Regional cerebral blood flow and glucose metabolism during propofol anaesthesia in healthy subjects studied with positron emission tomography.

BACKGROUND: General anaesthetics can alter the relationship between regional cerebral glucose metabolism rate (rGMR) and regional cerebral blood flow (rCBF). With the present study, we wanted to assess quantitatively the effects of propofol on rCBF and rGMR in the same healthy volunteers measured with positron emission tomography (PET). METHODS: (15)O-labelled water and (18)F fluorodeoxyglucose were used as PET tracers to determine rCBF and rGMR, respectively, in eight healthy volunteers during the waking state (baseline) and during propofol anaesthesia. Propofol was titrated to keep a constant hypnotic depth (Bispectral Indes 35-40) throughout the anaesthesia. Changes in rGMR and rCBF were quantified using region-of-interest and voxel-based analyses. RESULTS: The measured mean propofol concentration was 4.1 ± 0.8 µg/ml during anaesthesia. Compared with the conscious state, total CBF and GMR decreased during the anaesthetic state with 47% and 54%, respectively. In the white and grey matter, rCBF and rGMR were reduced by 37% and 49%, and by 45% and 57%, respectively. Propofol decreased rCBF in all brain structures by 46-55% (P ≤ 0.01) with highest significant decreases in the thalamus and parietal lobe. Regional GMR was reduced in all brain areas to 48-66% (P ≤ 0.01) with highest significant reductions in the occipital lobe, the lingual gyrus, parietal lobe, temporal lobe and thalamus. No increases in rCBF or rGMR happened anywhere. CONCLUSIONS: General anaesthesia with propofol is associated with a global metabolic and vascular depression in the human brain, with significant shifts in regional blood flow and metabolism indicating marked metabolic and vascular responsiveness in some cortical areas and thalamus.

Regional cerebral glucose metabolism during sevoflurane anaesthesia in healthy subjects studied with positron emission tomography.

BACKGROUND: The precise mechanism by which sevoflurane exerts its effects in the human brain remains unknown. In the present study, we quantified the effects of sevoflurane on regional cerebral glucose metabolism (rGMR) in the human brain measured with positron emission tomography. METHODS: Eight volunteers underwent two dynamic 18F-fluorodeoxyglucose positron emission tomography (PET) scans. One scan assessed conscious-baseline metabolism and the other scan assessed metabolism during 1 minimum alveolar concentration (MAC) sevoflurane anaesthesia. Cardiovascular and respiratory parameters were monitored and bispectral index responses were registered. Statistical parametric maps and conventional regions of interest analysis were used to determine rGMR differences. RESULTS: All subjects were unconsciousness at 1.0 MAC sevoflurane. Cardiovascular and respiratory parameters were constant over time. In the awake state, rGMR ranged from 0.24 to 0.35 mumol/g/min in the selected regions. Compared with the conscious state, total GMR decreased 56% in sevoflurane anaesthesia. In white and grey matter, GMR was averaged 42% and 58% of normal, respectively. Sevoflurane reduced the absolute rGMR in all selected areas by 48-71% of the baseline (P< or = 0.01), with the most significant reductions in the lingual gyrus (71%), occipital lobe in general (68%) and thalamus (63%). No increases in rGMR were observed. CONCLUSIONS: Sevoflurane caused a global whole-brain metabolic reduction of GMR in all regions of the human brain, with the most marked metabolic suppression in the lingual gyrus, thalamus and occipital lobe.

Regional cerebral blood flow responses to hyperventilation during sevoflurane anaesthesia studied with PET.

BACKGROUND: Arterial carbon dioxide tension (PaCO(2)) is an important factor controlling cerebral blood flow (CBF) in neurosurgical patients. It is still unclear whether the hypocapnia-induced decrease in CBF is a general effect on the brain or rather linked to specific brain regions. We evaluated the effects of hyperventilation on regional cerebral blood flow (rCBF) in healthy volunteers during sevoflurane anaesthesia measured with positron emission tomography (PET). METHODS: Eight human volunteers were anaesthetized with sevoflurane 1 MAC, while exposed to hyperventilation. During 1 MAC sevoflurane at normocapnia and 1 MAC sevoflurane at hypocapnia, one H(2)(15)O scan was performed. Statistical parametric maps and conventional regions of interest analysis were used for estimating rCBF differences. RESULTS: Cardiovascular parameters were maintained constant over time. During hyperventilation, the mean PaCO(2) was decreased from 5.5 + or - 0.7 to 3.8 + or - 0.9 kPa. Total CBF decreased during the hypocapnic state by 44%. PET revealed wide variations in CBF between regions. The greatest values of vascular responses during hypocapnia were observed in the thalamus, medial occipitotemporal gyrus, cerebellum, precuneus, putamen and insula regions. The lowest values were observed in the superior parietal lobe, middle and inferior frontal gyrus, middle and inferior temporal gyrus and precentral gyrus. No increases in rCBF were observed. CONCLUSIONS: This study reports highly localized and specific changes in rCBF during hyperventilation in sevoflurane anaesthesia, with the most pronounced decreases in the sub cortical grey matter. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve during hypocapnia.

The relationship between intracranial pressure and the degree of brain swelling in patients subjected to infratentorial surgery.

BACKGROUND: In patients with supratentorial tumours, intracranial pressure is a strong predictor of intra-operative brain swelling and thresholds for ICP associated with brain swelling have been defined. Whether these ICP thresholds can be applied during infratentorial surgery is uncertain. We studied the relationship between subdural ICP and the degree of brain swelling after opening of the dura mater in patients subjected to infratentorial surgery. Thresholds for ICP associated with brain swelling were defined. METHODS: One hundred and nine adult patients subjected to infratentorial surgery were studied. Subdural ICP was measured immediately before opening of the dura and the degree of brain swelling was estimated by the neurosurgeon according to a four-point scale. FINDINGS: At ICP less than 7 mmHg brain swelling did not occur. In the range from 7 to 13 mmHg 21 of 39 patients (54%) had moderate swelling, but not pronounced swelling. At ICP greater than 13 mmHg some degree of swelling occurred in all patients, and at ICP exceeding 24 mmHg pronounced cerebral swelling was found in all patients. Using logistic regression analysis specific thresholds for ICP associated with brain swelling were defined as follows: at an ICP equal to or greater than 13 mmHg, brain swelling occurred with 95% probability; and at an ICP less than 6 mmHg brain swelling occurred with 5% probability. CONCLUSIONS: Subdural ICP measured before opening of the dura mater can predict the risk of brain swelling during infratentorial surgery. Thresholds for ICP associated with brain swelling are close to thresholds defined in patients undergoing supratentorial surgery.

Effects of dose-dependent levels of isoflurane on cerebral blood flow in healthy subjects studied using positron emission tomography.

BACKGROUND: In this study, we tested the hypothesis that escalating drug concentrations of isoflurane are associated with a significant decline in cerebral blood flow (CBF) in regions sub-serving conscious brain activity, including specifically the thalamus. METHODS: Nine human volunteers received three escalating drug concentrations: 0.2, 0.4 and 1.0 MAC end-tidal inhalation. During waking, baseline and the three levels of sedation, aO PET scan was performed. RESULTS: Isoflurane decreased the bispectral index (BIS) values dose-dependently. Cardiovascular and respiratory parameters were maintained constant over time. No significant change in global CBF was observed. Throughout all three MAC levels of sedation, isoflurane caused an increased regional cerebral blood flow (rCBF) in the anterior cingulate and decreased rCBF in the cerebellum. Initially, isoflurane (0 vs. 0.2 MAC) significantly increased relative rCBF in the medial frontal gyrus and in the nucleus accumbens. At the next level (0.2 vs. 0.4 MAC), relative rCBF was significantly increased in the caudate nucleus and decreased in the lingual gyrus and cuneus. At the last level (0.4 vs. 1 MAC), relative rCBF was significantly increased in the insula and decreased in the thalamus, the cuneus and lingual gyrus. Compared with flow distribution in awake volunteers, 1 MAC of isoflurane significantly raised relative activity in the anterior cingulate and insula regions. In contrast, a significant relative flow reduction was identified in the thalamus, the cerebellum and lingual gyrus. CONCLUSIONS: Isoflurane, like sevoflurane, induced characteristic flow redistribution at doses of 0.2-1.0 MAC. At 1 MAC of isoflurane, rCBF decreased in the thalamus. Specific areas affected by both isoflurane and sevoflurane included the anterior cingulate, insula regions, cerebellum, lingual gyrus and thalamus.

The effects of 10 degrees reverse Trendelenburg position on subdural intracranial pressure and cerebral perfusion pressure in patients subjected to craniotomy for cerebral aneurysm.

The aim of the current study was to examine the effects of 10 degrees reverse Trendelenburg position (rTp) on subdural intracranial pressure (ICP), cerebral perfusion pressure (CPP), and dural tension. Additionally, the relationship between preoperative Hunt and Hess (H and H) grade and the subdural ICP in patients scheduled for cerebral aneurysm surgery was investigated. Twenty-eight consecutive patients with a cerebral aneurysm were subjected to craniotomy in propofol/fentanyl or propofol/remifentanil anesthesia. Subdural ICP was measured after opening of the bone flap and exposure of dura. After reference measurements of subdural ICP and mean arterial blood pressure (MABP), the measurements were repeated during 10 degrees rTp. No significant differences between the anesthetic groups were disclosed. During 10 degrees rTp, a significant decrease in MABP, ICP, and jugular bulb pressure was observed whereas CPP remained unchanged. In H and H 0 patients (unruptured aneurysm), the ICP decreased from 2.9 +/- 2.6 mmHg to 0.4 +/- 2.2 mmHg at 10 degrees rTp. In H and H I to II patients, the ICP decreased from 9.3 +/- 3.8 mmHg to 4.6 +/- 3.3 mmHg at 10 degrees rTp. A significant difference in the mean baseline subdural ICP and DeltaICP (change in ICP) was found between patients with unruptured aneurysm and patients with subarachnoid hemorrhage (H&H I and II). Furthermore, the relationship between the subdural ICP at neutral position and DeltaICP was significant. In patients without intracranial hypertension, 10 degrees rTp decreases subdural ICP and dural tension in patients with ruptured as well as patients with unruptured cerebral aneurysm; CPP is unchanged.

Effect of alfentanil on intracranial pressure during propofol-fentanyl anesthesia for craniotomy. A randomized prospective dose-response study.

BACKGROUND: The effect of alfentanil on intracranial pressure (ICP) in patients with supratentorial cerebral tumors has only been sparsely examined and with somewhat contradictory results. METHODS: Thirty-one patients were anesthetized with propofol and fentanyl. After removal of the bone flap a bolus-dose of alfentanil 10 (group 1), 20 (group 2), or 30 microg kg(-1) (group 3) was administered followed by an infusion of 10, 20, or 30 microg.kg(-1).h(-1) to patients in groups 1, 2, and 3, respectively. A control group received no alfentanil. Subdural ICP, mean arterial blood pressure (MAP), and cerebral perfusion pressure (CPP) were monitored and arterial and jugular bulb blood were sampled before and every minute for 5 min after the bolus administration of alfentanil and again after 5 min of hyperventilation to be able to calculate cerebral arterio-venous oxygen content difference (AVDO2) and carbon dioxide reactivity (CO2-reactivity). RESULTS: No changes in subdural ICP or AVDO2 from alfentanil in the study period were observed within the groups. However, alfentanil decreased MAP and CPP. The maximum CPP decrease (mean value of each group) was 4 mmHg, 8 mmHg, and 18 mmHg in groups 1, 2, and 3, respectively. There was no difference between groups as regards the CO2-reactivity. CONCLUSION: We conclude that administration of alfentanil to propofol-fentanyl anesthetized patients with supratentorial cerebral tumors decreases MAP and CPP in a dose-related way, but does not influence subdural ICP, AVDO2 or the CO2-reactivity.

Subdural intracranial pressure, cerebral perfusion pressure, and degree of cerebral swelling in supra- and infratentorial space-occupying lesions in children.

UNLABELLED: To our knowledge comparative studies of intracranial pressure (ICP) and degree of cerebral swelling during craniotomy for supratentorial or infratentorial space occupying lesion in children are not available. In this prospective study subdural ICP, cerebral perfusion pressure (CPP), dural tension, and the degree of cerebral swelling were analysed in supine and prone positioned children subjected to craniotomy for space occupying lesions. MATERIAL AND METHOD: 48 children with space occupying tumours were subjected to either isoflurane/nitrous oxide 50%/fentanyl (n = 22) or propofol/fentanyl/air/oxygen (n = 26). 25 children were operated supratentorially in supine position, while 23 patients were operated infratentorially in the prone position. Subdural ICP, mean arterial blood pressure (MABP), and CPP were measured just before opening of the dura. Dural tension was estimated before opening of dura, and the degree of cerebral swelling was estimated after opening of dura. RESULTS: The age and weight of children anaesthetised with isoflurane in the prone position were significantly lower than the propofol anaesthetised groups. No significant inter-group differences as regards tumour size, midline shift, rectal temperature, MABP or PaCO2 were found. ICP in prone positioned children averaged 16.9 mm Hg against 9.0 mm Hg in supine positioned children (p < 0.001). In prone positioned children the dura was significantly tenser, and the degree of brain swelling after opening of dura was significantly more pronounced. No significant difference as regard ICP was disclosed when isoflurane/nitrous oxide/fentanyl and propofol/ fentanyl anaesthetized children were compared, but MABP and CPP were significantly lower in isoflurane anaesthetised children. CONCLUSION: In children with cerebral tumours ICP is higher, and the degree of cerebral swelling more pronounced in the prone-compared with supine positioned children. Choice of anaesthesia did not influence ICP, but CPP was significantly lower during isoflurane anaesthesia.

Effects of subanaesthetic and anaesthetic doses of sevoflurane on regional cerebral blood flow in healthy volunteers. A positron emission tomographic study.

BACKGROUND: We tested the hypothesis that escalating drug concentrations of sevoflurane are associated with a significant decline of cerebral blood flow in regions subserving conscious brain activity, including specifically the thalamus. METHODS: Nine healthy human volunteers received three escalating doses using 0.4%, 0.7% and 2.0% end-tidal sevoflurane inhalation. During baseline and each of the three levels of anaesthesia one PET scan was performed after injection of . Cardiovascular and respiratory parameters were monitored and electroencephalography and bispectral index (BIS) were registered. RESULTS: Sevoflurane decreased the BIS values dose-dependently. No significant change in global cerebral blood flow (CBF) was observed. Increased regional CBF (rCBF) in the anterior cingulate (17-21%) and decreased rCBF in the cerebellum (18-35%) were identified at all three levels of sedation compared to baseline. Comparison between adjacent levels sevoflurane initially (0 vs. 0.2 MAC) decreased rCBF significantly in the inferior temporal cortex and the lingual gyrus. At the next level (0.2 MAC vs. 0.4 MAC) rCBF was increased in the middle temporal cortex and in the lingual gyrus, and decreased in the thalamus. At the last level (0.4 MAC vs. 1 MAC) the rCBF was increased in the insula and decreased in the posterior cingulate, the lingual gyrus, precuneus and in the frontal cortex. CONCLUSION: At sevoflurane concentrations at 0.7% and 2.0% a significant decrease in relative rCBF was detected in the thalamus. Interestingly, some of the most profound changes in rCBF were observed in structures related to pain processing (anterior cingulate and insula).

The effects of indomethacin on intracranial pressure and cerebral haemodynamics in patients undergoing craniotomy: a randomised prospective study.

We compared the effects of indomethacin (bolus of 0.2 mg.kg-1 followed by an infusion of 0.2 mg.kg-1.h-1) and placebo on intracranial pressure and cerebral haemodynamics in 30 patients undergoing craniotomy for supratentorial brain tumours under propofol and fentanyl anaesthesia. Indomethacin was given before induction of anaesthesia and the infusion was terminated after opening of the dura. Subdural intracranial pressure was measured through the first burr hole and before opening the dura. Cerebral blood flow velocity, cerebral perfusion pressure, jugular bulb oxygen saturation, arterio-venous oxygen difference and carbon dioxide reactivity were measured; dural tension and the degree of brain swelling were estimated. Before induction of anaesthesia, indomethacin administration was associated with a significant decrease in cerebral blood flow velocity compared with placebo. After induction of anaesthesia, cerebral blood flow velocity and mean arterial blood pressure decreased significantly in both groups. Indomethacin was not associated with a decrease in intracranial pressure. There were no differences in cerebral perfusion pressure, dural tension or degree of brain swelling between the two groups. Carbon dioxide reactivity measured after induction of anaesthesia was significantly lower in the indomethacin group (p < 0.05). After removal of the bone flap, no significant difference in carbon dioxide reactivity was observed. We suggest that these findings are explained by propofol-induced cerebral vasoconstriction.

No influence of the endothelin receptor antagonist bosentan on basal and indomethacin-induced reduction of cerebral blood flow in pigs.

BACKGROUND: The mechanism behind indomethacin-induced cerebral vasoconstriction is incompletely understood. We tested the hypothesis that the mixed endothelin-1 receptor antagonist bosentan would modify or prevent indomethacin-induced reduction of CBF in the anaesthetized pig. Furthermore, we investigated the effect of bosentan on resting CBF and CMRO2. METHODS: Twelve pigs were randomized in two groups of six, and received either bosentan and indomethacin (group 1), or placebo and indomethacin (group 2). Anaesthesia was induced with ketamine and midazolam and maintained with fentanyl, nitrous oxide and pancuronium. Baseline measurements of CBF and CMRO2 were performed before intravenous bolus injection of bosentan (10 mg/kg) or placebo (0.9% NaCl). The second CBF and CMRO2 measurement was performed 30 min after administration of bosentan/placebo. A 40-min infusion of indomethacin (0.05 mg/kg/min) was administered and the third CBF and CMRO2 measurement was performed 80 min after administration of bosentan/placebo. Independently, pharmacokinetic data of bosentan were generated in four pigs. RESULTS: In group 1, baseline CBF was 55 +/- 7 ml/100 cm3/min. Administration of bosentan i.v. did not change CBF significantly. Indomethacin decreased CBF to 41 +/- 5 ml/100 cm3/min (P < 0.002). In group 2, baseline CBF was 54 +/- 10 ml/100 cm3/min. Placebo did not change CBF while indomethacin decreased CBF significantly to 41 +/- 5 ml/100 cm3/min (P < 0.002). No significant changes in CMRO2 were observed. In group 2, a significant increase in MABP was observed after administration of indomethacin. No change in MABP was observed in the bosentan-treated animals. Total plasma concentrations of bosentan at the time of the first and the second PET measurement were 3.9 and 1.4 microg/ml, respectively. The corresponding values for the pharmacologically active metabolite Ro 48-5033 were 1.2 and 0.4 microg/ml. CONCLUSION: These findings indicate that endothelin receptor stimulation is not involved in indomethacin-induced cerebral vasoconstriction or maintenance of cerebrovascular tone in the anaesthetized pig. However, our results suggest that the increase in MABP is mediated through endothelin receptors.

The effects of 10 degrees reverse trendelenburg position on ICP and CPP in prone positioned patients subjected to craniotomy for occipital or cerebellar tumours.

BACKGROUND: Control of ICP-hypertension is of utmost importance during craniotomy. The effects of reverse Trendelenburg position (RTP) upon ICP and CPP have recently been studied in supine positioned patients. METHOD: In this study we investigated changes in intracranial pressure (ICP), mean arterial blood pressure (MABP), CPP and jugular bulb pressure (JBP) before and one minute after 10( degrees ) RTP in 26 prone positioned patients with either occipital (n=12) or cerebellar tumours (n=14). ICP was measured by a subdural approach after removal of the bone flap. Tension of the dura was estimated by the surgeons by digital palpation before and after change in position. FINDINGS: In patients with occipital tumours ICP decreased from 21.0 to 15.6 mm Hg (p<0.05). MABP decreased from 87.9 to 83.3 mm Hg (p<0.05), JBP decreased from 14.3 to 7.7 mm Hg (P<0.05), while CPP was unchanged. In patients with cerebellar tumours ICP decreased from 18.3 to 14.2 mm Hg (p<0.05). MABP decreased from 93,8 to 90.5 mm Hg (p<0.05), JBP decreased from 12.1 to 5.0 mm Hg (P<0.05), while CPP was unchanged. There were no significant differences between the two groups with regard to changes in ICP, MABP, CPP and JBP. The change in ICP was accompanied by a significant decrease in dural tension (p<0.05). INTERPRETATION: In prone positioned patients 10 degrees RTP significantly reduces ICP, JPB and MABP within one minute, while CPP is unchanged.

ICP is lower during propofol anaesthesia compared to isoflurane and sevoflurane.

OBJECTIVES: Propofol is a cerebral vasoconstrictor while inhalation anaesthetics like isoflurane and sevoflurane act as cerebral vasodilators in both animal and human studies. This difference of action upon cerebral vessels might implicate a lower ICP during propofol anaesthesia. Cerebral metabolism is decreased by all three anaesthetics. In a prospective, randomised multicenter study ICP was compared during anaesthesia with propofol, isoflurane and sevoflurane. METHODS: 117 patients subjected to elective craniotomy for supratentorial tumour. Propofol: N = 41; isoflurane: N = 38; sevoflurane: N = 38. Nitrous oxide was omitted and all anaesthetics were supplemented with a continuous infusion of fentanyl. ICP was measured subdurally after removal of the bone flap. MABP, CPP, PCO2, AVDO2, rectal temperature, tumour size and midline shift were registered too. STATISTICS: Kruskal-Wallis Variance on Ranks. All values in medians with range. P < 0.05 was considered significant. RESULTS: ICP (mmHg): propofol 7 (-1-20), isoflurane 12 (1-29), sevoflurane 11 (2-32). ICP was significantly lower in the propofol group compared to the isofluane and sevoflurane groups. CPP (mmHg): propofol 80 (45-104), isoflurane 60 (32-84), sevoflurane 63 (44-77). CPP was significantly higher in the propofol group compared to the isoflurane and sevoflurane groups. AVDO2 (mmol/l): propofol 3.1 (0.9-5.1), isoflurane 2.5 (1.1-4.5), sevoflurane 2.6 (0.8-4.1). AVDO2 was significantly higher in the propofol group compared to the isoflurane and sevoflurane groups. No significant differences in PCO2, rectal temperature, tumour size and midline shift were found. CONCLUSIONS: Subdural ICP is significantly lower during propofol anaesthesia compared to isoflurane and sevoflurane anaesthesia. CPP and AVDO2 are significantly higher during propofol anaesthesia compared to isoflurane and sevoflurane anaesthesia.

Effects of dihydroergotamine on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients undergoing craniotomy for brain tumors.

In a search for a nonsurgical intervention to control intracranial hypertension during craniotomy, the authors studied the effects of dihydroergotamine on mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral metabolism in patients who underwent craniotomy for supratentorial brain tumors. Twenty patients were randomized to receive either dihydroergotamine 0.25 mg intravenously or placebo as a bolus dose during craniotomy. Anesthesia was induced with thiopental/fentanyl/atracurium, and maintained with isoflurane/N2O/fentanyl at normocapnia. After removal of the bone flap and exposure of intact dura, ICP was measured subdurally and dihydroergotamine/placebo was administered. Intracranial pressure and MABP were measured continuously. Cerebral blood flow (after intravenous administration of 133Xe) and arteriojugular venous difference of oxygen (AVDO2) were measured before, and 30 minutes after, dihydroergotamine/placebo administration. Cerebral metabolic rate of oxygen (CMRO2) was calculated. After administration of dihydroergotamine, a significant increase in MABP from 74 to 87 mm Hg (median) and CPP from 65 to 72 mm Hg (median) were found. Simultaneously to the increase in MABP, a significant increase in ICP from 9.5 to 11.5 mm Hg (median) was disclosed, whereas no significant differences in CBF, AVDO2, or CMRO2 were found. Intracranial pressure was significantly higher after dihydroergotamine than after placebo. In conclusion, no ICP decreasing effect of a bolus dose of dihydroergotamine was found when administered to patients with brain tumors during isoflurane/N2O anesthesia. Corresponding increases in MABP and ICP suggest that abolished cerebral autoregulation might explain why dihydroergotamine was associated with an ICP increase.

Studies of regional subdural pressure gradients during craniotomy.

We investigated subdural pressure gradients within the operative field of the exposed intact dura in 53 patients with space-occupying lesions during craniotomy. In 37 patients with supratentorial brain tumour paired measurements of subdural pressure were studied in either the same horizontal or vertical plane. In 16 patients with infratentorial brain tumours the influence of a tumour was studied by measuring subdural pressure bilaterally over the right and left cerebellar hemisphere. Significant correlation between the vertical distance and the difference in subdural pressure was found, with the highest pressure in the most downward part of the brain. In patients with tumour in one cerebellar hemisphere, subdural pressure ipsilateral to the tumour was significantly higher than the subdural pressure on the contralateral side. The present study demonstrates subdural pressure gradients within the area of the exposed dura. The subdural pressure was influenced by the underlying tumour and/or gravity. This must be taken into consideration when a dura incision is made.

Cerebral blood flow in volunteers measured by PET and Xe CT/CBF. A comparison.

Aim of this study was to compare two quantitative CBF methods. Seven young, healthy volunteers were studied with PET (15-0 labelled water) and afterwards with Xe CT/CBF (30% xenon in oxygen, 3 minutes wash-in, 5 minutes washout protocol). Xe CT/CBF showed greater differences between high and low flow areas than PET CBF. Correlation was found within subjects between ROI's, but no agreement or correlation between the methods could be demonstrated. The disagreement in this study could be due to changes in PCO2.

Subdural pressure measurement during posterior fossa surgery. Correlation studies of brain swelling/herniation after dural incision with measurement of subdural pressure and tactile estimation of dural tension.

Thirty-two patients with posterior fossa tumours or arteriovenous malformations were subjected to elective craniotomy in the prone position. The intracranial pressure (ICP) was measured by a subdural approach in the open area of the exposed dura. Estimation of dural tension before dural incision and the degree of brain swelling/herniation after opening the dura were correlated with the subdural pressure measured with intact dura. The results indicate that at ICP < 10 mmHg, brain swelling/herniation rarely occurred, while at ICP > or = 10 mmHg some degree of brain swelling/herniation was always present. The neurosurgeon's tactile estimation of dural tension correlated poorly with any tendency to brain swelling/herniation. It is concluded that measurement of subdural pressure is a better predictor of the risk of brain swelling/herniation than the tactile estimation of dural tension during posterior fossa surgery.

Subdural monitoring of ICP during craniotomy: thresholds of cerebral swelling/herniation.

It is possible to define thresholds for cerebral swelling or herniation during craniotomy. In 178 patients subjected to craniotomy for space occupying processes subdural ICP was measured before opening of dura. The subdural ICP was correlated to the degree of cerebral swelling or herniation after opening of dura. At subdural ICP < 7 mm Hg cerebral swelling/herniation after opening of dura rarely occurs, while at ICP > or = 10 mm Hg cerebral swelling/herniation occurs with high probability. These ICP thresholds are independent of the pathophysiology (SAH, cerebral tumor), the anaesthetic agent (isoflurane, propofol) and the PaCO2 level (< or = 4.0 kPa, > 4.0 kPa). Generally, a good correlation between the tactile estimation of dural tension and the tendency to cerebral swelling or herniation after opening of dura was found. However, in 8.5% the surgeons were unable to predict swelling/herniation.

ICP during anaesthesia with sevoflurane: a dose-response study. Effect of hypocapnia.

In patients with a supratentorial cerebral tumor, an increase in sevoflurane concentration from 1.5% (0.7 MAC) to 2.5% (1.3 MAC) did not change the intracranial pressure (ICP) significantly (12 to 14 mm Hg (medians)). However, a significant increase in cerebral blood flow (CBF) from 29 to 39 ml/100 g/min (medians) was disclosed. During administration of sevoflurane 1.5% and 2.5%, a significant decrease in ICP (3.5 and 3.0 mm Hg (median) respectively) was found when PaCO2 was decreased by 0.8 kPa.

Cerebral blood flow measurements by magnetic resonance imaging bolus tracking: comparison with [(15)O]H2O positron emission tomography in humans.

In six young, healthy volunteers, a novel method to determine cerebral blood flow (CBF) using magnetic resonance (MR) bolus tracking was compared with [(15)O]H2O positron emission tomography (PET). The method yielded parametric CBF images with tissue contrast in good agreement with parametric PET CBF images. Introducing a common conversion factor, MR CBF values could be converted into absolute flow rates, allowing comparison of CBF values among normal subjects.