative assessment of cerebral physiology using respiratory-calibrated MRI and near-infrared spectroscopy in healthy adults

BackgroundFunctional near-infrared spectroscopy (fNIRS) and functional MRI (fMRI) are non-invasive techniques used to relate activity in different brain regions to certain tasks. Respiratory calibration of the blood oxygen level dependent (BOLD) signal, and combined fNIRS–fMRI approaches have been used to quantify physiological subcomponents giving rise to the BOLD signal. A comparison of absolute oxygen metabolism parameters between MRI and NIRS, using spatially resolved (SRS) NIRS and respiratory calibrated MRI, could yield additional insight in the physiology underlying activation. Materials and methodsChanges in the BOLD signal, cerebral blood flow (CBF), and oxygen saturation (SO2) were derived from a single MRI sequence during a respiratory challenge in healthy volunteers. These changes were compared to SO2 obtained by a single probe SRS NIRS setup. In addition, concentration changes in oxygenated (O2Hb), deoxygenated (HHb), and total haemoglobin (tHb), obtained by NIRS, were compared to the parameters obtained by MRI. ResultsNIRS SO2 correlated with end-tidal CO2 (0.83, p<0.0001), the BOLD signal (0.82, p<0.0001), CBF (0.85, p<0.0001), and also MRI SO2 (0.82, p<0.0001). The BOLD signal correlated with NIRS HHb (−0.76, p<0.0001), O2Hb (0.41, p=0.001), and tHb (r=0.32, p=0.01). ConclusionsGood correlations show that changes in cerebral physiology, following a respiratory challenge, go hand in hand with changes in the BOLD signal, CBF, O2Hb, HHb, NIRS SO2, and MRI SO2. Out of all NIRS derived parameters, the SO2 showed the best correlation with the BOLD signal.

Effects of Positioning on Cerebral Oxygenation

Postural change during anesthesia has a complex effect on the systemic and cerebral circulations which can potentially decrease cerebral blood flow and oxygenation. Cerebral oximetry is emerging as a monitor of cerebral perfusion with widespread application in many types of surgery. The technology is based on the differential absorption of oxygenated and deoxygenated hemoglobin to near-infrared light. However, the dynamic coupling that exists between cerebral arterial, venous and cerebrospinal fluid volumes may influence oximetric readings during postural change. Interpretation of cerebral oxygen saturation measurement must account for these changes in cerebral physiology if monitoring is to predict neurological outcome.

Visualizing Recovery of Cognitive Function in Stroke

Hippocrates (460-377 BC) first described stroke over 2400 years ago. Stroke is the 4th leading cause of death in Canada (3rd in the USA) and the primary cause of permanent motor and cognitive disability. The majority of strokes are ischemic. The extent of cerebral dysfunction and thus the severity of stroke are based on the location, severity and duration of ischemia. Stroke management and prognosis encompass early recognition of the onset of stroke and post-stroke determination of the extent of brain injury aided by clinical stroke scores and diffusion-weighted imaging. Cognitive domains most likely to be affected following stroke are memory, orientation, language, attention and executive function. While the vast majority of functional recovery occurs within the first 3 months post-stroke, the neural mechanisms promoting recovery are not well understood. Investigations into the neural plasticity of brain areas after a lesion demonstrate that the adult brain can be shaped by environmental inputs, such as rehabilitation techniques. Many rehabilitation techniques are actively being pursued, including brain-computer interfaces providing sophisticated methods for detecting rehabilitation-associated changes in cerebral physiology. The success of such strategies visualized with functional magnetic resonance imaging and positron emission tomography may provide an objective complement to clinical evaluations.

The Effect on Cerebral Tissue Oxygenation Index of Changes in the Concentrations of Inspired Oxygen and End-Tidal Carbon Dioxide in Healthy Adult Volunteers

A variety of near-infrared spectroscopy devices can be used to make noninvasive measurements of cerebral tissue oxygen saturation (ScO2). The ScO2 measured by the NIRO 300 spectrometer (Hamamatsu Photonics, Japan) is called the cerebral tissue oxygenation index (TOI) and is an assessment of the balance between cerebral oxygen delivery and utilization. We designed this study to investigate the effect of systemic and intracranial physiological changes on TOI. Fifteen healthy volunteers were studied during isocapneic hyperoxia and hypoxemia, and normoxic hypercapnea and hypocapnea. Absolute cerebral TOI and changes in oxy- and deoxyhemoglobin concentrations were measured using a NIRO 300 spectrometer. Changes in arterial oxygen saturation (SaO2), ETCO2, heart rate, mean arterial blood pressure (MBP), and middle cerebral artery blood flow velocity (Vmca) were also measured during these physiological challenges. Changes in cerebral blood volume (CBV) were subsequently calculated from changes in total cerebral hemoglobin concentration. Baseline TOI was 67.3% with an interquartile range (IQR) of 65.2%-71.9%. Hypoxemia was associated with a median decrease in TOI of 7.1% (IQR -9.1% to -5.4%) from baseline (P < 0.0001) and hyperoxia with a median increase of 2.3% (IQR 2.0%-2.5%) (P < 0.0001). Hypocapnea caused a reduction in TOI of 2.1% (IQR -3.3% to -1.3%) from baseline (P < 0.0001) and hypercapnea an increase of 2.6% (IQR 1.4%-3.7%) (P < 0.0001). Changes in SaO2 (P < 0.0001), ETCO2 (P < 0.0001), CBV (P = 0.0003), and MBP (P = 0.03) were significant variables affecting TOI. Changes in Vmca (P = 0.7) and heart rate (P = 0.2) were not significant factors. TOI is an easy-to-monitor variable that provides real-time, multisite, and noninvasive assessment of the balance between cerebral oxygen delivery and utilization. However, TOI is a complex variable that is affected by SaO2 and ETCO2, and, to a lesser extent, by MBP and CBV. Clinicians need to be aware of the systemic and cerebral physiological changes that can affect TOI to interpret changes in this variable during clinical monitoring.

Quantification of modulated blood oxygenation levels in single cerebral veins by investigating their MR signal decay

The transverse magnetization of a single vein and its surrounding tissue is subject to spin dephasing caused by the local magnetic field inhomogeneity which is induced by the very same vessel. This phenomenon can be approximated and simulated by applying the model of an infinitely long and homogeneously magnetized cylinder embedded in a homogeneous tissue background. It is then possible to estimate the oxygenation level of the venous blood by fitting the simulated magnetization-time-course to the measured signal decay. In this work we demonstrate the ability of this approach to quantify the blood oxygenation level ( Y) of small cerebral veins in vivo, not only under normal physiologic conditions ( Y native =0.5–0.55) but also during induced changes of physiologic conditions which affect the cerebral venous blood oxygenation level. Changes of blood's oxygenation level induced by carbogen (5% CO 2, 95% O 2) and caffeine were observed and quantified, resulting in values of Y carbogen =0.7 and Y caffeine =0.42, respectively. The proposed technique may ultimately help to better understand local changes in cerebral physiology during neuronal activation by quantifying blood oxygenation in veins draining active brain areas. It may also be beneficial in clinical applications where it may improve diagnosis of cerebral pathologies as well as monitoring of responses to therapy.

Changes in cerebral physiology following cranioplasty: a 15oxygen positron emission tomography study

Patients with skull defects report symptoms, which improve with cranioplasty (CP). We used 15O positron emission tomography (PET) to examine whether this resulted from improvements in cerebral physiology.

Use of spin echo T(2) BOLD in assessment of cerebral misery perfusion at 1.5 T.

Inadequate blood supply relative to metabolic demand, a haemodynamic condition termed as misery perfusion, often occurs in conjunction with acute ischaemic stroke. Misery perfusion results in adaptive changes in cerebral physiology including increased cerebral blood volume (CBV) and oxygen extraction ratio (OER) to secure substrate supply for the brain. It has been suggested that the presence of misery perfusion may be an indication of reversible ischaemia, thus detection of this condition may have clinical impact in acute stroke imaging. The ability of single spin echo T(2) to detect misery perfusion in the rat brain at 1.5 T owing to its sensitivity to blood oxygenation level dependent (BOLD) contrast was studied both theoretically and experimentally. Based on the known physiology of misery perfusion, tissue morphometry and blood relaxation data, T(2) behaviour in misery perfusion was simulated. The interpretation of these computations was experimentally assessed by quantifying T(2) in a rat model for cerebral misery perfusion. CBF was quantified with the H(2) clearance method. A drop of CBF from 58+/-8 to 17+/-3 ml/100 g/min in the parieto-frontal cortex caused shortening of T(2) from 66.9+/-0.4 to 64.6+/-0.5 ms. Under these conditions, no change in diffusion MRI was detected. In contrast, the cortex with CBF of 42+/-7 ml/100 g/min showed no change in T(2). Computer simulations accurately predicted these T(2) responses. The present study shows that the acute drop of CBF by 70% causes a negative BOLD that is readily detectable by T(2) MRI at 1.5 T. Thus BOLD may serve as an index of misery perfusion thus revealing viable tissue with increased OER.

The electro-encephalogram in hypnotic age regression.

The hypothesis that there might be changes in cerebral physiology accompanying the psychological phenomena of hypnotic age regression was tested by comparing the electro-encephalograms of 10 normal subjects before and during regression. No alterations of cerebral physiology during hypnotic age regression were discovered.