Supratentorial Lesions


Acknowledgment

We are thankful to Mr. Munish Kumar, Junior Research Fellow in the Department of Anaesthesia and Intensive Care, for the sketches of Figs 12.1, 12.2, and 12.4 .

Introduction

The supratentorial region accounts for major intracranial distribution in the intracranial compartment. The supratentorial region is bound superiorly and laterally by the tense dura mater and skull. The inferior boundary consists of the anterior cranial fossa, middle cranial fossa, posterior cranial fossa, and tentorium cerebelli. The supratentorial region is divided into the right and left halves by the falx cerebri. The contents include the subarachnoid space containing cerebrospinal fluid and major vessels of the two cerebral hemispheres and lateral ventricles.

The supratentorial region consists of the part of the brain that lies above the tentorium cerebelli. It consists of two cerebral hemisphere, ventricles and blood vessels. The two cerebral hemispheres are separated by falx cerebri ( Fig. 12.1 ). Each cerebral hemisphere consists of four lobes: frontal, parietal, temporal, and occipital. Individual lobes have specific neurological functions. The supratentorial lesions may be associated with either a compromise or loss of neurological functions depending on the site and size of the lesion.

Figure 12.1, Sketch of the coronal section of supratentorial compartment.

Classification

The supratentorial lesions can be broadly classified as follows ( Box 12.1 ).

Box 12.1
Classification of Supratentorial Lesions

Intra-Axial Lesions (Within Brain Parenchyma)

  • 1.

    Neoplasm

    • a.

      Primary

      • i.

        Glioblastoma multiforme

      • ii.

        Astrocytoma

      • iii.

        Primary central nervous system lymphoma

      • iv.

        Ganglioma

      • v.

        Oligodendroglioma

    • b.

      Metastasis

  • 2.

    Infections

    • a.

      Abscess

    • b.

      Neurocysticercosis

  • 3.

    Hemorrhage (intracerebral hemorrhage)

Extra-Axial Lesions (External to Brain Parenchyma)

  • 1.

    Neoplasm

    • a.

      Meningioma

    • b.

      Hemangiopericytoma

    • c.

      Pituitary tumors

  • 2.

    Hemorrhage

    • a.

      Subarachnoid hemorrhage

    • b.

      Subdural hematoma

    • c.

      Extradural hematoma

  • 3.

    Arachnoid cysts

Intraventricular Lesions

  • 1.

    Neoplasms

    • a.

      Ventricular wall and septum pellucidum

      • i.

        Ependymoma

      • ii.

        Central neurocytoma

    • b.

      Choroid plexus

      • i.

        Choroid plexus papilloma/carcinoma

    • c.

      Others

      • i.

        Intraventricular meningioma

  • 2.

    Colloid cysts

  • 3.

    Infections

    • a.

      Hydatid cysts

    • b.

      Tuberculoma

    • c.

      Neurocysticercosis

Although supratentorial lesions can occur due to causes related to tumors, trauma, and infections, the present chapter will focus on supratentorial tumors only.

Pathophysiology and Clinical Correlations

The supratentorial region is well protected within the confines of the tough dura mater and skull. The pressure within the right and left sides of the supratentorial compartment is in equilibrium as is the pressure within the supratentorial and infratentorial compartments. The supratentorial compartment follows the Monro–Kellie doctrine that states that the sum total of the volume of the compartment at any point remains constant. This would translate into a realization that the compensation for any expanding mass lesion would be limited and could lead to an increase in intracranial pressure (ICP).

During the initial phase of a slow-growing mass lesion there would be compensation in terms of egress of cerebrospinal fluid and reduction of blood volume (phase I, Fig. 12.2 ). At this point of time surgery can be planned as an elective procedure. As the mass lesion grows further, there comes a point whereby the compensatory mechanisms are exhausted (phase II, Fig. 12.2 ). With further growth of mass lesion, there is increase in ICP. Discordance in ICP between the two halves in the supratentorial compartment leads to shift of brain parenchyma from one half to the other, which is referred to as subfalcine herniation or midline shift (phase III, Fig. 12.2 ). A midline shift of more than 5 mm is usually considered to be associated with significant mass effect ( Fig. 12.3 ). At this point of time surgery is considered as an urgent procedure. The unabated growth of mass lesion may lead to differential pressure between the supratentorial and infratentorial compartments. The transtentorial pressure gradient may lead to herniation of the medial portion of the temporal lobe into the infratentorial compartment, called “uncal herniation/central herniation” (phase IV, Figs. 12.2 and 12.4 ). This leads to compression of the ipsilateral third cranial nerve, which clinically manifest as anisocoria. Radiologically this is manifested as obliteration of basal cisterns. This is the time when surgical procedure for decompression of mass lesion is an absolute emergency.

Figure 12.2, Intracranial pressure–volume curve.

Figure 12.3, Computed tomograpgic scan showing significant midline shift due to a supratentorial tumor.

Figure 12.4, Transtentorial herniation.

The enlarging supratentorial mass in animal studies has been associated with loss of autoregulation in the regions of brain ipsilateral and contralateral to the lesion. However, there is relative preservation of midbrain autoregulation. The understanding of the effect of supratentorial tumors with regard to the integrity of blood–brain barrier (BBB) is limited. The integrity of BBB as studied by contrast enhanced scanning will depend on the degree of the malignancy of the supratentorial tumors. The effect on the BBB depends on the type and stage of tumor development. BBB permeability is heterogeneous within the tumor site and depends on the type of tumor and stage of tumor development. Low-grade gliomas usually have preservation of the BBB. It has been found that BBB is intact in the initial steps of tumor development with significant increase in BBB permeability only during the later stages as tumor mass increases. Low-grade gliomas and tumor in early stages are least likely to impact the BBB. Nevertheless, even in later stages, BBB is still functional and limiting in terms of solute and drug permeability in and around the tumor. The regional blood cerebral flow can be affected ipsilateral as well as contralateral to the supratentorial mass lesion. The blood flow to the midbrain is preserved till the point of total decompensation and herniation.

Various animals studies have shown that the progressive expansion of a supratentorial epidural space gave rise to a series of pathophysiological reactions. The vital physiological variables and sequential magnetic resonance (MR) images were recorded simultaneously using intracranial expanding mass. When the expanding mass was increased into 4–5% of the intracranial volume (ICV), there was a progressive slow rise in systemic arterial pressure, along with changes in pulse and respiratory frequency. This volume is known as reaction volume. At a volume of 8–10% of ICV, apnea (referred to as apneic volume) and an isoelectric electroencephalogram were observed. Following apnea the systemic arterial pressure increased as part of the Cushing triad. The changes in vital physiological variables progressed in a rostrocaudal direction. Reaction volume associated with a marked transtentorial pressure gradient and magnetic resonance imaging (MRI) changes were consistent with tentorial herniation. Respiratory arrest (apneic arrest) was associated with occlusion of the cistern magna, consistent with some degree of foramen magnum herniation.

Epileptogenesis associated with tumors can be due to changes in peritumoral microenvironment, alterations of synaptic neurotransmitter release and reuptake and the exitotoxic effect of glutamate.

Clinical Features

The clinical features of the patients with supratentorial lesions will depend on the following three factors(S 3 ): (1) site of lesion (localizing signs), (2) size of lesion and mass effect (nonlocalizing signals), and (3) speed/rate of growth of lesion.

The clinical manifestations of a supratentorial lesion may be site specific and may produce localizing clinical manifestation. The lesion affecting the motor frontal cortex may be associated with contralateral hemiparesis. The tumors of speech area will result in aphasia. Affection of visual pathway at a particular site will help in localizing features (e.g., bitemporal hemianopia) in case of suprasellar lesion. Presence of a focal seizure can help in precise localization of a tumor.

Large tumors and associated mass effect may produce generalize signs and symptoms, which are referred as nonlocalizing clinical manifestations. Raised ICP is a feature of many supratentorial lesions. Raised ICP may manifest as headache and/or nausea and vomiting. Papilledema may be a common accompaniment. There may be elevation of blood pressure with increase or decrease in pulse rate. A slow pulse rate appears to be due to vagal excitation or a response of carotid sinus to acute rise in blood pressure. The rise of blood pressure has been hypothesized to be due to compensatory autoregulatory responses to decreased cerebral blood flow caused by the raised ICP.

An expanding mass lesion causes third nerve palsy due to compression by herniating temporal lobe at the edge of the tentorium. Sixth nerve palsy can occur as a consequence of stretching of the abducens nerve due to rostrocaudal displacement of brain stem. Compression of foramen of Monro or third ventricle can result in hydrocephalus. A supratentorial mass lesion may result in cognitive decline.

The speed of growth of the lesions determine the nature of onset and progress of the signs and symptoms. Slow-growing tumors have an insidious onset of presentation and are gradually progressive. Rapidly expanding masses have fast progression. Similarly, a bleed into the tumor may result in an acute presentation. A transtentorial herniation (TTH) is representative of an acute neurological deterioration. An acute neurological deterioration may manifest as sudden loss of consciousness.

Neuroimaging

Neuroimaging is a routine diagnostic procedure in patients with suspected intracranial lesions. This helps in precise localization as well as differentiating the type of lesion. The type of radiological imaging will depend upon the clinical presentation and urgency for evaluation and management. Patients who have slow onset and progression of neurological symptoms are more commonly subjected to MRI, which is more sensitive in the detection and differentiation of intracranial lesions as compared to computed tomographic (CT) scans. Various sequences of MRI can help in delineating the intracranial tumor and the associated mass effect ( Fig. 12.5 ). MR spectroscopy evaluates the chemical spectrum of the mass, and it helps in differentiating tumors from various mass lesions like abscess. Patients who present with acute neurological deterioration are usually subjected to CT scan as this procedure is faster and can help in emergency management of these groups of patients. Cerebral angiography may define the arterial supply of the tumor and help in planning tumor resection. In case of highly vascular tumor preoperative radiologically guided intravascular embolization helps in reducing the vascularity and intraoperative bleeding. Angiography is also helpful in distinguishing arteriovascular malformations and giant aneurysm, which may present as mass lesions.

Figure 12.5, Magnetic resonance imaging sequences of brain (T1, T2, and FLAIR, from left to right; showing ill-defined supratentorial mass in insular region with midline shift).

It is important for the neuroanesthesiologist to have a working knowledge of the imaging scans so as to estimate the mass effect and take appropriate intraoperative steps to optimize the brain conditions. In case of giant tumors it is possible that despite all the physiological, pharmacological, and mechanical methods advocated by the anesthesiologist to reduce the ICP, the brain may still be bulging. It is important to interact with the surgeons prior to the surgery regarding the possibility of refractory brain bulge and the need to drain the CSF if required. Imaging scans can also help to triage patients who may otherwise need an urgent surgery. Positron emission tomographic (PET) scan gives the amount of metabolic activity in the brain, thus differentiating the tumors from inflammatory lesions. PET scans are promising in differentiating between recurrent tumors and treatment-induced changes. PET scan can be superior to MRI for follow-up of patients who have been treated surgically or by radiation for brain tumors.

Intraoperative Considerations: The Team Approach

The conduct of neurosurgery is a team work, which includes the anesthesiologist, surgeons, operating room technicians, nursing staff, and at time radiographers and neurophysiologists. There should be good understanding and communication among the team members so as to conduct smooth anesthesia, perioperative management, optimal patient positioning, and maximal safe tumor resection.

The surgery for intracranial lesions is challenging and can be associated with variable intraoperative patient dynamics. Consequently it is important to be familiar not only with the disease process and presentation but also with the important surgical steps so as to anticipate complications and appropriately manage them. It is important in this regard for the anesthesiologist to interact with the surgeon prior to surgery and discuss various concerns regarding the patient. An understanding of the crucial surgical steps and anticipating blood loss keeps one vigilant and prepared to handle a critical situation. The surgical site should always to be confirmed and should be kept free from interference of monitoring sensors/electrodes like those used for monitoring the depth of anesthesia. Similarly the endotracheal tubes, drug delivery systems, intravenous fluids, various monitoring devices, and anesthesia equipment should be adequately secured and should be placed in such a way that they do not affect the working in the operation theater. It is important to advocate measures to facilitate maximal brain relaxation, which will enable the surgeons to conduct maximal tumor resection.

The anesthesiologist should brief the surgeons from time to time the hemodynamic changes during surgical stimulation so as to warn him against damage to vital brain structures. In situations in which intraoperative evoked potential studies are conducted there needs to be good communication between the anesthesiologist, neurophysiologist, and the surgeons. The surgical approaches and craniotomy depend on the tumor location. Most of the surgeries anterior to coronal suture are conducted in supine position. Pterional and frontal approaches are the most common surgical approaches. The lesion behind the coronal suture may require the patient to be positioned in the semsitting or lateral decubitus position. The lesion in the pituitary gland and the sellar and suprasellar regions can be approached through the transsphenoidal route. The nursing staff should ensure adequate sterility and absolute cleanliness of the operating room environment. The operation theater technicians should be well trained, should be alert, and should be ready with all the equipment required for the conduct of anesthesia and surgery.

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