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Year : 2009  |  Volume : 53  |  Issue : 4  |  Page : 395-398 Table of Contents     

What is New about Neuroanaesthesia ?

Professor, Department of Neuro anaesthesia, National Institute of Mental Health and Neurosciences, Bangalore 560 029, India

Date of Web Publication3-Mar-2010

Correspondence Address:
G S Umamaheswara Rao
Professor, Department of Neuro anaesthesia, National Institute of Mental Health and Neurosciences, Bangalore 560 029
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Source of Support: None, Conflict of Interest: None

PMID: 20640199

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How to cite this article:
Umamaheswara Rao G S. What is New about Neuroanaesthesia ?. Indian J Anaesth 2009;53:395-8

How to cite this URL:
Umamaheswara Rao G S. What is New about Neuroanaesthesia ?. Indian J Anaesth [serial online] 2009 [cited 2021 Mar 7];53:395-8. Available from: https://www.ijaweb.org/text.asp?2009/53/4/395/60308

When Dr. John W. Michenfelder coined the term "Neuroanaesthesia" in his pioneering review published in 1969 [1] , he would have least believed where the specialty has headed for in the past 40 years. From a service that provided anaesthesia to patients undergoingneurosurgery, it evolved to a subspecialtythat combines the rapidly advance ing basic and clinical neuroscience knowledge with the knowledge of anaesthesiato improve the outcomes ofneurological patients. The speciality also has been able to contribute to the understanding of some of the basic phenomena in neurosciences. Seminal changes have occurred in the concepts in many clinical and research arenas as discussed below:

Intraoperative Concerns during Craniotomy

Intraoperative concerns during craniotomy generally revolve around intracranial pressure (ICP) reduction and protection against inadvertent cerebral ischemia Maintenance of optimal systemic physiology still remains the mainstay to achieve both the goals. Mannitol and hyperventilation have been the most commonly usedtools for intraoperative ICP reduction. Hypertonic saline has emerged as amore physiological alternative to mannitol. But, the limited data available has not convincingly proved that it offers any advantage over mannitol for operative conditions of the brain during craniotomy [2] . With regards to hyperventilation, a recentstudy in patients undergoing surgery for supratentorial tumors has shown thatmoderate hyperventilation to a PaCO2 of 32-35 mmHg effects a significant change in subdural ICP and the surgeon's assessment ofbrain relaxation [3] . Whether such hyperventila­tion raises the same concerns of cerebral ischemiaas in traumatic brain injury (TBI), remains to be evaluated.

Anaesthetics have been relied upon for intraoperative cerebral protection. Controversy continues regarding the superiority of one agent over others [4] . Inhalational agents have been claimed to offer more predictable protec­tion than intravenous agents. Giventhe Experimental evidence that cerebral vascular occlusion caused under hal­othane anaesthesia produced smaller infarct volumes than under awake state raises the pons ibilitythat it is the anaesthetic state rather than the individual agentthat offers protection. Apart from their effects on cerebral metabo­lism, anaesthetics seem to offerprotection through othermechanisms such as ischemic preconditioning.

Functional Neurosurgery and Awake Craniotomies

Awake craniotomy has become an option to preserve function during surgery inthe proximity of eloquent areas of brain (speech area, motor area). Providing acaim and relaxed patient without the risk of airway obstruc­tion is achallenge. Monitored anaesthesia care and asleep-awake-asleep techniques have been used with success. [5],[6]

Minimally Invasive Neurosurgery

Endoscopic neurosurgery with its advantages of minimal invasion and clear depiction of the structures is becomingmore common [7] . Apart from surgical complications, of which vascular injury is the commonest, acute bradycardia and other arrhytlunias including ventricularfibr - illation have been documented [8],[9] during neuroendoscopy. Irrigation of the scope athigh flows has been shown to increase the ICP to levels causingtransient intracranial circulatory arrest and postoperative neurological complications [10] .

Interventional Neuroradiology

En dovascular treatment with cyanoacrylate glues, Onyx liquid embolic system and detachable coils is rapidly becoming a routine choice for the management of cerebral aneurysms. Intra-arterialpapaverine and nimodipine are being used in the treatment of cerebral vasospasm. General anaesthesia is preferred for these procedures. Laryn­geal mask airway has been used as an alternative to endotracheal tube. Simple sedation, though used as an alternative to general anaesthesia, may pose the problems of airway obstruction and undesirable movement of the patient at crucial steps during the procedure [11] . Anaesthesiologists providing care during endovascular procedure may also have to deal with the haemorrhagic and ischemic cerebral complications that might occur during the procedure.

Traumatic Brain injury

Traditionally, all efforts have been focused on optimising ICP in TBI. While there is some soundness in this approach, the need to look beyond ICPhas been appreciated recently. Cerebral perfusion pressure (CPP)-based management is a step in this direction. Aftera great deal of debate on the appropriate levelof CPP [12] , it is recog­nizedthat "one size does not fit all," and CPP should be individually optimized to maximize the cerebral oxygen­ation and avoid anaerobic metabolism [13] . This calls for direct cerebral oxygen tension and cerebral metabolite monitoring. Technology required forthis purpose is at present successful at experimental level and may soon be available freely for routine clinical use.

Cerebral Ischemia

From cumbersome technologies suited only for experimental conditions, practicalmethods for bedside as­sessment ofcerebral blood flow have been developed. With all its limitations, transcranial Doppler (TCD) remains an acceptable tool which is usefulfor repeated measurements. Its value has been established in subarachnoid haemorrhage, and'IBI. Monitoring jugular venous oxygen saturation has provided insights into practical methods of optimizing global cerebral oxygenation, though it fails to provide regional information. Positron emission tomog­raphy (PET) and single photon emission computed tomography (SPELT) promise to provide deeper insights into ischemic mechanisms in future.

On a therapeutic front, management ofcerebralischemiastill remains farfrom satisfactory Oncethe ischemic is established, very few interventions have been proven to be of unequivocal benefIt. Important among them is the emergency thrombolyis with rTPAin stroke [14] . Of some limited value are brain tissue 02 (PbtO2) guided manage­ment in TBI [15] and hypertensive therapy in cerebral vasospasm [16] . 'Therapies based on single specific molecular mechanisms in the ischemic cascade have been uniformly unsuccessful.

Benefits and Controversies beyond Neurosurgery

Depth of Anaesthesia: Knowledge of cerebral electrophysiology has prompted the development of moni­tors of depth of anaesthesia such as bispectralindex (BIS) [17] , and spectralentropy [18] . Though questions have been raised on the consistency of their performance, and arecent study found no difference between BIS and end tidal anaesthetic agent concentration monitoring in preventing awareness during anaesthesia [19] , for the moment, they have brought in some measure of objectivity in the quantification of the depth of hypnosis.

Mechanisms ofAnaestheticAction: Functionalstudies through magnetic resonance imaging (MRI) and regional CBF/metabolism studies through PET open newvistas in under tandingthe mechanisms ofanaesthetic action [20]

Anaesthetics, Neurogenesis and Neurological Dysfunction : Anaesthetics have apotentialto cause neu­rological dysfunction, which may take the formofpostoperativeneurocognitive dysfunction in the elderly, learning disabilities of the neonates exposed to anaesthetics in utero or early after birth, and precipitation or exacerbation of Alzheimer's in susceptible individuals [21] . Majority of this information comes from rodent experiments, the clinical relevance of which remains largely unexplored. There are a few clinical publications which are either retrnspective analyses or case-control studies. The drugs that have been predominantly implicated in the causation ofneurologi­cal dysfunction are bezodiazepines and ketamine, though evidence exists with other agents also including barbitu­rates, propofol, halothane, isoflurane, and sevoflurane.

The mechanism of anaesthetic-induced neurotoxicity remains unexplained. During normal CNS develop­ment, neurons are produced in excess and as much as 50%-70% of these neurons and pro genitor cells undergo apoptosis [22] . Disruption of this physiological cell death mechanism seems to lead to intrauterine malformation of the brain and premature death of the embryo [23] . General anaesthetics seem to inhibit the synaptic transmission medi­ated through gamma aminobutyrate (GABA)and % or N-methyld-aspartate (NMDA) receptors. Because GABA­and NMDA-mediated neuronal activity is essential for mammalian brain development, exposure to general anaesthetics could potentially interfere with normal brain maturation [24],[25],[26] .

In conclusion, neumanaesthesia has evolved from a clinical service catering to the needs of neurological patients to a scientific discipline that is also exploring the basics of nervous system with benefits extending beyond anaesthesiato neumsciences in general. Paradoxically, the goal of generating large clinical evidence-base to formu­late practice guidelines remains unfulfilled. Given the voluminous clinical material available in India, it should be possible focus to undertake this task in our country!

   References Top

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2.Rozet I, Tontisirin N, Muangman S, et al. Effect of equiosmolar solutions of mannitol versus hypertonic saline on intraop­erative brainrelaxation and electrolyte balance. Anesthesiology. 2007;107:697-704.  Back to cited text no. 2      
3.Gelb AW, Craen RA, Rao GS et al. Does hyperventilation improve operating condition during supratentorial craniotomy? A multicenter randomized crossovertrial. AnesthAnalg. 2008;l06:585-94.  Back to cited text no. 3      
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8.Anandh B, Reddy KRIvl, MohantyA, Umamaheswara Rao GS. Intraoperative bradycardia and postoperative hyperkalemia in patients undergoing endoscopic third ventriculostomy. Minim Invasive Neurosurg 2002;45:154-157.  Back to cited text no. 8      
9.Handler MET, Abott R, Lee M. A near-fatal complication of endoscopic third ventriculostomy: case report. Neurosurgery 1994;35: 525-527.  Back to cited text no. 9      
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12.LingGSF,NealCJ.Maintaining cerebral perfusion pressure isaworthy goal. NeurocritCare 2005;2:75-82.  Back to cited text no. 12      
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16.U11manJS,BedersonJB.Hypertensive,hypervolemic,hemodilutionaltherapy foraneurysmalsubarachnoidhemorrhage. Is it efficacious? Yes. Crit Care Clin 1996;12:697-707.  Back to cited text no. 16      
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23.Kuida K, Zheng TS, Na S, Kuan C, Yang D, Karasuyama H, Rakic P, Flavell RA. Decreased apoptosis in the brain and premature lethalityinCPP32-deficient mice. Nature 1996;384:368-72.  Back to cited text no. 23      
24.Campagna JA, Mi11erKW, Forman SA Mechanisms of actions of inhaled anesthetics. N Engl J Med 2003;348:2110-24.  Back to cited text no. 24      
25.Varju P, Katarova Z, Madarasz E, Szabo G GABAsignaling during development: new data and old questions. Cell Tissue Res 2001 X05:239-46.  Back to cited text no. 25      
26.de LimaAD, Opitz T, Voigt T. Irreversible loss of a subpopulation of cortical interneurons in the absence of glutamatergic network activity Eur JNeurosci 2004;19:2931-43.  Back to cited text no. 26      


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