Eloquent cortex is a term usually used to describe functional areas of the cerebral cortex associated with motor, language, and sensory activity. Traditionally, tumors or epileptic foci within or near these areas have been termed inoperable because of the devastation caused to the patient by injury to these neurons.

The underlying pathology requiring an awake craniotomy for mapping and resection within the eloquent cortex can be either a space-occupying lesion or epileptic foci. In either case, mapping of the cortical and subcortical structures with an awake and cooperative patient is necessary to minimize neurologic injury and maximize lesion resection. Mapping of the motor cortex is often done under general anesthesia, after reversal of any residual muscle relaxant, because the stimulated area(s) can usually be seen by an observer. Nevertheless,
there are several potential problems. In the case of a space-occupying lesion, the neuronal pathways can become distorted secondary to the expanding mass and mislead the surgeon who is searching not only for the functional area but also a “quiet” area of cortex through which to do the resection. In addition, these patients are frequently in a lateral decubitus position, with the side to be observed in the down position. Visualization of the patient can be further obstructed with sheets, blankets, forced warm-air blankets, and other patient-positioning devices. Hence, we tend to map the motor cortex in an awake craniotomy whenever possible.

Supratentorial brain tumors are about 31% gliomas (Fig. 19.1), 15% meningiomas, 12% metastatic lesions, and 8% pituitary tumors. Metastatic lesions are most frequently lung, breast, and gastrointestinal tract tumors. Additional space-occupying lesions include blood and blood vessels, infections, hydrocephalus, cerebral infarctions, radiation necrosis, arachnoid cysts, and cerebral edema.

These space-occupying lesions can present in various manners. The most common presentation of brain tumors is a progressive neurologic deficit (68%), usually motor weakness (45%), headache (54%), and seizures (26%). Others may present from progressive focal deficits resulting from destruction of brain tissue or compression of normal brain structures by the mass itself or peritumoral edema. Additional presentations include nausea or vomiting, vertigo, lethargy, apathy, and changes in mental status as several examples.

In addition to these various presenting signs and symptoms, asymmetric supratentorial tumors can enlarge to the point of causing a midline shift of the intracranial contents, possibly leading to herniation. The brain can be displaced across the midline beneath the falx or compressed through the tentorial incisura into the posterior fossa. As these various areas of the brain are compressed against these dense fibrous structures, stretching and shearing of the penetrating arteries can result in devastating neurologic injuries.

An area of cerebral edema surrounds most intracranial masses secondary to the disruption of the blood-brain barrier (BBB) usually associated with a localized acidosis. Vasogenic edema reflects a shift of fluid from the intravascular to the extravascular space. Cytotoxic edema represents a shift of fluid from the extracellular to the intracellular space. Vasogenic edema responds very well to corticosteroid treatment. Dexamethasone is frequently prescribed for this problem. This area of cerebral edema is known as the penumbral area and represents areas of autoregulatory dysfunction as well as BBB breakdown. The vasculature in this area of the brain is usually maximally vasodilated. Hypercapnia in surrounding normal brain causes vasodilation in the normal vasculature and may result in decreased flow to the ischemic area. Hypocapnia, on the other hand, causes vasoconstriction of the normal adjacent vascular beds, with the resultant redistribution of blood to the ischemic area. This has been referred to as the “Robin Hood” phenomenon. The formation of peritumoral edema increases the overall size of the tumor, which can lead to the same signs and symptoms as noted earlier.

Patients presenting for an awake craniotomy for excision of an epileptic foci have usually had a seizure disorder for many years and have been on numerous antiepileptic drugs (AEDs) in an attempt to control their disorder. Unfortunately, many of these patients develop adverse reactions or cannot tolerate the side effects of the AEDs and become, for practical purposes, medication failures. Table 19.1 lists the more common AEDs and the types of seizure disorder they treat.

Only patients with seizures in whom the foci are localized in an area of eloquent cortex require an awake craniotomy. Temporal lobe, hippocampal-localized foci are usually resected under general endotracheal anesthesia with intraoperative electrocorticography. Most of these patients have had preceding intracranial strips, grids, or electrodes placed to help localize the seizure foci.

The adult skull is a rigid, bony box with a fixed volume. Neonatal and infant skulls have several noncalcified portions, called fontanels, that allow the skull to deform during passage through the birth canal. These noncalcified areas also allow the volume of the skull to
increase in the presence of increased ICP such as congenital hydrocephalus. Once these areas have calcified, the pediatric skull is also a rigid, fixed volume box.

The intracranial constituents are intravascular blood, CSF, and the brain. As liquids, the blood and CSF are noncompressible. Although water can be extracted from the brain by use of osmotic diuretics and other hypertonic fluids, this does not result in much change in brain volume and its gel-like consistency also makes it virtually noncompressible.

ICP is a relationship of the homeostatic balance of the noncompressible contents within a fixed-volume container, the skull. The normal value is 10 to 15 mm Hg. In the early 19th century, the Monro-Kellie hypothesis was the first attempt to describe this relationship. Although several modifications of this doctrine have been made over the years as more has been learned, the basic principle still holds true: Because the intact skull is unyielding, an increase in volume of any one of the normal contents or the addition of a space-occupying lesion must be accompanied by a reduction in one or more of the normal constituents to maintain normal ICP.

There are limits to the balanced relationship described by the Monro-Kellie hypothesis. Figure 19.2 represents an idealized ICP-volume curve and diagrams these limitations.

The flat portion of the curve represents increasing volume with no increase in ICP. Several compensatory mechanisms are at work to keep the ICP steady. The most effective of these mechanisms is the dynamic nature of CSF. The rate of absorption increases or the rate of production decreases in light of an increase in ICP. Cerebral blood volume (CBV) is decreased by a redistribution primarily of the intracranial venous blood volume. These mechanisms work to keep the ICP at its normal value of 10 to 15 mm Hg. As the volume continues to increase, these compensatory mechanisms become exhausted and ICP starts to rise as represented by the “knee” of the graph. It is important to note that at this area of the curve, small increases in volume give rise to a much larger increase in ICP. The sharp rise in the graph demonstrates rapidly increasing ICP with even smaller increases in volume. It is vitally important to understand that as the volume continues to rise and ICP continues to increase, the risk of cerebral herniation also increases. Cerebral perfusion pressure (CPP) is also adversely affected with a rise in ICP. CPP is defined as: CPP = MAP – ICP (CVP), where MAP = mean arterial pressure and CVP = central venous pressure. This equation readily shows that an increase in ICP will lead to a decrease in CPP.

Figure 19.3 shows that CBF remains at 100% for CPPs ranging from 50 to 150 mm Hg. Some have recently advocated that the lower threshold for autoregulation should be shifted more toward 70 mm Hg and the upper threshold shifted more toward 180 mm Hg. In the supine position, ICP in the normal state is effectively zero, making CPP directly related to MAP.

In its simplest form, autoregulation is a myogenic response of the vascular smooth muscle of the intracranial cerebral arterioles to maintain a nearly constant CBF in the face of changing CPP. Not all of the mechanisms controlling this action are fully understood.

When CPP becomes less than 50 mm Hg or greater than 150 mm Hg, the CBF becomes pressure passive. This response is important to keep in mind when considering the use of deliberate hypotension. A MAP of less than 50 mm Hg could theoretically cause a decrease in CPP and thereby decrease CBF to the point of causing cerebral ischemia. On the other side of the spectrum, MAPs greater than 150 mm Hg can cause disruption of the BBB and cause
vasogenic edema throughout the brain, not only in the area of vasogenic edema surrounding the tumor.

The autoregulation curve is shifted to the right in the presence of chronic uncontrolled hypertension, as shown in Figure 19.4.

This is important because now the lower threshold for cerebral ischemia is higher than in the normal state. Although there is not a direct correlation between degree of hypertension and rightward shift of the autoregulatory curve, it is possible that where signs of cerebral
ischemia might not have become obvious until the CPP was 30 to 40 mm Hg in the normotensive person, these signs may now occur with the CPP at 80 to 90 mm Hg, a usually normal CPP. Therefore, great care must be taken to keep the MAP near the patient’s usual levels in the uncontrolled or poorly controlled hypertensive patient. On the other end of the curve, it is possible that the rightward shift adds some form of cerebral protection against perfusion breakthrough at the higher CPPs. Treatment with antihypertensive drugs modifies this rightward shift back toward the normal range. The degree to which this occurs depends both on the length of time the hypertension has been treated and the resultant decrease in blood pressure.

The type of drug used to treat hypertension may also determine the effect on autoregulation. Systemic direct-acting vasodilators without action on cerebrovascular smooth muscle and α-adrenergic and ganglionic blocking drugs should have no effect on cerebrovascular autoregulation. Systemic direct-acting vasodilators that do have an action on the cerebrovascular smooth muscle, such as hydralazine, sodium nitroprusside, nitroglycerin, and calcium channel blockers may influence autoregulation. Treating congestive heart failure may also improve CPP by lowering CVP and thereby decreasing cerebral venous outflow pressure.

CBF also responds to chemical modulation. Figure 19.3 demonstrates these relationships in the arterial carbon dioxide partial pressure (PaCO₂) and arterial oxygen partial pressure (PaO₂) curves. Carbon dioxide (CO₂) concentration is the most potent modulator of CBF. Insonating the middle cerebral artery of a volunteer by means of transcranial Doppler device and asking the subject to hyperventilate will show an increase in cerebral blood velocity reflecting a decrease in CBF secondary to cerebral vascular constriction, usually within 3 to 4 breaths, a very rapid response. This principle is utilized to treat increased ICP by decreasing CBV secondary to the hyperventilation. However, this mechanism is self-limited after approximately 6 to 10 hours and will no longer provide the decreased ICP.

As shown in Figure 19.3, there is a near linear response in CBF at a PaCO₂ between 20 and 80 mm Hg, with CBF increasing about 2% to 4% for each millimeter of mercury change in PaCO₂. In general, doubling PaCO₂ from 40 to 80 mm Hg doubles CBF and likewise halving PaCO₂ from 40 to 20 mm Hg halves CBF. This represents maximal vasodilation at extreme hypercapnia and maximal vasoconstriction at extreme hypocapnia, respectively.