Chapter 68 – Neurosurgery

1872 CHAPTER 68 Neurosurgery is defined as surgery of the brain, spinal cord, peripheral nerves, and their supporting structures, including the blood supply, and protective elements, spinal fluid spaces, bony cranium, and spine. Although it may be intuitive to think of neurosurgery as mostly concerned with the neural tissue itself, it is common that the pathophysiology and opportunity for therapy involve its infrastructure. Thus, it is easy to understand that neurosurgeons are often focused on intracranial pressure (ICP), cerebrospinal fluid (CSF) dynamics, cerebral blood flow (CBF), and compression syndromes of the spinal cord, nerve roots, and peripheral nerves. Whatever may be happening to the neural tissue, whose complexity often defies direct intervention, its environment must be optimized for improvement or recovery to occur. The rigid closed space around the brain and spinal cord is often said to set neurosurgery apart from other branches of surgery. A prime example is the contrast between intra-abdominal and intracranial hemorrhage. Whereas bleeding in the abdomen may focus concern on blood loss and hypotension, bleeding within the closed space of the cranium causes problems with an increased ICP, with attendant decreased CBF, infarction, edema, and obstruction of spinal fluid absorption. These intracranial mechanisms can be lethal at volumes of intracranial bleeding that have no effect on systemic blood pressure through the mechanism of hypovolemia. The chapter is intended for non-neurosurgeons who want to initiate a framework on which to add further knowledge and experience. It hopefully will also help personnel in a community hospital emergency room, or a medical student on the ward for the first time, communicate patient problems efficiently to neurosurgeons. The chapter first provides an overview of the underlying principles of neurosurgery, with a focus on intra- cranial dynamics. The remaining sections include a discussion of the following: cerebrovascular disorders, which include subarachnoid hemorrhage, intracerebral hemorrhage, aneurysm, and arteriovenous malformation (AVM); central nervous system (CNS) tumors, which include neoplasms of the brain, skull base, cranial nerves, spinal cord, meninges, and peripheral nerves; traumatic brain injury; degenerative diseases of the spine; func- tional neurosurgery, which includes stereotactic radiosurgery (SRS), epilepsy surgery, and surgery for the management of pain and movement disorders; hydrocephalus and pediatric neuro- surgery; and neurosurgical management of CNS infections. The field of neurosurgery is simply too broad to make a detailed encyclopedic overview realistic, but some introduction to these issues will hopefully be useful to the reader. INTRACRANIAL DYNAMICS A few basic principles concerning intracranial dynamics, CSF, CBF, and ICP are essential to grasp at the outset and are sum- marized here for quick review. Some of these principles are obvious whereas others might be considered counterintuitive. The first principle is obvious. The cranial cavity has a fixed volume comprised of (1) brain tissue (parenchyma), (2) CSF, and (3) blood vessels and intravascular blood. According to the Monro-Kellie doctrine, the sum of these components within the fixed volume of the cranial cavity implies that an increase in one component must be accompanied by an equal and opposite decrease in one or both of the remaining components.1 If this does not occur, the ICP will rise to levels close to the systemic blood pressure, producing a reverberating blood flow pattern with no net flow. The clinical implications are also straight- forward. For each intracranial component, there is a family of pathologic conditions of excess volume and a means to improve that excess (Table 68-1). A consequence of this principle is that if there is an elevation in the volume of any one compartment, there is a stage of compensation in which the volume of one or more other compartments can be reduced to avoid elevations in the ICP. The second principle is not obvious, and may seem coun- terintuitive. Spinal fluid is produced at a constant rate (≈15 to 20 mL/hr), by an energy-dependent, physicochemical process, mainly by the choroid plexus of the ventricles. It is essential to understand that production is little affected by any intracranial backpressure; thus, CSF production continues unabated, even to lethal elevations of intracranial pressure. Because production is almost always constant, it follows that derangement of CSF dynamics almost always involves some aspect of impeding CSF absorption through obstruction along the CSF pathways inside the brain, subarachnoid spaces at the basal cisterns or cerebral intracranial dynamics cerebrovascular disorders central nervous system tumors traumatic brain injury degenerative disorders of the spine functional and stereotactic neurosurgery hydrocephalus pediatric neurosurgery central nervous system infections NEUROSURGERY Jaime Gasco, Aaron Mohanty, Fadi Hanbali, and Joel T. Patterson Neurosurgery  Chapter 68  1873 SECTIO N XIII sPeC IALTIes IN g eN er AL su rg ery pronounced (i.e., smaller changes in blood pressure or PCO2) and affects the CBF dramatically (Fig. 68-1). If tissue demand exceeds autoregulation, or if CBF declines for pathologic reasons, the first defense is that the O2 extraction will increase (i.e., arteriovenous O2 difference, AVDO2). The tissue begins to dys- function at levels below 0.25 mL per g of brain tissue per minute. With levels between 0.15 and 0.20 we may encounter reversible ischemia; however, infarction will occur when levels range between 0.10 and 0.15 (Fig. 68-2). The metabolic con- sumption of oxygen in the brain (CMRO2) is decreased after traumatic brain injury to levels between 0.6 and 1.2 µmol/mg/ min. Complete loss of blood flow to any brain area results in infarction (irreversible damage) within a few minutes. Swelling of the infarcted tissue takes days to peak and weeks to resolve.2 An important implication is that if brain dysfunction is occurring clinically because compensatory mechanisms (e.g., autoregulation changing the vascular resistance, capacity to elevate mean systemic arterial pressure, ability to increase O2 extraction) have been exceeded, the tolerance for further decline in blood flow is low, and tissue damage is seriously threatened. Therapy to increase blood pressure or decrease ICP may be urgently needed. When time permits because the dysfunction FIGURE 68-1 CBF as a function of MAP. Note the upward and downward shifts with hypercapnia and hypocapnia, respectively. In traumatic brain injury, the curve is steeper, with large CBF changes occurring with small pressure changes. (Adapted from rangel-Castilla L, gasco J, Nauta HJ, et al: Cerebral pressure autoregulation in traumatic brain injury. Neurosurg Focus 25:e7, 2008.) Hypercapnia Traumatic brain injury 50 MABP (mm Hg) CB F (m l/g /m in) CB F (m l/g /m in) 15050 MABP (mm Hg) 150 Hypocapnia 100 80 60 40 20 100 80 60 40 20 table 68-1  Intracranial excess Volume Syndromes and therapy COMpONeNt eXCeSS VOLUMe SYNDrOMe SpeCIFIC treatMeNt Brain tissue edema: Cytotoxic, vasogenic, perineoplastic, inflammatory Diuretics: Mannitol, furosemide, hypertonic saline; steroids for perineoplastic and inflammatory vasogenic edema Vascular elevated PCo2: Hyperperfusion state with loss of autoregulation as in severe hypertension, after trauma or AVM removal; relative venous obstruction Increased ventilation; diuretics (in hyperperfusion state, avoid mannitol), barbiturates; clear venous obstruction; elevate head of bed (to reduce venous volume) Cerebrospinal fluid Impaired absorption with congenital, posthemorrhagic, or postinfectious hydrocephalus, communicating or obstructive; loculations; arachnoid or periventricular cysts; rare increased production of CsF with choroid plexus papilloma Ventricular external drainage (or lumbar drainage only if no threat of herniation) or shunt; with flocculation, or with some types of obstructive hydrocephalus, endoscopic fenestration or third ventriculostomy may be possible; acetazolamide and steroids may temporarily decrease CsF production Mass lesion Tumor, cyst, abscess, hematoma, radiation necrosis, or cerebral infarction necrosis remove, fenestrate, aspirate lesion (often with stereotactic guidance); less commonly, might be useful to enlarge intracranial volume by decompression convexity, or arachnoid granulations from which most absorp- tion occurs. In the following discussions on tumors, infection, intracranial hemorrhage, and trauma, many examples will become apparent whereby impaired CSF absorption contributes to the pathologic condition. The only exceptions to the almost constant CSF production are the excess production associated with the rare choroid plexus papilloma tumor and the occasional decreased CSF production seen with some gram-negative bacte- rial meningitis with ventriculitis, usually in neonates. The third basic principle is that the CBF normally varies over a wide range (30 to 100 mL/100 g brain tissue/min), depending on metabolic demand from neuronal activity within a particular area of the brain. The CBF may be considered in aggregate or of specific small regions, pathologic or normal. The blood flow to any brain area is generally abundant, exceeding demand by a wide margin, so that O2 extraction ratios are often low. The brain vasculature matches the blood flow to tissue metabolic demand and the CBF generally maintains what is needed, despite wide variations in systemic blood pressure, by a phenomenon known as autoregulation. Factors such as an elevated or decreased arterial PCO2 shift the curve as indicated. In the setting of traumatic brain injury, the curve becomes more 1874  SeCtION XIII sPeCIALTIes IN geNerAL surgery higher than 70 mm Hg is not supported based on systemic complications.3 A fifth principle concerns focal mass effect and its progres- sion in regard to the complex anatomy of the cranial cavity. The cranial cavity is not just a hollow spherical space but contains several almost knifelike projections of folded dura, the falx and tentorium, which divide the cavity into right and left supraten- torial compartment and an infratentorial compartment, the posterior fossa. The sphenoid wing is a prominent, mostly bony ridge that separates the anterior fossa containing the frontal lobe from the middle fossa containing the temporal lobe. A narrow opening, the incisura, edged by the tentorium, sur- rounds the midbrain and is the only passage between the supra- tentorial and infratentorial compartments. Apart from the small openings for the cranial nerves and arteries, the foramen magnum is the only sizable opening from the cranial cavity as a whole. The condition that classically illustrates the expanding mass lesion is the acute epidural hematoma, seen after trauma with skull fracture. Regardless of the source, however, the progression can be similar and has been termed rostrocaudal decay to reflect the early and late stages, as listed in order below: • Focal distortion only • Effacement of gyri and sulci • Compression of the lateral (or other) ventricle • Midline shift • Subfalcial herniation • Temporal lobe tentorial herniation • Third nerve compression (unilateral dilated pupil) • Obliteration of basal cisterns • Midbrain compression • Midbrain infarction, Duret’s hemorrhages (both pupils dilate, with irreversible damage to midbrain) fluctuates chronically, it may sometimes be appropriate to measure O2 extraction ratios as one index of the overall adequacy of the CBF. At a low CBF, O2 extraction is increased with a lower venous PO2. It is interesting to note that the variations in CBF and extraction ratios related to neuronal activity are said to underlie the ability to image function by functional magnetic resonance imaging (MRI), a technique that is finding wider usage in the clinical neurosciences. A fourth principle derives from the other three and the fact that injured tissue swells, making obvious the potential for a cascading injury by a vicious cycle mechanism (Fig. 68-3). If the stage of compensation (see earlier), even with therapy, is exceeded, and ICP is elevated high enough by some mechanism so that cerebral perfusion pressure (CPP) declines, CBF can decline to levels at which tissue injury occurs. CPP mean arterial pressure MAP ICP= −( ) Brain edema swelling within the closed cranium will lead to further increases in ICP with even further decreases in CPP in a stage of decompensation. When the capacity for autoregula- tion is exceeded or damaged so that it can no longer play a role, CBF is linked directly to the CPP. In the management of intracranial pathology, ICP and CPP are easy to measure continuously and thus serve as highly practical surrogates for the more fundamental, but much more difficult to measure, CBF. However, these are not equivalent, and the limitations of these parameters for guiding therapy need to be remembered. Regardless of causation, when concern arises about the possibility of cascading injury, every effort is made to keep the CPP in the realm of 60 mm Hg (range, 50 to 70 mm Hg) and ICP below 20 mm, Hg if possible. Rou- tinely using pressors and volume expansion to maintain CPP FIGURE 68-2 relationships among cerebral flow, metabolism, and oxygen extraction in normal and pathologic circumstances. (From rangel-Castilla L, gasco J, Nauta HJ, et al: Cerebral pressure autoregu- lation in traumatic brain injury. Neurosurg Focus 25:e7, 2008.) Infarction 0.0 0.4 CBF (ml/g/min) 0 1 2 3 4 Ischemia CMRO2(µmol/mg/min) 1.8 1.5 1.2 .9 .6 .3 Hyperemia Normal Hypoperfusion AV D O 2 (µm o l/m l) 5 6 0.8 1.2 FIGURE 68-3 relationship among increased ICP, reduced CPP, devel- opment of ischemia and infarction, and cerebral edema. ↑ICP Ischemia Edema ↓CPP Neurosurgery  Chapter 68  1875 SECTIO N XIII sPeC IALTIes IN g eN er AL su rg ery initially worse on far vision or gaze directed toward the side of the palsy. The papilledema is a mostly chronic phenomenon and is not seen acutely. The sixth nerve palsy of raised ICP can occur regardless of its cause and does not imply direct involvement by a mass lesion, large or small, on the sixth nerve. In this situation, the sixth nerve palsy is a false localiz- ing sign. With raised ICP, there may also be obscurations of vision, in which patients report that their vision temporarily fades or becomes gray, in combination with headache. Again, these obscurations are caused by the effect of diffusely increased ICP on the sensitive optic nerves. They do not imply the presence of a focal mass lesion directly affecting the optic nerves or pathways. Intuitively, it seems that if there is a slow increase in a process raising ICP, the pressure would also rise slowly and evenly, in pace with the evolving process. However, as first shown by Lundberg in 1960,5 the intermedi- ate stages of decompensation are characterized by transient pronounced elevations in ICP (to 60 mm Hg) that character- istically plateau for up to 45 minutes and then transiently cycle down again to a more normal range. The original form of this condition of chronic, diffuse, raised ICP is known by the old term pseudotumor cerebri or the more descriptive idiopathic intracranial hypertension. Because it is often not benign, causing disabling chronic headache and visual loss, sometimes even to permanent blindness, the term benign intracranial hypertension is falling out of favor. The basis for the condition is not entirely understood. It usually occurs in obese young women. Treatment is with acetazolamide diuretics, steroids, and intermittent lumbar puncture. Severe cases with threatened permanent visual loss may require a lumboperitoneal or ventriculoperitoneal CSF shunt or optic nerve fenestration, in which the meninges around the optic nerves are opened to vent CSF in the orbit. Pure ventriculomegaly—specifically, enlargement of the lateral ventricles—is characterized by gait disturbance and incontinence early in the clinical picture. As the process worsens, cognitive disturbances may be added on. The early appearance of gait disturbance and urinary incontinence is attributed to dysfunction of the medial cerebral hemispheres in which the leg area of the primary motor cortex and bladder control area reside. Nerve fiber pathways inside the brain must pass around the lateral ventricles to reach these areas on the medial hemisphere and therefore are especially vulnerable to pressure or distortion by the enlarged ventricle. This syndrome is called NPH. The usual diagnostic difficulty is in differentiat- ing the condition from cerebral atrophy. Ventricular enlarge- ment more prominent than enlargement of the CSF subarachnoid spaces over the cerebral convexity is typically seen in NPH. The clinical impression that gait disturbance and incontinence occur early and predominate over dementia is considered an important feature of NPH. Treatment is with CSF shunt, lumboperitoneal or ventriculoperitoneal. The dif- ferentiation between NPH and cerebral atrophy is important because of the increased risk for subdural hematoma with shunting in cerebral atrophy. Table 68-2 summarizes the relationships among ICP, mass lesions, and ventriculomegaly. CEREBROVASCULAR DISORDERS Cerebrovascular disorders encompass a host of disorders, con- genital and acquired (Box 68-1). • Further brainstem compression • Loss of brainstem reflexes: Progression from flexor pos- turing to extensor posturing; vestibulo-ocular and ocu- locephalic reflexes; corneal reflexes • Medullary compression syndrome: Respiratory reflexes; vasomotor reflexes, Cushing’s reflex with elevation of the systolic blood pressure, widening of the pulse pres- sure, bradycardia. • Foramen magnum herniation At stages beyond tentorial herniation, it is unusual for focal mass effects not to be accompanied by an overall increase in ICP. The point at which focal mass effect evolves to include a rise in overall ICP depends largely on the compliance within the cranial cavity. Young patients with so-called tight brains can develop raised ICP, even with relatively small volumes of mass that produce only effacement of the cortical gyri. On the other hand, patients with advanced cerebral atrophy can, for example, toler- ate large frontal intracerebral hematomas or chronic subdural hematomas with compression of the lateral ventricle and midline shift while maintaining a tolerable ICP and a surprising degree of intact neurologic function. The Glasgow Coma Score (GCS; see later, “Traumatic Brain Injury”) provides a clinical functional measure of the degree of mass effect and advanced raised ICP. Although it is a useful standardized functional measure of the more advanced stages of mass effect or raised ICP, it was never really intended to focus on more subtle functional changes. A recently intro- duced coma scale by Widjicks and colleagues4 has delineated the FOUR score ( full outline of unresponsiveness) consisting of four components (eye, motor, brainstem, respiration). Each has a maximal score of 4 and takes into account the subtleties related to brainstem activity and breathing patterns occurring during the rostrocaudal decay described. A sixth principle concerns the separateness of the phe- nomenology of the following: (1) focal mass effect (as described earlier); (2) diffuse raised ICP; and (3) ventriculo- megaly (enlargement of the cerebral ventricles). Although these three processes often occur in combination, the notion that they are separable comes from the observation that the