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Year : 2008  |  Volume : 52  |  Issue : 5  |  Page : 494 Table of Contents     

Current Concepts in the Intensive Care Management of Neurosurgical Patients

Professor of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, (NIMHANS), Bangalore 560 029, India

Date of Acceptance02-Aug-2008
Date of Web Publication19-Mar-2010

Correspondence Address:
G S Umamaheswara Rao
National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore
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Source of Support: None, Conflict of Interest: None

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There have been some major conceptual changes in the approach to patients with both traumatic and nontraumatic cerebral injury, in recent years. These changes have their basis in a better understanding of the cerebral pathophysi­ology and availability of some recent monitors of cerebral function. Both traditional and modern therapeutic innova­tions are being subjected to extensive investigation. Evidence-based guidelines are now available for the management of traumatic brain injury. Increasing emphasis is being laid on monitoring not only intracranial pressure and cerebral perfusion pressure, but also cerebral blood flow, oxygenation and metabolism. Alternative osmotherapeutic choices are being explored. With a large pool of high quality evidence, more focused and precise therapeutic innovations are likely to emerge in near future.

Keywords: Intensive care, Neurosurgery, Head injury, Monitoring, Guidelines, Evidence-based medicine

How to cite this article:
Umamaheswara Rao G S. Current Concepts in the Intensive Care Management of Neurosurgical Patients. Indian J Anaesth 2008;52:494

How to cite this URL:
Umamaheswara Rao G S. Current Concepts in the Intensive Care Management of Neurosurgical Patients. Indian J Anaesth [serial online] 2008 [cited 2020 Oct 31];52:494. Available from: https://www.ijaweb.org/text.asp?2008/52/5/494/60666

Rapid evolution of concepts in basic and clinical neurosciences combined with intensive care technol­ogy has helped to change the outcomes of some of the neurosurgical conditions over the past few decades. The following review is intended to cover some of the areas where recent advances have had some impact on the practices in neurological critical care. It can by no means be considered an exhaustive or comprehen­sive account of all the advances in this field.

   Management of head injury Top

Approach to a patient with traumatic brain injury (TBI) has been changing over the past decade based on the evidence emerging from neurological monitor­ing. The traditional obsession with intracranial pressure (ICP) has given way to approaches based on monitoring cerebral perfusion, oxygenation and metabolism. Evidence-based guidelines have been formulated and updated periodically.

Brain trauma foundation guidelines for the management of traumatic brain injury

The Brain Trauma Foundation (BTF) has pub­lished evidence-based guidelines on various aspects of management of head injury for the first time, in 1996 and has been revising them periodically. The latest guidelines published in 2007 [1] are summarized in [Table 1] and [Table 2]. The evidence is classified into three levels based on the strength of the relevant clinical studies. It is to be noted that much of the currently available evidence falls into Class II and III. Class I evidence is available on very few issues.

Management of cerebral perfusion pressure

Two major schools of thought exist currently re­garding management of cerebral perfusion pressure (CPP) in patients with TBI: CPP-based management as proposed by Rosner and colleagues [2] and the intrac­ranial pressure (ICP)-based management as proposed by the Lund group [3] . While the former advocates high CPP (>70 mmHg), the latter supports aggressive ICP control and modest CPP values (50 mmHg).

The basis of CPP-targeted management

Pathological studies have shown evidence of is­chemia in about 90% of patients who died of TBI [4] im­plicating ischemia as a major cause of unfavourable outcome. Ultra-early evaluation of cerebral blood flow (CBF) following head injury has documented lowest CBF values during the first six hours following injury [5] . Cerebral perfusion early after injury has been corre­lated with the long-term neurological outcome [6] . Rec­ognizing the role of cerebral ischemia in causing poor neurological outcome, some authors have suggested that CPP should be maintained above 70 mmHg. The ad­vantage claimed for such an approach is that CBF in­creases passively with CPP when CBF autoregulation is impaired. In addition, an increase in CPP causes ce­rebral vasoconstriction and reduces cerebral blood volume (CBV) and ICP if the CPP is in the autoregula­tory range.

CPP management strategy

In the original strategy of CPP-based manage­ment employed by Rosner [2] , a CPP of 70 mmHg was targeted initially, by draining CSF until the ICP de­creased to 15 mmHg. In addition, CSF was continu­ously drained whenever CPP dropped to below 70 mmHg. If CPP did not increase to 70 mmHg, vaso­pressors were added. Phenylephrine or norepineph­rine with or without dopamine was used to achieve the required mean arterial pressure (MAP). Mannitol in a dose of 0.5 - 1.0 g/kg was used whenever CPP de­creased to below 70 mmHg due to ICP elevation. If CPP was maintained at an acceptable level with high but stable ICP, efforts were made to minimize or avoid mannitol. Barbiturates, active hypothermia and decom­pressive craniectomy were not a part of the protocol. With this strategy, Rosner and colleagues demonstrated better neurological outcome compared to the other contemporary series.

The desirability of high CPP has been questioned and attempts have been made to find out the ideal CPP threshold. Some important evidence suggested that CPP values greater than 70 mmHg do not necessarily achieve the goal of avoiding hypoperfusion and hypoxia. Steiner et al [7] evaluated the response of CBF in the pericontusional tissue at 70 and 90 mmHg of CPP. Higher CPP caused only a modest increase in CBF that does not justify pharmacological elevation of CPP. A large volume of evidence suggests the critical CPP threshold to be around 60 mmHg. Using cerebral oxy­gen extraction as an index of adequacy of CBF, Stochetti et al showed that a CPP lower than 60 mmHg was associated with inadequate perfusion [8] . A signifi­cant correlation between CPP and brain tissue oxygen tension (PbtO2) was found below a CPP of 60 mmHg [9] , but not between 60 and 130 mmHg [10] .

Interventions used to achieve high CPP may pose special risks to the patients. Robertson et al [11] com­pared a CBF-targeted protocol (where the goals were a CPP higher than 70 mmHg and normocapnic ventila­tion) with an ICP-based protocol (target ICP of less than 20 mmHg and a CPP greater than 50 mmHg). There was a substantial reduction in ischemic episodes in the CBF-targeted group. This was, however, asso­ciated with a five-fold increase in the incidence of acute respiratory distress syndrome (ARDS) caused by the use of epinephrine and high dose dopamine to maintain the target CPP. Based on this evidence, the latest BTF recommendations advocate a CPP threshold of 60 mmHg and oppose aggressive attempts to maintain CPP above 70 mm Hg with fluids and pressors should be avoided.

There is growing evidence that CPP therapy guided by cerebral oxygen tension (PbtO2) monitoring may result in better outcomes than therapy with arbi­trary ICP or CPP thresholds. Meixensberger et al re­ported a series of 93 patients of severe TBI who were managed by an ICP target of less than 20 mmHg and a CPP target greater than 70 mmHg. In 53 of these pa­tients, CPP was manipulated to maintain a PbtO 2 greater than 1.3 kPa (10 mmHg). Cerebral hypoxic events were significantly reduced by PbtO 2 monitor­ing. There was also a positive trend towards better outcome in patients monitored by PbtO2 [12] . In another series with ICP and CPP targets of 20 and 60 mmHg respectively, patients who had concomitant PbtO2 monitoring had a significantly lower mortality (44% vs25%) [13] .

   Role of hypothermia in cerebral protection Top

Histopathological evidence of neurological pro­tection has been demonstrated in experimental models of cerebral ischemia, head trauma and cardiac arrest when the body temperature was maintained at 32-35 0 C temperature. Depression of cerebral metabolism alone cannot explain such protection. Alternative explanations offered are: 1. Alterations in ion homeostasis (Ca ++ , K+),2. Increased membrane stability (blood brain barrier), 3. Altered enzyme function (phospholipase, xanthine oxidase, nitric oxide synthase), 4. Alterations in neurotransmitter release or uptake (glutamate and aspar­tate) and 5. Changes in free radical production or scav­enging. Cerebral protection was consistent when mild hypothermia was induced prior to or along with the ischemic event. The role of post-ischemic hypothermia remains controversial. Not withstanding some success in small clinical series, a large multicentre randomised trial of mild hypothermia during the first 48 h after head injury, had to be discontinued as no benefit could be demonstrated[14] . But a more recent Chinese study re­ports lower mortality and better outcomes at two years after TBI; the hypothermic patients in this study had a higher incidence of pulmonary infection and thromb­ocytopenia[15] . Two human studies in cardiac arrest re­ported improved survival and cerebral function with 12 and 24 h of post-arrest hypothermia[16],[17] . In an obser­vational study of spontaneous intraoperative hypother­mia in 50 patients undergoing surgery for ruptured ce­rebral aneurysms, we found that patients who had no neurological deterioration within 24 h after surgery had a significantly lower intraoperative nasopharyngeal tem­peratures than patients who had neurological deterioration. Mean temperature for 2 h starting from the time of temporary vascular occlusion was 35.3 ± 1.5 0 C in the deteriorated patients as against 34.2 ± 1.5 0 C in the non-deteriorated patients[18] . A major randomized clini­cal trial of patients with aneurysmal subarachnoid haemorrhage did not show any improvement in the long term neurological or neuropsychological outcome of the patients subjected to intraoperative moderate hypothermia[19] .

   Monitoring in Neuro-Intensive Care Top

Accurate monitored information forms the basis of appropriate therapeutic interventions in patients with cerebral injury/insult.

Systemic monitoring

Unequivocal evidence exists at present about the role of secondary injury on the outcome of cerebral insults of varied aetiology. Systemic arterial hypoten­sion and hypoxia are the two major determinants of poor outcome in patients with brain injury [20] . In a pa­tient with cerebral injury, optimisation of cardiovascu­lar and respiratory function requires monitoring systemic parameters such as arterial blood pressure, central venous pressure, arterial oxygen saturation, blood gases, biochemical parameters, haemogram and urine output. Specific neurological monitoring optimizes the therapeutic interventions.

Neurological monitoring

Monitoring cerebral blood flow, oxygenation and metabolism using transcranial Doppler flowmetry, jugu­lar venous oximetry, direct brain tissue oxygen tension monitoring, electroencepahlography, and microdialysis, have provided insights into practical management of patients with both traumatic and nontraumatic cerebral injury.

Transcranial doppler

Transcranial Doppler (TCD) ultrasonography pro­vides indirect information on blood flow in the branches of circle of Willis. A 2 MHz pulsed ultrasound signal transmitted through the skull (usually through the tem­poral window) provides a measure of red cell flow ve­locity (FV) using the Doppler shift principle. Insonation of one of the arteries (most commonly the middle cere­bral artery (MCA) produces an arterial flow velocity waveform. Changes in FV correlate closely with changes in CBF provided the angle of insonation and the diameter of the insonated vessel remain constant. In the absence of vessel stenosis, vasospasm, change in arterial blood pressure or blood rheology, FV changes parallel changes in CBF. The pulsatility index (PI) (calculated as PI = (FVsys - FVdias)/ FVmean, where FVsys is the systolic velocity, FVdias diastolic velocity, and FVmean is the mean velocity) reflects the downstream cerebrovascular resistance.

TCD finds its major application in the diagnosis of high velocity states such as cerebral vasospasm or hyperaemia. The differentiation between the two con­ditions is important in order to target appropriate therapy. MCA flow velocities > 120 cm/s are consid­ered significantly high. If the ratio of MCA flow veloc­ity to extracranial internal carotid flow velocity (Lindegaard Ratio) is > 3, vasospasm is the likely di­agnosis.

The major limitation of TCD lies in the fact that what is measured is velocity and not flow. Secondly, the values are highly operator-dependent. Continuous monitoring is possible only by using a specialized head frame with which the probe can be fixed in a given po­sition.

Jugular venous oximetry

Continuous monitoring of jugular venous oxygen saturation (SjVO 2 ) is an indirect method of assessing cerebral oxygen utilisation. When cerebral oxygen de­mand exceeds the supply, the brain extracts greater amount of oxygen from the CBF, resulting in a decreased jugular bulb oxygen saturation. If CBF decreases to a point at which brain cannot compensate for the decreased CBF, cerebral oxygen consumption decreases and anaerobic metabolism ensues. Increased SjVO2 suggests that cerebral oxygen supply exceeds the demand.

The catheter for SjVO2 monitoring is placed into the internal jugular vein on the side of dominant cere­bral venous drainage, usually the right [21],[22] . In the pres­ence of a focal brain injury, it is controversial if the catheter should be placed on the side ipsilateral to injury or on the dominant side, if different. The dominant side of venous drainage may be determined by comparing the ICP increase caused by manual compression of each internal jugular vein separately [23] ; it may also be deter­mined by computed tomographic assessment of jugu­lar foramen size [24] , or by ultrasonography.

The normal value for SjVO2 is approximately 55- 75%. SjVO 2 monitoring provides an early diagnosis of ischemia resulting from either intracranial or systemic causes [25],[26] . SjVO 2 monitoring has been used to guide hyperventilation or barbiturate therapy, fluid manage­ment and oxygenation [27] , and to optimize cerebral per­fusion pressure [28],[29] . Used along with transcranial Dop­pler monitor, SjVO2 helps to distinguish cerebral hy­peremia from vasospasm.

The major limitation of SjVO2 is that it is a mea­sure of global cerebral oxygenation and is not particu­larly sensitive to small areas of focal ischemia. The re­sults may be affected by contamination of the jugular bulb blood flow with extracerebral blood flow during sampling. However, there are negligible (approximately 3%) chances of extracerebral contamination if the blood is sampled at a site within 2 cm of the jugular bulb and at a rate of < 2 mL/min [30] .

Brain tissue oxygenation

Continuous monitoring of brain tissue partial oxy­gen pressure (PbtiO2) is now possible through microsensors placed into brain parenchyma. PbtiO2 had been shown to have a good relation with the out­come in TBI; its ability to predict the outcome is com­parable to that of other powerful predictors such as age, GCS score, and pupil reactivity [31],[32] . PbtiO 2 and SjVO2 were compared in some studies. Kiening et al [32] showed a good correlation between different CPP val­ues and both the neuromonitoring parameters (PbtiO 2 and SjVO 2 ). Gopinath et al [34] monitored SjVO 2 and PbtiO 2 in 58 head-injured patients. The reduction in CBF on decreasing PaCO 2 from 36 to 26 torr, was better detected by SjVO 2 . PbtiO 2 also decreased, but not in all patients, and it even increased in some. In another study, when the inspired oxygen concentration was changed from 40 to 100%, PbtiO 2 reflected the modification better than SjVO2 [34] . The prognostic value of PbtiO 2 in TBI was demonstrated by Valadka et al [36] ; the length of time the PbtiO 2 remained low (less than 15 mm Hg) correlated with the outcome.


Electroencephalography (EEG) is an important tool for monitoring seizures (especially the non-con­vulsive status epilepticus) and detecting ischemic cere­bral events, arising from intracranial hypertension [37] . Certain EEG features may also be useful in predicting the survival and outcome. Metabolic suppression using intravenous anaesthetic agents for cerebral protection may be monitored using EEG, where burst suppression or isoelectricity is a useful target.

Several automated EEG processing systems have been developed recently to facilitate continuous EEG monitoring. Power spectral analysis by fast Fourier transformation of EEG provides a graphical represen­tation of the relative power content in the various fre­quency bands. These spectral diagrams can be helpful in diagnosing changing EEG patterns as the cerebral pathology evolves over time. The same spectral moni­toring can also provide some numeric descriptors (e.g.. mean frequency, spectral edge frequency etc.) that can be tracked over time to follow the progress of the dis­ease.

Bispectral index (BIS), normally used for mea­suring the depth of sedation during anaesthesia, has also been used in neurological intensive care patients. BIS scores obtained prior to sedation in patients of trauma, have been found to be predictive of TBI and neurological outcome at discharge [38] . The probability of re­covery from unconsciousness based on BIS monitor­ing has also been investigated in unconscious neuro­surgical patients [39] . In a study involving patients with mild and moderate TBI, we showed a statistically good cor­relation between BIS and GCS. Mean BIS values, in this study were significantly different between moder­ate and mild head injuries [65.7±16.1 vs 85.76.1, p = 0.006]. However, the scatter of BIS values for any GCS score was high limiting the practical utility of BIS as a measure of depth of coma [40] .


Clinical studies have shown correlations between adverse clinical events (such as high ICP, low blood pressure, and hypoxia), and brain lactate, glucose, an­tioxidant, and excitatory amino acid levels. Correla­tions have been demonstrated between jugular bulb oxygen desaturation and lactate, glutamate adenosine, and xanthenes [41],[43] . Microdialysis helps to monitor the extracellular fluid concentration of various brain me­tabolites.

Various studies examined the effects of therapeu­tic interventions on the levels of extracellular metabo­lites after cerebral injury. Thiopental coma was associ­ated with a reduction in lactate, glutamate, and aspar­tate [44] . Hypothermia significantly reduced glutamate and aspartate levels [45] . Hyperoxia led to a reduction in lac­tate [46] . One study has shown a reduction in lactate, glutamate, lactate/pyruvate ratio, and glycerol after a controlled reduction in the cerebral perfusion pressure in TBI according to the Lund protocol [47] . Being a moni­tor that provides information only from a focal area, location of the probe has a very important bearing on its usefulness.

Multimodality monitoring

The concept of multimodal monitoring involves continuous monitoring of more than one parameter us­ing two or more of the techniques described above. Multimodal monitoring helps to overcome the limita­tions of each individual method of monitoring. For ex­ample, a change in the ICP associated with an increase in CBF or ischemia can be accurately interpreted when TCD flow velocity information is combined with ICP data. Multimodal monitoring is expensive, and requires highly trained staff. The data generated needs to be acquired in a format that allows quick and easy analy­sis.

   Hypertonic saline for control of intracranial hypertension Top

Hypertonic saline has emerged as an alternative to mannitol for hyperosmolar therapy in patients with intracranial hypertension. An intact blood brain barrier (BBB) is less permeable to saline than to mannitol. Hypertonic saline is therefore a more effective and more durable osmotic agent. In clinical and experimental stud­ies, hypertonic saline effectively lowered ICP that was refractory to mannitol[48],[49].

In TBI, hypertonic saline has been used for initial resuscitation, as an infusion for prophylaxis against in­tracranial hypertension and as a bolus substitute for mannitol. Prospective randomized trials have failed to show any overall benefit from resuscitation with hyper­ tonic saline in TBI [50],[51]. However, hypertonic saline doubled the survival rate of a subgroup of patients with both hemorrhagic shock and TBI[52] . Numerous case reports and small cohort studies have reported the ef­ficacy of hypertonic saline bolus dosing to reduce TBI­induced intracranial hypertension that was refractory to mannitol[53],[54],[55] . The concentration of NaCl boluses used in these reports varied from 7.5% to 23%. Qureshi et al[56] examined continuous maintenance infusions of 3% NaCl-acetate in a retrospective series of 27 pa­tients with cerebral edema from various causes, 8 of whom had TBI. HS infusions were started although all patients had initial ICPs ranging from 8 to 18 mmHg. A significant trend in ICP reduction and an improvement in midline shift were noted in the hypertonic saline co­hort. In a comparative study, 20 patients with TBI were randomized to receive either 20% mannitol or 7.5% HS boluses for ICP elevations of greater than 25 mm Hg for more than 5 minutes[49] . Patients in the mannitol group experienced more frequent ICP episodes requir­ing interventions; there were significantly fewer refrac­tory ICP episodes in the hypertonic saline group. No difference in clinical outcome was demonstrated be­tween the two groups.

The role of hypertonic saline in hemispheric stroke remains controversial. In a prospective comparison of 20% mannitol versus 7.5% hypertonic saline boluses to control ICP episodes in nine patients with large hemi­spheric strokes [48] , hypertonic saline was more reliable in reducing ICP. Bhardwaj et al [57] examined the effect of continuous hypertonic saline infusion on infarct size in a rat model of middle cerebral artery occlusion. They noted that a continuous infusion of 7.5% NaCl was necessary to increase serum sodium content to 145 to 155 mmol/L. While comparing normal saline, 20% mannitol, 3% NaCl, and 7.5% NaCl, they found that 7.5% NaCl decreased brain water content in the con­tralateral hemisphere and increased infarct volumes in the ipsilateral hemisphere. They conjectured that hy­pertonic saline has a deleterious effect on stroke pen­umbra.

Complications of hypertonic saline therapy

The central pontine myelinolysis resulting from acute increase in serum sodium concentration remains only a theoretical concern. Metabolic changes that may accompany prolonged hypertonic saline therapy include hypo- or hypernatremia, hypokalemia, and hypocalcemia. Volume overload associated with this therapy may have implications in patients with cardiac disease. Acute renal failure may occur if serum osmolality ex­ceeds 320 mOsm/kg. Rebound oedema has been noted with hypertonic saline too. Some authors recommend limiting the infusion to 48-72 h and slow withdrawal to avoid the rebound effect.

   Ventilatory management Top

Optimal ventilation remains a major goal in man­aging patients with cerebral injury. The role of hyper­ventilation is now clearly defined and the beneficial role of hyperoxic ventilation is under investigation.


Hyperventilation is normally used for acute treat­ment of raised intracranial pressure. But cerebral vaso­-constriction caused by hyperventilation has the poten­tial to decrease CBF. In a study of TBI, patients who received severe hyperventilation had high cerebral arterio-venous oxygen difference and CBF values, in the ischemic range [58] . Hyperventilation was the second common cause for decrease in SjVO2 in patients with TBI [59] . In a study comparing clinical outcomes of hyperventilated and normoventilated patients, better outcomes were observed at 3 months in normoventilated patients [60] . A xenon CT study in pae­diatric TBI showed 28.9% frequency of cerebral is­chemia when PaCO 2 was > 35 mmHg as against 73.1% when the PaCO 2 was decreased to 25 mmHg [61] . Re­cent Brain Trauma Foundation guidelines advocate against hyperventilation particularly during the first 24 h after injury. Brief periods of hyperventilation may be justified when there is acute neurological deterioration. Prolonged hyperventilation may be used only if the in­tracranial hypertension is refractory to sedation, pa­ralysis, CSF drainage and osmotic diuretics [1] . In con­tradiction with the above evidence, a positron emission tomographic study showed that hyperventilation de­creased CBF, but did not cause energy failure. The authors concluded that CBF reduction associated with hyperventilation is unlikely to cause brain injury [62] .A recent Cochrane review indicates that the data avail­able at present is inadequate to assess any potential benefit or harm caused by hyperventilation [63] .

Hyperoxia and brain injury

Recent evidence suggests that hyperoxic ventila­tion may mitigate, to some extent, the adverse effects of hypoperfusion in patients with cerebral pathology. CBF reduction ranging from 9% to 27% and a de­crease in cerebral (A-V)DO 2 have been reported in response to hyperoxia [64],[65],[66] .

Hyperbaric oxygen therapy

The amount of oxygen dissolved in the plasma increases linearly with an increase in PaO2. For every atmosphere of pressure increase, 1.8 mL of oxygen/100 mL of blood is dissolved in plasma. Hyperbaric oxygenation thus induces a dramatic increase in blood oxygen-carrying capacity and tissue oxygen diffusion. Despite this theoretical advantage, in a randomized trial where the patients received either standard care or stan­dard care plus hyperbaric oxygen therapy at 1.5 atm, the overall mortality in the treatment and control groups was not significantly different [67] . Though the mortality was low in a subgroup of patients, this treatment was not associated with an increase in favorable outcomes among survivors. A recent review of the literature also does not support routine use of hyperbaric oxygen therapy for TBI [68] .

Normobaric oxygen therapy

Normobaric hyperoxia is easily and quickly per­formed in an ICU setting by increasing the fraction of inspired oxygen (FiO 2 ) on the mechanical ventilator. Menzel et al [69] tested hyperoxia over a period of 6 hours by raising the FiO2 from 35% to 60% and then to 100% during the first 24 hours after injury. Hyperoxia did not have any effect on ICP and CPP. PbtiO 2 increased in all the oxygen-treated patients. Patients subjected to hyperoxia showed a 40% decrease in lactate by the end of oxygen treatment. The levels of glucose did not show a clear trend during the oxygen enhancement period. Magnoni et al [65] tested the hypothesis that hyperoxia could improve oxidative metabolism after TBI, by evaluating the lactate/pyruvate ratio. But the data suggested that, in a condition of sufficient oxygen supply, hyperoxygenation does not change oxidative metabolism.

In summary, there have been significant changes in the concepts related to the management of cerebral blood flow, and metabolism and intracranial pressure dynamics. A major proportion of this development has its basis in the developments in technology that enabled a closer observation of the cerebral physiology in dis­ease. Refinement of our concepts with routine use of these newer techniques should pave way for better treatment protocols in the near future.

   References Top

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