Atlanta, Georgia, October 20, 1995.

James C. Eisenach, MD, Editor.

The Society of Neurosurgical Anesthesia and Critical Care (SNACC) held its 23rd annual meeting on October 20, 1995, at the Atlanta Hilton Towers, Atlanta, Georgia. The program was prepared and organized by Dr. Arthur Lam.

The meeting began with the invited presentations by Dr. Rune Aaslid, Research Professor of Neurological Surgery, University of Washington, Seattle, and by Dr. Lawrence Litt, Professor of Anesthesiology, University of California at San Francisco.

Dr. Aaslid: Transcranial Doppler Ultrasonography for Monitoring of lntracranial Pressure and Cerebrovascular Tone. Dr. Aaslid, the developer of transcranial doppler (TCD) ultrasonography, discussed some of the more recent applications of TCD monitoring. The use of TCD to monitor middle cerebral arterial flow (Vmca) as a marker of cerebral blood flow (CBF) and for detection of emboli has been well established. TCD also can be used for the measurement of dynamic autoregulation. Dynamic autoregulation is determined by the measurement of Vmca immediately before and after a transient decrease in mean arterial pressure (MAP). This is accompanied by a reduction in Vmca. Flow velocity, however, recovers more rapidly than does MAP, suggesting that cerebral autoregulatory response is rapid. Previous work by Aaslid has shown that the rate of this autoregulatory response is more rapid when the cerebrovascular tone is high (e.g., during hyperventilation). Therefore, relative cerebrovascular tone can be inferred from a measurement of the rate of the autoregulatory response.

Dr. Litt: Functional Magnetic Resonance Imaging of the Brain. Recent advances in magnetic resonance imaging (MRI) have provided investigators with the ability to obtain information about the function of specific structures in the brain. Dr. Litt explained that blood flow in a specific brain structure (e.g., visual cortex) increases if the metabolic activity of that structures increases. This increase in flow, which is slightly greater than required, results in an increase in the oxygen saturation of hemoglobin, and signal intensity is increased. Of relevance is that functional magnetic resonance imaging can be used to map eloquent regions of the brain in patients undergoing temporal lobectomy for intractable epilepsy. Given that it is noninvasive, does not require the administration of isotopes, and can be performed repeatedly in individuals and that images can be obtained almost in real time, the impact of this technology on our understanding of the functioning of the human brain is large.

The problem of postoperative hyperperfusion syndromes in the patient undergoing postcarotid endarterectomy and postarteriovenous malformation resection was addressed by Dr. William Lanier and Dr. William Young.

Dr. Lanier: Carotid Endarterectomy. In patients with chronic carotid stenosis, CBF to the ipsilateral hemisphere is maintained by collateral flow. When the stenosis is relieved, an increase in CBF occurs. In the majority of patients, this increase in flow is transient and does not result in any symptoms. In a minority (2-15%), hyperemia will become manifest clinically. The symptoms include headache, lateralizing epileptiform discharges to frank seizures, and rarely, cerebral hemorrhage. The latter complication occurs in only 0.7% of patients. The patients at greatest risk are those with severe bilateral carotid stenosis, severe unilateral stenosis with poor collateral flow, or chronic symptoms of cerebral hypoperfusion.

Dr. Young: Arteriovenous Malformation. Resection of arteriovenous malformation (AVMs) often is accompanied by an increase in CBF. Traditionally, this swelling has been attributed to perfusion pressure breakthrough. According to this theory, the vessels in brain tissue that surrounds AVMs are maximally vasodilated and "paralyzed." Dr. Young indicated that a number of lines of evidence suggest this simplistic concept needs revision. For instance, vessels in brain tissue surrounding an AVM have preserved pressure autoregulation and reactivity to changes in PaCO2. Furthermore, the surrounding vessels have been shown to be responsive to vasodilating agents (e.g., papaverine and acetozolamide). This suggests that these vessels are far from being "paralyzed."

A brief introduction to the Internet and the world-wide-web was provided by Dr. Ira Rampil. Dr. Keith Ruskin discussed anesthesiology-related sources on the Internet. He drew attention to the web page "Gasnet," which he maintains. The universal resource locator for this page is

The last of the formal presentations was a debate, "The New Inhalational Anesthetics Desflurane and Sevoflurane Are Valuable Additions to the Practice of Neuroanesthesia," between Dr. Kristy Baker and Dr. Rene Tempelhoff. After a spirited discussion, both speakers agreed that successful outcomes in neuroanesthetic practice depend more on the skill of the individual practitioner than on anesthetic drugs used.

Each year, SNACC recognizes research performed by new investigators in the field of neurosciences. This year, the New Investigator Award was presented by Dr. Patricia Petrozza to Dr. Kiichiro Taga, from Niigata University, in Japan. Dr. Taga was a Neuroanesthesia Research Fellow in the Neuroanesthesia Research Laboratories of Dr. John Drummond and Dr. Piyush Patel, of the University of California at San Diego. Dr. Taga's studies indicate that preischemic cortical spreading depression (CSD) reduce subsequent ischemic injury. Dr. Taga concluded that prior CSD preconditions the brain and induces ischemic tolerance.

Crowder and colleagues measured core body, jugular bulb, and brain surface temperature and found that the latter was consistently lower than core temperature (on average, 1 degree C less). Cooling of the patients can be accomplished consistently with the new Polar Bair device (Theard et al.). Rewarming, however, occurs at a slower rate, and many patients remain hypothermic at the conclusion of surgery (Seifert et al.). In an attempt to increase the rate at which rewarming occurs, Baker and colleagues administered nitroprusside to produce cutaneous vasodilation; this approach was unsuccessful. Although rewarming is often incomplete, recovery from anesthesia and the time of extubation of patients was not delayed by intraoperative induction of hypothermia (Young et al.).

Significant complications attributable to the use of hypothermia were not reported. Sitzwohl and colleagues reported that moderate hypothermia reduced CBF velocity but preserved the carbon dioxide responsiveness (under alpha-stat management) of the cerebral circulation. Baumann and colleagues found that, in the absence of surgical intervention, induced hypothermia to a temperature of 32 degrees C did not significantly affect either the coagulation or the fibrinolytic system. In humans, hypothermia did not lead to an increased incidence of wound infection (Baker et al.).

Warner et al. compared the effect of two doses of pentobarbital (a burst suppression dose and a lower dose that resulted in mild attenuation of the electroencephalogram (EEG) on brain injury in rats subjected to focal ischemia. Low-dose pentobarbital reduced injury, but increasing the dose did not decrease injury further. Amadeu and colleagues evaluated the effect of etomidate on transmission damage in brain slices subjected to anoxia. They found that etomidate did not reduce injury. Similarly, Sano et al. showed that cerebral metabolic rate (CMR) suppression, either with isoflurane alone or with isoflurane in combination with thiopental, did not reduce ischemic injury. Collectively, these investigations add to the growing body of evidence that suggests that CMR reduction per se is not the major determinant of pharmacologic protection.

The role of nitric oxide received considerable attention. In an interesting study, Pelligrino et al. showed that oophorectomy severely reduced endothelial nitric oxide synthase (NOS) activity and blood flow during incomplete forebrain ischemia. Estrogen supplementation decreased the severity of ischemia. The demonstration by Farrell et al. that hypoxia-induced flow increases might be mediated by increases in nitric oxide is consistent with this suggestion. By contrast, in dogs subjected to global ischemia, reduction of nitric oxide synthesis with L-NAME or augmentation with L-arginine did not influence neuronal outcome (Kirsch et al.). This study questions the relevance of nitric oxide in the pathophysiology of global cerebral ischemia. Koenig et al. demonstrated previously that inhibition of neuronal NOS reduced ischemic injury. However, these authors were not able to reproduce the favorable results they had obtained with neuronal NOS inhibition in diabetic rats.

A considerable amount of data now suggest that hyperglycemia aggravates ischemic brain injury. Sieber et al. showed that, in diabetic dogs in whom blood glucose was poorly controlled, ischemic injury and mortality were increased greatly. The detrimental effect of hyperglycemia was demonstrated further by Wass and colleagues. Corticosteroid-induced hyperglycemia augmented neurologic injury in rats subjected to forebrain ischemia.

Hennes et al. demonstrated that tirilazad improved neurologic outcome in newborn pigs subjected to cerebral asphyxia. Another investigation by Davis et al. showed that desferroxime improved electrophysiologic and biochemical recovery after global ischemia in dogs. Cerebral edema develops rapidly after the onset of ischemia. Maktabi et al. showed that antagonism of vasopressin receptors augmented edema formation.

The use of cerebral oximetry (Invos 3100 Cerebral Oximeter) to detect changes in cerebral oxygen saturation in patients was evaluated by four groups of investigators. Shah et al. demonstrated that, in normal volunteers made hypoxic, cerebral oximetry correlates well with system oxygen saturation measured by pulse oximetry. However, in patients undergoing carotid endarterectomy, cerebral oximetry did not distinguish between patients who experienced EEG and somatosensory evoked potential changes on carotid cross-clamping from those without such changes (Gogarten et al. and Duffy et al.). By contrast, Plyushcheva et al. found that changes in cerebral oximetry during carotid clamping correlated well with EEG changes and Vmca changes. In the discussion that followed, the general consensus was that cerebral oximetry shows promise, but its utility in the operating room setting needs to be investigated further. In patients undergoing craniotomy, Hoffman et al. demonstrated the feasibility of directly measuring tissue PO2, PCO2, and pH using a commercially available electrode.

The monitoring of the motor function of the spinal cord is receiving more attention. Kalkman et al. monitored motor evoked potentials (MEPs) in response to transcranial electrical stimulation in patients undergoing repair of thoracoabdominal aneurysms of the aorta. They found that MEP monitoring provides the anesthesiologist with almost immediate feedback about spinal motor neuron function. However, MEPs are sensitive to anesthetic agents. Ghaly et al. demonstrated in monkeys that the amplitude of the MEP decreased significantly with the administration of nitrous oxide. Similarly, Sloan demonstrated that the administration of isoflurane in concentrations greater than 0.7% resulted in a significant decrease in amplitude. These studies suggest that MEP monitoring is useful in certain clinical situations but that the anesthetic technique must be tailored to obtain meaningful information.

The bispectral index (BSI; Aspect Medical Systems) as an indicator of the depth of sedation induced by isoflurane was assessed by Bloom et al. These investigators demonstrated that BSI had the best correlation with the degree of sedation, whereas median frequency and spectral edge did not correlate with sedation. However, in human volunteers made hypoxic, neither the BSI nor any other EEG parameter was useful in detecting moderate hypoxemia (Shah et al.). The utility of the BSI remains to be defined.

Pieron and colleagues evaluated the accuracy of several pharmacokinetic models in predicting blood propofol concentrations. Their data suggest that the three-compartment model of Gepts with central elimination provided the best agreement between expected and measured blood propofol levels. Levati et al. suggested that infants undergoing MRI scanning require a higher dose of propofol to prevent movement than do older children. The data of Cheng et al. and McFarlane et al. support the contention that propofol is a proconvulsant.

The effect of the volatile anesthetics isoflurane and sevoflurane on nicotinic acetylcholine receptors was studied by Scheller and colleagues. Both anesthetic agents significantly reduced the current by applied acetylcholine. Lu et al. demonstrated in rats that sevoflurane anesthesia resulted in a greater increase in CBF and intracranial pressure than did desflurane.

Synthetic opioids commonly are used in neurosurgical patients. In a provocative investigation, Sinz et al. demonstrated that high-dose opioid administration (titrated to seizure activity) resulted in neuronal death. The administration of naloxone or the anticonvulsants midazolam and phenytoin reduced this injury significantly.

The physiology of cerebral vascular tone was investigated by McPherson and Koehler. They demonstrated that, in the dog, ventriculocisternal perfusion of the alpha2agonist dexmedetomidine reduced resting CBF and the increase in CBF produced by hypoxia. In an in vitro study, Wendling and colleagues determined that the administration of phencyclidine (an NMDA antagonist) resulted in the dilation of preconstricted bovine middle cerebral artery. The authors concluded that NMDA antagonists dilate cerebral arteries via calcium entry blockade.

Nemoto and colleagues demonstrated that subarachnoid hemorrhage results in localized cortical hyperemia. However, the trend was toward global cerebral hypoperfusion. This hypoperfusion and the subsequent neuronal injury can be reduced by hemodilution produced with diaspirin-linked hemoglobin (Cole et al.).

Young and colleagues demonstrated that the vessels in the normal brain parenchyma that surrounds an AVM can dilate in response to papaverine infusion. These data are consistent with the premise that, in hypoperfused brain that surrounds AVMs, the vessels are not "paralyzed." Matta et al. monitored Vmca during AVM resection and found that Vmca decreased ipsilateral to the AVM as the AVM was resected.

Perkins and colleagues presented a retrospective review of 1,769 patients from the Mayo Clinic who underwent carotid endarterectomy between 1982 and 1993. The overall stroke rate was 2.5%, with the majority of strokes occurring in patients who were neurologically unstable. Two-thirds of the strokes occurred in the postoperative period and, of these, most were thromboembolic in origin. Doblar et al., by monitoring Vmca, demonstrated that emboli can be detected in all patients undergoing angioplasty of the carotid artery.

The issue of complications related to anesthetic management of neurosurgical patients was addressed by several investigators. Black et al. prospectively evaluated the incidence of complications related to three-quarter prone position in 34 patients. Minor complications, such as skin breakdown and shoulder pain, were noted in 18% of patients. Complications related to endotracheal intubation included vocal cord paralysis in 0.5% of patients (Kimovec et al.). In a preliminary investigation, Farrell and colleagues evaluated C-spine motion during laryngoscopy in normal patients. They showed that about 10 degrees of extension occurred at the occiput and C1. Minimal flexion was evident in the lower cervical spine segments.

The number of abstracts at this meeting was the largest ever presented at SNACC. Judging from the quality and scope of the abstracts, it is apparent that the SNACC annual meeting is becoming an important forum for presentation of scientific work by investigators. The abstracts of the meeting have been published in the Journal of Neurosurgical Anesthesia and Critical Care (1995; 7:300-24), the official journal of SNACC.

Piyush Patel, MD, F.R.C.P.C., Assistant Professor of Anesthesiology, University of California, San Diego, Staff Anesthesiologist, VA Medical Center, San Diego, 3350 La Jolla Village Drive, San Diego, California 92161.