The aim of this article is to describe the up-to-date use of different specialized monitoring modalities used perioperatively during neurosurgery or in critically ill neurosurgical patients submitted to surgery obtained from consideration of recent literature. In different sections the main factors that affect CNS function are considered: brain oxygenation, cerebral blood flow, electrophysiological activity, intracranial pressure, ischaemia, air embolism and temperature, as well as clinical monitoring of consciousness. It should always be remembered that any claims or results reported in the literature need to be evaluated carefully.
Neuronal oxygenation is the final objective of all clinical procedures in neuroanaesthesia. Presently available monitors of brain oxygenation are only able to provide an incomplete picture of what is happening.
Jugular venous oxygen saturation
Monitoring of the jugular venous oxygen saturation (SjvO2) is an index of cerebral oxygen uptake. Its usefulness is in large part due to availability and ease of obtaining the information. The normal SjvO2 is 55–75%. This value assumes a normal oxygen delivery (cerebral blood flow × arterial oxygen content) and a normal concentration of circulating haemoglobin when the oxygen saturation is 100%. Changes in SjvO2 provide indirect information on the state of the cerebral metabolic rate of oxygen (CMRO2); and because cerebral blood flow (CBF) is normally linked to CMRO2, SjvO2 provides indirect information on CBF as well. An increase in SjvO2 indicates a lowered CMRO2, increased CBF, or both. A decrease in SjvO2 indicates an increased CMRO2, inadequate delivery of oxygen to the brain, or both . Monitoring SjvO2 provides different data to the anaesthesiologist, but cannot be used as a single source of information: although we can determine the dominant venous drainage of the head, only a fraction of the blood passing through the brain is sampled when SjvO2 is measured in one or both internal jugular veins. The jugular sample is more representative of the forebrain than of the venous blood draining from the posterior fossa.
In 1994, Matta and his colleagues published an interesting study examining the intraoperative use of jugular venous bulb catheters in 100 consecutive patients undergoing neurosurgical procedures . He concluded that this technique is feasible and may be beneficial both for detecting and treating cerebral venous desaturation, and for calculating the cerebral arteriovenous oxygen content difference (AVDO2). They were able to detect at least one episode of cerebral venous desaturation due to hyperventilation in approximately 50% of patients studied. They did not deliberately institute excessive hyperventilation in their patients, and without this monitor they would not have suspected this level of desaturation on clinical grounds. Cerebral venous oxygen desaturation may occur when hyperventilation is deliberately employed during neurosurgical procedures to diminish cerebral blood volume. In a further study, they concluded that hyperoxia during acute hyperventilation in the anaesthetized patient improves oxygen delivery to the cerebral circulation, as measured by a higher cerebral venous oxygen content and saturation . An increased PaO2 should be considered for those patients in whom aggressive hyperventilation is contemplated.
Monitoring of SjvO2 is used during aneurysm surgery to control ischaemia periods. Temporary vessel occlusion of the proximal parent artery is an integral component of aneurysm dissection and clipping. The use of temporary occlusion permits reduction of the pressure and size of the aneurysm hence facilitates its dissection; it also reduces the risk of rupture of the aneurysm during surgery. The safe limits for arterial occlusion and the benefits – or detrimental effects – of intermittent reperfusion are yet to be determined; SjvO2 can be a useful sign of impending ischaemia . Jugular bulb catheters are routinely placed in many centres to detect brain desaturation during surgery of large tumours or repair of aneurysms. Moreover, its usefulness in the management of head trauma patients is accepted world-wide.
Regional brain oxygen saturation
Recent advances in optoelectronics have enabled near-infrared spectroscopy (NIRS) to measure oxyhaemoglobin saturation in the cerebral vasculature and provide a sensitive indicator of cerebral hypoxia . NIRS measures, non-invasively and continuously, regional changes in oxyhaemoglobin, deoxyhaemoglobin and cytochrome aa3 redox status; NIRS interrogates arterial, venous and capillary blood and, therefore, the derived oxygen saturation is an average value for these three compartments. However, most of the NIRS signal is from the venous blood because it contributes to approximately 70% of the intracranial blood volume . This technique indirectly assesses flow by detecting changes in venous saturation and can provide information about tissues several centimetres below the probe. NIRS has greater tissue penetration than pulse oximetry and does not need pulsatility. Nevertheless, at present, NIRS methods in adults strikingly underestimate CBF and this is likely to relate to the contribution of non-cerebral tissue overlying the cerebral tissue in the field of view of the probe .
Normal values have not been defined for regional brain oxygen saturation (rSO2). A post-mortem study found in eight of 18 subjects that after cessation of systemic circulation rSO2 measurements had values of over 50% or were in the range we would find in healthy volunteers . The potential usefulness of NIRS is as a monitor of changes in cerebral oxygenation rather than an indicator of an absolute condition of the oxygenation in the mixed venous blood of the brain. Trend values of NIRS may help to detect ischaemic events and rSO2 is being used during interventional neuroradiological procedures . NIRS may prove useful as an early warning of cerebral hypoxaemia because it may detect reduced oxygenation. Saito used a two-wavelength NIRS (INVOS 3100; Somanetics Corp., Troy, MI, USA) to show that electroconvulsive therapy (ECT) decreases rSO2 immediately after application of the current; rSO2 then increases to values exceeding those obtained before ECT .
Further development of cerebral monitors is assisting research. The NIRS monitor (INVOS 4100, Somanetics) is now provided with two probes and displays the rSO2 value of each cerebral hemisphere simultaneously. In this way, trends in total cerebral oxygenation can be followed, and NIRS used as a monitor of changes in rSO2.
Brain tissue oxygen tension
The intraparenchymal measurement of brain tissue oxygenation (PtiO2) is made via an oxygen sensitive Clarke-type electrode. Monitoring of PtiO2 is being increasingly used whenever intracranial pressure (ICP) monitoring is indicated. This technique may be used for patients with head injury, subarachnoid haemorrhage or intraoperatively during aneurysm surgery.
Dings assessed the technical and diagnostic reliability of PtiO2 . He concludes that brain PtiO2 monitoring, reflecting an area 17–27 mm below the dura, is a safe and reliable technique for monitoring cerebral oxygenation. Except for the first hour after insertion of the probe, data are reliable with almost 100% accuracy. Doppenberg measured brain PtiO2, brain PCO2, pH and haemoglobin oxygen saturation before and after temporary occlusion in 12 patients with cerebral aneurysms . A multiparameter sensor (Paratrend 7; Biomedical sensors, Malvern, PA, USA) was placed in the relevant cortex and locked in position by means of a specially designed skull bolt. Data were collected every 10 s. A wide range in baseline PtiO2 was seen, although a decrease from baseline in brain PtiO2 was found in all patients. During temporary occlusion, brain PtiO2 in patients with unruptured aneurysms (seven patients) dropped significantly, from 60 ± 31 mmHg to 27 ± 17 mmHg (P < 0.05). In the subarachnoid haemorrhage group (five patients), the fall in PtiO2 was not significant. Removal of intracranial haematoma in four severely head-injured patients resulted in a significant increase in PtiO2, from 13 ± 9 mmHg to 34 ± 13 mmHg.
Hoffman looked for differences in brain PtiO2 adjacent to arteriovenous malformations (AVM) compared with control patients (non-ischaemic patients scheduled for cerebral aneurysm clipping) . He found that during baseline conditions before the start of surgery, PtiO2 was decreased in patients with AVM. However, PCO2 and pH were unchanged compared with a control group. During resection of AVMs, PtiO2, and pH increased and PCO2 decreased compared with baseline measurements. These variables did not change in control patients during a similar time period. The results suggest that cerebrovascular or metabolic adaptation occur in those patients with AVMs, with decreased tissue perfusion pressure as an adjustment for decreased oxygen delivery. During resection of AVMs this adaptation produces a relative hyperaemic environment with tissue hyperoxia, hypocapnia, and alkalosis that remains uncorrected at the end of surgery.
Gupta and his colleagues, studying brain oxygenation in head-injured patients, found that the SjvO2 was not as reliable as the PtiO2 as an indicator of regional oxygenation . He used a multiparameter sensor (Paratrend 7TM, Diametrics Medical, High Wycombe, UK) inserted into the brain tissue.
Robertson’s group analysed the brain PtiO2 . Their data suggest that the likelihood of death increased with increasing duration of time at or below a PtiO2 of 15 mmHg, or with the occurrence of any PtiO2 values < 6 mmHg. More studies are needed in this clinical setting.
Cerebral blood flow
Measuring cerebral blood flow continues to be difficult, especially intraoperatively, in the clinical setting. The most reliable methods are used in research laboratories and are technically complex and non-continuous; monitoring CBF changes is still much more accessible for the anaesthesiologist than assessment of absolute CBF values.
Regional blood flow can be determined by the intravenous 133-Xenon (133Xe) method. Ostapkovich and his colleagues used this technique (Cerebrograph 10a, Novo Diagnostic Systems, Bagsvaerd, Denmark)  to compare the effects of remifentanil–nitrous oxide on CBF and carbon dioxide reactivity, with fentanyl–nitrous oxide anaesthesia during craniotomy. After dural exposure and a minimum of 15 min at a stable drug dose, 15–20 mCi of 133Xe in saline was injected into the saphenous vein, followed by a saline flush. 133Xe gas was sampled from the expired circuit monitor to construct the arterial input function. Tracer washout was recorded over the middle cerebral artery distribution contralateral to the operative site with an NaI (sodium iodine) scintillation detector for 11 min; CBF was calculated using the initial slope index. Both regimens had similar effects on absolute CBF and cerebrovascular CO2 reactivity was maintained. This technique is routinely unavailable for surgical procedures.
Double-indicator dilution technique
Wietasch and his colleagues have recently described a bedside method for the assessment of CBF . The investigation was performed in 14 anaesthetized patients before coronary bypass surgery during which CBF was altered by hypocapnia, normocapnia and hypercapnia. Measurements were made simultaneously by the Kety–Schmidt inert-gas technique with argon and with a newly developed transcerebral double-indicator dilution technique (TCID). For the TCID measurements to be made, boluses of ice-cold indocyanine green were injected through a central venous line, and the resulting thermo-dye dilution curves were recorded simultaneously in the aorta and the jugular bulb using combined fibre-optic thermistor catheters. The value of CBF was calculated from the mean transit times of the indicators through the brain. The authors conclude that TCID is an alternative method to measure global CBF at the bedside and it offers a new opportunity to monitor cerebral perfusion of patients. However, its use is far from being applied in the operating theatre.
Positron emission tomography
Positron emission tomography (PET) is being used both as a diagnostic and a clinical research tool. It allows examination of the CBF and cerebral oxygen consumption. Alkire and his colleagues recently published a study evaluating regional cerebral metabolic activity in the human brain using functional brain imaging with the F-18 fluorodeoxyglucose PET . He found that halothane caused a metabolic reduction in the whole brain with significant shifts in regional metabolism. Propofol compared with halothane or isofluorane was associated with greater absolute metabolic reduction and a suppression of relative cortical metabolism, and caused significantly less suppression of relative metabolism in the basal ganglia and midbrain regions. The need for the use of radioactive substances, which have to be manufactured close to a special scanner, makes this method very complicated and expensive.
Transcranial Doppler ultrasonography
Routine transcranial Doppler (TCD) ultrasound examination of the intracranial arteries was shown to be possible in 1982. It is used with ease at the bedside or intraoperatively. The waveform resembles that of an arterial pulse and is easily quantified into systolic, mean and diastolic flow velocities and pulsatility index. One fact that has to be kept in mind when using TCD is that the value obtained for a particular artery is the velocity of blood flowing through that vessel. Unless some means or other can establish the diameter of that vessel it is impossible to determine the actual blood flow. Thus, TCD is primarily a technique for measuring relative changes in flow but does not facilitate quantitative measurements of CBF . For instance, in patients with subarachnoid haemorrhage and vasospasm, an increase of blood flow velocities paradoxically indicates a decrease rather than an increase of CBF .
Transcranial Doppler has been used to assess the cerebrovascular reactivity. Piechnick and his colleagues placed TCD probes (Neuroguard, 2 MHz; Medasonics, Fremont, CA, USA) over the temporal window, just above the zygomatic arch, on both sides . In all subjects the middle cerebral artery was insonated at a depth of 50 mm bilaterally. End-tidal CO2 (ETCO2) was measured using an anaesthetic facemask that was attached via a small diameter tube to a CO2 monitor. By these means the authors could investigate the moving correlation between slow waves in arterial pressure and blood flow velocity at different levels of cerebrovascular vasodilatation provoked by changing ETCO2. Gupta and his colleagues suggested that hypoxaemic cerebral vasodilation may be measured non-invasively using TCD . They studied normal human volunteers, and found that the threshold for hypoxaemic cerebral vasodilation was a SpO2 of 90%, which is higher than previously reported.
Transcranial Doppler is being used intraoperatively in anaesthetic research and has shown that inhalational anaesthetics produce a dose-dependent increase in CBF. The magnitude of this increase is dependent on the balance between the intrinsic vasodilatory action of the agent and the vasoconstriction secondary to flow-metabolism coupling. A 2-MHz transcranial Doppler ultrasound probe (DWL Multidop; Sipplingen, Germany) was used by Mattat and his colleagues to measure the time-averaged mean blood flow velocity in the middle cerebral artery . Once the optimal signal was obtained, at a depth between 45 and 55 mm, the probe was secured in position using a special frame so that the angle of insonation remained constant throughout the study period.
Transcranial Doppler may be a good monitoring device during carotid endarterectomy, and continuous measurement of blood flow velocity in the distribution of the middle cerebral artery may be helpful in differentiating intraoperative haemodynamic vs. embolic neurological events. Embolization detected by TCD occurs in more than 90% of patients during carotid endarterectomy. It has been suggested that surgical intervention such as more careful dissection of the artery and more meticulous attention to back-bleeding and flushing to avoid embolization can be guided by acoustic evidence for embolism. TCD may also indicate which patients should have aggressive haemodynamic interventions and/or be anticoagulated after cerebral embolic events; decreased CBF velocity can be differentiated. Failure to obtain interpretable signals occurs in 15–20% of cases because of temporal hyperostosis or other technical difficulties .
Oscillating flow or systolic spikes are typical Doppler-sonographic flow signals in the presence of cerebral circulatory arrest, which if irreversible, results in brain death. Similar wave shapes could be seen during some neuroendoscopic procedures with increases of ICP during surgery . Extracranial and intracranial Doppler sonography is a useful confirmatory method to establish irreversibility of cerebral circulatory arrest as an optional part of the protocol to confirm brain death and it is of special value when the use of sedative drugs renders electroencephalography unreliable .
Laser Doppler flowmetry
A craniotomy or burr hole is needed to insert a Laser Doppler flowmeter to detect cortical blood flow. The depth and area of the tissue involved limit the technique. Moreover, it is possible that areas that are beyond the monitor could be subjected to deleterious flow reduction without being detected. The technique requires the cortex to be exposed and so cannot be used to follow changes in physiological variables during the earlier or later phases of neurosurgical operations. For these reasons, reliance on such measurements alone to predict the risk of ischaemic injury may be unwise .
Neurophysiological monitoring performed during operative procedures provides information about the functional integrity of accessible neuronal pathways. The modality of neurophysiological testing must assess the portion of the nervous system at greatest risk of injury. Despite technical advances electrophysiological monitoring in the operating theatre is technically demanding. Displacement of surface leads, effects of anaesthetic drugs, interference by electrical equipment, and the absence of reliable baseline data can diminish its usefulness.
The electrical activity of the brain is closely coupled to CBF. In the progression of acute cerebral ischaemia, a failure of electrical activity precedes the deterioration of ionic homeostasis; monitoring this activity should be an important tool in predicting the development of cerebral ischaemia before irreversible damage ensures.
The most commonly used evoked potentials are those produced by stimulation of the sensory system, somato-sensory evoked potentials (SSEP). Several studies have confirmed the efficacy and cost effectiveness of intraoperative monitoring. The American Academy of Neurology has published an assessment on SSEP monitoring during surgery which concluded that ‘considerable evidence favours the use of monitoring as a safe and efficacious tool in clinical situations where there is significant nervous system risk, provided its limitations are appreciated’ . Perhaps the most common application of SSEP monitoring is during spinal correction surgery such as for scoliosis or spinal trauma. Standards of care have defined this monitoring as essential in scoliosis repair .
During posterior fossa surgery spontaneous or evoked electromyographic (EMG) activity, SSEP or brainstem auditory-evoked responses are frequently monitored . In general, brain stem auditory-evoked responses are less susceptible to anaesthetic agents than SSEP. The cortical component of SSEP is very sensitive to anaesthetics and can be abolished at 0.5 minimum alveolar concentration of inhalational anaesthetic. While both volatile and intravenous anaesthetics increase the latency of SSEP and brainstem auditory responses, the amplitude of the response may be unaffected by intravenous agents .
Several groups have reported the application of electrophysiological monitoring during aneurysm repair [4,30]. The most common variables monitored during the surgery of anterior cerebral artery aneurysms are changes in amplitude or latency of SSEP and central conduction time, which is the interval between the peaks N14 and N20 and is preserved with values of CBF as low as 30 mL 100 g−1 min−1. During temporary arterial clipping, significant SSEP changes were found in 17 patients reported by Scharmm and his colleagues . Despite the advantage gained by electrophysiological monitoring, the tolerance for temporary vascular occlusion in each patient remained unpredictable. Evoked potentials can reliably predict the occurrence of ischaemic deficits only if continuous monitoring is performed on pathways that include all regions at risk. This is not possible with current technology . Intraoperative occlusion of a perforator vessel, for instance, which may result in a catastrophic event, may not affect the somatosensory or the auditory pathways, and thus goes completely unnoticed .
Neurogenic motor evoked potential (NMEP) involves the stimulation of the spinal cord by electrodes placed near or on the vertebral bodies cephalad to the region of spinal surgery. The responses can be measured in the distal spinal cord, peripheral nerves and muscles. This monitoring, like epidural stimulation, appears to assess motor as well as sensory tracts of the spinal cord. Its use in scoliosis repair has reduced the practice of classical ‘awake testing’ .
Pure motor tract monitoring is best accomplished using motor cortex stimulation using transcranial electrical or magnetic stimulation. The high incidence of paraplegia after extensive type II postdissection thoracoabdominal aortic aneurysm has stimulated interest in developing techniques for intraoperative monitoring. Recordings of myogenic motor potentials evoked by transcranial pathways can be made during these procedures . Myogenic responses to transcranial cortical stimulation are entirely specific for motor tract conduction; it is also the most challenging monitoring technique in terms of anaesthetic management because it is incompatible with high concentrations of volatile agents and requires careful titration of neuromuscular blocking drugs .
Auditory evoked potentials (AEP) are being used for monitoring awareness, depth of anaesthesia and sedation. Changes in the latency of the waves are highly correlated with the transition from the awake to the unconscious state. Subsequent decreases and increases in the amplitude of the waves reflect the interplay of general anaesthetics with the responses to surgical stimulation, which are modified by the effects of analgesics. The early cortical AEP is valuable in distinguishing between the awake and the anaesthetized state and subsequent CNS depression .
The electroencephalogram (EEG) is useful for the detection of electrical seizure activity and for detection of cortical ischaemia. The EEG has, therefore, become indispensable for intraoperative mapping of seizure foci that are to be removed, but are not associated with any structural abnormality such as a tumour. Because the EEG is altered during periods of ischaemia, its use has been advocated during procedures that involve the vascular supply to the brain, e.g. for cerebral aneurysm or carotid endarterectomy. In these procedures the EEG may help in the management and reduce the risk of intraoperative stroke .
Matta and his colleagues used propofol to induce isoelectricity of the EEG and were able to demonstrate that isoflurane and desflurane produce more cerebral vasodilation than an equipotent dose of halothane . The same group, studying the cerebral vasodilatory effect of sevoflurane, showed that burst suppression could be monitored by the EEG . Brain electrical activity was measured using a two-channel bipolar frontal montage (A-1000 EEG monitor, Aspect Medical Systems, MA, USA), which displays the unprocessed EEG and the burst suppression ratio. The burst suppression ratio is defined as the percentage of epochs in the past 63 s during which the EEG signals are considered to be suppressed: a burst suppression ratio of 100% implies EEG silence. It is often assumed that the cerebral metabolic and protective effects of qualitative burst suppression are similar to those of the isoelectric EEG. Doyle examined the effect of different degrees of EEG suppression on blood flow and arteriovenous oxygen difference during general anaesthesia for resection of acoustic neuromas . He concludes that if flow-metabolism coupling is maintained, the assumption that cerebral metabolism during 50% EEG burst suppression is equivalent to isoelectric EEG may not be justified. If cerebral protection is related to brain metabolism, then an isoelectric EEG may give more cerebral protection than 50% burst suppression. It should not be assumed that pharmacologically induced burst suppression would lead to a better neurological outcome . In models of transient focal ischaemia, burst suppression with either isoflurane or etomidate does not confer the same degree of brain protection as does burst suppression with a barbiturate . Reduction of CMRO2, burst suppression, or both, are probably not the essential elements of brain protection by barbiturates. Thus, pharmacologically induced burst suppression by itself would seem to have little to do with clinically relevant brain protection . This interesting field deserves more extensive research.
Electroencephalographic activity can be displayed in an unprocessed (raw) or processed format (compressed spectral array – CSA; density spectral array – DSA) that is easier to interpret by less experienced personnel. Bispectral index (BIS), which examines the phase relationship – or coherence – between different EEG frequencies, is the most recent widely applied EEG measurement of the effect of anaesthetics on the brain. It has been ‘designed’ to measure depth of hypnosis and it is beyond the scope of this review.
Patients with refractory epilepsy are often scheduled for brain surgery. Watts performed an electrocorticographic (EcoG) study in patients with refractory epilepsy scheduled for insertion of subdural electrodes . Eight-channel digital EcoG recordings were obtained from freshly implanted subdural electrodes using a Neurotrac I Monitor with a sensitivity of 40 μV mm−1 and a bandpass filters of 0.5–50 Hz. In one patient, 16 EcoG channels were recorded using a Grass Model 8 electroencephalograph with a sensitivity of 30 μV mm−1 and bandpass filters of 0.3–70 Hz. The subdural electrodes were made of 316 stainless steel embedded in implant-grade silicon sheets. The electrode positions were confirmed by fluoroscopy during the surgical procedure. Attempts were made to record from the mesial cortex in all patients and bilateral mesial temporal recordings were obtained wherever possible. In addition, recordings were made from electrodes located at the seizure focus if this was suspected to be at a location other than the mesial temporal area. The authors found that under sufficiently rigorous conditions, both sevoflurane and isoflurane can provoke interictal spike activity at near burst-suppression doses (i.e. 1.5 MAC values of inhalational anaesthetics). The results of this study suggest that the capacity to modulate neuroexcitability is a dose-dependent feature of volatile anaesthetics that is manifested most prominently at higher doses (> 1.5 MAC) and is minimal or absent at lower doses. Manninen and his colleagues found that alfentanil and fentanyl activate epileptiform activity in patients with temporal lobe epilepsy . Thus, these opioids can be used to assist in the localization of the epileptogenic focus during surgery .
Facial nerve monitoring is considered as a standard of care in surgery for acoustic neuroma . With large cerebropontine angle lesions, monitoring spontaneous or triggered EMG activity in the motor domain of cranial nerves can help identify structures and guide surgical dissection. To facilitate EMG monitoring, the intensity of neuromuscular block is optimally reduced and supplemental i.v. anaesthetic agents or opioids are used to prevent coughing or bucking.
Consciousness during some surgical procedures allows for the detection of neurological focal insults that are almost impossible to detect by instrumental monitoring.
Conscious sedation may be defined as a minimally depressed level of consciousness, whereby the patient is able to maintain an adequate airway and respond appropriately to commands. This simple method of monitoring is commonly employed during interventional neuroradiology and is well known in dentistry . Communication with the patient provides a way of monitoring cerebral function during the critical periods of embolization of arterio-venous malformations and vascular tumours, and balloon occlusion of the arterial supply of these lesions. Similar patient conditions are needed during stereotactic procedures.
Clinical monitoring is also used during carotid endarterectomy conducted under regional block. Here awake testing is sensitive to CBF reductions at 25 mL min−1 100 g−1, above levels where the EEG and SSEP are affected (15–20 mL min−1 100 g−1). Moreover, awake testing can continually assess areas of the brain at risk (e.g. speech) that are not assessed by electrophysiological methods .
Delivering optimal sedation and analgesia during an awake craniotomy is an anaesthetic challenge. Adequate sedation and analgesia for the removal of a bone flap followed by an appropriate level of consciousness for cortical speech or seizure focus mapping, while at the same time keeping the patient comfortable and immobile over long periods of time, can be difficult to achieve .
Rapid emergence from anaesthesia is important for the early assessment of postoperative neurological function. During neuroanaesthesia, there are periods of intense stimulation (e.g. laryngoscopy and intubation, head pinning, scalp incision, craniotomy) alternating with periods of minimal stimulation (e.g. preparation of the surgical site, intracranial dissection). The ideal opioid-based technique for neuroanaesthesia would allow for rapid changes in the depth of anaesthesia during surgery while providing a short recovery time regardless of the duration of surgery. These requirements seem to be easily achieved with remifentanil . A delayed emergence may be expected if the tumour is larger than 30 mm in diameter or shows mass effect . Moreover, from the study by Bruder and his colleagues we know that delayed recovery cannot be recommended as a mechanism for limiting the metabolic and haemodynamic consequences from emergence after neurosurgery . Early awakening is still the best monitoring technique to detect neurological damage after surgery that will indicate radiological or surgical examination.
Intracranial pressure monitoring, intraventricular or intraparenchymal, is extremely valuable in severe cranial injury. However, its use during surgery is limited to specific situations (e.g. large tumours with mass effect, surgery for hydrocephalus, brain oedema, etc.) in which it is important to record the pressures particularly when the patient can not be awakened after surgery. In the intraoperative setting, ICP has been recorded in the epidural, subdural and subarachnoid space at lumbar level. Guy and his colleagues used a Gaeltec ICP monitor (Medical Measurements, Hackensack, NJ, USA) inserted into the epidural space to measure ICP intraoperatively during elective supratentorial craniotomy .
Budgaard and his colleagues wanted to define a threshold for cerebral herniation so they measured subdural ICP in 178 patients subjected to elective craniotomy . This was carried out immediately before the dura was opened. A thin cannula (Venflon 22 G, 0.8 mm), connected via a water-filled polyethylene catheter to a pressure transducer, was introduced tangentially through the dura. The subdural ICP correlated with the degree of cerebral swelling or herniation after the dura had been opened. When the subdural ICP < 7 mmHg cerebral swelling or herniation after opening the dura rarely occurs; however, at ICP ≥ 10 mmHg a high probability of cerebral swelling or herniation occurs. These ICP thresholds are independent of the pathophysiology, the anaesthetic agent and the concentration of PaCO2. Intracranial pressure may be monitored through the pressure obtained in cerebrospinal fluid (CSF) at lumbar level . Patients’ anaesthetized for intracranial surgery undergo many different positions that can affect ICP. Mavrocrodatos and his colleagues demonstrated in patients with ICP < 20 mmHg that an increase in the ICP only occurred in the head-down position or when the head of the patient was rotated and/or flexed, but not when it was extended . They monitored the ICP by means of a 20-gauge malleable spinal needle inserted into the L3–L4 space; thus when indicated they could proceed to perioperative CSF drainage. Although patients with a brain tumour may have a normal ICP (< 20 mmHg) intracranial compliance is abnormal.
The insertion of a lumbar intrathecal catheter is often used for transsphenoidal hypophysectomy procedures. This catheter is used to facilitate the exposure of the hypophysis by injecting small volumes of saline intrathecally. Talke and his colleagues found that sevoflurane, 0.5 and 1.0 MAC, increased lumbar CSF pressure . Intraventricular or intraparenchymal ICP monitoring is particularly useful in the postoperative period after surgery for severe head injury, but as the need for it should be identified very early the procedure must be established either before, or immediately after, surgery has commenced in the operating theatre.
Neuroendoscopic procedures, although considered a minimally invasive procedure, may have a high risk of postoperative morbidity. During these surgical approaches, high pressures inside the endoscope, due to the force of the irrigating liquid perfusion, can occur without haemodynamic warning signs. The pressure inside the endoscope can be measured, as described elsewhere , by means of a fluid-filled catheter connected to a stopcock located in the irrigation lumen. The catheter is attached to a pressure transducer which has been zeroed at the skull base level. In this way pressure waves may be continuously displayed on the anaesthesia monitor. With this monitoring the anaesthesiologist can warn the surgeon when the pressure increases in order to stop the irrigation and allow the irrigating liquid to escape.
The duration of an ischaemic episode, as well as the density of ischaemia, has been shown to be a significant factor in the evolution of injury. Determination of the ischaemia metabolites in the brain and their evolution can help to establish the magnitude of the ischaemic insult as well as the response to therapeutic manoeuvres. This is one of the most recent and promising monitoring fields.
Microdialysis allows the detection of changes in the composition of the extracellular space. Excitatory amino acids (EAA) are important mediators of brain injuries after direct trauma, hypoxia or ischaemia. There is a rise in extracellular EAA after brain injury and surgery . Baunach and his colleagues focused their study on the relationship between PtiO2 (intraparenchymal measurement of brain tissue oxygenation) and the amount of EAA in peritumoural oedema in glioma surgery . Measurements were performed in nine patients with a high-grade glioma in the frontal or temporal lobe. Microdialysis probes were constructed according to the method of CS Robertson (Baylor College of Medicine, Houston, TX, USA). These sterile loop-type microdialysis probes have a molecular weight cut-off of 13 000 D (Daltons), an outer diameter of 1.5 mm, a 2 × 0.5 cm loop and a total length of 4.5 cm. The probes were perfused at a rate of 2 μL min−1 with sterile 0.9% NaCl solution. The microdialysis probe and tissue-PO2 catheter (Licox, GMS, Kiel, Germany) were placed in close vicinity but outside the visible tumour tissue in the peritumoural oedema. The tip was inserted to a depth of about 2 cm. Samples were collected every 10 min and analysed by high-pressure liquid chromatography starting 30 min after placement of the probe. In the majority of patients (seven out of nine) initial PtiO2 was below 10 mmHg at an inspired oxygen concentration (FiO2) of 0.45. Elevation of FiO2 to 1 lead to 2.5- to 4-fold increases in PtiO2 and 50–80% decreases of glutamate and aspartate concentrations.
In head-injured patients similar results were found in a recent study by Menzel and his colleagues . In addition to standard monitoring of ICP and cerebral perfusion pressure, they measured brain tissue PO2, PCO2, pH, and temperature continuously in 24 patients with severe head injury. Microdialysis was performed to analyse lactate and glucose concentrations. In one cohort of 12 patients, the PaO2 was increased to 441 ± 88 mmHg over a period of 6 h by raising the FiO2 from 0.35 ± 0.5% to 1 in two stages. The results were analysed and compared with the findings in a control cohort of 12 patients who received standard respiratory therapy (mean PaO2 136.4 ± 22.1 mmHg). The mean PtiO2 values increased in the patients who received oxygen up to 359 ± 39% of the baseline level during the 6 h of FiO2 enhancement, whereas the mean dialysate lactate concentrations decreased by 40% (P < 0.05). A simplistic interpretation of these data suggests that lung ventilation with 100% O2 should be considered at least for the first 6–8 h after any severe head injury, when metabolic demands on the neural energy systems are greatest. However, as Menzel and his colleagues have stated further validation of this study is needed, and it must first be shown that oxidative metabolism, with increased adenosine triphosphate (ATP) generation, increases as a result of this O2 enhancement in severe head injury .
The use of the sitting or upright position for patients undergoing posterior fossa and cervical spine surgery facilitates surgical access but presents unique physiological challenges with the potential for very serious complications. These include haemodynamic instability, venous air embolism (VAE) with the possibility of paradoxical air embolism, pneumoencephalus, quadriplegia and compressive peripheral neuropathy . Occurrence of VAE has also been described in sedated patients during spontaneous ventilation . Monitoring of VAE can be accomplished by a variety of techniques. It is generally recommended that at least three of these have to be used to ensure that VAE can be detected .
Transoesophageal echocardiography (TEE) is the most sensitive monitor to detect air in the right atrium and paradoxical air embolization to the left atrium through a patent foramen ovale. TEE is capable of detecting a single air bubble as an echo dense structure. However, TEE is not specific for VAE, fat emboli and microemboli will also be detected. Monitoring is non-continuous . Besides, it is an expensive semi-invasive device not affordable in the majority of operating theatres.
Doppler ultrasonography is the most sensitive of the generally available monitors capable of detecting intracardiac air. Commercially available Doppler systems generate and detect an ultrasonic signal (approximately 2.0–2.5 MHz), which is reflected from moving erythrocytes and cardiac structures. The reflected signal is converted into a continuously audible sound. Air is an excellent acoustic reflector and its passage through the heart is noticed by a change from the previous sound to an erratic noise . This monitor is capable of detecting 0.015 mL kg−1 of air . The probe is positioned over the right heart, usually at the third to sixth intercostal spaces to the right of the sternum: correct functioning may be verified by rapid i.v. injection of saline into a central venous cannula and the signal produced is immediately audible.
Pulmonary artery pressure
Pulmonary artery pressure is the next most sensitive VAE monitor. Entry of air into the pulmonary circulation causes an increase in pulmonary artery pressure. Unfortunately, only small quantities of air can be aspirated from the pulmonary catheter . In some instances, systemic air emboli may be due to the passage of air through the pulmonary capillaries .
Mass spectrometry or other methods to detect end-tidal nitrogen (ETN2) are extremely sensitive. It is highly specific for the nitrogen in air that gains access to the circulation. The method is expensive and, thus, not widely available. The concentration of exhaled nitrogen is usually less than 2%, which is below the threshold of some commercial mass spectrometers. With venous air embolism occurs the ETN2 immediately increases beyond this value.
End-tidal carbon dioxide
The progressive decrease in lung perfusion caused by air trapped within the pulmonary circulation leads to an increased physiological dead space, which is reflected by a decrease in end-tidal carbon dioxide (ETCO2). This decrease is not specific for venous air embolism: hyperventilation, low cardiac output, other types of emboli and chronic pulmonary disease can also decrease ETCO2.
Right atrial pressure
A central venous catheter is usually inserted during or before surgery when there is a high risk for venous air embolism. The tip of the central venous catheter is positioned close to the junction of the superior vena cava with the right atrium. The method provides a measure of intravascular volume status and can be used to confirm (but not to detect) the presence of intravascular gas in addition to providing some means for the evacuation of air. Multi-orifice catheters have been designed to enhance bubble recovery . The position of the catheter tip should be checked radiologically, by pressure wave recordings or by intravascular ECG using special catheters (a biphasic P wave indicates the appropriate position). The proper position for the right atrial catheter during craniotomy in the sitting position has been clearly defined. However, the optimal position of the right atrial catheter for other procedures, such as lumbar spine surgery in the prone position, is not known . The right atrial catheter is of limited therapeutic value, although it gives the opportunity of diminishing the intravascular air volume after it has entered the vascular system. Nevertheless, the most important manoeuvre for preventing the consequences of air embolism is eliminating the source of the venous air embolus entrance.
The classic method of monitoring for intracardiac air uses an oesophageal or praecordial stethoscope. The observer listens for a change in heart sounds to a splashing ‘mill-wheel’ murmur; detection is dependent on quite large amounts of air in the right ventricle and provides little advance warning of impending cardiovascular collapse. It is the least sensitive monitor for venous air embolism. Nevertheless, because of its non-invasive nature and mechanical simplicity, the oesophageal stethoscope should be retained as a monitoring device for the detection of air embolism .
Metabolic suppression is not the major mechanism by which anaesthetics provide neuroprotection. Perhaps the most widely studied anaesthetics have been the barbiturates, long known to be neuroprotective in focal cerebral ischaemia in numerous animal models, and the only intervention that has proved of some use in humans . Small differences in intraischaemic brain temperature critically determine the extent of neuronal injury in experimental models of global cerebral ischaemia . When ischaemia reduces oxygen supply, hypothermia remains the sine qua non for reducing demand. The importance of diligent monitoring and control of brain temperature in experimental paradigms of cerebral ischaemia and reperfusion cannot be overemphasized .
A survey conducted in 1994 indicates that a large majority of neuroanaesthesiologists use mild to moderate hypothermia during surgery for aneurysms . Preliminary results of the use of mild hypothermia for the surgery of aneurysm clipping have been encouraging . The National Institute of Health has funded a world-wide, multicentre ‘hypothermia during intracranial aneurysm surgery trial’ which has just been started by Michael Todd. Perhaps their results will establish anaesthetic standards for aneurysm surgery?
The temperature of the human brain can be measured with the use of epidural, intraventricular or intraparenchymal probes. There is a temperature gradient within the central venous system (0.4–1°C); the epidural space is cooler than the cerebrospinal fluid in the ventricular system . For practical purposes, core temperature may be used to estimate overall brain temperature during routine anaesthesia ; if a pulmonary arterial pressure catheter is in place the central blood temperature can be recorded continuously. Tympanic temperature has been proposed as the best approximation of average cerebral temperature . The temperature in the lower oesophagus will also give a reliable approximation of cerebral temperature  provided the thorax is closed and not irrigated with cold solutions.
The acutely ischaemic or traumatized brain is inordinately susceptible to the damaging influence of even modest rises in brain temperature. Available evidence is sufficiently compelling to justify the recommendation that fever should be combated assiduously in acute stroke and trauma patients, even if ‘minor’ in degree and even when delayed in onset. Ginsberg and his colleagues suggested that body temperature should be maintained in a safe normothermic range (36.7°C to 37°C) for at least the first several days after acute stroke or head injury . The correct temperature for neurosurgical patients during surgery remains to be determined. Table 2 summarizes the characteristics of the monitors described in this article and their place in clinical monitoring during neuroanaesthesia.
1 Dearden NM, Midgley S. Technical considerations in continuous jugular venous oxygen saturation measurement. Acta Neurochir (Wien)
1993; 59 (Suppl.): 91–97.
2 Matta BF, Lam AM, Mayberg TS, Shapira Y, Winn RH. A critique of the intraoperative use of jugular venous bulb catheters during neurosurgical procedures. Anesth Analg
1994; 79: 745–750.
3 Matta BF, Lam AM, Mayberg TS. The influence of arterial oxygenation on cerebral venous oxygen saturation during hyperventilation. Can J Anaesth
1994; 41: 1041–1046.
4 Taylor CL, Selman WR, Kiefer SP, Ratcheson RA. Temporary vessel occlusion during intracranial aneurysm repair. Neurosurgery
1996; 39: 893–906.
5 McCornick PW, Stewart M, Goetting MG, Balakrishnan G. Regional cerebrovascular oxygen saturation measured by optical spectroscopy in humans. Stroke
1991; 22: 596–602.
6 Owen-Reeve H, Smith M, Elwell CE, Goldstone JC. Near infrared spectroscopy. Br J Anaesth
1999; 82: 418–426.
7 Schwarz G, Litscher G, Kleinart R, Jobstmann R. Cerebral oximetry in dead subjects. J Neurosurg Anesthesiol
1996; 8: 189–193.
8 Luer MS, Pharm D, Dujovny M, Slavin KV, Hernandez-Avila G, Ausman JI. Regional cerebral oxygen saturation during intra-arterial papaverine therapy for vasospasm: case report. Neurosurgery
1995; 36: 1033–1036.
9 Saito S, Miyoshi S, Yoshikawa D et al
. Regional cerebral oxygen saturation during electroconvulsive therapy: monitoring by near infrared spectroscopy. Anesth Analg
1996; 83: 726–730.
10 Dings J, Meixensberger J, Jäger A, Roosen K. Clinical experience with 118 brain tissue oxygen partial pressure catheter probes. Neurosurgery
1998; 43: 1082–1095.
11 Doppenberg EMR, Watson JC, Broaddus WC, Holloway KL, Young HF, Bullock R. Intraoperative monitoring of substrate delivery during aneurysm and hematoma surgery: initial experience in 16 patients. J Neurosurg
1997; 87: 809–816.
12 Hoffman WE, Charbel FT, Edelman G, Ausman JI. Brain tissue gases and pH during arteriovenous malformation resection. Neurosurgery
1997; 40: 294–301.
13 Gupta AK, Hutchinson PJ, Al-Rawi P et al
. Measuring brain tissue oxygenation compared with jugular venous oxygen saturation for monitoring cerebral oxygenation after traumatic brain injury. Anesth Analg
1999; 88: 549–553.
14 Valadka AB, Gopinath SP, Contant CF, Uzura M, Robertson CS. Relationship of brain tissue PO2
to outcome after severe head injury. Crit Care Med
1998; 26: 1576–1581.
15 Ostapkovich ND, Baker KZ, Fogarty-Mack P, Sisti MB, Young WL. Cerebral blood flow and CO2
reactivity is similar during remifentanil/N2
O and fentanyl/N2
O anesthesia. Anesthesiology
1998; 89: 358–363.
16 Wietasch GJK, Mielck F, Scholz M, von Spiegel T, Stephan H, Hoeft A. Bedside assessment of cerebral blood flow by double indicator dilution technique. Anesthesiology
2000; 92: 367–375.
17 Alkire MT, Pomfrett CJD, Haier RJ et al
. Functional brain imaging during anaesthesia in humans: effects of halothane on global and regional cerebral glucose metabolism. Anesthesiology
1999; 90: 701–709.
19 Romner B, Bellner J, Kongstad P, Sjöholm H. Elevated transcranial Doppler flow velocities after severe head injury: cerebral vasospasm or hyperemia? J Neurosurg
1996; 85: 90–97.
20 Piechnick SK, Yang X, Czosnyka M et al
. The continuous assessment of cerebrovascular reactivity: a validation of the method in healthy volunteers. Anesth Analg
1999; 89: 944–949.
21 Gupta AK, Menon DK, Czosnyka M, Smielewski P, Jones G. Thresholds for hypoxic cerebral vasodilation in volunteers. Anesth Analg
1997; 85: 817–820.
22 Matta BF, Mayberg TS, Lam AM. Direct cerebrovasodilatory effects of halothane, isoflurane, and desflurane during propofol-induced isoelectric electroencephalogram in humans. Anesthesiology
1995; 83: 980–985.
23 Tuman KJ. Anaesthesia for surgery of the carotid artery. 50th Annual Refresher Course Lectures and Clinical Update Program
. Park Ridge, Ill: Am Soc Anesthesiologists 1999; 557–564.
24 Valero R, Fàbregas N, Carrero E, Caral L, Zavala E, Ferrer E. Episodes of intermittent high peak pressures inside the endoscope, during surgical neuroendoscopies, occur simultaneously with transcranial Doppler wave pattern of ‘near intracranial circulatory arrest’ (Abstract). Eur J Anaesthesiol
2000; 17 (Suppl.): 94–94.
25 Ducroq X, Hassler W, Moritzke K et al
. Consensus opinion on diagnosis of cerebral circulatory arrest using Doppler-sonography. Task Force Group on cerebral death of the Neurosonology Research Group of the World Federation of Neurology. J Neurol Sci
1998; 159: 145–150.
26 Anonymous. Assessment: Intraoperative neurophysiology. Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology
1990; 40: 1644–1644.
27 Nuwer MR, Dawson EG, Carlson LG, Kanim LE, Sherman JE. Somatosensory evoked potential spinal cord monitoring reduces neurologic deficits after scoliosis surgery: results of a large multicenter survey. Electroencephalograph Clin Neurophysiol
1995; 96: 6–11.
28 Sloan TB. Evoked potential monitoring. Int Anesthesiol Clin
1996; 34: 109–136.
29 Lopez JR. Intraoperative neurophysiologic monitoring. Int Anesthesiol Clin
1996; 34: 33–54.
30 Schramm J, Koht A, Schmidt G, Pechstein U, Taniguchi M, Fahlbuah R. Surgical and electrophysiological observations during clipping of 134 aneurysms with evoked potential monitoring. Neurosurgery
1990; 26: 61–70.
31 van Dongen EP, Beek HT, Schepens MA et al
. Effect of nitrous oxide on myogenic motor potentials evoked by a six pulse train of transcranial electrical stimuli: a possible monitor for aortic surgery. Br J Anaesth
1999; 82: 323–328.
32 Kalkman CJ, Ubags LH. Motor-evoked potential monitoring. Curr Opin Anesthesiol
1997; 10: 327–332.
33 Thornton C, Sharpe RM. Evoked responses in anaesthesia. Br J Anaesth
1998; 81: 771–781.
34 Matta BF, Heath KJ, Tipping K, Summors AC. Direct cerebral vasodilatory effects of sevoflurane and isoflurane. Anesthesiology
1999; 91: 677–680.
35 Doyle PW, Matta BF. Burst suppression of isoelectric encephalogram for cerebral protection: evidence from metabolic suppression studies. Br J Anaesth
1999; 83: 580–584.
36 Roach GW, Newman MF, Murkin JM et al
. for the multicenter Study of Perioperative Ischaemia (McSPI) Research Group: Ineffectiveness of burst suppression therapy in mitigating perioperative cerebrovascular dysfunction. Anesthesiology
1999; 90: 1255–1264.
37 Drummond JC, Cole DJ, Patel PM, Reynolds LW. Focal cerebral ischaemia during anaesthesia with etomidate, isoflurane or thiopental. A comparison of the extent of cerebral injury. Neurosurgery
1995; 37: 742–749.
38 Hindman BJ, Todd MM. Improving neurologic outcome after cardiac surgery (editorial). Anesthesiology
1999; 90: 1243–1247.
39 Watts AD, Herrick IA, McLachlan RS, Craen RA, Gelb AW. The effect of sevoflurane and isoflurane anaesthesia on interictal spike activity among patients with refractory epilepsy. Anesth Analg
1999; 89: 1275–1281.
40 Manninen PH, Burke SJ, Wennberg R, Lozano AM, El Beheiry H. Intraoperative localization of an epileptogenic focus with alfentanil and fentanyl. Anesth Analg
1999; 88: 1101–1106.
41 Hewitt PB. Anesthesia for epilepsy surgery. In: Oxbury J, Polkey C, Duchovny M, eds. Intractable Focal Epilepsy
. Philadelphia: W.B. Saunders, 2000: 761–770.
42 National Institutes of Health (NIH) Consensus Development Conference. [consensus Statement 9]. December, 1991.
43 Manninen PH, Chan ASH, Papworth D. Conscious sedation for interventional neuroradiology: a comparison of midazolam and propofol infusion. Can J Anaesth
1997; 44: 26–30.
44 Sloan TB. Clinical monitoring of the brain and spinal cord. In:American Society of Anesthesiologists Annual Refresher Course Lectures.
Orlando, FL, 1998; 245: 1–7.
45 Johnson KB, Egan TD. Remifentanil and propofol combination for awake craniotomy: case report with pharmacokinetic simulations. J Neurosurg Anesthesiol
1998; 10: 25–29.
46 Gesztesi Z, Mootz BL, White PF. The use of remifentanil infusion for hemodynamic control during intracranial surgery. Anesth Analg
1999; 89: 1282–1287.
47 Schubert A, Mascha EJ, Bloomfield EL et al
. Effect of cranial surgery and brain tumor size on emergence form anaesthesia. Anesthesiology
1996; 85: 513–521.
48 Bruder N, Stordeur JM, Ravussin P et al
. Metabolic and haemodynamic changes during recovery and tracheal extubation in neurosurgical patients: immediate versus delayed recovery. Anesth Analg
1999; 89: 674–678.
49 Guy J, Bradley JG, Hindman BJ et al
. Comparison of remifentanil and fentanyl in patients undergoing craniotomy for supratentorial space-occupying lesions: immediate versus delayed recovery. Anesthesiology
1997; 86: 514–524.
50 Bundgaard H, Landsfeldt U, Cold GE. Subdural monitoring of ICP during craniotomy: thresholds of cerebral swelling/herniation. Acta Neurochir
1998; 71 (Suppl.): 276–278.
51 Jacot A, Bissonnette B, Favre JB, Ravussin P. Effet de l′ ondansétron sur la pression intracrânienne et la pression de perfusion cérébrale chez le patient neurochirurgical. Ann Fr Anesth Réanim
1998; 17: 220–226.
52 Mavrocordatos P, Bissonnette B, Ravussin P. Effects of neck position and head elevation on intracranial pressure in anaesthetized neurosurgical patients. Preliminary results. J Neurosurg Anesthesiol
2000; 12: 10–14.
53 Talke P, Caldwell JE, Richardson CA. Sevoflurane increases lumbar cerebrospinal fluid pressure in normocapnic patients undergoing transsphenoidal hypophysectomy. Anesthesiology
1999; 91: 127–130.
54 Fàbregas N, López A, Valero R, Carrero E, Caral L, Ferrer E. Anaesthetic management of surgical neuroendoscopies. Usefulness of monitoring the pressure inside the neuroendoscope. J Neurosurg Anesthesiol
2000; 12: 21–28.
55 Hillered L, Persson L, Ponten U, Ungerstedt U. Neurometabolic monitoring of the ischaemic human brain using microdialysis. Acta Neurochir (Wien)
1990; 102: 91–97.
56 Baunach S, Meixensbergber J, Gerlach M, Roosen K. Intraoperative microdialysis and tissue-pO2
measurement in human glioma. Acta Neurochir (Wien)
1998; 71 (Suppl.): 241–243.
57 Menzel M, Doppenberg EMR, Zauner A, Soukup J, Reinert MM, Bullock R. Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury. J Neurosurg
1999; 91: 1–10.
58 Porter JM, Pidgeon C, Cunningham AJ. The sitting position in neurosurgery: a critical appraisal. Br J Anaesth
1999; 82: 117–128.
59 Suarez S, Ornaque I, Fàbregas N, Valero R, Carrero E. Venous air embolism during Parkinson surgery in patients with spontaneous ventilation. Anesth Analg
1999; 88: 793–794.
60 Black S. Venous air embolism. Problems Anaesthesia
1997; 9: 113–124.
61 Gildenberg PL, O'Brien P, Brett WJ, Frost EA. The efficacy of Doppler monitoring for the detection of venous air embolism. J Neurosurg
1981; 54: 75–78.
62 Tommasino C, Rizzardi R, Beretta L, Venturino M, Piccoli S. Cerebral ischaemia after venous air embolism in the absence of intracardiac defects (case report). J Neurosurg Anesthesiol
1996; 8: 30–34.
63 Bunegin L, Albin MS, Hesel PE, Hoffman A, Hung TK. Positioning the right atrial catheter. A model for re-appraisal. Anesthesiology
1981; 55: 343–348.
64 Zaidan JR, Klochany A, Martin WM, Ziegler JS, Harless DM, Andrews RB. Effect of thiopental on neurologic outcome following coronary artery bypass grafting. Anesthesiology
1991; 74: 406–411.
65 Busto R, Deitrich WD, Globus MY-T, Valdes I, Scheinberg P, Ginsberg MD. Small differences in intraischaemic brain temperature critically determine then extent of ischaemic neuronal injury. J Cereb Blood Flow Metab
1987; 7: 729–738.
66 Bhardwaj A, Kirsh JR. Anaesthetic agents and hypothermia in ischaemic brain protection (editorial). Anaesthesiology
1998; 89: 289–290.
67 Craen RA, Gelb AW, Eliasziw M, Lock P. Current anaesthetic practices and use of brain protective therapies for cerebral aneurysm surgery at 41 North American Centres. J Neurosurg Anesthesiol
1994; 6: 303–303.
68 Hindman BJ, Todd MM, Gelb AW et al
. Mild hypothermia as a protective therapy during intracranial aneurysm surgery: a randomized prospective pilot trial. Neurosurgery
1999; 44: 23–33.
69 Mellergård P. Monitoring of rectal, epidural, and intraventricular temperature in neurosurgical patients. Acta Neurochir (Wien)
1994; 60 (Suppl.): 485–487.
70 Spiss K, Illievich UM. Mild and moderate hypothermia for neuroprotection. Eur J Anesthesiol
2000; 17 (Suppl.): 22–24.
71 Mariak Z, Lewko J, Luczaj J, Polocki B, White MD. The relationship between directly measured human cerebral and tympanic temperatures during changes in brain temperatures. Eur J Appl Physiol
1994; 69: 545–549.
72 Ginsberg MD, Busto RBS. Combating hyperthermia in acute stroke. A significant clinical concern. Stroke
1998; 29: 529–534.
Keywords:© 2001 European Academy of Anaesthesiology
SURGICAL PROCEDURES, OPERATIVE, monitoring, intraoperative; MONITORING, PHYSIOLOGICAL, monitoring, intraoperative